Speaker 1:
0:00 My medical background is I'm board certified in both emergency medicine and family medicine. I've taken a personal interest in cardiology early on in my career, mainly from my work in the emergency department where I see the end stage of cardiovascular disease.
Speaker 2:
0:17 Is there any positive impacts this can have on heart function or cardiovascular function?
Speaker 1:
0:21 It's easy to answer for testosterone because we've got a wealth of data in that area. Now the synthetics, it's a little bit different. I call it testosterone phobia within the research community out there that they're just. They are afraid of doing proper studies with the sort of levels that where men truly get the most benefit, which tends to be higher than what they do in the studies. So it's great that you have a zero score. I had a zero score at age 40. I had a score of 16 at age 50. So it's not like I still had plaque at 40. It just didn't get picked up because my score just wasn't calcified yet.
Speaker 1:
1:06 You would need an angiogram. There's even issues with those. You can still miss it because plaque doesn't always grow into the artery lumen. It actually can grow something called positive remodeling. You actually could have a significant amount of plaque within the wall that's growing outward here. So a CTA is, yeah, vastly superior to a coronary calcium scan. But you can, in these admittedly less likely and somewhat rare conditions, you can still miss plaque. So the best way is with a coronary catheter where they put in the wire into the heart and it has a little ultrasound probe on it intravascular ultrasound. So it's angiogram with IVUS they call it, and there's a couple other ways too, but most places don't do that.
Speaker 2:
2:00 I think it's about time I got a formally trained physician on the podcast Today, my guest Dr Andrew Wingy. We discuss the effects anabolic steroids and testosterone can have on the heart. Now, I know there are a lot of podcasts which discuss this very topic. However, my gripe, if you will, with a lot of the podcasts out there is the lack of specificity. What do I mean by that? Okay, we have normal testosterone levels without exogenous testosterone use. We have normal testosterone levels with exogenous testosterone use. Then what is normal? Then we have super physiological levels of testosterone. What are those levels? Then we have combinations of testosterone and anabolic steroids and then we have different doses of those combinations of steroids. So we have five or six different things going on here. However, I do tend to see a lot of physicians, or fear mongers, bucket this whole thing either in one bucket of TRT and then another bucket of super physiological levels is a weasel word, if you will. What number are we talking about? Because from one physician to the next, their definition of what's normal can be different.
Speaker 2:
3:32 So, within this podcast, not only do I ask specific questions about all of those different factors, but I also ask specific questions within segments of the cardiovascular system. Now I'm the layperson, I don't know that much about the heart, but I do know that there's the heart structure, so what you're born with. Then there's also the channeling of the heart. Say how your heart's beating. Then we have what's called the disease of the arterial system, if you will, ascvd or atherosclerosis, and that's a progressive form of heart disease. So we got three different segments there, probably more, and I asked specific questions on could option A or medication A improve one area of the cardiovascular system but be potentially damaging in another area? It's important that we cipher between each area of the cardiovascular system and then also the dose of the drug and which drug.
Speaker 2:
4:39 I really don't think it's fair to put anabolic steroids and testosterone even in the same bucket, which is a little contrarian seeing as how the title of this is anabolic steroids and testosterone's effects on the cardiovascular system. However, they do have some similarities in action as to what areas of the cardiovascular system they do affect. But, as you will learn in this podcast, there is a difference. So, without further ado, here is an excellent chat with Dr Andrew Wingy. As always, everything you witness here is not medical advice. Please seek the care from your health practitioner before making any decisions with your health. Enjoy.
Speaker 2:
5:31 Okay so today we're talking about the heart and the interactions of anabolic steroids and testosterone on the heart. But before we do that, why would you be a good authority to talk on this? Could you introduce us?
Speaker 1:
5:49 Sure, yeah, as you can see that on the screen there, my name's Andrew Wingy. I'm a traditionally trained medical doctor from the United States, so my medical background is I'm board certified in both emergency medicine and family medicine. I've taken a personal interest in cardiology early on in my career, mainly from my work in the emergency department, where I see the end stage of cardiovascular disease, which is usually heart attacks, obviously strokes, cardiac dysrhythmias, all of the very late end stage complications of the things that you and I are going to talk about today end stage complications of the things that you and I are going to talk about today. So you know, quite naturally, as a young medical student and a resident, you know, as I was taking care of these people, I got interested in like, first of all, how do we prevent this? And also for myself, like how do I keep myself from going down this pathway? You know, as a 27, 28 year old resident and student, coming from a family that is riddled with heart disease, my dad had his first angioplasty in his iliac vessels in his early 50s We'll talk about that. I have a genetic lipid condition that we'll get into a little bit. That has devastated it's kind of like devastated all the men in my family. So I've just been acutely aware of cardiovascular disease from like very early on in my career and so naturally, you know, in medicine everybody tends to find a little niche that they're interested in, and for me, outside of trauma and you know sepsis and all the normal things I take care of in the emergency department it's preventive medicine and particularly preventive cardiology. Now, I'm not a cardiologist and I'm not a lipidologist. I'm interested in all those things, but not enough to go and do another residency or a fellowship in it. But I really feel like the role of prevention with cardiovascular disease it shouldn't really be up to the cardiologist, it shouldn't be up to the lipidologist, because this is a problem that affects the entire world, affects both men and women. I'm here in the UAE now and I activate the cath lab for ST segment elevation myocardial infarctions on an almost daily basis here, and it's in young guys, young guys in their 40s and 50s, so it's actually it's very pervasive over here. We don't have there's not the same obesity problem here, yet we still have massive amounts of cardiovascular disease in the UAE. So this is a global problem and so this needs to be taken up by family physicians, which, you know again, I'm boarded in family medicine, so I feel like this is definitely within my wheelhouse.
Speaker 1:
8:29 On the side, you know, I run a telemedicine men's health practice as well that's focused on health optimization. Testosterone therapy is obviously a part of that, but a big focus of it is in preventing cardiovascular disease. I really don't think you can't have a men's health sort of a medical practice without addressing the number one killer of men, which is cardiovascular disease. Everybody focuses on testosterone, and I get it. It's crucially important. It can be a game changer for a man's health.
Speaker 1:
9:02 But there's no point in having optimal testosterone levels and optimal libido and a six pack If you're all, your arteries are clogged and you kill over from heart attack at age 60, which is kind of what my genetics would lead me to If I did nothing. I would sort of follow down the path of of most of the men in my family and have events you know, an event in my 50s or 60s. I'm 51 right now, so I'm getting close to the point where many of the men in my family don't survive, and so this is something I've been, you know again, acutely aware of for quite some time.
Speaker 2:
9:40 So I take it very seriously and on that, if you could elaborate, is that familial hypercholesterolemia or something like that? It's not, but that's yeah, good guess.
Speaker 1:
9:50 So there's a number of genetic syndromes in the lipid world that, like rapid, that are massively increased your risk. One of them is FH familial hyperlipidemia, as you mentioned. You can be either homozygous where you have that's the really bad one where you have two bad copies of the gene, you know, and these are people that run around with LDLs of like 500, 600. They develop heart disease Many of them. They have myocardial infarctions as teenagers. So not uncommon.
Speaker 1:
10:19 I have something called elevated lipoprotein A, LP, little a, which is extraordinarily common. It's totally underappreciated even today, which kind of boggles my mind. Uh, 20% of the world's population has elevated lipoprotein A levels and they are uh, significantly associated with, you know, with high risk in terms of both stroke, heart attack and also like thrombosis, DVT and whatnot. So my LDL levels have always been perfect. I mean, they've always been like traditionally what any lipidologist would be very happy with. They've been like under a hundred. But my LP little a levels are my entire life because this is genetically determined have been twice the upper limit of MAMMA, which in the grand scheme of things is not too bad. There are people out there that have even higher LP little a levels and they develop really early heart disease, Maybe not quite to the extent that the FH people do, but it's still.
Speaker 1:
11:20 It's still rapidly accelerates. You know the whole process of atherosclerosis which I'm sure we'll we'll get into. So, um, I inherited it from my dad, he got it from his dad and, um, my, the advantage that I had over them was I have known about this, for I've known about it for about 20 years, so I've been able to make some interventions to minimize my risk. But, having said that, I had a CT coronary calcium score done a couple years ago now and I have developed plaque now in my right coronary and one of my other vestibules. So, even despite having pristine lipids, I still developed some atrial sclerosis as a result of that. So it just caused me to double down and be even more aggressive with, uh, all the things we'll talk about, I guess, today sure now this could be the start of a beautiful multi-series on cardiovascular health I mean before we do that, I think, I would like to ask you the first question.
Speaker 2:
12:25 If, if you had to break down the segments of cardiovascular health, how would you do it? So, as I understand it, there's the structure of the heart, then there's channeling, then there's obviously ASCVD. How would you put that into different segments? Is there four? Is there five? How would you? Yeah, good question.
Speaker 1:
12:46 I haven't been asked that before, but I'll try to work through it logically. So yeah, the first part is, of course, structural. So you're born into this world with certain heart structures. Ideally you have two atria, two ventricles. You don't have any holes that shouldn't be there where blood is communicating right to left, left to right, et cetera. So you hear, actually it's interesting in the UAE, here we see a lot of kids with congenital heart disease and that's a whole different ballgame. So you come into the world with, hopefully, a structurally normal heart. All the valves work, nothing's leaking, et cetera.
Speaker 1:
13:26 Now you have to have, you know, in order to have, obviously, a functioning heart, you need the proper structures. But you also need a properly formed electrical system where the electrical conduction starts in the SA node and it works its way through. It's not that important that people really understand all of the electrical structures and the different bundles and things like that. But you want to have it's like a house you have to have a good foundation, you have to have the house, but then the electrician comes in and does the wiring. You have to have the wiring done correctly and you can have a structurally normal heart, but you can have an issue with the wiring, and so you'll have people that have SVT or supraventricular tachycardias. They sometimes refer to them as something called AVNRT atrioventricular neural reentry tachycardia. It's not really important. Maybe there's a little cluster of abnormal cells that are not firing in the way that they're supposed to. They set up these little what they call reentrant circuits, and then that's when you wake up at two in the morning and your heart rate is 220 and you're sweaty and you're short of breath. There's nothing structurally wrong with the heart. You've got a problem with the electrical conduction system. So that would be part two to that.
Speaker 1:
14:42 Again, that's usually something that you're born with. It can be a result of trauma or damage to the heart, like, obviously, if you've had a heart attack and you've got an area of dead or compromised tissue that involves the electrical system, now you've got a scar there and that can interfere with the electrical systems of the heart. So those are the first two, and then, as time goes on, we have the development of atherosclerotic cardiovascular disease, as you mentioned, and that's the thing I'm really interested in, because I can't do anything about your structural heart disease. I really can't do anything other than refer you to an electrophysiologist if you've got an electrical issue, I can manage it medically with certain medications in some cases. But again, most of that stuff that really needs to be those are high-level problems that should be managed by a very good cardiologist or an electrophysiologist. But what I can do as a primary care physician, as someone who's interested in prevention, is address the development of atherosclerosis, which is fascinating to me that people don't know this. But honestly, I was never taught this in medical school.
Speaker 1:
15:53 But atherosclerosis begins in childhood. So we have very good, consistent autopsy studies of children that were killed in motor vehicle accidents, going back like even to the 1970s. So we're talking about like seven and eight year old kids and on autopsy, sure enough they've got these first signs of these fatty streaks in their aortas and some of the vessels of their heart vessels and other parts of their body. So this is something that starts I. You know it may be controversial, people might disagree with me, but I think that atherosclerosis is probably part and parcel of just being a human being. Like everybody will get atherosclerosis. In my opinion, Again, there might be some pushback on that, but I think it you'd be hard pressed to find anybody that dies without any atherosclerosis. There might be a few genetic mutants out there, people with mutations in the PCSK9 system that never develop atherosclerosis, but even they do develop a small amount of it. So I think it's part and parcel of being a human being. We have mummified remains that are up to 4,000 or 5,000 years old who clearly were not overweight, had a very vigorous lifestyle and ate as close to a paleo diet as you could possibly eat, because they were close to being in the paleolithic Not quite, but they have in the preserved tissues they've got atherosclerosis. So I have a feeling that this is part of being a human being.
Speaker 1:
17:27 But that doesn't mean, you know, just because you die with atherosclerosis doesn't mean you have to die from it, or certainly it doesn't mean you have to die prematurely, which is what we're seeing now. So you know, we all got to go at some point. But you know I would rather die of a heart attack at age 99 than at 59. And and that is something that we have control over now, especially with new medications we just know more about lifestyle exercise. We know a lot more about hormones. So that's the intervention, that's that third piece that we really should be putting 98% of our effort into. Is the prevention of alpha-scribed disease, or at least like slowing it down. So maybe you'll die of something else, you know, when you're in your nineties. So that's how I think about those.
Speaker 1:
18:16 I guess there's probably three main areas. Maybe I'm leaving something out there. I suppose you could also maybe the fourth one. You know, everything is tied in together, right? The heart doesn't function independently. So I like to think of like the cardiorenal system, so the kidneys and the heart are very intimately related. There's obviously a cardiorespiratory system, so the heart and the lungs are intimately related. So you know, if something goes wrong in one it affects the other. So that's where everything is sort of integrated, maybe in that fourth aspect of what you were talking about. So that's kind of just generally how I think about it.
Speaker 1:
18:53 Other physicians or cardiologists, they might have a different order of priorities, but I think about those two, and it's those last two the development of atherosclerotic disease and then the interaction with other organ systems. That's where I think we can do the most for ourselves and that's where somebody who understands this type of medicine can intervene and make the biggest difference in their patients. The first two you're kind of out of luck. That's congenital stuff. You didn't do anything wrong. That's out of luck. That's congenitalist stuff, that's nothing. You didn't do anything wrong, that's just bad luck.
Speaker 2:
19:29 That's a great answer and, if I may, double-click here for just a moment for the general audience, so we have the structure of the heart you're born with it, the channeling or the electrical part of the heart, the wiring of the heart, and then we have ASCVD. Could we get a layman's definition on it, because I'm not even sure I fully understand the definition myself in terms of explaining it to my mother or my father Exactly.
Speaker 1:
19:56 Yeah, Well don't feel bad about that.
Speaker 1:
19:58 I mean, the more I read and learn about atherosclerotic disease, the more I guess I just have a more and more of appreciation of how complicated it is. And I, the more I read, the more questions I have. So it's an incredibly complex process and unfortunately, on the internet and physicians are guilty of this I'm guilty of this too is we kind of we oversimplify this process. It's incredibly complex and that's why you have people fighting back and forth about oh, it's all A, but it'll be no, it's all inflammation. You have the carnivores and the vegans and they're all well, the thing is, they're all they all have a piece of the truth right, they all have a.
Speaker 1:
20:34 They're all right about what they're right about, but they're also wrong about what they're wrong about, and and so it is confusing for a lay person to try to get a handle on this and to try to figure out, like, who to trust is really tough. It's really really tough. There's a lot of noise there. So, in general though, I mean I think of atherosclerosis as it's a. It's a slow, indolent, progressive process of arterial not the vein, not the venous system. It affects just arteries arterial narrowing and stiffening and then, at the micro level, arterial and endothelial dysfunction. So atherosclerosis starts at the microscopic level, before you even have plaque, you have dysfunction within the artery and then it sets up a situation that sort of self-perpetuates over time, where you get progressive, progressive narrowing of the lumen of the vessel and so, obviously, when you take a pipe and you, let's say, you limit its, cut its diameter in half, well, now everything distal to that is not going to be perfused as well and you're going to have issues. You could well, you could have issues.
Speaker 1:
21:51 A lot of people walking around with 50% blockages have no idea that they have 50% blockages. They can exercise normally. They're totally asymptomatic. But there does come a point generally because, like I said, it's a big part of atherosclerosis is that it's a progressive disease. It gets worse with time. So the number one risk factor for atherosclerosis is age. It's not LDL, it's not blood pressure, it's age. So that's how I think of it Progressive narrowing, stiffness and dysfunction within the arterial system. That's a good answer.
Speaker 2:
22:24 Okay, now to the fun stuff. I was thinking about this before the podcast because I know on other podcasts they aren't specific enough, at least for me. So this is how I categorize things we have natural testosterone levels that are in normal range. We have low testosterone levels. We have physiological levels of testosterone replaced exogenously, then we have high exogenous testosterone levels, and then we have combinations of testosterone and anabolic steroids and or other.
Speaker 2:
22:58 PED. So we've got six different things going on here, but I feel like a lot of people are bucketing anabolic steroids and testosterone in the same bucket. So how do we separate each of these and what do you think about each individual thing either impacting the heart in positive ways and or negative ways? That's a loaded question, I know Totally, but it is confusing, you're right question, I know, but totally.
Speaker 1:
23:29 But it is confusing, you're right. Because yeah, it's. I mean etrt. Uh, no matter how well you do it, you know with yeah, you could do three times a day micro injections of bioidentical testosterone, it will never be precisely physiologic, it will never mimic exactly what your, your body, was making in its prime or hopefully was making in its prime.
Speaker 1:
23:50 So, yeah, trt on one end and then the sort of androgen use that we see like at the professional bodybuilding level. These are like two totally different animals, like physiology, like it's just you've got human, you know human physiology on one side and like superhuman, abnormal physiology there. And so you do have to be careful about conflating the two and making assumptions in one group and applying it to the other group. You have to be very careful doing that, because it's probably not going to work. Doing that because it's probably not going to work. And the other thing, of course, is that we don't have anywhere near as much research in the TRT world as I would like to have, but we have a hell of a lot more than we do in the second group, where we have virtually none.
Speaker 1:
24:40 We have very few human studies looking at populations of, like professional bodybuilders, with all of the cocktail of drugs that they take, and following them over time. We have observational studies, you know we have case reports. So this is, you know, this happened to this individual, this is what we found on autopsy. So you know we can't discount those because they do seem to show some very consistent things. But, like most of the anabolic steroid research out there is in animals and usually is in rats, which, again, you know, it may or may not apply to various degrees to humans. So we just have to be careful about, you know, conflating things. I forgot the second part of your question, but I think you were talking about both the benefits and the drawbacks, potentially, of these different sort of scenarios.
Speaker 2:
25:35 Is that right? Yes, well, that was a good answer, but I'll follow up okay, so I can be a little more specific here. So I live in that world. I live in that bodybuilding world. I'm not a bodybuilder, I am on TRT myself, but I've used anabolic steroids before and this is what I see, and I think a lot of the other experts, if you will see the same thing. I see a lot of the larger dudes dying a lot earlier, even the users of anabolic steroids who are lighter and leaner. I don't see them dying early or having the same issues early nearly as much as the big guys. So how much of this is the drugs itself and how much of this is the size the drugs make you?
Speaker 1:
26:17 That's a great question, because I've observed the same thing. Right, the mass monsters all die early. Um, I mean, we could, we could rattle off the names, but we don't, really we don't need to. I think we anybody that follows bodybuilding probably can rattle off four or five top pros that have died prematurely, you know, over the last decade or so. It's.
Speaker 1:
26:39 It's pretty tragic and you're right, it doesn't seem to be quite the same in the light, lighter weight categories. The lightweight guys that I've seen die prematurely, it seems to be like more related acutely to like diuretic abuse and like contest prep misadventures, like I think about I'm a bit of an older guy. So Mohammed Benaziza died. He was a smaller guy but he died. I think about I'm a bit of an older guy. So Mohammed Benaziza died. He was a smaller guy but he died. I think I heard it was like acute hyperkalemia related to, you know, like kidney failure and diuretic abuse. So it wasn't anything to do with. He didn't die of a heart attack per se, like atherosclerotic disease or chronic kidney disease. He just prepped too hard, basically.
Speaker 1:
27:25 So but yeah, I've wondered about the size thing too. So you know, it's interesting, like if you look in the animal kingdom. Um, large body size is not necessarily correlated with um shortened lifespan. In fact, it's exactly the opposite. Like the biggest mammals on Earth tend to have the longest lifespans. So you look at, like elephants and blue whales and the Galapagos tortoises that live over a century, those are like pretty big animals. So being big in and of itself, you know, at least in the animal world, doesn't seem to convey a shortened lifespan. In fact, maybe it's the opposite. And you know, it's small, little furry animals that have very short lifespans. We think about rodents, for example, small insects, those sorts of things. So, but how does that correlate with humans? Now, is it the body size that's prematurely killing these guys? Or is it all the things that they do to get the big body size that is killing them prematurely? And you know, if you hold my feet to the fire, I'm going to say it's probably the latter more so than anything else.
Speaker 1:
28:37 Now, being bigger than you're genetically meant to be, obviously there's going to be a cost to that. Sleep apnea, for example, is like a very obvious thing. Um, you know these, all of these like world's strongest men guys, I'm willing to bet, you know, almost everybody on the olympia stage, uh, has sleep apnea? Uh, certainly, or at least in the off season they do, and and that's just a function of just being a big human. Um, by the way, like I see that in the hospital all the time with obese people, they what if I have to intubate them and put them on a ventilator, like they're very difficult to ventilate, sometimes I have to use very high pressures simply because they're laying prone and all of that fat tissue, all of the, so all the abdominal fat is pushing up, compromising their lung volume, when their spine and then all the you know, obviously the fat from, you know, from the neck to the xiphor here, is pushing down and so just mechanically, like it just makes it really difficult to take care of those people. So there's that part of it, but I think that mostly it's the, it's the massive amounts of androgens that these guys are using, um, specifically, like the long-term effects of that.
Speaker 1:
29:52 We can, we can dive into that a little bit, but the cardiac hypertrophy is like that's one of the universal things I was alluding to on autopsies that you see, like I've never seen an autopsy of a pro bodybuilder, professional wrestler, that didn't have massive cardiomegaly, like two to three times the normal size, and not just the heart too, but like other organs as well. So, um, you know, we can name some names. So like um, because these are, this is out in the public domain, like rich Piana's autopsy is out there. I mentioned it in one of my videos because I'm a child of the 80s and 90s, but the ultimate warrior, when he passed away shortly after turning I think he was 51 or 52, it was my age Massive cardiomegaly. I forget how big his heart was. It was like 600 grams, so well over double the size, upper limits of like a normal, fit, adult male heart. So that's almost certainly like a result of chronic hypertension, so chronic high blood pressure, as well as the direct effect of androgens, like on the heart tissue itself, and so that not only affects the pumping ability of the heart but those androgens affect the electrical system as well, as I was talking about earlier. So you know, that's the issue.
Speaker 1:
31:18 I think that that causes the premature death in these guys. It's, you know, and the kidneys go along with it because, remember, it's a cardio renal system, these things you know, and the kidneys go along with it because, remember, it's a cardio renal system. These things are connected. So when the heart starts to go, the kidneys start to fail. When the kidneys start to fail, the heart is also affected as well, and that's what I see.
Speaker 1:
31:36 If you look at the cause of death of you know the pros that we have autopsy results in the public domain, I mean, that's universally. What you see is, you see, like massive cardiomyopathy issues organomegaly, and then a lot of them have chronic kidney disease as well. So so I tend to think it's more related to the, the things that these guys do to get big, as opposed to just physically being big in and of itself. Now, you're good, there's going to be again differences Like there's. Guys like that have acromegaly, you know that are just massive human beings. There's going to be. You know they have issues from their size, but a lot of their issues come from their hormonal problems, diabetes and things like that as well.
Speaker 1:
32:21 So it's a little bit of both, but I think it's more about what you do to get the size, and again it's a size like above your genetic Like if you reach your ultimate genetic limit, naturally in terms of size, my general feeling is that that is not going to compromise your lifespan, assuming you don't get some sleep apnea or some other issues with that. Because muscle tissue I say this a lot, but of course the composition matters and what I'm getting at is muscle tissue is really one of the it's one of the most health-promoting, if not the most health-promoting tissue in your entire body In general. The more muscle tissue you have, the healthier you are metabolically. You actually have lower blood pressure in many cases, lower levels of systemic inflammation. Your body benefits generally from more muscle tissue and you can't really say that about any other body tissue, whether it's connective tissue or, obviously, fat tissue. The more you have, it's actually the opposite.
Speaker 1:
33:26 So putting on muscle tissue up to your genetic natural limit is going to be something I think will. If anything, at the worst would be neutral if and I think in most cases will probably be beneficial and maybe prolong your life. But now, when you're using substances and doing all the things that these guys do to go beyond your genetic limit, now we start seeing the issues. So that's kind of my take on it and again, this is just me. A lot of this is going to be my opinion, and so feel free. Guys out in the audience, if you want to disagree with me. I'm open to hearing alternative explanations for this sort of thing, but that's just sort of what I've seen over the years and I think about this stuff too. Most of my meds health clients are not bodybuilders and not in that world, but I have a handful that are and I do worry about them a little bit. So we talk about neurointroduction a lot.
Speaker 2:
34:23 That's a great answer and my head is going here and here and here, but I'm trying to do my best to focus in on one thing at a time. So I'm going to start with the cardiomegaly, if I pronounced that correctly.
Speaker 1:
34:37 Yeah, yeah.
Speaker 2:
34:37 So for the lay audience, what you're saying is the heart gets bigger. Yeah, and in these anabolic steroid users let's say someone is 300. In these anabolic steroid users let's say someone is 300 pounds anabolic steroid user, his heart is likely bigger than a fat person not using anabolic steroids. He's also 300 pounds. Is that correct? Um it?
Speaker 1:
34:57 maybe, maybe, oh, so it's interesting. So, uh, the you know lv we'll call it lvh left ventricular hypertrophy, because that's pretty much what we see you can have. The right ventricle can be involved in in certain cases too, uh, and it often is in bodybuilders. But you know, the heart is physicians, cardiologists, er physicians. We think about the left side of the heart and the right side of the heart because they're involved in different things. The right side pumps blood to your lungs where it's oxygenated, it comes back and then it goes into the left ventricle and that's the thicker ventricle, the one that pumps blood out into the systemic circulation. So that's what keeps your brain perfused, your kidneys, all of the tissues in your body. So we think about the left ventricle.
Speaker 1:
35:42 I see a lot of left ventricular hypertrophy in fat, old, diabetic men, but also in young men who have had chronic hypertension. I just had a guy just it was just a couple of weeks ago here a taxi cab driver here who came in with he had passed out in his cab, probably had a little bit of heat exhaustion, but on his EKG he had these big waves. You know, you can see this when you look at like a 12-lead EKG. And this guy. I went over with the resident. We have an ultrasound machine, we did a bedside echocardiogram and I mean his ventricle was just massively dilated or it wasn't dilated, sorry, it was thickened, it was very, very thick. So what happens when the ventricle gets thick? The chamber on the inside where the blood fills it starts to get narrow. So now there's less blood in there to pump.
Speaker 1:
36:40 Every time the heart pumps during systole there's diastole and systole Diastole is when the heart relaxes and fills and then systole is when it contracts. So you want to have a healthy chamber size. You want to be able to fill the heart nicely during diastole and then, of course, when it contracts, you want to be able to pump, you know, pump out most of that blood. It's called an ejection fraction. So you want to. You don't want to pump out less than 40% for an ejection fraction. It is generally considered to be a proud thing but, as you can imagine, like if you've got these, like instead of if your walls of your ventricle are normal, like this, if they all of a sudden are thick like this, you know the space in here when this opens up, it only opens up a little bit. So they're the chamber size.
Speaker 1:
37:29 I don't know if I'm gonna do a good job explaining this, but the amount of blood that that is available at the end of diastole to then be pumped forward starts to go down, and so these guys, they're not perfusing their body, so they develop a type of heart failure. It's called heart failure with preserved ejection fraction, and then as time goes on, the blood pressure is more and more of an issue. The heart has to work, it finally gives out and it just kind of balloons out and then it becomes like this sort of soft, squishy heart that can no longer adequately contract. So it leads to like the more classic heart failure that we see, where people are swollen all the time, their lungs are congested full fluid, and I deal with that like on a daily basis.
Speaker 1:
38:28 What anabolic steroids do is, you know they? They induce cardiobaggly or ventricular hypertrophy through mainly like there's like two big mechanisms. One, of course, is something called the, generally called pressure overload, so which makes it basically means high blood pressure, so hypertension. So whenever your heart squeezes, it has to squeeze against that resistance of high blood pressure. It has to work harder and so, just like any muscle that's working harder in the gym, what does it do, it hypertrophies, right. It gets thicker and stronger and up to a certain point that's adaptive. Natural athletes that exercise hard and train hard, they have something called the athlete's heart, which is a type of cardiomegaly per se. They have slightly larger hearts and they have slightly thicker ventricles, but it's beneficial to them. It's a beneficial adaptation to exercise.
Speaker 1:
39:20 What you see in people who use high levels of androgens is it goes beyond that. So not only do they get a thick vegetable because they're chronically exposed to high blood pressure, but the androgens themselves like directly stimulate the growth and probably the hyperplasia. So maybe you get like more heart cells developing. So it like directly stimulates the growth of the cardiac tissue, but not in a good way, a pathological way. So it's kind of a double whammy. So that's why it's you know I harp on this a lot with my guys but, like blood pressure control is incredibly important.
Speaker 1:
40:01 Especially if you're going to use high levels of androgens, you really need to make sure that your blood pressure is under control Because there's a whole the renin-angiotensin system is like massively activated as you go up and up in your androgen use and you know you're going to need pharmaceuticals to manage that and it's all part of this like damage control, you know and it's all part of this like damage control, you know philosophy that I think if more guys who used high levels of androgens had somebody that could help them do that, I think you could certainly offset a lot of the risk that these guys take.
Speaker 1:
40:36 It's never, you're always taking a risk when you, when you take high levels of androgens. It's, I mean, you know what you're getting into, you're you're, you're getting into you, you're um, you're taking a risk, but with proper medication and proper um approach. You know there's things you can do to mitigate that to a certain extent, but blood pressure is like, first and foremost like and it's one of the easiest ones to do okay, a lot to unpack there and again, I'm one of the lay people, I'm one of the stupid people.
Speaker 2:
41:04 I'm one of the stupid people and I guess that sort of answers, at least for me, why I never could understand the large heart thing. So on one hand, I'm exercising a lot, my heart gets bigger, it's a good thing. But then if my heart gets too big, it's a bad thing. How much is too big? How much is too small? So I went and did an echocardio myself. I have one millimeter of lvh, good or bad yeah, that's, that's probably okay.
Speaker 1:
41:31 Yeah, yeah, now I would. I would follow that up, especially if you're going to continue to use as you get older, um, make sure that you know. I would probably repeat that in three years, uh or so, depending on what you're up to and what you're doing. But it also is a sign that just be very diligent with your blood pressure, be very diligent. We can talk about this if you want, or we can save it for another podcast. But there's sort of a of prescription medications that you know can potentially offset this issue to a certain degree. That, um, that I think you know people can consider if they're going to go down this road.
Speaker 1:
42:16 Um, but blood pressure control is like the cornerstone of it. You just you can't be walking around with 140s, 150s. You can't be walking around with 140s, 150s, 160s, systolics year after year after year and not expect to have some sort of negative outcome eventually. Now it may be a decade or more before that's a problem. These are slow, indolent processes, but why would you even get it started to begin with? Yeah, I'm really big on keeping blood pressure under control if you want. You got to make your heart last.
Speaker 2:
42:51 You know you don't want it to work any harder than it has to yeah, so my blood pressure is 115 over 70 now I've had to work at that. We're talking about four or five hours of cardio per week. But with the go back to the lvh, what the cardiologist told me. He asked me if I exercise. I told him my protocol. He goes oh, that that's normal.
Speaker 1:
43:13 Yeah, yeah, like that's within the range of, like the athlete's heart range. So, yeah, so that's, that's fantastic. Yeah, that's fantastic. You just want to monitor that, keep an eye on it and just make sure that it is at least staying within that range as you get older. So not everybody needs to do that.
Speaker 1:
43:34 By the way, this is just for guys that are using high levels of androgens. I just think it's kind of a smart thing to do, but it can be a little problematic to get an echo. For some people it depends on where you are in the world. But it's, it can be a little problematic to get an echo, um, for some people it depends on where you are in the world, but it's, it's usually not problematic to get a blood pressure reading anywhere, um, and that's easy. So that's like the poor man's test right there. You know, if you're consistently 115s, I mean it's hard to argue with that.
Speaker 1:
44:01 That that's like any LVH that you get from. That is either just going to be from like the athlete's heart or it's going to be from huge amounts of androgens, because you know the androgens will directly stimulate the hypertrophy of the cardiac cells themselves. So, but that's, that's good. I mean, that's, that's really really good. The problem is, you know these guys I mean I'm not privy to their medical records per se these guys that have died prematurely, but you know, I bet, if you strapped an ambulatory blood pressure monitor on some of these guys that died prematurely, that they were not walking around at 115, over 70. They were probably walking around at 160, 170, even 180. That's just my guess, and they were probably at that level for a very long period of time, most of the time.
Speaker 2:
44:52 Yeah, I mean, we have the famous example of John Meadows, who was very well measured but still suffered the cardiovascular fate, didn't he?
Speaker 1:
45:01 Yeah, yeah, he did. Yeah, and it's really sad. You know, I I don't I never met him, but um, by all accounts, he was a really great guy and, uh, yeah, died premature. I think he had a pulmonary embolism, if I'm not mistaken.
Speaker 2:
45:15 Yeah, and a heart attack prior to a year prior. No, did he okay, okay, yeah, I didn't know that, but that's again you know um.
Speaker 1:
45:20 Okay, yeah, I didn't know that, but that's again you know um the these are the choices, right? I mean, uh, I, I respect professional bodybuilders. I have a tremendous amount of respect for the, what they put themselves through, the amount of discipline it takes um and just the rigorous um adherence to like to the training and the diet, adherence to the training and the diet.
Speaker 1:
45:51 But they do tend to not live as long, and so if a young person wants to be, if that's your goal in life is to be a pro bodybuilder, then who am I? Of course I'm not going to tell you not to do it, but uh, I would just say damage control. You got to do damage control from very early on in your career. Uh, get with a physician who uh understands the risks the cardiovascular risks of anabolic steroid use, and just do every, every single thing you can do. Um, just like you do everything you can possibly do to get in shape for a contest, you should be doing everything you can possibly do to minimize the amount of damage that the drugs are doing, because they're part of the game. Obviously You're not going to do well in the bodybuilding world as a natural athlete, sadly, at least at the high levels. That's just how it is, that's right. You know where my podcast is a little different is I'm not the moral police, at least at the at the high levels.
Speaker 2:
46:44 You know that's just how it is. That's right. So you know. Where my podcast is a little different is I'm not the moral police, I'm not here to preach health or anything like that, but I guess a lot of my audience want to know how can they uh do a healthy, an unhealthy sport the healthiest way possible? That's kind of my audience, right, right, yeah, yeah yeah, exactly, and that's a way to approach it.
Speaker 1:
47:04 Just understand that what you're doing is inherently unhealthy. It is inherently, it's inherently bad for you in terms of longevity. And again, I'm just like you as a and just from the physician side. I'm not the police, I don't judge. I'm only here to give the best advice that I can give, and then I want you to be able to have the information you need to make a decision that's best for you. I don't, I, I give it up telling people what to do. I don't tell people what to do, um, I rarely even tell people to stop smoking these days, believe it or not, because they already know they already know they don't need to hear me wave, you know, wag my finger at them.
Speaker 1:
47:45 They know If they need some help doing it, we'll have that conversation, of course. But yeah, I've become a little bit more libertarian as I've gotten older. It's not my job to tell you what to do with your life. It's not my job to tell you what you can and can't do with your body, but I will absolutely do my best. If you want my advice or opinion in order to mitigate some of these things, that's where I can step in and be useful.
Speaker 2:
48:13 But I don't get to those tools as well. We'll get to those tools from you, maybe in another podcast, because we'll go through the segments of his heart. We've. We've started with the. This is a known mechanism. Anabolic steroids and testosterone at higher doses at least make the heart bigger, in particular the left ventricle. So we'll put that aside for the moment. Yep, the next thing I wanted to talk about, less discussed, is anabolic steroids, um negative or positive impacts on this electrical system. So I'll give you an anecdote of myself. The reason I stopped using anabolic steroids, or one of, is it made my heart palpitations way worse, like I had to stop. It was so uncomfortable. So how can anabolic steroids affect this electrical system?
Speaker 1:
49:07 Yeah, super, super interesting. Again, I'll caveat this by saying I'm not an electrophysiologist. I don't consider myself an expert in anabolic steroids per se. There are a lot of folks out there that know quite a bit more about the. You know the minutia of, like all of these synthetic anabolic steroids. I do know a fair amount about testosterone, of course, and I know a fair amount about how the heart works so well, I'll kind of approach it from that. So from that standpoint.
Speaker 1:
49:37 But yeah, it was a bit of a revelation to me years ago when I learned about how, you know, I understood the structural impacts of anabolic steroids on the heart I think most people could get a handle on that but to also have learned that it really can profoundly affect the electrical system as well. And so what we found and I'll speak just in general, general terms there seems to be a bit of a difference between testosterone per se, this natural testosterone, and these other synthetic uh, androgen, you know, testosterone derivatives, your, your nandrolones and your echopoises and um oxandrolones and all those sorts of things. So, in general, what you can see with the synthetics is a prolongation of the action potential, and the action potential is the electrical discharge that happens in the membrane of the cardiac cells and so you get this electrical discharge and what that looks like is you have sodium channels that are I'm trying not to get too geeky and technical for the audience, but sodium channels open up. Sodium rushes in, potassium rushes out, you have release of calcium within the cells. It's just like precisely orchestrated. It's incredibly detailed and you want this to go off without a hitch and you want it to go off perfectly every single time, so with every single heartbeat. You want this little system to work and it generally does. Unless you've got pathology of some kind or there's a drug involved, it generally works well. So you don't want this action potential to be prolonged.
Speaker 1:
51:22 You don't want to develop something on an EKG and it's called a prolonged QT interval. So there's a Q wave and a T wave on the EKG, which is not important that people can Google that if they want to see, but it's. It's the distance between those two things on an EKG. The longer that is, the more likely you are potentially to go into like sometimes a lethal cardiac dysrhythmia. So that system can be disrupted when you have this prolonged QT.
Speaker 1:
51:53 Now you can get prolonged QT from a bazillion different things. There's congenital genetic causes. There is a list of medications that's as long as your arm and longer that can influence the QT cycle, but synthetic androgens are one of them in some cases. So the problem is, you know, unless you've never had, you know if you've never had an EKG, you may not know where your QT interval is. It's probably normal. But you know, if you have one of these congenital syndromes where it runs a little bit long, and then, let's say, you're on high doses of nandrolone or oxandrolone or some other synthetic anabolic steroid, now that's going to be a little bit longer. And then now let's say you've got a sinus infection, your doctor puts you on a macrolide antibiotic or something that also prolongs the QT interval. Now all of a sudden you're in my office in the emergency department and I've got the Pavas out to try to put your heart back into a normal rhythm.
Speaker 1:
52:53 The interesting thing is that testosterone actually seems to have the opposite effect, in that it actually stabilizes and perhaps shortens the duration of those action potentials. Stabilizes and perhaps shortens the duration of those action potentials, maybe shortens the qt interval. I say maybe because so much of this is is like in like in rats. So these are animal studies. So there's not a lot of like solid human data that I have seen, um, but it kind of makes sense. I mean, the body knows what to do with testosterone and and so it's a bit more tolerant, especially of even higher doses of testosterone milligram per milligram that it would be of a synthetic androgen.
Speaker 1:
53:32 So it's interesting that they you know, we think people lump testosterone in with all the other anabolic steroids, but when it comes to these electrical changes, it seems like at least the animal data shows that testosterone in some ways is not as dangerous per se as high doses of these synthetics, at least when it comes to these changes in the electrical activity, the action potential, that sort of thing. So I don't know, maybe you can speak to um, if you don't mind, like what you were using when you started having your tachycardia issues. Was it high? Was it just like? Would it be? Were you on a testosterone only cycle? Or was it were you throwing in synthetics? Because maybe it was the synthetics and not so much the testosterone.
Speaker 2:
54:19 I mean, I don't know I have good anecdote for this. I like to consider myself a very accurate n of one, okay, excellent. So I have in the past used up to a gram of testosterone, loved it, did not suffer the heart palpitations, at least not as frequently. The moment I add in any DHT derivative, I'll explain to the audience. So this is the normal heart boom, boom, boom, boom. This is what happens to me when I get what I call a heart palpitation flare-up. Now it could happen from, like circadian rhythm disruption. Other medications, yes, but with steroids. Every time, and it's the worst, it's like this boom, boom, boom, boom, boom, boom, yeah, boom, and it's just uncomfortable, even if it's not necessarily dangerous in the acute term, it just you can't stand it.
Speaker 1:
55:09 It's horrible well, and the danger with that is, especially as you get older, is that that boom, boom, boom, those three beats turns into boom, boom and it keeps going. And now you're that's when you come see me, me, and that's a big problem. And so that's interesting that you say that, because that's kind of in line with what I've seen in the electrophysiology literature, with testosterone being at least neutral, in some cases somewhat protective against these dysrhythmias, versus the synthetics, the DHT derivatives, all these other drugs where, like universally you seem to see, you know, perturbations in the QT interval that sets people up for, or at least sets up the rats for, cardiac dysrhythmias. The interesting thing too is that, with when they would like, there's a study I'm thinking of in particular where they induced heart attacks in mice.
Speaker 1:
56:08 If they had higher levels of synthetic androgens in their system, they were more likely to go into a lethal dysrhythmia, something called ventricular fibrillation, which that's how you die of a heart attack. You know you have a, you know you're not getting enough blood flow, you go into usually ventricular fibrillation, and then it's lights out, much more likely to go into ventricular fibrillation when you add high doses of, say, nandrolone in these animals versus high doses of testosterone. So it took it took more time for them to go into their trick of fibrillation if they were on testosterone versus the synthetics. So you can imagine the correlator there. Let's say you're a 300-pound bodybuilder, you rupture plaque, you have a heart attack and you happen to be on high levels of these synthetic androgens.
Speaker 1:
56:56 You may be more likely to die it was also harder to get these mice, by the the way, it's harder to get them out of ventricular fibrillation. They needed more shocks, higher and higher, uh, higher electricity, more and more joules to get them out of it, as opposed to the ones that were either on nothing or on testosterone. So again you know, um, as a bodybuilder, probably testosterone only cycles are probably, if you're going to go down that road seems to be like the safer alternative. It's still, you're still. I mean it's not good for you, it's.
Speaker 2:
57:33 It's clearly going to still be a negative, but it may be less of a negative that's a great answer and, at least on my youtube algorithm, I'm seeing a lot more of these test only or high testosterone only cycles being promoted due to tolerability in general. I guess one of the reasons why Sorry.
Speaker 1:
57:55 It does, it makes sense.
Speaker 2:
57:57 Yeah, it honestly does, but you know I'm not a pro and pros know they need Tremblone so I won't recommend them. Otherwise. I guess one of the reasons why this channeling discussion is less appreciated is because, yes, it's fond to my own heart, but I honestly haven't heard a lot of friends or people in the community reporting these symptoms. It does seem more rare.
Speaker 1:
58:23 Yeah, it's, you know, but things are underreported. You know, a lot of men in particular fall into two categories. From what I've seen, slightest little twinge. But then there are. There's a whole group of guys out there that they basically have to be dying for them to be, and they have to be dragged in by their wife or their girlfriend before they'll come in and see a doctor for anything. So you have to wonder um you know how many guys are out there experiencing this and just not seeking medical care for it or not talking about it? Um, it's hard, it's hard to know, it's hard to know that is a good point.
Speaker 2:
59:08 Apparently, at least on the ekg, I think it's called I have these heart palpitations even when I don't notice them, and I tend to notice them more when they become more frequent or harder. How interesting is that? Like it could be happening. It's super common, I don't know.
Speaker 1:
59:23 Super common, super common, yeah, and it all depends on what these things are. I mean they're probably what's called pvc's premature ventriculitis. It's super common. I don't know. It's super common, super common, yeah, and it all depends on what these things are. I mean they're probably what's called PVCs proven sure ventricular contractions, which everybody has them. If I've been hooked up to a monitor and if I've had a little bit too much coffee, for example, I will see them.
Speaker 1:
59:43 I don't always feel them either, and it's very interesting to me. Some people are just perhaps more in tune with their body. They're just a bit more sensitive. They're able to detect it, and some guys they could be just pounding away with a heart rate Like.
Speaker 1:
59:58 I see guys coming in with atrial fibrillation, which is a slightly different arrhythmia Heart rates 140s, 150s, up to 180s. Occasionally they just like I just feel a little off. I'm like do you feel your heart? I don't feel. No, I don't feel anything in my heart, I'm just, I'm just a little short of breath, uh, or I just feel, I just feel weird. That's what I get. I feel weird like, yeah, I see why you feel weird. Your heart's going's going 180 beats per minute. But then other guys they feel it immediately. And if you have to choose, you want to be the guy that feels them, in my opinion, because you want to know if they're sustained. If it's sustained, you need to come in. You need to come to the emergency department. If it's just a couple flip-flops here and there, that's different. But if it's sustained, if you're having this going on for two, three, four or five minutes, you need to come in.
Speaker 2:
1:00:56 Sure, okay, before we get to your wheelhouse. The ASCVD the reason I don't say the word I can't pronounce it. I have a lisp. I literally can't pronounce it. That's okay. Atherosclerosis I can't pronounce it. I have a lisp. I literally can't pronounce it. It's a sclerosis. I can't Okay. So A-S-C-V-D it is Testosterone. I want to, instead of being Negative Nancy, all the time, because that's all I see on YouTube. Testosterone and anabolic steroids are bad for the heart. We know that. All right, Right, positive Pete, let's play positive pete for a moment. Can you list me any positive impacts outside of what you just mentioned? A shortening of the qt interval with either or testosterone or optimal testosterone level, so, for example, a worsening if it's low and or even an anabolic steroid. Is there any positive impacts this can have on heart function or cardiovascular function?
Speaker 1:
1:01:49 yeah, well, for testosterone, that's it easy. It's easy to answer for testosterone because we've got a like a wealth of data um in in that area. Now the synthetics it's a little bit different, like all the synthetics that. You know they came onto the market for legitimate medical uses, it's just that they're just not either. You know they came onto the market for legitimate medical uses, it's just that they're just not either. You know they've been taken off the and then like late, late stage, stage four metastatic breast cancer, like way back in the day, but nobody uses it for those situations anymore. So so there really is, there is no like legitimate beneficial use, I don't think, for those medications at this stage of the game. You could make a few arguments here and there, people with like cancer, cachexia and like HIV wasting and sort of those sorts of things, like these little niche medical issues, that maybe there's a use for some of the synthetics. But honestly, like I think testosterone does the job better and it does it more safely. Like I think testosterone does the job better and it does it more safely. So it's like why not just use testosterone in those cases? But as far as testosterone goes, so first of all, it's like, well documented, all of the like.
Speaker 1:
1:03:17 The adverse effects of low testosterone are pretty well known. It's obviously associated with higher just all cause mortality it's. It's associated with worsening heart failure. It's associated with dementia. It's associated with worsening, worsening fatty liver disease, type two diabetes, chronic kidney disease, like the list goes on. So you know testosterone is a hormone that, uh, there are, you know, the androgen receptors exist throughout the body. For a reason it's a crucial hormone. So when you're low, it's not hard to imagine you're going to have problems in a lot of different areas, from the brain all the way down to your penis and everything in between is going to be affected by that. So what you see when you replace that is that obviously all of those areas, if there are issues, they tend to improve. So we, you know the cognitive effects are well-documented.
Speaker 1:
1:04:11 The effects on the heart, outside of the electrical system, are well-documented. Men who, by the way, men who suffer heart attacks, tend their testosterone levels tend to plummet after having, like, their first macronutrient infarction and oftentimes they don't recover. So men that are put back on therapeutic testosterone after a heart attack and it's debatable about, like, how long you should wait. I personally don't think you should wait at all. But the cardiology world doesn't agree with me. They usually say about six months. But that's you know. Honestly, they pulled that number out of you know where out of just an abundance of caution. But putting men on therapeutic testosterone after a heart attack, especially when they're low, reduces their all cause mortality. It improves their quality of life and in so many different ways. So, yeah, replacing it really makes a big difference.
Speaker 1:
1:05:05 The other cardiac scenario where it can be really helpful too is in heart failure. So congestive heart failure. Again, the heart is not pumping, you're not able to adequately perfuse all of the tissues in your body. It can be. It's actually one of the really serious problems. After a heart attack People become we call them cardiac cripples. So basically, your heart function has become so compromised after the heart attack that just like getting up out of your recliner and walking to the bathroom, you're just like profoundly, you get profoundly short of breath. It's a major, major hit to somebody's quality of life. I mean there's people that commit suicide over it because they just can't. They're functionally debilitated after a heart attack. So the interesting thing about heart failure is, if you give a man with heart failure testosterone and up to a third of men with heart failure meet even the strict endocrine society guidelines for hypogonadism. A third of them are below the reference range, but I'm willing to bet that probably at least two thirds are still significantly low, even though they don't quite hit that threshold. But my point is, if you give a man with heart failure testosterone, you significantly improve their functional capacity. So what I mean by that so there's this New York Heart Classification 1 through 4 is how we rate heart failure symptoms.
Speaker 1:
1:06:37 So one if you're class 1, you're basically like asymptomatic or it takes like extreme exertion for you to get symptomatic, and usually it's shortness of breath. All the way to stage four, which is basically you're symptomatic at rest, so even just sitting in your recliner At that point the gig is up. Like those are guys that are on the transplant list. What therapeutic testosterone can do is it can lower. At least in the studies that we have, it can lower your class by one point, which is actually a major win. So class one is you can pretty much do whatever you want minimal symptoms. Class two is it takes a pretty heavy exertion for you to become symptomatic. Class three is you're okay at rest, but getting up to use the bathroom going up a flight of stairs. You can't do that, or you can, but you have to stop to catch your breath. That's class three.
Speaker 1:
1:07:34 So if you could take a man with class three which is class three is sort of like that's when things really impact your quality of life Class one or two, most people seem to get by okay, but you could take them from a three to a two, just with therapeutic testosterone, that is a major, major improvement in somebody's quality of life, major improvement. And so and they've documented this with um something called a six minute walk test. So they basically just get the patient up and say how far can you walk on a treadmill for six minutes, you know, before you have to stop? Essentially, how far can you walk on a treadmill for six minutes before you have to stop? Essentially, how far can you get within six minutes, even if you have to rest along the way? And so major improvements in their ability on the six-minute walk test and major improvements in VO2 max, just with testosterone. In fact, it's as good as the other prescription drugs that we use for heart failure. You know the ACE inhibitors, arbs, beta blockers, these nephrolysin inhibitors, which are newer agents. Everybody talks about those Like cardiologists, don't bat an eye. They'll throw a cocktail of these heart failure meds at these guys. But testosterone is as effective as those drugs. Yet nobody's using it, or very few people are using it, but it could have a major, major impact on quality of life.
Speaker 1:
1:08:50 The other part that guys don't again this is not talked about either is like very high rates of sexual dysfunction after an MI, both sexual function and clinical depression. So something like 50 to 70% of men will have erectile dysfunction after a heart attack and sometimes that comes back, sometimes it doesn't. But you know testosterone's role in erectile function is very well documented and we know that it can improve. You know vascular, you know regeneration of, you know development of like collateral circulation in the penis and in the heart. You know sex is a cardiovascular activity and so it makes sense that it would improve that. So you can certainly use it for that as well. But then you know, the one that people don't talk about is depression is extremely common in men. It's like a third to half of men after an MI will go through a period, sometimes like really profound depression. And of course, what do doctors do about that? Well, either nothing or they put them on an SSRI and very few of them even bother to check to see that they've got low testosterone which, as I mentioned earlier, is, like, extremely common. So there's these roles for testosterone to help people with cardiovascular disease that I think it's like vastly underutilized.
Speaker 1:
1:10:12 It used to be used commonly for angina or angina depending on where you're from. Back in like the 40s and 50s, I did a video on this kind of going back and looking at how they used to take care of heart blockages before we had bypasses and stents and they were giving people testosterone propionate and relieving angina. You know, with testosterone propionate back in the 40s there's some really interesting studies both in the US and Ireland and the UK. So you know, testosterone is a natural hormone. It exists for a reason it's exceedingly beneficial. The issues happen, of course, when levels Everything's dose-dependent right. It's always we learned in toxicology training that it's the dose that makes the poison right. So you take a Tylenol because you have a headache. It will work great. If you take a bottle of Tylenol now, you're on the liver transplant list, so the dose makes the poison.
Speaker 1:
1:11:13 But, testosterone is underutilized, in my opinion.
Speaker 2:
1:11:18 Great answer. I have a follow-up. Okay, you're familiar with the term weasel words, right? You've heard of this before Weasel words. I think I could probably figure it out.
Speaker 1:
1:11:30 Yeah, yeah, sort of like academics like to use them, right? Is that what you're getting at? Like to sort of weasel around answers and not answer directly?
Speaker 2:
1:11:39 Not answer directly but, moreover, with numbers. So here's where my bone to pick is. Here, it's never the data that I have an issue with, it's the interpretation of the data. The data is the data right. And, yes, I'm a bit of a bookworm, so I've read most, if not all, of the major studies that are cited online and, I've got to be honest with you, none of them are using the doses of testosterone I am, and not just me, but within this popular clique, the Dave Lee clique I forgot his name he does up to 200 plus milligrams per week. He's a physician you had him on once, I think Tier 1 Health.
Speaker 1:
1:12:22 Oh yeah, yeah, I forgot his name, sorry.
Speaker 2:
1:12:24 Yeah, yeah, dr Keith Nichols. Keith Nichols, yeah, yeah, fantastic, and I guess, yeah, yeah, yeah, yeah, yeah, dr Keith Nichols yeah, yeah, fantastic, and I guess, yeah. So look, we're all getting symptom resolution, but my only bone to pick is if we're going to take these doses. I think we should take the papers with a grain of salt.
Speaker 1:
1:12:41 Yeah, so so I have the same bone to pick as well, because, um, there there's this I call it testosterone phobia within the research community out there. That they're. They're just, they are afraid of doing proper studies with the sort of levels that where where men truly get the most, uh, benefit, which tends to be higher than what they do in the studies, and they just, like you know they I think it was the Traverse trial where if your levels went over I think I don't have it in front of me, but I think it was if you went, levels went over 700, they kicked you out of the study. You know, but that's precisely we we should be, that's the group we should be studying, is the group above 700, um, so this is where, like anecdote and real world experience, is what we have to go on, and what you see almost universally not always is that when those doses are pushed a bit, a little bit higher I'm not talking a grand a week, but the kind of doses that Keith alludes to, and others as well you see, men get better. They get significantly better than they did when their levels were 500, 600, which is generally where the endocrinologists and many of the urologists want them to be.
Speaker 1:
1:14:05 So it's uh, it gets back to like well, where do you want your levels to be? You know, I want my levels to be at whatever level, my health is optimized and I feel and function the best. And I'm stealing that from Neil Rousier, because those are the words that he uses and I really like them. Um and so, if and if I'm a type two diabetic and I want to improve my insulin sensitivity to the greatest degree without using other prescription drugs, do I want to have? Do I want to use Androgel and have a total T of 450, maybe? Or do I want to get on injectable testosterone or hypoxic cream and be 11, 12, 13, 14, 1500? And I mean, I know which one I would pick, and it's going to be option number two well, this is why I have you on, because I'll give you another personal anecdote.
Speaker 2:
1:15:01 I feel like I'm getting a free consult here, so yeah, look no problem, no problem. Look, no problem, no problem. You guys are my idols. Honestly, I'm a big fan. So, first and foremost, I'm so honored to have you on the podcast. I watch all your videos. Oh, thanks All of them.
Speaker 1:
1:15:19 I really appreciate that I've got time, so I watch all of yours as well, by the way.
Speaker 2:
1:15:26 So super fascinating, yeah, fascinating. Thank you, it was great to have you on, it's like my pleasure, all right, so I did bring my levels too. I think it was. You know, with these other assays you get different scores each time because we don't have access to LCMS here, right? But anyway, the dose was 200 milligrams. The only reason I brought it back to 150, I looked at myself in the mirror and I said you're too muscular for this to be your genetic potential. And I went back down to 150. I didn't feel worse. I felt the same, if not better. Libido was better. I only brought it down because I was unsure. So what do you say to someone that is not exhibiting any negative side effects? They go to 200 milligrams. They feel the same, if not better. But they say hey, this is probably too big. I'm 100 kilos at 5'10". If I get lean, I'm like 92 kilos. I look at natural bodybuilders I'm bigger than all of them. I feel like this is too big to be natural, right?
Speaker 1:
1:16:28 yeah, I have the same sort of build that you do I'm. I fluctuate 100 kilos. Well, I mean, yeah, I'm 5 foot 11. I'm in pounds, I'm about 230 pounds, ish, you know. But uh, but this is sort of. I've been this size since I was 18. So some of it is genetics, I guess.
Speaker 1:
1:16:51 But to answer your question, just like all drugs whether I have you on an antibiotic, a blood pressure medicine or whatever the case may be I really like the concept of minimum effective dose. So we spend some time, like, if you're one of my patients, we spend some time over the first year usually trying to find if there is such a thing, a sweet spot, because you're absolutely right, there are guys. I've done the same thing you've done, by the way. I've gone up to 200 milligrams. I felt no different, there was no difference. And so I've settled in at to 200 milligrams. I felt no different, there was no difference. And so I've settled in at about 160 milligrams total per week. Now, when I very first started testosterone, I was at 120 milligrams a week and I was profoundly low before I started. So of course I felt amazing low before I started. So of course I felt amazing. But as time went on I did. There was a noticeable improvement from 120 to 160. I went to 180 and then 200 and that there was no difference. So you know, I I practiced what I preach and I backed it back down again, and so that's kind of for now, where I've settled, um as well.
Speaker 1:
1:18:04 Um, you have to also be objective with some of this stuff too. I mean, it's the way that you feel on a day-to-day basis has a lot. It's not just your testosterone level, right? I mean we were talking earlier. I have a newborn in the house. You know I'm exhausted. It has nothing to do. There's not enough testosterone in the world to fix that right now. You know I work really long hours at the hospital, I work nights, I work swing shifts. I can't testosterone my way out of that. So it also is important to have realistic expectations about what testosterone can and can't do for you.
Speaker 1:
1:18:39 Um, but yeah, minimum effective dose. I think is is the prudent thing to do. Um, if you're a bodybuilder and your goal is to put on muscle tissue, then there is a dose response curve. There More generally is better. I don't know where it plateaus, but there's a reason guys take a gram a week is because it freaking works, you know, and, and then they add, and that's just their base, and then they add more. You know, in terms of muscle hypertrophy, more generally is better, but when it comes to health, more is not better in so many different ways. So, and that's what I'm interested in, you know, at this point I want to live to be 100. I want to be the outlier in my family. So I'm acutely aware of, you know, my own mortality, especially as I get into my 50s, as I said earlier. That's when a lot of the men in my family start having issues. So I want minimum effective dose.
Speaker 2:
1:19:36 That's a great answer. And just to point out what you said before on the potential positive impacts of testosterone, I think you're referring to doses between 100 to 250 milligrams per week. Correct me if I'm wrong. Is that Reasonable, right? Yeah, I think we can ballpark.
Speaker 1:
1:19:54 That that will probably you know, there's a bell curve. Of course, that will probably get us 85 to 90% of men. If you're somewhere in that range, that's probably where you're going to help the most people. But again, there's always outliers. Right, there's always outliers.
Speaker 2:
1:20:15 Of course. Now, the reason I wanted a ballpark number is because I don't want people thinking okay, testosterone improves my heart health. What if they start using doses 500 milligrams per week? Is? This is a good question, I think, because I had someone popular, broderick chavez. I asked him. I said honestly, what have you seen from 500 milligrams? He goes, I can't tell you everything, but he goes. Honestly, testosterone only 500 milligrams compared to 200, not much difference, still pretty good.
Speaker 1:
1:20:45 Yep, yeah so broderick broderick's you know he's a super smart guy. I don't know him personally again, but you know he knows a lot about animal exterior. He's got a lot of personal um anecdotes with it, not just himself but with his clients. So, yeah, I mean, again, I don't have the um, I don't have the same client base that he does. So none of my guys take 500 milligrams, at least not that I'm prescribing them. But yeah, I think that's probably correct. Especially, again, we're talking about testosterone here. We're not talking about Tremblone, right? It's totally different ballgame.
Speaker 1:
1:21:24 So, yeah, there is a dose response in terms of you are going to see more negative effects the higher you go. It's going to be different for each guy. I've had just a good example. I've had guys who have had underlying mental health issues you know, bipolar and anxiety disorder who do not tolerate if they get close to 200 milligrams. They can't sleep, they're anxious. It just does not suit their physiology. And then you're going to have guys like yourself. You said you felt amazing on a thousand milligrams a week, you felt great on that, so right. So there's clearly a difference right between those, between you and these other individuals.
Speaker 1:
1:22:10 So I think what broderick is saying is likely very accurate. But the other thing you know we have to look at is like okay, 500 milligrams over what length of time? You know are we does. Does broderick have 20 years of guys that are on 500 milligrams a week? He might. I mean, I know there are guys out there that do that, but they're they're not well studied, you know.
Speaker 1:
1:22:35 So you're that you're kind of venturing. It's all about time, time scale, right. Um, you, you can take a toxic substance for a short period of time and do okay. If you take even a low dose of a toxic substance for years and years and years, now you could run into some problems. So if you're going to do 500 a week, let's just say we have our hypothetical amateur or non-competitive bodybuilder who likes the look and wants to keep that look and feels like he needs that much. That's the guy that needs a damage control um plan, a philosophy, a, an agenda to go along with that over time to help mitigate some of those unknowns. So the hypertrophy, the lipids, the ascvd, the renal, all that sort of stuff.
Speaker 2:
1:23:28 I think that these people need to find you. I think you could take on a lot more of these clients. I really do think it's up your alley. You haven't mentioned it in this podcast, but I know you're into grappling. You're obviously hyper muscular. I'm a jujitsu guy. Yeah, I mean, you seem like the Joe Roggan of the medicine world here, man, yeah, without the multi-million dollar contract it's coming. It's coming, man, I'm telling you so let's let's flex some of your knowledge.
Speaker 2:
1:23:59 Let's talk about some tools here before we get into ascvd, because we know there's a lot of tools there. But just from a structure of the heart and then the electrical system of the heart, what are some of the tools we can use if we're either high or sports TRT guys or anabolic steroid users? Is there anything?
Speaker 1:
1:24:21 Yeah, yeah, and of course it's. You know everybody individual. So you know the cornerstone of practicing medicine is, like I always would teach us, is like a good history and physical exam. So I want to know your family history. What are the things that run in your family? So, like the lipoprotein A thing I'll use myself as an example like that's something I would want to uncover because that, out of the gate, we need to. That that changes the calculus a little bit in terms of how aggressive we're going to be. But let's just say you're the average average guy. You don't have any, you know, major. Uh, let's say you pick the right parents. You don't have any major like genetic issues and things like that. Um, you know, the cornerstones are always the cornerstones.
Speaker 1:
1:25:04 In In an emergency medicine it's the ABCs right, airway, breathing, circulation. It's the basics that make the difference. Like we have a lot of fancy drugs for people's hearts, but what really will save your life is good CPR. So I stick with the basics at first and that's just going to be a very healthy, low inflammatory diet. So what does that look like? I mean you can check that box a lot of different ways. The best data is in a sort of Mediterranean style diet. So you want to have like a fair amount of, you know, healthy fats, obviously monopolyunsaturated based. You want to limit your saturated fat intake. I know that'll ruffle the feathers of some of the carnivores out there. I love red meat. I'm not a vegan, but you do have to sort of take things in moderation in that regard. So good, healthy diet, lots of cardiovascular exercise and obviously strength training is going to be important there too. Now, as far as offsetting some of this cardiovascular stuff, let's talk about the trigonohypertrophy thing. So a lot of it gets back to just understanding the mechanisms and it's not important that the average person knows the molecular causes for all of this stuff. But I mentioned the first one Again. We want low-hanging fruit blood pressure. But I mentioned the first one Again we want low-hanging fruit blood pressure. Blood pressure control 120 over 80 or less is generally where you want to spend the majority of your time. Now you're going to be outside of that range depending on what you're doing. I've checked when I'm working in the trauma bay and I'm especially working night shifts. My blood pressure is higher than that, but for the majority of the time during the day I'm consistently under 120 over 80. So that's something that guys should shoot for If you can get there without medication. Absolutely, I mean, I think that that's important.
Speaker 1:
1:27:01 Make sure that you don't have sleep apnea. There's so many I can't tell you how many guys have told me there's no, I don't have sleep apnea. There's so many I can't tell you how many guys have told me there's no, I don't have sleep apnea. I don't snore. My wife's never said I've snored. I've sent them for a sleep study and they've got like moderate to severe sleep apnea. So, um, you know, if you're over 200 pounds, I think it's worthwhile to get a sleep study and make sure that that's not in the background. Um, uh, I I've seen like end-stage congestive heart failure solely from sleep apnea, and so that is a thing. So just make sure that that box is checked. You probably are going, especially if you're a bigger guy, when you start getting again above 100 kilos, there's probably going to be medication in the mix, especially if you're going to be pushing doses. So there's a bazillion different blood pressure medicines out there.
Speaker 1:
1:27:51 I'm a fan of ACE inhibitors and angiotensin receptor blockers, as are most people in the TRT world, for obvious reasons. They're very well tolerated. They don't cause an erectile dysfunction like diuretics and beta blockers do. That's one of the worst things a doctor can do is put a 25-year-old male on a beta blocker or like a thiazide diuretic. He'll be compliant with that for about four days and then he's just not going to take it. So ACE inhibitors and ARBs are usually first line. If that doesn't get you there, I will usually add in a calcium channel blocker. So something like amylodipine is well-tolerated in young athletes, also not associated with erectile dysfunction.
Speaker 1:
1:28:37 The thing about ACEs and ARBs I won't go too far down the rabbit hole with the renin-angiotensin system. But one of the things that high levels of amines do is they activate this renin-angiotensin system. But one of the things that high levels of anhydrins do is they activate this renin-angiotensin-aldosterone system. So it's a very complex but elegant system. It involves the liver, the lungs and the kidneys, essentially leads to retaining sodium, and wherever sodium goes, water goes with it. So this is a survival mechanism that's evolved to get you through times when you're going through famine or a drought, you're dehydrated, or if you're hemorrhaging to death because you got bit by a saber-toothed tiger. These are mechanisms to increase blood volume, so that signal is turned on all the time with androgens, and some probably do it more than others. And again it's a dose-related thing. The ACE inhibitors and the ARBs short-circuit that and they bring it back down to an acceptable level in most guys.
Speaker 1:
1:29:38 Angiotensin 2, which is one of the molecules in this pathway, is strongly implicated in atherosclerosis and endothelial dysfunction, which is dysfunction in the, in those you know sliding of your, your blood vessels where atherosclerosis gets started. It's strongly, strongly implicated in LVH, so it can be part of your anti-LVH cocktail is getting on. I prefer angiotensin receptor blockers, but if you're somewhere where you can't get that, you can use an ACE inhibitor. There's anything that ends in pril, like centipril, ramipril, et cetera, and there's other names out there Telmasartan, I mean, everybody loves Telmasartan, I love Telmasartan too. Telmasartan I mean, everybody loves Telmasartan, I love Telmasartan too. That's usually my go-to, but it's generally a class effect. So if you can't get Telmasartan, there's Valasartan and anything that has a sartan on it. Mainly it's a class effect. So those are good drugs. So the other thing to consider too and this is so interesting there are anti-diabetic drugs that now have, just sort of by accident, found to be helpful for cardiac and kidney issues.
Speaker 1:
1:30:55 One of them is these SGLT2 inhibitors, so these are the flozens. So basically they just cause you to urinate out glucose. And I have to admit, when these drugs first came on the market, I wasn't really that impressed with them. I was like, yeah, they'll be helpful, but you're just peeing out blood sugar. What else could they possibly do? And I was completely wrong. They have widespread beneficial effects. They're still figuring out all the effects that it has, but it can affect the transcription of mRNA in the heart. It can be protective against LVH. It does function as somewhat of a mild diuretic, so it helps lower blood pressure as well. It helps protect the kidney from the ravages of hypertension and diabetes, and so they're using them now in people who don't have diabetes for kidney protections. You have chronic kidney disease. These SGLT2 drugs are useful and they're first line now in heart failure, even if you don't have diabetes. So fascinating drugs. We could do a whole podcast on those. But ACE inhibitors, arbs and SGLT2s are like right up there with sort of like frontline.
Speaker 1:
1:32:12 If you're going to be abusing androgens, those are things I think that you should strongly consider. Talk to your doctor about it. Don't go do it on your own, because there are issues with these drugs. Sglt2 inhibitors increase your chances of urinary tract infections in some populations because there's sugar in your urine all the time. They do raise hematocrit a little bit two to four points. So if that's an issue for you, you know, or benefit it could be. A benefit Depends on how you feel about hematocrit. I've talked about that a little bit. But just you know, you just have to kind of be aware of that. So don't just find a professional, find somebody who knows what they're doing, preferably a physician, but there's, honestly, there's a lot of health coaches out there. They're very knowledgeable about this stuff. They know more than physicians do in some cases about it. But that's sort of the baseline.
Speaker 1:
1:33:04 Now, additional things you could consider. Like you know, most beta blockers are not going to be good agents for exercising athletic young men. But there is one in particular that's a bit better tolerated by athletes nabivalol. It is more commonly used in the bodybuilding world, like Vigor. Steve has talked about nabivalol quite a bit. If I'm going to use a beta blocker, I will use that one at a low dose as well.
Speaker 1:
1:33:29 Beta blockers can also be somewhat protective in the treatment of LVH, whether it's from anabolic steroids or not. So beta blockers are a mainstay of treatment of congestive heart failure and so that's why, you know, grandma and grandpa will get put on the Bivolol as well for their LVH and their congestive heart failure. It could also potentially be used by a bodybuilding athlete. That's a little bit further down the line, but that could be considered as well.
Speaker 1:
1:33:58 So that's sort of the initial approach, but really, again, it's the blood pressure thing is really really important. It's chronic exposure to elevated blood pressures that causes the damage, causes the hypertrophy in the majority of people, even the ones that guys who don't abuse androgens, like I said in the emergency room. The guy I mentioned at the beginning, the taxi driver his blood pressure was 250, over like 130 when he came in and I think he probably lived close to that most of the time. So and he wasn't taking anabolic steroids. So there's, you know, blood pressure is super important. That's the low-hanging fruit and then you can start adding in medications as needed, you know, for that.
Speaker 1:
1:34:45 As far as the lipid, we haven't really talked about lipids very much. That's my other area that I really have a lot of interest in as well. But you know, apob is crucially important. It's one of the, if not the fundamental cause of atherosclerotic disease. So testosterone tends to be somewhat neutral in terms of ApoB, again, it's a dose response thing.
Speaker 1:
1:35:10 But the synthetics like some of the worst ApoB or LDL levels I've ever seen are with Tremblone. I've seen guys that normally had LDLs of like 130 shoot up to like 350, 400 when they take Tren. And you know you can argue that, oh, if you only do that for six weeks or so, that's probably not a problem and that's probably true. However, it's not like it immediately goes down. But if you're repeatedly using Tren and you're exposed to these high LDL levels, it's a problem. So you need to at least keep tabs on your lipids.
Speaker 1:
1:35:45 I know that's an area that there's some controversy in for some people, but it's super important. And then you got to make sure it gets screened for LP little a. That's going to be my public service announcement. 20% of you have high LP little a levels. That's going to be my public service announcement. 20% of you have high LP little a levels. And if you do, you have to get very aggressive with your APOB lowering, much more so than if you didn't have LP little a, because, as it stands right now, we don't have a good pharmacological agents, uh, to treat LP little a um, we could save it for later, but, uh, I treat it with hormones. We could save it for later, but I treat it with hormones personally. But in the general cardiology world we don't have any good drugs for L-pilate currently there's so much for me to unpack there, but let's double-click on that.
Speaker 2:
1:36:32 That was going to be one of my questions, because I heard it on a round table with More Plates, more Dates. I think it was vigorous, steve, and also you know, rest in peace now. This guy I forgot his name, but he was referring to some data that anabolic steroids could reduce LPA yes, yes, yes.
Speaker 1:
1:36:53 So interesting, right. So yeah, lp little a, it doesn't. It doesn't follow the script when it comes to, like the other lipids. So nandrolone we have studies with nandrolone. It will cut Lp-lil-A 20, maybe 30%, depending on which study you look at. Pretty much all androgens will have a lowering effect on Lp-lil-A. The problem with the synthetics, of course, is that, like, that's offset by an increase in all the other APOB containing particles, ldl, et cetera. So there's a bit of an offset there, but it is interesting. Yeah, the LP little a is is is lowered by there's.
Speaker 1:
1:37:34 There's three hormones that can that can impact it. Androgens in general will bring it down, including testosterone, estradiol very effective. So, side note, I take estradiol. That's how I manage my LPLA. I take a milligram of oral estradiol every day. Okay, and you know what? I haven't grown breasts and I don't watch. You know I'm not watching the Lifetime channel and crying when the kitty cats come on the TV and stuff. I feel fine. But you can lower LpA and again another 20%, maybe 30% with estradiol and then thyroid hormone will lower LpA as well to some extent. So thyroid hormone can be beneficial for all of your lipids.
Speaker 1:
1:38:17 If you have a dysfunctional thyroid, it can be very difficult to get your lipids in line. I learned that many, many years ago as a resident. I had a patient that was subclinical hypothyroidism and high-dose statins, high doses of niacin, and I couldn't really make an impact on his lipids. And then I had a smart attendant say, hey, knucklehead, why don't you fix his thyroid? And lo and behold, everything fell in line and I could take him off a lot of his lipid drugs. So as it stands right now, hormones are probably the best way to treat LP little a. There's a few other little things like low dose aspirin might impact it a little bit as well, but it's tough to like.
Speaker 1:
1:39:02 We can make. We're at the point now with drugs that we can make the LDL or the ApoB, whatever you want it to be. I could, we could give you a single. If you want single digit ApoB. We could do single digit ApoB with enough medications. But we can't do that. We're not there yet with lipoprotein A, but we can make a dent in it. You know, I brought my trying to remember my numbers. Uh, I generally run about 150 to 170 nanomoles per liter. I brought it down to about 90. So oh, wow is yeah. Upper limit is 70 ish, so nanomoles per liter. So that's with testosterone and estradiol. Yeah, that's a lot, all right. I mean, for me it's a lot. It's I. The question is well, is that enough? Is it enough to make a difference down the road? I don't know. I hope so. I also have an ldl of 25 because I'm on medication, so, um, but yeah, that's that's how I approach it for everyone this is a great question because, again, free consult, stuff, right, I am going to turn 35 next year.
Speaker 2:
1:40:06 Now my APOB, whether I'm dieting or not, it's at the high end of normal. Most cardiologists will let you, you're fine on, you go, but then we all watch Peter Addy. He's not happy with it and I have to admit, all of this stuff makes sense. So I would like a 25 apob. What would you? What would you tell me if? If I said hey, I don't, I don't want a heart disease or progressive ac cvd too early, do do I need to take medication? If this is my goal, well, let's put it this.
Speaker 1:
1:40:39 It this way. I mean, if you want an ApoB or an LDL of 25 from where you're starting, you probably do need medication. And Atiyah talks about this. And the other guy who's really good out there is Tom Dayspring. He's getting up in years now but he's a lipidologist. He's really good at explaining this. So if you want to Google Tom Dayspring listeners out there, if you want to take some of, get some really good information on lipids, he'll. He'll take you to school on it, yeah. So the question is you know, ultimately, I think that the question you're asking is at what level will your're like right? What level if we lower your APOB, will you no longer build atherosclerotic plaque Like we'll be mine Zero?
Speaker 2:
1:41:27 by the way, right now, what's up? My CAC, my CAC score right now, as of last year, zero, okay, good.
Speaker 1:
1:41:34 As it should be. But here's the result, not to diverge too much, be very careful with that though. Um, the the only problem with calc scores and especially the young guy like yourself is that you can get false rear shots. So coronary calcium scans detect calcified plaque only, not soft plaque. So calcified plaque is late stage plaque. So and here's the thing it's not the old, like calcified plaque that is as prone to rupture. That's not what kills you, although obviously it can. It's the soft, non-calcified, inflamed plaque that's like a 40% like. It's almost better to have a 70% lesion that blocks 70% but is hard and calcified. It has a very thick fibrous cap. It's almost better to have that than to have a 40% non-calcified, highly inflamed, rapidly growing atherosclerotic plaque. That's the one with a very thin fibrous cap that's likely to rupture. That's what kills people, or more likely to kill people is these smaller and those don't show up at all on a, on a C, on a corner excuse me on a calcium scan. So I need to die.
Speaker 2:
1:42:55 Do I need to?
Speaker 1:
1:42:56 you would need it, you would need the, you would need an angiogram. There's even issues with those. There's even issues. You can still miss it, because plaque doesn't always grow into the artery lumen. It actually can grow, something called positive remodeling.
Speaker 1:
1:43:11 I know we're going down a different tangent here, but the plaque that builds up in the wall of the artery you would think that it would always. You know, if this is the lumen, that it always grows inward. Well, it doesn't, especially early on as it expands. You know the artery whether it's doing this consciously or not is, you know, debatable, but it will balloon. It wants to maintain the patency of this vessel, right? So it will balloon outward. So the plaque will sort of grow away from the lumen. So you'll have a very thick plaque here, but the diameter of the lumen remains intact and that's where the dye goes. So when you look at the CT, you're like oh, I've got this nice, wide, open vessel, no stenosis, no plaque.
Speaker 1:
1:43:59 Probably, but not necessarily, you actually could have a significant amount of plaque within the wall that's growing outward here and then it reaches a critical stage and then it will grow inward and compromise the women. So if you need a visual, this is a visual thing. So if people are listening to this. You can just type in, like our artery positive remodeling, and you'll get some diagrams and shows what it looks like. So, uh, a cta is, yeah, vastly superior to a coronary calcium scan.
Speaker 1:
1:44:31 But you can, in these admittedly less likely, in somewhat rare conditions, you can can still miss plaque. So the best way is with coronary catheter, where they put in the wire into the heart and it has a little ultrasound probe on it intravascular ultrasound, so it's angiogram, with IVUS, they call it, and there's a couple other ways too, but most places don't do that. So so it's great that you have a zero score. I had a zero score at age 40. I had a score of 16 at age 50, so it's not like I still had plaque at 40. It just didn't get picked up, um, because my score just wasn't calcified yet.
Speaker 1:
1:45:16 So so, anyway, amazing want to throw that out there, man, Because again guys, they'll run around with an LDL of 180 and be like, hey, man, I got zero calcium, I'm good. Like no, no, you're not good.
Speaker 2:
1:45:29 You're not good. Okay, we are going to stay on topic here your wheelhouse, if you will. Ascvd Again, the whole weasel word thing. The reason I bring that up is because a lot of my friends or a lot of people in the community and I understand there is controversy as to what number is best. But if we all can agree that lower is better and we can all agree that there almost is no other way to get there other than medication, sadly, is it fair to say that these drugs if heart disease is the number one killer are making us live longer Good?
Speaker 1:
1:46:09 question. Good question. I mean, we're all going to die of something. Of course you know my concern, honestly, in the I was talking about this in a different podcast last night actually but my concern is that we're going to get a handle on heart disease in terms of, you know, slowing progression and that sort of thing, but we're seeing an uptick in cancer deaths as a result of probably multifactorial, but you know, processed chemical exposure and endocrine disrupting issues and perhaps vaccines. I don't know if we can say that here or not, so I don't know if we will extend the lifespan per se, but we may skew. I mean, at the very least I think we can take cardiovascular disease off the peak at.
Speaker 1:
1:47:03 You know, it is the number one cause of death worldwide. I think we have the potential to knock that down a few notches, but it's going to get replaced by something else, of course, which is probably going to be cancer. So so I don't know that, population wise, we will see. I could be completely wrong, but we will see a major increase in the human lifespan. But we will maybe be changing the things that he has said and I can't quite decide some days I'm on board with this and some days, I'm not. He said it's possible to completely eradicate Athens sclerosis from the population, and what he means by that is basically aggressive ApoB lowering from very early in life, however early. I've never heard him actually say. I'm presuming he's talking about teens and early 20s. So whether that's feasible or not is a whole other question.
Speaker 2:
1:48:07 He actually did say.
Speaker 1:
1:48:12 He did.
Speaker 2:
1:48:16 Well, I think I lost you there for a second. Yeah, sorry. Again, it's our connection connection, but I'll do my best here so I don't yeah sorry um, yeah, he actually said as early, as from the moment you could walk right, right.
Speaker 1:
1:48:30 So you know there's practical implications to that. Whether we could actually ever institute anything like that on a global scale is probably up for debate. You know whether we could do that, but you for debate. You know whether we could do that, but you know there's a lot of things we could do as individuals. So you were asking me before you know, like, what should your ApoB be, so to speak, or what level should you personally shoot for in order to no longer develop or not to develop any more atherosclerotic disease, no longer develop or not to develop any more atherosclerotic disease? And I say that, I say that very specifically because you and I, we both have.
Speaker 1:
1:49:05 You have atherosclerosis, you just it's subclinical, it's everybody has it to some extent. This is like ubiquitous. The question is, you know, what do we need to do to not let you get any more over the next five decades? And you know that I think takes a comprehensive approach. That you know. Again, I said this earlier. But atherosclerosis is complicated. It is a disorder of lipids. Clearly, and I think Peter Atiyah and Tom Deschpring are probably correct that, yeah, if you just can crush ApoB and you get an ApoB level like well under 50, you know, if we're talking like you, get down in the 40s or 30s. Some people are getting them even lower than that. That, yeah, you could probably halt the progression of atherosclerosis. I think that's a reasonable thing to do.
Speaker 1:
1:50:02 This is just my personal bias, but atherosclerosis is also an inflammatory disease. It's also a metabolic disease. So that doesn't mean that we ignore insulin sensitivity. It doesn't mean that we ignore free radicals. It doesn't mean that we ignore blood pressure. We ignore chronic inflammation. So the way that I think about it is that if you're in a disease, if you're an unhealthy, chronically inflamed individual, in order to stop the progression of atherosclerosis, you will probably require a very low ApoB level because you have unhealthy vessels to begin with. So you have blood vessels that are fertile ground for ApoB to come and to build atherosclerotic plaque. Ideally, what you want is blood vessels that are not fertile ground for ApoB to become stuck and then to initiate that entire cascade. So the way that I approach atherosclerosis, obviously I do lower LDL, slash ApoB levels significantly.
Speaker 1:
1:51:09 But the other side of that coin is endothelial health and managing chronic inflammation. You know managing chronic inflammation. So that involves, you know, a healthy diet, a healthy lifestyle, supplementing with, you know various micronutrients. It involves managing blood pressure, and when you do that then maybe we don't have to lower your ApoB to 30 to stop atherosclerosis. Maybe 60 would be sufficient for you to no longer develop plaque because you've got a healthy vessel. I don't know if I'm explaining that well enough, but if you have a super sticky, diseased vessel, any amount of ApoB is going to want to stick to that, and so naturally you're going to have to bring that level way, way down, which means more drugs. If you've got a very healthy endothelium, you're doing all the things from your lifestyle standpoint, and maybe also with some medications in terms of controlling inflammation and glucose and insulin and all those sorts of things that the carnivore guys talk about there's kernels of truth to what they talk about then maybe you don't have to lower ApoB quite as aggressively.
Speaker 1:
1:52:23 I do think you still need to lower it significantly because you're never going to have zero inflammation, nor would you want to. I mean, we're always in a balance between pro-inflammatory processes and anti-inflammatory processes. So yeah, if you had zero inflammation, maybe you would have zero plaque, but you'd also die. You're going to have some degree of inflammation. It's just part of human life being an air-breathing organism on earth. So it's not practical that you, but what you want to limit is excess inflammation, you, but what you want to limit is excess inflammation, excess, you don't. You want to limit issues with insulin resistance, et cetera. You want to lower visceral body fat so that you're not spewing out these toxic adipokines which are, you know, deleterious hormones secreted by visceral body fat. You want to lower angiotensin too, as I mentioned earlier, which again promotes atherosclerosis, promotes inflammation.
Speaker 1:
1:53:22 So there's two sides to that equation. There's maintaining the health and integrity of the vessel and then lowering ApoB, and you've got to do both, in my opinion. So when you tell me or you ask me, what should my ApoB level be, to be honest I say I don't know. I don't know what it should be, but it should probably be lower than what it is currently. I think you know. So if you're upper lip, what are you? Probably 90? Are you like 90, 100, something like that, 100.
Speaker 2:
1:53:50 100.
Speaker 1:
1:53:51 Yeah, yeah, so I think in general most people, even if you're metabolically healthy you're probably better off being closer to 60.
Speaker 1:
1:54:02 Why not bring it to zero? Well, it's a good question. It's theoretically possible to do that, and believe it or not? I mean, there are studies where they have brought A, b and LDL levels to like single, low, single digits and maintain them for five, six, seven years. There does not appear to be any deleterious effect. You know, the brain makes its own cholesterol, the tissues themselves make their own cholesterol for local use. So what we're really doing is lowering serum levels and we're not lowering levels in other tissues to the same extent, and so there doesn't appear to be any deleterious effect. But the question is like do you need to? You know, because again, lowest effective dose, you're going to require a larger dose of whatever cocktail of drugs it takes to get to zero, and then you know you're going to be subject to potential side effects.
Speaker 2:
1:54:56 So that's the only reason I haven't done it yeah, if you can get away with.
Speaker 1:
1:55:01 You know, let's say rosuvastatin, uh, which is a Crestor, which is what is one of the high potency statins. You know, if you can get away with using 10 milligrams, you'd rather do that than use 40, because your chances of getting you know the muscle aches, the myopathies and you know other potential side effects is it's a dose related thing, so I want to be on the lowest effective dose. I take 10 milligrams of rosuvastatin, I take 10 milligrams of azetamide rosetia, so, um, and that does it for me. How about go ahead?
Speaker 2:
1:55:35 if I fly over there to the uae and I look the risk of. The statin side effects are already giving me no SIBO. How about we start me on a PCSK9 and and or Zetamibe?
Speaker 1:
1:55:48 or Bepidocacid. So it's just a cost. You could do it. It's a cost issue. Those, those drugs are not inexpensive. So yeah, you totally. I mean the data is there for those. They're definitely. It's definitely there for the pcs k9s, um. They do lower lp la, by the way too, not a lot like 15, 20, so um that seems that, yeah, that's an option.
Speaker 1:
1:56:13 That's an option you could could do. That it's um, you know they, just until they get we get generic versions of those medications yeah, they're going to be very, very pricey so, but worth it?
Speaker 2:
1:56:26 right? It seems to be, and correct me if I'm wrong. You can control almost everything with lifestyle that we have discussed, or peter adia has discussed, except this one. You can get it.
Speaker 1:
1:56:40 So there's yeah, I mean, that's precisely right. You can get a handle on it and you can. You can, you can improve it within the limits of your genetics. You know, there there's a we haven't really talked about this, but you know there's genetic differences in how much ap you know your liver makes versus my liver, versus somebody else. And there are people who are naturally quite low and they get less. They do get less. They're less prone to cardiovascular disease. And there are people like the extreme example is the FH people, where it's three roof and they they died prematurely. So, yeah, so all of the keto and all of the whatever diet you want to choose in the world is not going to fix familial hyperlipidemics. Ldl Might improve a little bit, but yeah, they need drugs. So to get to the levels that we're talking about, I probably think probably 90% plus of the population will require at least a low dose of at least one drug, and probably two.
Speaker 2:
1:57:47 That sucks, man. I hate taking that. Yeah, it does suck. I don't like it either.
Speaker 1:
1:57:51 I'm an MD, obviously, so people occasionally accuse me of being a pill pusher, and I'm I'm like the last I'm, that's like the last thing I am. But I'm also a realist, um, and I live in the real world and I see the outcome of letting these things go and not doing anything about it, um, and that's, that's worse than taking the drugs in most cases. So I'm not a pill pusher, I don't. I don't get any kickbacks from big pharma. I'm still waiting for my paycheck, you know, for all the statins that I've written over the last 25 years, and it hasn't come yet. So I'm not a huge advocate.
Speaker 1:
1:58:31 Lifestyle we gloss over it, but it's the cornerstone of any longevity program is lifestyle. I think I'll just say it's the cornerstone of any longevity program is lifestyle. I think I'll just. I'll just say it for the record. I mean, we're talking about drugs and hormones, but it's lifestyle, lifestyle, lifestyle, um, that's that's what really matters, and all the rest of this is sort of ancillary and extra there's so much to it that I guess I've been with my head in the books for 20 odd years learning about sleep apnea, mass, elevating the bed.
Speaker 2:
1:59:03 But for most bodybuilders, most athletes, they don't have the time or interest for this stuff. They really just need to see a physician like you to sort it.
Speaker 1:
1:59:11 Honestly, they do. Yeah, they just need some good advice and they just need um, you know, it's not. It's not important that you as an individual, the average person, your average bodybuilder, like it's not important that you understand the physiology of atherosclerosis I mean, it's this is just. You know specific stuff unique to my profession and other doctors and stuff, but you know you don't have to know the how, but you should understand the why. You know you don't have to know the how, but you should understand the why, meaning like why is it important for me to care about this stuff? You don't need to know the how, the how. You can look it up or you can look on Google, but I think it's important for an average person to have some understanding of like. Okay, this is why I'm doing this. This is what I'm trying to avoid, this is what I'm trying to achieve. Is what I'm trying to achieve so kind of more qualitative understanding of, of just longevity?
Speaker 2:
2:00:03 okay, just uh. Going back to acvd, why do anabolic steroids, and particularly the derivatives of testosterone, why do they raise apob and ldl so much and then lower hdl? Why do they do that? Good, good question.
Speaker 1:
2:00:20 Yeah, the testosterone does this too, but again to a lesser extent. You know, again we'll get back to the synthetics. These are unnatural substances that your body is not accustomed to dealing with, and it's not accustomed to dealing with the downstream metabolites either, so the effects can be somewhat unpredictable. But there's an enzyme in the liver that gets activated, that essentially drives down HDL and raises LDL. If I remember correctly, it's a hepatic triglyceride lipase enzyme and it shuttles, like vldl and ildl, towards making more ldl. That's the the what, the geeky mechanism there there are. There are probably other ones as well, but that's just off the top of my head, what I'm remembering. So so that's what you'll see with the synthetics. So we use trump tremble out as like the obvious example, because that's like by far the worst offender. So you see, ldl, apop slash. When I say ldl, I think for the listeners, just keep.
Speaker 1:
2:01:30 I'm also that's sort of part and parcel with apob. Most of your apob particles are contained within the LDL, but also ILDL and VLDL and lipoprotein A, but LDL tends to run with ApoB in most cases. So I'm going to just use those interchangeably. But what you'll see with TREN and some of these other drugs is yeah, as you will see a big increase in LDL and then variable amounts of HDL suppression as well. Trigosurides tend to be neutral or actually drop a little bit in some cases. Again, it's all dose-related. The other thing I guess too we should probably mention is the oral steroids. There's obviously much worse effects on the lipids in general than the intramuscular, you know, than injectable steroids.
Speaker 2:
2:02:25 How is it going with your media campaign? If you will? What was the intention behind getting online and speaking about this stuff?
Speaker 1:
2:02:34 Oh yeah, that's a good question. It's something that I've been, I was kicking around for at least a couple of years. You know, I'm naturally I'm a very introverted guy. I like my privacy. I have no desire to be a public figure of any kind. But I also, you know, saw the writing on the wall in terms of my career that I do need to eventually, especially as I get older, now that my career that I do, I do need to eventually, especially as I get older, now that I've got young kids, I'm going to be transitioning out of the crazy, you know, emergency medicine world more into men's health and hormones. And you know, over the years, as I've gotten into that particular field, I mean I just truly enjoy it.
Speaker 1:
2:03:15 I really I, I I've said this on other shows but I, I and it sounds crazy to people who don't really understand emergency medicine, but there's definitely days where I don't feel like I really help anybody at the hospital. What I do is is pull people back from the edge and and really like put a bandaid on their bad decisions, to speak, that have led them there. Um, not always, I mean it's it's actually quite a bit different here, but in the us there was. I was just dealing witha lot of like self-inflicted chronic problems and not really feeling like I was able to help people to the same extent where in my men's health practice, um, you know, I can honestly say that I've been able to like radically change the trajectory of certain men's lives, helping them lose, you know, 50 kilos, you know that sort of thing and like, given I've saved multiple marriages, you know, in my men's health practice you know I can't say that about my emergency medicine practice so I started the channel one to help promote the practice.
Speaker 1:
2:04:25 But also I kind of felt that there was there's just not a lot of evidence-based sort of more mainstream doctors that are talking about this sort of stuff. There there was a, there was always been a few, but there was a lot of fringe, you know, for lack of a better term like just wackos out there just just saying things that are not based on good scientific evidence and they're just like not medically sound in my opinion. Um, so I just kind of wanted to be a voice of, you know, somebody who I have one foot in the mainstream medical world. I'm a nerd, you know, I'm a proud nerd and I like evidence, but I also care about people. I want to improve their health and I want to, you know, make this sort of information accessible to the general public. So I wanted to make a platform where I talk about the research studies. This is why things are the way they are. This is what you can do to fix them, without the agenda of like selling anything you notice, like I don't plug products products there will never be an Athletic Greens spot on my show or anything along those lines. I just want to give people good, solid information that they can use and that they can use to improve their own lives.
Speaker 1:
2:05:54 My little tagline in my videos is to help men escape the collapsing US healthcare system, which you know. The healthcare system in the US and in many other parts of the world it is collapsing and so you know your personal health is your responsibility. So I've always said to my patients it's not my job to make you healthy, it's your job to make you healthy. I'm here to help you. I'm here to give you good advice and give you good information and obviously I can prescribe medications if need be.
Speaker 1:
2:06:24 But I really want guys to take personal accountability and ownership for their health because the way the healthcare system is going, as we talked about offline before we started filming here. You know the government and you know big pharma and the medical industrial complex in general doesn't always have your best long-term interests at heart. They have their own interests which may or may not overlap with yours. So it's important that everybody has some degree of buy-in and some degree of personal responsibility for their health care. So in order to make good decisions, you need good information. So my goal with the channel is just to put out good information so that people can make better decisions and really, ultimately, that's it but it was.
Speaker 2:
2:07:17 It took me a long time to get the guts to get in front of a camera man, you're gonna blow up one big guest appearance on joe rogan or something like that, because you have the, the maturity, the formal education and you know you're walking the talk, you know you're jack. That it is important, like it's important if you're if you're a physician talking about men's health, to be the sort of man that most men will want to look like.
Speaker 1:
2:07:45 You know it's important, yeah yeah, I, I feel sorry for anyone that wants to look like this, but, um, you know it is what it is, but you know, all joking aside, I mean I, yeah, I do. I I'm not going to give advice that I don't take myself um, um or that is um is not something that I'd be willing to consider for myself either. I, um, I, you know, I do my best. I'm not perfect, I, and I don't expect any. You know, nobody's perfect.
Speaker 1:
2:08:11 I, I try to do the right thing, uh, in terms of my body, 85% of the time, and that's enough, and that's enough. So that's what I want guys to do. And just because I do a certain thing, like I take oral estradiol, that doesn't mean that you should take oral estradiol. I take that from the lipoprotein A. If you don't have lipoprotein A probably don't need to be taking oral estradiol. So I want to be careful about people mimicking what I do. Um, because that's unique to me, but I do in general. I mean I do, I try to eat healthy. I'm not perfect, but I, I do, I do my, I try to walk the walk, talk the talk. So to speak.
Speaker 2:
2:08:50 Yeah, I look forward to you being on bigger podcasts because you're definitely one of these what I call fingerprint medicine doctors. Have you heard of this term before? I haven't. No, so fingerprint meaning individual medicine, right?
Speaker 1:
2:09:03 individual, yeah, yeah, yeah that's how it should be. Yeah, yeah, yeah, that's one of my big beefs with with the trt world is that, um, you know, at least in the us, these sort of big box I call them clown clinics, but that's probably not nice windmill clinics where, yeah, people just get put on sort of these standard protocols. There's no individualized care. That's why I keep my medical practice is tidy and I keep it tidy on purpose, because I want to develop a good relationship with the guys that are with me and all of them are different, all of them have different needs, so none of them are on the same sort of protocol and you need somebody that can sit down.
Speaker 1:
2:09:43 It's one of the reasons I got out of general primary care is, you know, it doesn't matter how good of a doctor you are and I can't help somebody in 15 minutes or 20 minutes, 20 minutes with an office visit to untangle grandma's kidney disease, diabetes, heart failure and chronic you know arthritis pain. You know, in 15 minutes this is impossible. So, like my guys, you know, my new intakes are usually two hours. So I and that's the kind of medicine I want to practice. So when I, when I finally hang up my stethoscope in the emergency department, then that's, I will be 100% into that. I'll be switching gears into that field. I still I still have the adrenaline bug. I still like the ER a little bit. I like a little too much. So but eventually, you know that's a young man's sport.
Speaker 2:
2:10:36 So I'll be, I'll be moving on you know that's a young man's sport, so I'll be, I'll be moving on, sure. And what are you thinking? Sort of how peter adia started, like fewer clients, high net worth individuals who are motivated.
Speaker 1:
2:10:48 You know easier to deal with that type of thing yeah, yeah, I think so and, and not necessarily, I don't really care what your net worth is, but what I insist upon is that you are motivated and, um, you know, I'm not going to waste my client's time, but I also don't want them to waste my time, like I want you to be on board and follow the protocol. I'm not a dictator, I'm not going to say you know, it's my way, or the highway, but I want guys that are ready to put in work, because, because I put in the work for you as a patient, so you better put in the work for me, and not for me, but truly for yourself. So I, um, yeah, I want guys who really are motivated and, um, again, it's not the high net worth, so to speak, I don't charge very much, I, I don't think, but it's uh, I.
Speaker 2:
2:11:33 I want guys who are in this for the right reason sure, the diagnostics, though, that you may want to see in a client can be expensive though. Yeah, like they can be 10, 20k plus.
Speaker 1:
2:11:46 Yeah, I mean, it depends on how, yeah, how deep a dive we need to take. But you know, lab work is not terribly expensive. But you know, and I I get it, I mean people there, people, you know, and and I I get it, I mean people there are, people have financial constraints and stuff, and so I keep my margins pretty low, but you know.
Speaker 2:
2:12:07 I tell guys listen, I understand.
Speaker 1:
2:12:09 you know some of this stuff can be expensive, but I think it was Rob Kamenorek said. I said this I'm probably going to butcher his quote, but you know it's you can spend money being sick or you can spend money being healthy. You're going to spend money either way, so you just decide what you're going to spend your money on. So that's, that's how I look at it. I, I, I spend. You know, I purchase all of my own healthcare. At least I did in the United States. I have the VA, so the Veterans Administration, so nothing against the VA, but I took care of myself, I did my own primary care. I paid for all my medications out of pocket, all my own labs, that sort of thing, because um, that sort of thing.
Speaker 2:
2:13:05 Um, because I had to, it's just the way it is so. But that's money well spent in my opinion, absolutely, yeah, I guess I've set aside the certain budget that I'm going to need for these sk9s, or yeah, it's. It can be thousands per year. A lot.
Speaker 1:
2:13:18 Those are expensive drugs. Those are expensive drugs. They're going to come down eventually, but right now, yeah, you're going to be spending thousands of dollars on those, so sure sorry where we cut off before.
Speaker 2:
2:13:32 I think that we'll pick up on that next time, because that is something I don't want to just brief over. Today was a really good overview on the many ways in which anabolic steroids and testosterone can impact the heart, both positively and negatively. But I guess the conclusion is here and you correct me if I'm wrong the larger the individuals they tend to take take more. More drugs means more problems. Lifestyle is understated in terms of how much risk prevention you could do there if you will, and it seems like a lot of bodybuilders just are lazy. I have to admit I know off the top of my head 100 of them, 100 acquaintances. Not all of them do their cardio, and when they do, it's like I don't include steps, it's cardio, but you know what I mean. So it seems to be understated. And then another one what you're mentioning here for people on the flip side, you've got the lifestyle, only guys. They may also not be correct in terms of prescribing a sufficient protocol in order to not die prematurely. We may need medications too, absolutely, yeah.
Speaker 1:
2:14:56 Again, I'm not traditionally trained MD, but I'm just interested in what works and I want all the options on the table for me when I'm seeing a patient. That includes hormones, that includes traditional medications, it includes supplements and it includes lifestyle things. So I have no agenda, no bias. I just want what works and I want what's best for you as an individual. If some of that includes prescription drugs, so be it man, it's a fantastic answer.
Speaker 2:
2:15:32 Thank you for coming on, man. It was a pleasure, man, thanks for having me. It was everything I thought it would be and more. I learned so much I'll tell you. I'll tell you the thing that surprised me the most, the thing that I always learn something from a podcast that just completely changes the trajectory of my life, and in this podcast it was that scan the CTA with a dye doesn't detect all the soft plaque. I never knew that.
Speaker 1:
2:15:54 Yeah, yeah, if you want, I'll send you some information on that. You can share it with people. Again, I'm not telling guys to not get that test, but under four, especially under 40, you know it takes time to calcify that plaque. So it's it's expected if you're your age to have a score zero. But it just doesn't mean anything, it's not, it's not as helpful as if you have a score at 70 or 60. Ah, okay, now I'm impressed, but you, it doesn't get like. It doesn't get you anything. You still got to do with all the all the stuff we talked about sure fascinating.
Speaker 2:
2:16:30 Yeah, thank you, man. Uh, when it's ready for publishing, I will give you the.
Speaker 1:
2:16:36 You can preview it first and then I'll publish it oh sure, yeah, I'd love to yeah, okay, man, and I'd be happy to happy to do a part two with you anytime, anytime, please. I think I think you're gonna blow up honestly. Um, you know, you said that about me. I from very early on. I started watching your, your channel. I just came through on my feed and super impressed. Your interview style is really good and the guests you get are really good as well. So keep it up, thank you, thank you.
