Mark Bell's Power Project - Doctor Said He Was Healthy. Then He Found a 40% Heart Blockage | Joel Jamieson

Episode Date: October 21, 2026

You can be fit, eat healthy, have good bloodwork, and still have serious heart disease.In this episode, I'm joined by Joel Jamieson, creator of Morpheus, to discuss something we both have firsthand experience with: cardiovascular disease. Despite years of training and taking care of his health, Joel discovered significant plaque buildup and a blockage of more than 40% in his widowmaker artery after his cardiologist repeatedly reassured him that his numbers looked good.We break down why exercise alone may not prevent plaque buildup, the role of genetics, ApoB, LDL cholesterol, and inflammation, and why traditional bloodwork doesn't always tell the complete story.We also get into coronary calcium scores, CT angiograms, statins, Repatha, bempedoic acid, nattokinase, and other approaches to managing cardiovascular risk. Joel explains how he's using HRV, VO2 max training, and recovery to improve his health while managing heart disease.This is an important conversation for anyone who assumes being strong, lean, or physically fit means their heart is healthy.Find Joel Jamieson:https://trainwithmorpheus.comInstagram: @coachjoeljamiesonThis conversation is for educational purposes and is not individualized medical advice.Chapters0:00 The shock of a heart disease diagnosis3:15 Why standard blood work can be misleading7:40 The importance of CT angiograms for athletes12:20 Genetics and the baseline for plaque formation16:50 Study results on plaque in healthy populations21:15 Can exercise actually prevent heart disease26:30 The role of ApoB and LDL in cardiovascular health31:10 How endurance training affects calcified plaque36:45 Longevity and the ideal frequency for lifting weights41:30 The impact of performance enhancing drugs on the heart46:15 Essential blood markers to test for heart health51:40 Using DEXA scans and MRIs for visceral fat56:20 Supplements vs medications for lowering risk1:01:05 Understanding HRV and the Morpheus system1:06:40 Structuring Zone 2 and VO2 max training1:11:35 Conclusion and where to find JoelSpecial perks for our listeners below!🥩 HIGH QUALITY PROTEIN! 🍖 ➢ https://goodlifeproteins.com/ Code POWER to save 20% off site wide, or code POWERPROJECT to save an additional 5% off your Build a Box Subscription!🩸 Get your BLOODWORK/TRT/PEPTIDES! 🩸 ➢ https://marekhealth.com and use code "POWERPROJECT" for 10% off Self-Service Labs and Guided Optimization®.🧠 Methylene Blue: Better Focus, Sleep and Mood 🧠 Use Code POWER10 for 10% off!➢https://troscriptions.com?utm_source=affiliate&ut-m_medium=podcast&ut-m_campaign=MarkBel-I_podcastBest 5 Finger Barefoot Shoes! 👟 ➢ https://Peluva.com/PowerProject Code POWERPROJECT15 to save 15% off Peluva Shoes!Self Explanatory 🍆 ➢ Enlarging Pumps (This really works): https://bit.ly/powerproject1Pumps explained: https://youtu.be/qPG9JXjlhpM?si=JZN09-FakTjoJuaW🚨 The Best Red Light Therapy Devices and Blue Blocking Glasses On The Market! 😎➢https://emr-tek.com/Use code: POWERPROJECT to save 20% off your order!👟 BEST LOOKING AND FUNCTIONING BAREFOOT SHOES 🦶➢https://vivobarefoot.com/powerproject🥶 The Best Cold Plunge Money Can Buy 🥶 ➢ https://thecoldplunge.com/ Code POWERPROJECT to save $150!!

talked to the cardiologist, and he looked at my blood work. He's like, all your numbers look good. You're obviously taking care of yourself. You're doing a great job, keep it up. I went and got the test done, and then honestly, I was expecting them to come back and tell me, oh, yeah, you're great, you're clean. You know, I had a 40 plus percent blockage to wintermaker, very high calcium score, lots of plaque, and it was just a shock.

It's great that we're both here with heart disease, and that's what we're here to talk about. The radiologist that's done my CT angiogram, she's like, we have people who come in here that run marathons and have blockages all the time. She's like, this is not uncommon thing. What we know is exercise itself does not stop plaque from forming. You can't get rid of the disease. You can make it more stable.

You can make your risk lower. But cheers and welcome to the show. And it's great that we're both here with heart disease. And that's what we're here to talk about. That part's not great. Talking about it helping other people not have it as great. Right. So let's talk about it a little bit because for me, I haven't had any real noticeable symptoms.

I haven't had like pain or anything like that. But what has your experience been like? And how did you learn that you have any sort of heart issue? Yeah, I mean, I think that's a problem with most people with cardiovascular disease. They don't know they have it until they have a heart attack or something serious, right? And so in my late mid-30s, I had gone to a cardiologist because he was treating my mom for her cardiovascular disease. My dad had had had cardiovascular disease and died from a heart attack. My grandpa on both sides had died from a heart attack.

So I was really aware that this was in my family. And I really believed that doing all the right things from a lifestyle and training standpoint, were going to be enough. And that was reinforced, actually, because I talked to the cardiologist, and I said, hey, what do I need to be doing? What advice you have for me? I really want to make sure I'm doing everything possible to prevent this. And this is actually more like mid-30s now, I think about it.

And he looked at my blood work. He's like, all your numbers look good. You're obviously taking care of yourself. You're doing a great job. Keep it up. You know, come back and see me when you're in your early 40s or 40. And we'll just do so we can do some more tests. But it was really reassuring, to be honest with you.

Because I'd measured my blood work for a long time. And all my know. You've also always been fit. I've always been fit. I don't drink. Athletics and sports and different things. Exactly. And so on my family's side, both my grandpa's drank heavily. My dad didn't really drink. That was one, he was kind of an outlier. But I kind of in my head was like, well, my family that's had it has also had poor lifestyle choices. And so maybe that's the cause and think that makes sense. So anyway, I go back. I couldn't go back when I hit 40 because that was COVID and preventative cardiology was not on the top of the radar at that point. So I went back a couple years later and went to the same cardiologist, again, who had treated my mom.

And at that point, my brother, who was also, he was about in late 40s, he had had two stents put in already. He also had not the best lifestyle choices, but not tremendously terrible. And so anyway, I go back to cardiologist. I said, hey, I'm coming back here, you know, five years after you told me to or when you told me to and I want to get more thorough testing done. So he does a stress test. He does basic stuff. Again, looks at my blood markers. He's like, you're doing all the right things.

I'm not worried about you at all. You know, keep it up and I'm confident that you're on the right path and, you know, like, nothing to worry about. And so my mind, again, it's very reassuring to her cardiologists tell you like, oh, you're doing everything great. And at the time, I dug a bit more into the research and I'd come across the CT angiogram as probably a much better way to truly know whether or not you had plaque because all they're doing is using risk factors to determine this, right? They're saying, oh, your cholesterol is this, your triglycerase are this, you know, and they are basing their decisions on risk factors alone without actually knowing whether you have a disease. So I said, well, what do you think about me getting a CT angiogram so I can actually see? And he was like, well, it's not a bad idea.

You know, it's expensive. Insurance isn't going to cover it. You know, the risk factors you have are very low, so it's not really something I would necessarily recommend. But if you want to go do it, like, it's not a bad thing. It was very kind of like, oh, you know, it's up to you, but I don't think you really need to. It's more or less the attitude. I didn't take that advice. I went and got the test done.

And then honestly, I was expecting them to come back and tell me, oh, yeah, you're great, you're clean. And that didn't happen. You know, I had a 40 plus percent block. It's a wintermaker, very high calcium score, lots of plaque. And it was just a shock because you just think, again, I think it's clear if you're living a healthy life, you have this idea.

That means you're not going to get cardiovascular disease. But that's just not how it works, unfortunately. And the more I've learned about it, the more of this sort of story that I have is very common, much more common than people think. I think. Looking back at it, do you think there was something that you could have done? Like, let's hypothetically say that, let's say 10 years previous to that, that you were getting blood work done. Sure.

Would there be something in your blood work you think that would show up and you would go, oh, there it is. That's how I was accumulating plaque. No, it's the problem. So what I've learned over the years is there's kind of two things to consider. One is everyone has like a genetically set baseline of their, cholesterol levels that are going to be just their normal baseline. And you can make them worse, obviously, by eating. You can make them better by eating better.

So your diet has a pretty big influence here. But the second thing that you don't really know or have control of is how much plaque you will build at a given level of cholesterol. So in my case, I was right around the norm, maybe very slightly elevated. My LDL back then was like 100, 105, 110, which again is maybe above the optimal. But the cardiologist is like, ah, you're just barely above optimal and all your other numbers look great. like it's not something to worry about.

But what we now know, and it's more clear and more testing has been done, is different people will build a lot of plaque at different levels of cholesterol. And so that's part of where my family probably has this disease, is we can have fairly normal level cholesterol and still accumulate plaque very rapidly. Somebody else can have much higher levels of cholesterol

and not build any plaque at all. And so that's where I think a lot of confusion misinformation comes in is like, oh, I know somebody has really high cholesterol, they don't have any plaque. Well, that's them. That's not everybody. We're all individual.

and I don't think my testing would have at that point revealed anything that was so far out of the norm that you would have expected me to have the plaque that I did. So the only thing I really could have done would have been getting CT angiogram earlier. And when I was my 30s, I still would have been able to detect that. But again, the doctor was like, oh, you're doing anything great, you know. And it was very uncommon back then in my mid-30s for someone to get a CT angiogram with no symptoms and no risk factors other than family history. So it would have been difficult to do a whole lot more.

though, you know, if I knew now back then, obviously, I would have made some changes. I saw a clip of you, and I'd like to get a little bit more context of this. You said something about, and you and I've talked on the phone about this as well, but you mentioned something of the effect of, like, 90% of this population in, like, Denmark, had plaque over the age of 60 or something like that. Can you share that with this? Yeah, so the study was done recently called React, and so they did 16,000-something people between Denmark and Spain,

and they deliberately took people who had never been diagnosed had no known history of cardiovascular disease. So they had no idea if they had or not, they'd just never been told they had it. So 16,000 people, first of all, I would say that Denmark and Spain haven't been to both countries. Those people are generally healthy than Americans.

So I imagine whatever numbers they had are probably worse here. And very relaxed, like kind of seemingly stress-free, right? Especially Spain that take half the year off. But, yeah, so they took 16 plus thousand people and they looked at whether or not they had plaque by three different ways. They looked at the carotid artery scan

to see if you have plaque and crudids. They did the full TTI angiogram, and they also did some arteries in the legs. And again, they looked at people between age 18 and 70 plus, a wide range. And they found across the entire study, 57% of that population had plaque. And again, this is people that didn't know they had any plaque. And, of course, that's all the way down to 18, which is probably low. But yes, by the time they got in their 60s, 90% of people in that age group had plaque. Now, it doesn't mean they all had enough that was going to kill them, but they all had it.

or 90% had it at least. And again, that's in a population I imagine is healthier than the average American. So I think we have to understand that the vast majority of people are going to have black accumulated across their lifetime. The bigger question is, is it going to accumulate fast enough to kill them before they die of something else? And for a third of the population, who dies of cardiovascular or something related to it, that's going to get them first.

For the other two thirds, they probably have some, but maybe they get cancer or maybe they have some other disease or something else that gets them down the road. and the plaque never kills them, but they still have some amount of it. So it's something we just now are starting to understand way more people have it than we think. And again, the fact that a third of the population, one and every three people dies from it tells you it's not just people that are unfit. It's also some people that are fit doing the right things in there as well. It's really tough, you know, being someone who's in fitness and into exercise and nutrition so much, you know, you just tend to like, you know, point the finger at someone. they turns out they have diabetes turns out they have this they have that and even like type 2 diabetes

i used to think well it's just simple like somebody's they're overeating yeah overconsumption of energy and uh they become insulin resistant and boom they get but not everyone's the same like i know a lot of people that have type 2 diabetes that aren't they're not heavy yep so it's like well where's the energy toxicity how could you have yeah exactly how could you have an over consumption of if with the models that we have now and our understanding, you know, how could you be overconsuming, but then also- Not gaining much of weight. Yeah, yeah, also not gaining the weight and stuff. So it's pretty complicated.

And hopefully I'm not misspeaking on this, the late John Meadows, RIP, I believe he had, and I'm not sure if he had a C-A-C or a C-T-T-A, but I remember them talking about how he had some plaque. And I think it was like low. I think it was like, well, low considering like the numbers I've heard before. but it was maybe just a few hundred or it was like maybe like 60 or something and then I remember he kind of died shortly after that and there was a guy and yes like we know what bodybuilders do and I have stated what what I've done and stuff like that too but there's a lot of people that

there's a lot of people that are dying of heart attacks that don't take steroids right but I don't want to scare people I want people to take initiative I want them to start to get some blood work done I think that's probably the easiest place to start. The CTTA, maybe it's a little on the pricey side. Maybe it's hard to figure out. I think you have to have a doctor's, whatever the hell, note to get it or whatever. But I want people to get these tests done, scan, kind of see where they're at. And then from there, just try to live an appropriate lifestyle.

That's going to help. But then it's like, well, shit, how do you live the appropriate lifestyle when it seems like a lot of people seem like you have lived pretty healthy. I don't think you were blasting steroids or anything, right? So you're not someone I know that drinks a lot or anything like that. Yeah, I don't drink at all, honestly. So people that hear this, you know, how do we empower them a little bit to be like, okay, man, I know you're a little bummed.

You know, he got this news that you have, you know, a 500 scan or whatever the hell. And it appears that you have some soft plaque and stuff. What can they do? Yeah, so the more I've learned about this, the more, it comes back to one thing and people don't like often hearing this but your cholesterol particularly the type of cholesterol it builds black is the single biggest driver of this let's let's cut this because it's obvious that he works for big pharma yeah exactly so who sent you in here to yeah i mean look there's there's so much information internet and even

like when i look online there's there's no there's so much out there that's like no no no you can't get cholesterol you can't get cardiovascular disease unless you're insulin resistant no no no you can't get cardiovascularis unless you have diabetes. No, like there's so many people out there making these claims that you can't get cardiovascularies if these other things aren't there. And that's simply not true. I've never been insulin resistant. Every single test I've done is shown great insulin sensitivity. You don't look like you're insulin resistant. There's lots of variables here. But at the end of the day, it's very clear. It comes down to what is your baseline level of atherogenic particles. We can measure an APOB. LDL is also a pretty good proxy. Apobo B is a little

better, that level is the single biggest determinant combined with how you as an individual build plaque at a given level. Like, that's just what it comes down to. And the problem with that is exercise as much as we love it does not necessarily move the needle very much on lowering it by itself. That's just doesn't. And so there's, so there's some pictures. But exercise can help stabilize.

Yes, exactly. That's what I was going to say. Yes. That's exactly. Well, so what we found out, what we know better now is the plaque itself, the plaque itself, doesn't slow down massively because you're exercising. In some cases, it might actually accelerate on the high end. So there's a couple studies people look at the Mark 1 and Mark 2.

It's measuring athletes risk for cardiovascular disease. And they find that people exercise 10 plus hours per week tend to actually have more calcified plaque than someone else their age. But what we don't know is that just because it's stabilized the soft plaque and it's actually more, it's risk reducing in just doing the exercise or does it actually contribute some way. They're a little bit of open and in question. But again, what we know is exercise itself does not stop plaque from forming.

It makes it more likely that you're not going to die from it. It reduces the risk of disease you have because it does likely stabilize the plaque in some ways. It increases blood flow, increases the size of arterial networks. It helps the blood pressure. So it does all these things that makes it less likely that you're going to die from it, but it doesn't stop you from getting it. And I think that's an important thing that people need to understand. The radiologist that's done in my CT angiogram, she's like,

we have people who come in here that run marathons and have blockages all the time. She's like, this is not an uncommon thing. It's just that you want to believe that the lifestyle and exercise can prevent the disease. It can contribute significantly to reducing your risk of, again, dying from it for multiple reasons. But it's not likely going to prevent you from getting it because it's not significantly reducing the plaque forming particles in the cholesterol that you have. And it's just not how the effect we think it does in that area. Let's talk a little bit about training. You have Morpheus, HRV, you know, kind of goes off of HRV,

and you've been studying this for so long. So I think it's awesome that you have a good understanding of how do we train and how do we get better at something, but how do we manage the training? Because it's like it can be very stressful. But to your knowledge and some of the studies that are out there, I believe they've studied, and I could be wrong, but I think it was specifically runners, or maybe it was just endurance athletes. And I don't know what they did to quantify the endurance athletes,

but it did appear that they oftentimes had more plaque than even like the almost the general population. Yeah, that's the test as I talked about. So you can look up MARC, measuring athletes risk, cardiovascular disease. There's been a couple other follow-up studies. And like I said, exactly. And what kind of athletes are we talking about? They were endurance athletes. Okay.

So like I said, they found basically that the athletes that trained the highest volumes did have higher levels of calcified plaque than their counterparts in the general population. Now, again, is that because it just calcified the plaque that was already there from just normal causes? Everyone else has that it made it more stable. Is it that it actually caused more total soft plaque to accumulate as well in the same process? We don't necessarily know, but what we do know, which is the benefit, is those people still are less likely to die cardiovascular disease, even though they have it. So exercise does not reduce your risk of getting the disease. It reduces your risk of dying from the disease.

That's just what all the data points do, because, again, if you're not lowering the particles that lead to the formation of plaque, then you're not really reducing the risk of getting the disease. Is there information in terms of like heavy lifting, power lifting, Olympic lifting, sprinters? Yeah, unfortunately not. I've never seen, I'm not aware of a study where they've looked specifically at power lifters or, like said, Olympic lifters or the strength athletes across different timeframes. I would venture or guess that extreme levels of it probably accelerate it to some extent just because there's very high blood pressures. And that could be why the endurance athletes maybe have higher levels is because spending hours and hours above high blood pressure or above what normal blood pressure would be combined

with massive extra blood flow just maybe creates more turbulence in arteries and can facilitate some of the stress interior wall when it's done high volumes. Just for a second, let's just talk purely about strength training and powerlifting in particular. That seems to be pretty extreme. Blood pressure seems to go through the roof. But, you know, it's training, right? And so, like, sometimes, you know, some of this poison can be a good thing.

But power lifting, especially the way that I did power lifting, I have no problem admitting, like, the way that I did it, was very unhealthy. On top of taking steroids, I also was very heavy for a long time. It wasn't really that long, but it was long enough to probably, cause some disruption in my cardiovascular system. Is there any information on like just raising blood pressure and like going to the gym and like just, you know, smashing some heavy weights and pushing yourself? I mean, again, from a research standpoint, not a time.

Like, there's really not. Because I know people that are on the powerlifting side or they're on the short distance sprinting side. They're like, yeah, I hate those damn runners. They want to be excited almost. Not that they're excited that people are dying, but they're excited. that they think that their sport has the answer. Yeah, vindicated. Yeah, I mean, there isn't that data I've ever seen. What there is is they've done observational studies where they basically ask people what type of exercise they do. How do you do cardiovascular training, if so, how many

minutes per week or how often? Do you lift weights? If so, how many times per week? And then they've tracked those people across decades. And what's interesting is the people that had the lowest risk of death over the study period said they lift weights two or three times a week. The people that said four, five, times plus a week, their longevity actually was decreased compared to the people who lifted two to three times a week. Now again, this is an observational studies. We can't make any definitive conclusions about cause and effect, but you just see in these big studies where they look at hundreds of thousands of people across decades, again,

the people that said they lifted two to three times a week, those are people who had the lowest risk of dying across the study period. The people that did way more, their benefit actually went down the wrong direction. Not that it was a negative effect necessarily, but they didn't have the same long is the people lifted two or three times. The only study I've seen where it's linking lifting weights and some sort of longevity correlation. My gut instinct just tells me from being around a lot of power lefters

and strong people my entire lives, they have a lot of heart attacks. Like just personally, people I've known, people you've probably known. It's not a low number. So I would be, again, some of this is extremes. I think for most people that are just average people going to gym, lifting weights two, three times a week, it's great. But maybe lifting weights five, six times a week.

driving your blood pressure super high, obviously taking anabolic, doing crazy things in your diet. That probably has a negative effect over the long run, a lot of people. What do steroids do in terms of cardiovascular health? A bunch. So, number one, your blood count, red blood pills. Steroid abuse. Sure.

Your red blood cell count's going to go up, right? So that's going to make your heart, your thicker blood be hard to pump around. That creates some left ventricular hypertrophy that's negative. Okay, I'll just donate blood. Okay, I'm going over the... Yeah, I mean, maybe you can try that. that a lot of them depends on which ones you're using can can ruin the HDL function. So HDL number itself doesn't seem to be as predictive as people thought, but it's the function

of the HDL. So long story short, LDL and other cholesterol particles that are in that category gets stuck in the interior wall and the HDL function is to pull them out before it becomes problematic. It's called reverse cholesterol transport. So if you have poor HDL function, you tend to accumulate plaque at a much higher level. So it can do that. And then also, like we talked about, if you have higher blood pressure because you have more blood and more plasma and all this sort of stuff, higher blood pressure is creating a force against the arterial wall.

That arterial wall is your protector against the plaque being stuck in it. So if you're creating high blood pressure with extra blood and create more force against the walls, you are probably more likely to cause that interior wall over time to be a bit damaged. And that damaged arterial wall is a big part of what determines how quick you accumulate plaque. The interesting thing that I found in my genetics is I've got a gene where my arterial wall doesn't function like it should. It's an endothelial dysfunctional gene. That gene raises your risk of heart attack by about 50 to 70 percent. Are they like maybe stiff and not pliable or something like that?

So in my case, it's the vascular smooth muscle cells proliferate, which is a whole other detail people don't need necessarily know about. But there's just arterial function that seems to play a really big role in this because, again, you have to not just have the plaque to hit the wall, but you also have the wall to not work the way that should because the wall should be a barrier. You should have the single glyco calyx. There's parts of arterial wall. It should prevent it from being stuck. And some people's arterial walls are much better genetically than others. And lifting weight to new and cardio should, again, in theory, make those walls better. In many cases, they do.

But my guess is that doing it to extreme levels might go the opposite direction and cause damage that wall over time. But this is, again, we don't have great research on this, am I aware of. How do we manage listening to this podcast today? and getting scared, you know, scared to death. Like we go and take some of this information, you're like, man, you know, I'm probably in a rough spot. I'm 55, and I'm listening to the show. I know they're right.

I know I need to get my blood work done. And you're already kind of getting nervous. And then, you know, you do get a scan. You do get your test scores back. We've talked a little bit about what you can do. Like, what I guess, like, let's maybe walk through, like, what are some tests that we think that people should consider? Sure.

And then once they consider those, if they have kind of poor results, like what do they start to think about? Yeah, so I think the first thing is talking about the blood work because that's important. Blood work is a way to measure your risk factors like we talked about. So you look at your APOB particles, your LDL, you can look at inflammation, you can look at all these different markers that measure your risk. And the problem we have to understand is that those risk factors are based on population-wide norms, right? So they're taking the whole population, they're looking at people, how these different risk factors, and measuring how many of them end up having disease or dying from it, so they create these risk models. They also typically work off a 10-year risk, although the newer models are a little bit better. And so they say, hey, Mark, here's your numbers.

Your 10-year risk is 1% or your 10-year risk is 5% or whatever the case may be, and that helps them decide what you should do. The problem is cardiovascular disease happens over decades, and the biggest thing that's going to determine your 10-year risk is your age. So someone who's 35, they're going to make, oh, you're 10-year-re risk. risk is low because not that many people in the mid-40s have heart attacks. And so you're like, oh, I have a very low risk over the next 10 years. And so you make decisions to not do anything until you get 10 years later. So we just have to realize that our risk factors don't tell us whether or not we have the disease. They just tell us the probability. And in my case, it told me my risk was very low. And yet it turned out I had a significant disease. Now, there are

other people who we've talked about who have all the risk factors and then they have zero disease. The problem, again, is that the medical field just uses that model generally to just do one thing. If your risk factors are high, you get on a statin or some drug. Your risk factors are low. You don't get a statin or some drug. Like that's kind of this very simple equation that most doctors are using based on standard guidelines, standard of care. And again, the problem is you're taking population-wide data and applying to each individual. And that's the problem in my mind.

It's why my doctor neurologist, oh, you look great. Your risk factors are low. So it sounds kind of interesting because you can get some blood work done, and we can give people some of the markers. They should definitely get tested. But you do some blood work. And then from there, you end up starting to tailor and customize. That's exactly what you have to do.

Because you look at it, you're like, okay, the APOB is a little high. And, you know, if you're, I think that the way that most people should probably proceed after they listen to this show is you should probably just pretend that you have calcification. Because it seems like the odds are fairly high. As you get old and older, then, yeah, the odds are shipping. And there's no reason for you to mess around with medications and stuff until you have further information, but it wouldn't hurt to, you know, engage in some training and engage in some cardiovascular training, all things that aren't redlining, all things that are kind of just in a little bit more maybe casual zone.

You're not powerlifting. You're not, you know, stepping on stage and bodybuilding or anything like that. And then you're going to continue to get test done in association with some of the results that you're going to get from the blood work and some of the communication back and forth with the doctor. Yeah, I mean, again, we're not doctors, so I don't want to give medical advice. But I would say we now know the process starts much earlier than we thought it did. And the number one risk factor I've seen, and we can talk about, is this family history because your genetics play a really big role in cardiovascular disease, bigger than people realize.

So I would say that should inform decision-making as well. If you have a family history, your dad, your mom, your aunts, your uncles, your brothers, grandpa, parents, all that. If there's a history of heart attacks, diseases, strokes, you probably need to be much more cautious and aware of this and be more proactive in your earlier years than if nobody your family has it because it does have a strong genetic component.

And we know this because of the genes. Like I just mentioned it because of one called LP little A, which is very genetically determined, which is another cholesterol particle. We know that your genetics play a big role and your lifestyle can accelerate or decelerate it, but it's your genetics that sets that baseline risk. So if I'm 30 years old and half the people in my family have cardiovascular disease,

I should probably be more proactive about measuring things, scans and various options, that if not one person my family has it. I'm not saying that's a get-out-jail-free card. I'm just saying that should inform how much I want to be, how proactive I want to be in my younger years to make sure I'm not accumulating. Because the problem right now is you don't do anything until you're 45, 50 years old, 60 years old, and now you have it. And we really can't reverse it at that point.

we can reduce our risk through various forms of medication and exercise and all these things, reduce the risk of dying from it, but the risk is still much higher than if we just didn't have the disease. So I really think the most important thing for anybody who has family history is just being very proactive in your 20s and your 30s and keeping your numbers where we know your risk is the lowest. And then when you get in your, you know, let's say 30s, 40s, depending on family history, you decide to go get a scan done. And then that provides much more detail, do you actually have the disease or not? Because we have to remember, you can't tell if you have the disease without a scan. The risk factors are just the risk. It's probability.

It's the lottery. You either have, you're likely to get it or you're not likely to get it by some extent. But we can't tell whether or not you have it without measuring it with scans. It's really disappointing. It'd be great if we could just train it away. Great if we could just say like, hey, you know, do 20 minutes of lifting every day and 20 minutes of cardio. I mean, the good factor is, yeah, look, I don't want to be depressing. We do know that exercise has a significant ability to reduce.

your risk of dying from it. Significant, 30, 40% reduction in a lot of studies. So it's big. Like, we don't want to downplay exercise. I just want people understand it's not going to prevent you from getting it. It's going to prevent you from dying from it. And best case is obviously you do both. You prevent getting it and you exercise because exercise, aside from his cardiovascular disease, has a whole bunch of other benefits in cognitive function and movement capacity and preventing cancers and a whole bunch of diseases. So exercise is not just do it for cardiovascular disease. it's preventative of a lot of other things and improves quality of life. So they should do that regardless of family history risk or any of that.

What are maybe like five or so things that they should be looking for when they get their blood work done? Sure. So you want to look at your total cholesterol risk. And the problem right now is a lot of people just do LDLC, which is not a bad starting point. It is the one that's been used the most in research, but it doesn't get the total picture of the different types of particles. So a lot of the, I wouldn't say newer cardiologists, but a lipidologist will recommend also APOB. It's just a marker of the total particles. When we look at LDLC, we're looking at a total amount of cholesterol, but it can be spread amongst different amounts of particles. The actual APOB

measures a number of particles you have that can cause atlaschlerosis or cardiovascular disease. The other one people can break out is what I said LP-L-A. That one's very genetic, as we've talked about, and diet and x-trace does not really move that one much at all. There's some drugs now that can influence it, but that one is something that's completely familial inherited. and you can measure that as well. So I would start with APOB, LP-L-A, and just like a basic lipid panel. That'll give you a big, broad picture of your wrist from cardiovascular disease from the lipid standpoint, which, again, is the single biggest driver,

no matter what anyone the Internet tells you. I don't think there's any serious cardiologist, lipidologists, any of these people that have been doing this for a whole lives, they'll tell you that it's not the main driver. It is. Now, the other things make it worse. So you should get a metabolic profile. Look at HB-A-1C.

Look at fasting glucose, fasting insulin. And then those sorts of markers will give you an idea of your metabolic glycemic control, which is really important. And then inflammation, two, I'd recommend HSCRP, which is a general inflammatory marker. And if you want to add another one that's run called LPPLA2, which is a measure of inflammation in the arterial system itself, in the arterial walls. So LPPLA2 is a more specific inflammation marker to the arteries themselves. You look at those areas, then you can look at obviously blood pressure if you want to.

That's also really useful to track over time. You can go home, exactly. That's a really useful thing. And then, you know, other basic markers of health could just be a complete blood count. You can look at hormones, stuff like that. But looking at the core of inflammation, lipids, and metabolic control, those are going to give you the biggest bang for your buck in terms of understanding the risk profile you have. Dr. Sean O'Mara checks out a lot of people that have, you know, he has him do an MRI, full-body MRI scan,

and he's really big on preventing, I guess, or getting rid of visceral fat. Yep. What are some of the thoughts there? He seems to think that the visceral fat is like the bigger problem. I think, you know, it seems like, you know, kind of why not work on both? Sure. But what are some of your thoughts on some of his theories? Yeah, I mean, I'm not too familiar with him honestly.

Visceral fat is tight instance sensitivity and other markers of health. So visceral fat is a bad thing in general. So, yeah, it's good to get a Dexas scan. You don't need a whole body MRI to actually get visceral fat. You can get that from a dexas scan, which is a couple hundred dollars usually. And again, it's pretty easy to get. Really easy to get. It shows you body fat and shows you bone density.

Yeah, I think that's a good thing for people get in general. It shows you, like said, body composition, visceral fat, bone density. I think Omera is just more of a fan of the MRI, just my understanding, and just to defend him a little bit. It's not here to talk about it, but like it gives you much more. Yeah, it gives you like better shots and better imaging, I think, around the heart and liver. Yeah, yeah, yeah. Those things are all are advanced tools. I'm not downplaying that.

But for most people who don't want to go spend the money for the full body MRI, you can get the, the Dexascan for... I think they're like $2,500. Yeah, Dexas scan is a couple hundred bucks and it'll give you least visceral fat. It won't give you all the organs same day, the MRI will. Probably a nice start. You could start, yeah. And so, yeah, again, visceral fat has negative health consequences across the board.

It's more pro-inflammatory. It's more insulin affecting and makes you more likely to have, again, all the other things we've talked about from a metabolic standpoint. So it's one of those things that'll accelerate and make things worse if you have cardiovascular disease and it's just a good thing to not have. So that's diet, exercise, all that sort of stuff. So we get those blood markers checked. Maybe we do a Dexa, like we're kind of investigating. We're looking through all this stuff. Have you found that there's, and each person is going to vary because I would imagine some people probably aren't so severe that they need pharmaceutical intervention.

Maybe they could just get away with just some supplementation. But what are some supplements that if you saw, you know, someone, and again, neither one of us are doctors, but, you know, if you have a family, member and their LP little A is high and their APO B is high. And things are just kind of slanted in a direction of like, oh, I don't really love the look of this, but they're not in like crazy danger. Do things like berberine help? Does natokinase help? We're hearing so much about garlic and all these different things.

First, I think we need to understand that when you take a metabolic or blood test, you're just looking at where you are right now. So it's snapshot. And again, cardiovascular disease happens over decades. it's your lifetime exposure to APOB particles and all their stuff that's causing this to accumulate or not. So I want to be cautious of somebody getting one test done and their numbers are great and then their lifestyle changes and all these other things change. And they're like, well, my last time I got my blood work, it was great. Or, again, someone has bad blood work doesn't mean they can't change that over time.

So we just need to recognize cardiovascular disease is not a snapshot. It's something that accumulates over a very, very long period of time. So one blood test does not mean you have it or don't have it and doesn't identify your lifetime risk from just where you are right now. I'm not about you, but I was different in my 20s and I'm in my late 40s. 100%. So that said, again, if we come back to the standpoint that the single primary thing, the geradic cardiovascular disease is the cholesterol that gets stuck in a material wall. Let's just call it APOB. That is the single most important thing.

Anything you can do to lower that is going to be the most beneficial. And the other things can be effective, but they're less effective. So the one thing that's got some decent research on it from lowering APOB, and the cholesterol is is red rice yeast, which actually is a naturally occurring type of statin, colomobostatin, alibostatin. So that one can definitely lower it. It's a naturally occurring statin, yeah.

That's cool. There's actually a paper on that, a few papers on red rice yeast. So it is a naturally occurring statin that has been shown to decrease it. You know, berberine can help with glycemic control and those sorts of things. you know, you'd are in the high dose lumbrokinase and nato-kina study. I think that does seem to have some benefits. The problem, even talking with the people running that, is they tested a ton of supplements, and very few of them actually came out with the right doses and had as much of the study.

Yeah, we're actually here at legendary food. This is where they have Bioshift, and Bioshift has a giant-ass machine that they can, like, run everything through and check to see, you know, whether it's like 100% of what it says it is. Yes, exactly. 50%. Yeah, and they found that very few of them actually did. And so that's a problem is if you're spending the money and you're taking a supplement, you want to make sure that it's actually got the doses of things that you're trying to get.

And if it's got a fraction of that, it's brutal. It's brutal. And they said they had very, I think they tested 15 or 20 things. And only a couple of them were even close to what the label said, unfortunately. So that's when you've got to be careful of. But again, this comes back to my mind, if you're going to take a supplement to reduce a risk factor, you want to compare it to blood work over time. So you say, okay, my apobie's little.

but higher, I'm going to see what a naturally occurring statin can do. I'm going to take red rice yeast for three months or whatever else you want to try, and then I'm going to retest my blood work and see if it got better or not. If it didn't get better, it's probably not translating to much benefit. If it got better, then keep taking it or make adjustments or whatever else. So I have a hard time just saying, take these supplements forever and hope it works. I think whatever supplement regimen or drug regimen, you need to be looking at your blood work to see if those are actually impacting it a positive way.

Yeah, it's such an interesting thing. I mean, it always seems like the answer always lies in the middle, right? Everything always kind of comes back to that principle where with some of what we're talking about here, if somebody had their APOB is like 200 or something like that, and they have a couple other risk factors. You know, the objective is not to annihilate the LDL cholesterol and the APOB and put it down in the basement of some sort of crazy number because we don't really know what the cost of that is.

I don't know. Is there research on that? Like having an A-B-B? Yeah, I mean, to be honest with you, so, I mean, my APOB now is the mid-30s, upper 30s, which is very low. And that's because my risk at my age is very high. I mean, do everything possible. From all the research that I've read, the risks are pretty low compared to having it much higher. And I'm an extreme case because I'm very young, relatively speaking, and I want to make it as low as possible,

because there is very clear evidence that lower is better from a risk factor perspective. What people don't know, and I think this is not discussed very widely, is the LDL that's circulating your blood is really not being driven to tissues to do anything. People don't necessarily know this. Most of the LDL that's in your blood is being transported back to the liver for recycling because it was picked up out of tissues that had more than needed. So most of the LDL, most of the cholesterol is produced locally in cells, and when it has more than it needs, it shuttles it back to the liver to be recycled.

That's mostly what's in your blood. Your blood is not taking LDL and delivering it to tissues to be used. People think that, that's not actually what's happening. The LDL can be produced. The cholesterol itself, I should say, can be produced in the tissues as they need it. They're producing as much as they need. And so, again, it's not that the LDL in your blood or cholesterol in your blood is necessary for those tissues to have cholesterol. They all have it.

They all make it themselves. And then they shift it back to the liver. And it's the LDL going back to the liver that's causing the plaque. It's not the LDL that the tissues aren't getting because we've loaded it so much. So people will say this again. You read the Internet. If your LDL is too low, your testosterone is going to be low, it's going to kill your hormones. Last testosterone tests I did, again, my LDL was 19.

My APOB was in the 30s. My testosterone was 792. I don't use any exogenous hormones. Like that was just my testosterone level. So I've seen personally, again, this is only number one. I've seen zero impact on any of my hormone levels despite having an LDL and APOB about as low as you're going to get them. Let's talk about the Joel Jamison stack. Yeah, sure.

I'm on it as well. So maybe you can share that with people. And again, this is not medical advice by any means. It's just like what you and I are messing with. Yeah. So look, again, it comes back to one simple statement. Different people will accumulate different black at different levels of these cholesterol markers.

Because you and I both have pretty expensive disease for our ages in particular. Lower. I think we're both in the 2000 or something for a scan, right? Lower is going to be better for us. It's going to mitigate our risk. We know that for every, I think it's one millimeter, I think it's like 30. 39 you drop your LDL or I think it's LDL was research you have a 22% reduced relative risk of dying from it. Like that's pretty significant.

So there's benefits to dropping it lower. I have seen zero evidence from studies that it causes these crazy side effects to get that low. I'm not noticing them. I don't know you are. So that being said, we can take different categories of medications to get there. Obviously statins are the most common. So I started with 10 milligrams of resuvvastatin. I think you did some of that.

I personally noticed at high doses of it, well, actually, so I started at 10, and then the cardiology swammy go to 40, which is not a good idea. I had 40 milligrams. I got some soft tissue injuries that were not normal to me. Muscle pain and stuff like that's muscle pain, but also I just was like pulling quads and pulling cab, like weird stuff without even, like without training. I was just like pulling my calf walking down the street. It was very odd.

Drop down to 10 and 5, and those things went away. But what I noticed is at high intensities, I was getting winded much faster. Because they do at high doses and an effective doses, some extent, impact mitochondrial function, which I don't think matters for... Is it like mitochondrial respiration? Yeah, it impacts how it respirates more or less. It impacts on the chain, the electron transport chain. But I only noticed that at very high intensities.

I didn't notice it any other time. And so also, it didn't lower my LDL enough. For some people, like 5 milligrams, might do more than enough. for them and they're not training at high intensity or maybe they don't have the same impact. So that might be just fine for them. Then my insurance approved repatha, which you're also on. So the difference is statins slow down the production or inhibit the production of LDL and other LDLRREPOB particles. So it reduces production.

Right. The problem is your liver can just not take as much in the bloodstream and increase circulation that way. So repatha works differently. It increases receptors in the liver that pull out the the LDL. So there's the amount in your blood is how much is being filtered back to the liver and how much the liver is actually pulling in. My understanding is the repath is a little bit more targeted towards APOB, right? No, it's really, it's really just particles themselves. Okay. Well, APOB is just a broad term for all, right? Apal B is just all LDL. APOB is just all LDL. APA should make it's clear is all types of athergenic particles. So most that's LDL, it's LPDL, it's other particles that are athergenic. So APO B is just any particle that could basically get stuck in your

material wall and cause plaque. So broadly term apobie is all these put together. So yes, I mean, it is pulling out all those particles to the liver. Um, so I went on that one, was on the statin and that got my, that got my apobie down to, I want to say 60 or 50 somewhere around there. And to me, I wanted to go lower. And again, this is, this is not what your average cardiologist is going to tell you, but this is what the top target cardiologist and the prodologist I've talked to. If people want to hear somebody's, people, Dr. Thomas Dayspring is a guy that's out there talking about this. He's a very, very, very experienced lipidologist. I talked to him personally, got his advice, shared some of my members with

them. And I think the other lipidologists out there that are doing the research that they'll all tell you, if you have a severe case, lower is better. And you're not going to have a downside by going lower. So I want to eat my number under 40. And that was really his advice was, and a couple other lipidologists, get it below 40. Just flatline that shit. Just get it below 40. Basically, again, You're not taking cholesterol away from the tissues. You're just taking it out of the bloodstream. Those are different things. So then I added benpidoic acid.

I added Zedia, which, again, is another way of reducing the absorption, or increasing the absorption, I should say, rather than reducing production. That got me down to 50 or so. And then I added one called benpidoic acid, which is a non-muscular one. These are all just different variations of how it lowers cholesterol. But anyway, the combination between right now,

I did get rid of the statin itself. So, repatha, benpidoc acid, zedia, those three. And that's gotten me, again, my apobie's in the 30s, mid-depper 30s. So that's kind of technically without a statin? Yeah, I got off the statin entirely because I didn't need it at this point. So you got your apo-b down to 30.

That's huge. Yeah, mid-depper 30s depending on the test. And again, I was, if I needed the statin to go lower, I would use it. But I don't need the statin to get lower. The problem, the big problem for this, is these drugs are not cheap. Statenes are dirt cheap, right? You can get a statin probably for free. Your insurance will pay for that all day long. Zeti itself is pretty cheap, but Benpidoic acid,

which is not super strong, but in combination, it does work the other ones, is not cheap. It's super expensive for no reason, for whatever reason. And then the Repatha is also 300 bucks a month. So Repatha is 300 plus a month. If you were to cash pay, I think the Benpidilic acid can be the $300 dollars a month so that's the unfortunate thing is if you want to get away from statin for whatever reason it's much more expensive there's no way around it yeah it's expensive uh well it's just a heart disease in general is just expensive in terms of like just trying to figure out ways of managing and i think all disease is that way we get into people having diabetes and uh needing insulin and then needing uh you know continued glucose monitor it's just like a lot of a lot of ways to try to figure

out how to like monitor yourself it is we talked a little bit about um about blood pressure like that's something you could do at home where some other like easy things you can do like have you seen studies or have you had an experience with like just maybe someone just measures their waste or the uh i know you i know using morphias is a great idea checking your hrv maybe there's some tests someone can do like they could go on a bike and do like a 12 minutes something or yeah i mean so if you want like a just a broad fitness marker for for VO2 max cardiovascular health there's a Cooper test so that's a 12-minute test where you go all out basically to run you enter your number how far you went into a calculator and spits out your VO2 max number that's a really good measure of overall cardiovascular fitness

resting heart rate is another good surrogate there lower resting heart rate is generally higher cardiovascular fitness average HRV and morphias is a really good number because that represents autonomic function autonomic fitness back up just a second to the resting heart rate so resting heart rate is different than your heart rate when you're sleeping? Well, it depends on how you're looking at, but they're very similar. You're going to get a bit lower resting heart rate overnight. You're taking an average of your resting heart overnight. That is a good gauge of your overnight resting heart rate.

Measuring in the morning when you're awake is just another way of doing it. If you're going to do one or the other, just make sure you're consistent. And if you're using overnight resting heart rate, it's going to be lower than the morning. So most of the data is based on measuring your resting heart rate, not just looking average overnight because overnight resting heart rate really wasn't possible for. for the average person to measure until wearables started doing it. And all the data is mostly built on resting heart rate that was measured in a special, you know,

and special, but like a consistent basis in the mornings. I haven't done the HRV in the morning in a while, so I brought my thing with me because I had to get a new one. But anyway, I'll get back on that. But what is HRV and how did you become, you know, we've talked about this on previous podcasts, but I think it's relevant to our topic today.

How did you become, obsessed with it and then I mean I know that you create you created morphius I understand that but it seems to be weird that it it helps with the exact disease that you have yeah I mean it's interesting so I was introduced to it by a track coach named randy huntington 25 plus years ago he coached the USA track and field jumps he'd coached michael mike paul to break carlos his long jump record oh damn very very experienced coach and I don't know where he was introduced to it but this is again back in like the early 2000s. And he had used the first system

called a Mega Wave. It was built by the Russians. The Russians were really the pioneers in using HRV. Most people don't know this, but they'd use it back in the 50s and 60s, like long, long time ago. Damn Russians. They were head of the technology curve. And they had started using it in their athlete programs in the 1980s during the Olympics where they just crushed us

at every Olympic Games possible. And yes, they were on drugs, but I hate to tell most people so were most of other countries at that point. But they had used it back then. they pioneered the use of HRV for athletic performance. So Randy told me about it, and back then it was just computer system. It was like $30,000. You had to hook up six electrodes on people in order to measure it.

It was super cumbersome. But at the first time I saw it, I was just amazed because I think it answered so many questions of like, why did this person get better or why did that person not get better? And I think a lot of training without data is just kind of guesswork and intuition. And you try this and you see if it works or not. and you're kind of spending weeks or months doing that. It's different than lifting. You know, if you're trying to train your cardiovascular system, like,

it's nice to have some markers. You know, when you go in the gym and lift, you can clearly see that there's two things on there. And yeah, you can determine, and in the next week, you could actually, like, maybe miss a lift, and you'd be like, hmm, I wonder what I'm doing wrong. But running is like a little harder or cardiovascular training is a little bit harder without some sort of measure. Yeah, exactly. I would say that. But also, look at an HRV can tell you why you're lifting is or is.

getting better. So you can see whether or not you're getting better. You're like, oh, my lifts got better or my lifts didn't get better? But the question is it because you did too much or is it because you did too little? Often you don't necessarily know. And so what HRV is showing us is how our body is going to this process. So we have to understand we work out and then we set off the signals in our body for our body to improve. It's not, you don't get stronger in the middle of the workout. Like you're just causing these signals to happen to your body that makes your body get better or stronger, more muscular or whatever, more fit over the recovery period. It doesn't happen immediately. It takes hours and days, right? And those accumulate

over time for you to get better. And so HRV is looking at that process. And the way this works is when I do something stressful, whether it's lifting weights, doing cardiovascular disease, doing something psychologically stressful, my fight or flight system turns on, which people have probably heard of. It's called the sympathetic part of our nervous system. It's just increasing our body's metabolism to create more energy to deal with the stressful thing we're doing right now. So I lift weights, my sympathetic nervous system turns on, my heart rate goes up, my blood pressure goes up, all these things happen to create more energy for me to go ahead and do the exercises or do whatever I need to do, right?

Afterwards, that has to shut back down. That dial has to turn down. And then the other part of my autonomic nervous system, the parasympathetic, has to turn up because its job is to store energy. It's anabolic. It's now restoring all the things that were broken. It's turning off the inflammation. It's facilitating energy directed towards bigger muscles or energy towards more mitochondrial.

It's it's directing the process that your body has to go through for your fitness to improve. And so when we're measuring HIV, we're measuring that part of the system. We're measuring that parasympathetic function that's driving rest, digest, recovery, and adaptation. And that's what's driving the actual fitness results you've got from this workout. It's not workout automatically better. It's workout, drive energy into the body, make sure all the things are need to be improved, or improving that need to be improved. And then I get better.

And so by looking at our HRV, we're understanding is our body actually going through the process where we're getting more fit? Or are we spending too much energy on stress and not enough energy on recovery because we're doing too much? Or because our lifestyle is short-serging it. If your sleep is poor, if your diet's poor, if your psychological stress is high, those are all taking energy away from turning your training into results. And so HIV shows us that. It gives us a gauge of how your body is managing energy correctly and whether or not that. or not, it's being driven into recovery. Has there been any studies on, you know, like seeing people that have really,

because I think HRV, you want your score to be high, right? That's to represent a little bit more health, right? Well, so I would say in general, people with higher average HRV baselines tend to have better outcomes across a wide range of things. People with higher average HRV tend to be able to adapt to programs faster. They tend to recover from all stresses better. They tend to have less disease or if they do have disease, they have better outcomes because it's a marker of your body.

resilience. Like you need to be able to deal with stress when you need to deal with it and then you need to turn off and focus on inward repair and maintenance when you're not in those stressful periods. If you can't shift back and forth very well, you're stuck more in a stress date. Those have, that has a long-term negative consequence. So people with higher baseline HRV, it just tells us that their systems are operating better and able to manage the stress of life. And to me, it's the stress of life across decades that determines how fast or slowly age because we have to constantly repair ourselves from all the damage of the stress. If we don't do that well, then that damage accumulates to me age faster.

Yeah, those inputs come in all the time. All the time. How are you managing it? And what does HRV mean? Like, I know it's heart rate variability, but is that like within a minute or within a second? Yeah, so there's two ways to measure this, and there's, I think one is bad in the other. So you're measuring it over some period time.

The way that traditional research has been done, the way the Russians did it, the way that almost all the research papers was you measure it at a specific time. generally, ideally in the morning where you're not having something that would artificially influence it, like caffeine, you didn't do a workout. You measure the morning after you've gone to bed and woken up because that's the completion of like one cycle, let's call it, right? Most of the recovery happens when you're sleeping, not when you're awake. So we stress ourselves out during the daytime. We hopefully recover during our sleep and then we repeat that pattern over time. So we want to wake up and see where are we at in that process.

And that gives us a very good window of where HRV is at to help us make. decisions. And so that's where how Morpheus works. That's again how almost all the research has ever been done and that to me is the best way to approach it the It was a two and a half minute test with Morpheus other ones can use different as short as 60 seconds One thing I liked about it when I was using it consistently was the Almost like meditative aspect of it. It's like I put this thing on you know you put the heart the heart rate monitor on And I just kind of look at my phone for a minute kind of put it to the side and then it was like just you know just calm down just try to you know have a nice relaxed heart rate and you're trying to to get a good score. So you kind of gamify it. And who does that? Like who it's rare for people to take even just two minutes, right? It's rare for people to take just two minutes and just

breathe and be calm for a little bit. So I like that aspect. Yeah, I think it puts people the right mindset. So personally, I get up. I measure my HRV. I step on the scale and then I'll check my blood pressure most times. And to me, like, that's my morning habit. It gets me in the right frame of mind to know what I'm going to do today and make decisions about what I should or shouldn't do that day and give me information. I just like having that to start my day. versus jumping out of bed and doing something stressful and not being thinking about the exercise piece and recovery piece. But the second way you measure HRV, and it can become more common with wearables, is you just wear it overnight, and it gives you your average across the night. And that's more convenient.

I wouldn't argue that, but it's less accurate from understanding where did you actually finish up. Where were you by the end of the night? Because let's say you did a workout, and you ran, let's say, six miles an hour for an hour, right? and let's see your average heart rate was 135. Let's say the second workout, you did a bunch of interval training, you took a few minutes off, you did a bunch of interval training. Your average heart rate could be literally identical if you look across that period. Does that mean the workout was identical?

No. And so when you're completely different input. So if we look at HIV patterns overnight, we can have completely different patterns that will tell us the averages the exact same. The other problem with it is whatever you did close to bedtime will dramatically influence your HIV in the first part of your sleep. So if you had some wine or you did a workout closer to bed or you did these things that were close enough to your sleep period to influence your HRV, it completely alters a huge part of your HIV and throws your average way off. Versus if we measure in the morning, we know where your body is at based on how it recovered overnight. And so, again, I think a lot of the wearables are willing to just trade accuracy for convenience because the average person wants convenience and that's, you know, is what it is.

but if you want the true picture, you want to take the two minutes, three minutes, whatever, to measure it first in the morning and get a very clear understanding of where you are. It's the same to me as if you were wanting to check your body weight. You wouldn't randomly step on the scale all day and take an average. You would just weigh yourself first in the morning to see where you're at, and that's what you should do. Some of what we've talked, we talked a lot about, you know, getting scanned and all these different things and blood work and so forth.

But a lot of the, just because we're saying here today that you can't really see, you can't see cardiovascular disease. You can't just look at someone and be like, oh, that guy's, that guy is overweight. He definitely has it. But on the same token, it's still useful, all the normal stuff that we know, all the things that we've learned over the years of trying not to, you know, have excess body weight and so forth. These are still important. Yeah, yeah, there's no doubt that you can't say that every single person that's lean or overweight is this or that. It's just risk factors.

So yeah, somebody who has diabetes and smokes and drinks, they're certainly much more likely to have it. It's just no guarantee either way. You can be lean and healthy and have it. You can be overweight, smoke, and do all the wrong things and not have it. And each person is only able to determine that by looking at the risk factors themselves and then measuring it. And so, again, I don't think either of us are saying, hey, don't worry about it.

If you have no family history, just go do all the stuff you want. and you're not worried about it. We all need to be aware of trying to improve our risk as much as we can and doing all the right things from an exercise standpoint, a lifestyle standpoint. We just need to be aware that just because our probability is higher for this or it's lower ability for that. That's not a guarantee of anything. It's just a probability. You have been doing this for so long and studying it so much that you actually know a radiologist and you communicate with this radiologist frequently. What have you learned from some of that?

because some of the information you were sharing with me was really interesting. Yeah, I mean, I think it goes back to what I just told you earlier. She's been doing it for 20 plus years. There's actually not that many radiologists that specialize in CT angiograms across the country. It's strange how few there are to do this. But she just kind of reinforced what we've talked about. She's like, I get people that run marathons. I get people that are doing all the things right.

And they come in and we have to send them to get stents right away because they have 90% blockage they had no idea about. And she just made it very clear. Again, that we can't judge this book by its cover. And, you know, she just reaffirmed people come in that look like they should have tons of plaque and have zero. People come in and look physically like they're in the great shape of their lives and everybody else's. And then they show up and have 90% blocked it. She's like it's much less straightforward than people would like to believe.

And then the other things she talked about just in general is a whole other conversation. But in general, you know, you don't see people's plaque, especially calcite plaque, generally. doesn't reverse to the point where the arterial wall looks like it did before. You can't get rid of the disease. You can make it more stable. You can make your risk lower. But she doesn't see any cases where someone did a CT angiogram and then a year, two, three years later, they come back and it's gone.

Like, there's claims online of people taking, you know, D3K2 or nanokinase and saying, oh, reversed it. It's completely gone now. Like, that's internet lore. I don't think that's real life. Again, we know in the Luna study and other things can probably help. stabilize it and reduce some of the soft plaque and increase some of the stability so you're less likely to die from it about i think some like 80 percent of heart attacks come from non-calcified

plaque so the more calcified you have relative to the soft plaque the better um but it's there's just nothing out there it's going to say you have you have really bad cardiovascular disease mark and then you do this thing and then it's completely gone like the damage has been done to arterial wall it never reverses itself and probably the surrounding tissues exactly yeah so it's by time you have calcified plaque the calcification has walled it off more or less. It's made it harder. It's made it more stable. It's less likely to rupture. The calcification process is the healing process of the artery. It's the last stage it goes through to make it less likely to rupture. It's the earlier soft plaques and the mixed plaques

that are much more likely to rupture for people. So having a high calcium score is not good. It means we have more total disease. But a higher percentage of your plaque being calcified actually lowers your risk than if you had much lower amounts of calcified plaque is much higher amounts of soft plaque. So she just kind of, again, she reinforced, like, we don't see people coming in here and seeing all their plaque disappearing. That doesn't happen. What you see is over time, people's calcified plaque becomes a bigger percentage of their total plaque, and that's where the risk reduction comes in. I've also seen people say, like, oh, I don't want to take statins because my calcium score will go up. It's going up because it's making the getting, it's stabilizing it.

So it's not a negative thing because it's taking the calcium, making it more stable and making it less likely that's going to rupture and kill you. So at this very moment, I mean, I know we're here, you know, at Bioshift and there's some things happening here in the background and hopefully those continue to be successful and hopefully they work the way that we think they're going to work. But currently, there is not, as far as I know, no one's done CTTAs and compared them and had people dropping considerable amounts of plaque, whether it be hard or soft plaque. I mean, not a huge amounts.

No, I mean, again, we do. generally do not see the total amount of calcified block or plaque decreasing. We might see the volume it takes up slightly decreasing because it becomes more dense. It becomes a bit smaller and more compact. So you see that happening a little bit. And you see the soft plaque becoming more calcified plaque. In the more aggressive treatments like you and I are at, getting our ABOB is very, very low. You do see some of the soft plaque reducing without becoming calcified plaque.

But it's very small amounts. So for example, like the studies that have looked at this, They'll usually quantify it in terms of total arterial volume. Let's say your one artery has 12% of that volume as plaque. In the most extreme studies, it might see go down to like 11% or 10.5%. It doesn't go down to like 1%. So, yeah, it can regress in the total volume because it becomes more compacted. It becomes a little bit more dense.

And that reduces the total volume. But you just don't see it where you go from a 19 or 20% arterial volume. to five or two like it decreases a bit it stabilizes but it just never is going to go back to the way it was and then my understanding is you know for people that maybe have been scanned maybe they don't know but like there can be a little variation from one scan another so you know uh probably not try not to be too excited and probably trying not to be too scared either way because there's going to be a little bit of percentage off potentially there is some of these machines I think they're using some types of AI

and they have different technology depending on when you got this thing done. Just in general, there's a margin of error. So if you were to do a calcium score and then measure it two weeks later, it can be 5% different, 10% different, depending on the machine. The more calcium you have,

and you and I have lots of calcium, obviously, the more difficult it actually gets for machines to read them because there's just what's called motion blur and artifacts and blooming, all these technical things you don't need know about. But yeah, you're never going to get the exact same scores on a calcium

skin or a CT angiogram, even if you did them a week apart. And if you do them in different machines, if you do them where one time your resting heart rate is way high and otherwise it's lower, that impacts things. There's a lot of variables here. It's not meant to be read as like a, this is going to change by 1.1%. It's much more broad than that. So most doctors will tell you once you've got the CT angiogram, again, the disease happens over decades.

So most of them will tell you like you don't need to do another one, maybe five years down the road or eight. They're not going to tell you like, hey, go get it. get five CT angiograms, it's not usually something that changes very fast. And so it's not something you would measure very frequently. And again, most doctors will say, look, this is where disease is at. We want to do everything we can to slow it down or stop the progression as much as we can. You might want to do a follow up in five years. It's not a test you would do frequently. What was the study that was done on natokinase that everyone kind of goes crazy about?

There's a few of those. I think there's one in Japan that are Japan or China. I think it might have been China. I can't remember which the which country was but yeah they've used high dose in what was the patient group I think it was older and older population they saw some decreases in the soft plaque remember correctly but then that's been replicated yet in the US or in random control trials or any of that wasn't like a placebo arm that wasn't a full study the way that we would see here in the US but it did show some promise and I think those things again they do seem to potentially help from when we've seen it's not a replacement for lowering your APOB but it probably could be an adjunctive thing that benefits it and maybe has some additional benefit that

there. There's any risk of, uh, high, high, yeah, high dose you can get, you can get blade a little bit increased, uh, clotting time. And so I noticed that really high doses, I got bloody noses quite a bit personally, but that's not a common thing that everyone gets. And we're doing, again, we're doing a high dose that was using the studies that are much more than the average person to get from a normal supplement. If there's someone even has it in it is a problem, right? So, I mean, look, we see people, D3K2. We see people talking to autokinase. These things to me can be helpful. but it's not a substitute for lowering APOB. Like nothing that doesn't lower APOB at all is going to have a dramatic effect

or be as likely to have as much effect as just lowering APOB. You have to start there. Like there's no other way around. If you want to lower the risk, you have to lower APA to some extent. And these other things can help, but it's not an option. It's not a substitute for it, Mike, everything I've seen. How big of a difference do you think it makes to have a healthy heart, even when your arteries might be compromised.

Yeah, I mean, massively, obviously. The heart itself is the one pumping the blood and the engine of the whole thing. So you want the heart itself be healthy, but also strength training, ideally in the right volumes and cardiovascular training. It does improve the arterial function even when there is calcified plaque in there and soft black in there. And you can build a word called corollaries. So the body will actually create new blood vessels there and have it. So it can bypass them the blockages. So you can create extra supply there, basically.

and that happens to cardiovascular training, right? So the body is very, very good at adapting to things and it is good at, you know, keeping you alive as long as it can. And exercise is a big piece of that because it's just, it's testing the system to, or it's training the system, how to get better at training recovery, training recovery. The more you train it, the better it gets within reason. If you manage that process correctly,

if you just overload it consistently, then you're overloading it. But if you're going through the process of do this training, allow it to recover, do this training, allow it to recover. You're making the body's, recovery engine better. Do you do some V-O-2 Max training? Because it seems like V-O-2 Max has been, have pretty good correlations with longevity.

It does. Yeah, I think V-O-2 Max is a good thing to increase in the sense that it's increased. It's a measure for cardiovascular's total engine performance. It's how much oxygen we can put through our system. I think it's, A, yes, it is better to have a higher V-O-2, but it's also the training process that you have to go through to get there that makes you more likely to survive these different things. Yeah, the same getting stronger, right?

Yeah, it's the process of trying to. training. It's the process of building autonomic system. It's the process of, again, allowing your body to go through these stress recovery cycles and increase their autonomic function, focusing on recovery through lifestyle change. All those things that are what you need to do to have a higher V02 max are also a big part of the process and big part of the benefit. So I focus on building a high VO2 max and I focus on my strength, mobility, and then I spend a lot of time of recovery stuff for generation, sauna, cold plunge, pool floating, soft tissue, you know, all that sort of stuff helps. to kind of build out some of this engine, you know, this build out your heart a bit.

I'm imagining, like, you need a little bit of zone two-ish. Not everyone needs, I guess there's different ways of tackling this, but you're maybe probably doing a little bit of zone two along with the V-O-2 Mac stuff. Like, what are some forms of exercises that you do personally and, like, how strenuous, you know, you're going, I guess I'm just trying to make the point here that, you know, not all of your training needs to be, like, so hard. Most of it shouldn't be. Be honest with you.

Yeah, it needs to be hard. And when I think about the data that we have currently on runners, I can't help but think, like, I wonder what their heart rate is, you know, because I'm thinking that probably for a lot of those people, I'm imagining that their heart rate is probably higher than what we'd like to see when someone's, you know, even just running various distances and stuff. So I would say in general, most of your training should be in the lower bracket of cardiovascular fitness, at least cardiovascular training.

And so, I mean, the old thing that endurance athletes do, like 80% of their stuff for the lower intensity is probably not a bad range for most people. What I've seen not just myself, but all the people I've coached over the years and looking to Morpheus data is it doesn't take that much high intensity. And the average person who's busy with their lifestyle and they don't get amazing sleep and they're dealing with stress of life, once a week of what I would call true high intensity is enough for most people. And so I bracket my train to three buckets.

And that's what Morpheus does. one is my low intensity. I try to get somewhere between two and three hours a week of that. Again, that's just me where I'm at. You can certainly get benefit much less than that. There's what I call moderate intensity, and that's where we're trained up around our anaerobic threshold. That determines kind of what percentage of our aerobic engine we can use for a longer period of time,

so I'll spend somewhere between 20, 30 minutes in that range across the week, and then three would be my highest intensity up closer to my DO2 max. It's like five to 10 minutes a week for me. It's not much. We don't need as much high intensity as we think we do across the board from everything that I've seen. And again, it comes down to what can you individually recover from. The only way to really know that is use HRV.

Morpia's a similar tool to see how much do I benefit from over time. Better genetics, younger age, better lifestyle, I can do more. Worst genetics, older, worst lifestyle, I got to do less. Like that's really what it comes down to. The VO2 max training can be pretty short. It could be very short, a few minutes. So I'll put this way. The lower intensity stuff is what builds the potential for a higher VO2 max ceiling.

Why? Because ultimately it's how much blood and oxygen your heart can pump out with each beat that sets the upper limit of VO2 max. Because VO2 max, again, it's the maximum amount of oxygen you can put through. And that happens at high heart rates. The bigger, the left ventricle chamber is, the more it can pump out in terms of blood and oxygen, each beat. That's called stroke volume. Stroke volume only really increases significantly over time with volume, with longer times of lower intensities. Because it's like a balloon filling up.

If I fill up a balloon and I left it for five hours, it would stretch. If I only fill it up for 10 minutes, it wouldn't stretch as much. So it really is the same thing. The lower intensity of work builds the size of the left ventricle over long periods of time. And that sets the ceiling. To me, the best analogy I get to people that usually makes sense is I said, hey, Mark, I want you to increase your max strength. We're going to start by just doing like one and three rep maxes.

And you would get stronger for a while, right? And then you would hit a plateau based on the muscle mass that you have. And you said, well, I can't get any stronger. I've spent two years or whatever. I can't increase my lifts. Okay, well, we're going to put 10 pounds of muscle on you. Now what's going to happen? Your strength isn't going to go up because you've increased the amount of muscle you have.

It's the same thing in the cardiovascular system. If all you do is high intensity, you will max out that stroke volume. The only way to continue to increase it is to make a bigger left ventricle. That's the hypertrophy. It's the same thing is I'm going to have to build more muscle. I'm going to build a bigger left ventricle. That will allow me to have more top-end V-O-2 max. So it depends on how how you want to get.

And specifically, what kind of training do you do? So I do a mix of the lower intensity stuff. I have elliptical. I have a bike. I just do a mix of stuff in that lower intensity range. And then typically for the higher intensity stuff, I'll play racquetball or pick a ball or do something athletic. You were saying racquetball, your heart rate. Yeah, record is the high intensity stuff.

I think it's just good to bring up because, you know, let's not forget games and sports. Yeah, they're all very good for you. Go play a pickup game of basketball. There's other risks. right? But you're getting a lot of cardio training and you're having a lot of fun. Yeah. I play picketball for a number of years. It's the easiest way I'm going to get my heart rate up into where I need to get it once a week. And it just makes it more fun.

It's more engaging and more fun to do than sitting in treadmill and sprint. If I had to do that, I would do that, but I find it more enjoyable to go play. And then, like I said, my lower intensity stuff, I live in North Pacific Northwest. It's beautiful. I hike a lot. I get in the pool. I do things like that. So I try to do a variety of exercise at low intensity so I don't bore myself bored to death as I'm doing it.

Any helicopter rides coming up? Yeah, any time you want to go, we should definitely go fly. I know. My wife's always like, you're not going in a helicopter. You've got much higher risk of dying from a lot of things other than helicopter that way. I've been flying helicopters for 12, 13 years now, and airplanes for 30, whatever it is. That's awesome. That sounds pretty cool.

It is. Thank you so much for being on the show. Where can people find you? Trainethmorphus.com. That's please find me or at Coach Joel Jameson on IG. Strength is never weakness, weakness, weakness never strength. Catch you guys later.

Bye.