Transcription
What was your first reaction when you saw my CT angiogram results? Can't say I was shocked. You just never know what to expect. I am comfortable saying you have. All righty, friends. This one is personal. After 10 years of pretty perfect blood tests on a plant-based diet, I decided to find out what is really going on inside my arteries. Do I have heart disease despite doing everything quote unquote right?
In this episode, I share the results of my recent CT angiogram and coronary artery calcium scan alongside my latest cardiovascular related blood tests. Together, we'll unpack what they mean for me and potentially for you too, especially if heart disease runs in your family like me or you have other risk factors like high cholesterol or elevated blood pressure.
Now, going into these scans, while I do like to tell myself I'm invincible, in the back of my mind, I did suspect that I might have some plaque or what's known as subclinical atherosclerosis in people without symptoms or a history of cardiovascular events. For the past decade, I've done everything by the book to lower my risk. But I am also aware that for the first 29 years of my life, I wasn't managing my modifiable risk factors anywhere near as well. So, did I have plaque? And if so, how much? We'll get to that shortly with expert commentary from Dr. Thomas Daypring and Dr. Dan Sofur along the way.
If you're new here, I'm Simon Hill. Nice to be with you. I have a masters in nutrition science and my interest in heart health goes back to a very pivotal moment in my teens, watching my dad experience a severe heart attack in his early 40s. Thankfully, he survived, but that experience ended up changing the trajectory of my life. His father, my grandfather, also had his first heart attack in his 40s, albeit in his late 40s. Ever since that experience, I've been curious about cardiovascular disease, how it develops, and what we can do to prevent it. Especially for those of us with a genetic predisposition.
In 2015, 10 years ago now, I made a major change to my lifestyle after learning that my LDL cholesterol, which typically hovered between 120 to 130 mg per deciliter, was putting me at higher risk of atherosclerotic heart disease, which is the most common form of heart disease. I shifted from what was a very meat-heavy paleo style dietary pattern where I was quite the steak enthusiast to a plant-based dietary pattern. At the time, I had all the usual doubts. Where would I get my protein? Could I live without meat, god forbid? Would I even like tofu? And what about soy and its effect on testosterone? These are all questions that I've since answered, not just for myself, but for this community since launching this show in 2018.
Why the change in diet? Well, there's consistent evidence all the way from animal studies to human studies in support of high-fiber plant-rich dietary patterns for lowering risk of heart disease. Hence, national dietary guidelines in almost all countries around the world encouraging this way of eating. It was a big shift, but with an open mind and the memory of my dad's heart attack still vivid, it was one that I was very determined to make. And within months, my LDL cholesterol dropped below 100 milligrams per deciliter. Within a year, it was between 70 to 80 milligrams per deciliter, which is a level that most cardiologists would consider excellent for preventing cardiovascular disease.
Since then, I have kept very close tabs with annual blood tests, my lipids, my blood glucose, HBA1C, and markers of inflammation have consistently come back in the optimal range. So, that's the context here. A family history of heart disease, considerably elevated cholesterol in early life and the past decade with much lower cholesterol thanks to these changes in my nutrition.
Before we get into my results, a few definitions so that we're all on the same page here. First, let's define atherosclerosis. Bit of a tongue twister. This is a fancy word for plaque building up in the walls of your arteries. And this plaque is made up of cholesterol and other substances and over time can narrow or block blood flow. It's what leads to most heart attacks and strokes. In fact, it is the number one killer globally and most people don't even know they have it until it's very well established.
And second, let's define apo. For a long time, LDL cholesterol was seen as the best predictor of atherosclerosis. And that's because LDL particles, which stands for low density lipoproteins, are the main carriers of cholesterol that get trapped in the artery wall. But it's not just LDL. Other lipoproteins like VLDL, LDL and IDL can also contribute. What all of these lipoproteins have in common is one protein, apolipoprotein B or apoB. Each atherogenic particle carries one apo molecule. So by measuring apoB, we're getting a direct count of all of the particles in the blood that can drive plaque formation or atherosclerosis.
With those definitions out of the way, now let me explain why I decided to do a CT angiogram and a coronary artery calcium scan. I'm almost the same age as my dad when he had a heart attack pretty much out of nowhere. And I say out of nowhere because like me today, he wasn't on any medications, nor did he have any diagnosis. And while my LDL cholesterol and more importantly ApoB are now at a pretty healthy level, there is a case to be made that they could be further optimized with lipid-lowering medications, especially if I knew I had more subclinical atherosclerosis than other men.
The rationale for getting a CT angiogram was that this test specifically looks at soft plaque, which is generally considered more valuable for people under the age of 40. And it's pretty common practice these days that when you get a CT angiogram, a coronary artery calcium scan is done at the same time, together giving a more complete picture of what is going on in your arteries. My prediction was that I would have some soft plaque, but how much I wasn't sure. We know from studies like the Pisa study that it's not uncommon for healthy people without cardiovascular disease risk factors to have some subclinical atherosclerosis. In fact, over 50% of people in Pisa with a cholesterol level like mine before I changed my diet had atherosclerosis. These subjects were 46 years old on average, so just a little bit older than me. I'm 39 years old as we record this.
I was a little less convinced that I'd have any calcification or hard plaque. Calcification being the body's way of patching up damaged arteries, part of a healing response that helps stabilize existing plaque. So, not necessarily a bad thing in and of itself, but isn't overly common for men under 40 years of age. While I couldn't find a study looking specifically at men aged 35 to 40 years of age, I did find a 2024 study of subjects in the USA and Canada that found that 31% of men under the age of 45 years old had calcified plaque. With the way that I've lived over the past decade, my hope was that I fell into the 69% of men under 45 that didn't have calcification. That said, I know that you can be fit and healthy on the outside and have calcification in your 30s. It's certainly possible.
I remember actually Peter Attia reporting a few years back that despite being super fit himself and seemingly healthy on the outside, he had a coronary artery calcium scan done when he was 36 years old and his score was six, which is actually what originally prompted him to lower his ApoB and LDL cholesterol to a level that halted atherosclerosis and presumably why he takes the topic of cardiovascular health so seriously today. So what's interesting here, so in 2009, I was 36 years old, woke up and said, "Man, every dude in your family died of a heart attack when they were young. I wonder what your risk is, even though you've been a lifelong exerciser." So in 2009, I got a calcium score and the score was six. So I had a speck of calcium in the left anterior descending artery. Even though six is a pretty low score for a 36-year-old, it's awfully high, placing me between the 75th and 90th percentile. That was 2009. That's when I started, you know, really be really becoming concerned about lipid management, uh, you know, all the things that I care about now. Of course, I know much more now than that.
With all of that context out of the way, let's look at my CT angiogram results. I had my CT angiogram done in Los Angeles with Dr. Matthew Budoff, a name that many of you will recognize. As many would expect at my age with my family history and prior lifestyle, and as I alluded to earlier, I did have some plaque. Was it a lot of plaque? Not really. It was described in the report from Dr. Matthew Budoff as minimal non-obstructive plaque. Specifically, the findings on the report read, and I quote, "Findings: The left anterior descending coronary artery with mild disease. The left circumflex coronary artery and obtuse marginal branches are without disease. The right coronary artery, acute marginal vessels, posterior descending and posterior lateral branches are without disease." End quote.
To get even more granular, we then had Clearly AI powered software review the CT angiogram images and provide specific measurements of plaque. Results are on screen for those watching on YouTube. And I'll read them out too. In the left main and left anterior descending artery, the one that Budoff's report described as having mild disease, there was a total of 46.1 mm cubed of non-calcified plaque volume. In the right coronary artery, there was 6.8 mm cubed of total non-calcified plaque volume. And in the circumflex artery, 8.1 mm cubed of total non-calcified plaque volume. All other arteries scanned including the first obtuse marginal, second obtuse marginal, first diagonal branch, right posterior descending branch, and the right posterior lateral branch were all clear with zero plaque observed. That means that my total non-calcified plaque volume measured across all of my coronary arteries with very sensitive software was 61 mm cubed. We'll come back to what this means in a bit.
To put things into perspective here, while I would certainly rather have no plaque, the average plaque progression in the recent ketoCTA study that I covered, which used the same Clearly software to analyze CT angiogram data was 31.5 mm cubed of plaque in a 12 month period for those following a ketogenic diet. So they were laying down on average about half of the plaque that I've laid down across 39 years in a single year. Now to better compare me to them, I would need to do a follow-up scan at 12 months to see how my rate of plaque progression looks. My percent atheroma volume or PAV, another way of measuring plaque, was 1.8%. This suggests minimal atherosclerosis. There is some early plaque, but it occupies a very small proportion of my artery walls at this stage. In other words, the disease process has started, but we're catching it early at a stage that, as you'll hear later, may be reversible with the right interventions. For context, in the reversal trial, a statin study in patients with established heart disease, PAV values at baseline were 40% or more. So, my 1.8% and 8% is low but still meaningful.
I also had a coronary artery calcium scan done and my coronary artery calcium score was four, indicating a small amount of calcium is deposited in my arteries, which really isn't too dissimilar to Peter's score of six that he identified when he was 36. The CT angiogram analysis by Clearly also measures calcium but gives you a better idea of the volume of calcium. And my total was 0.3 millimeters cubed, which I've been told is considered a trace amount of calcium. That's something that I'm going to follow up in a future episode with a cardiac imaging expert. Dr. Matt Budoff's report says that this score of four puts me in the 50th percentile for my gender and age, meaning that based on 30,000 persons scanned at Harbor UCLA, my coronary artery calcium score is average for my age. While this may seem reasonable given my lifestyle and my interest in living a long healthy life, I'm not really interested in being average here. And based on other data sets like the 2024 one that I mentioned earlier, there's actually an argument to be made here that I could be closer to the 75th percentile for my age and gender.
I'm sharing these scan results publicly even though they aren't quote unquote perfect because I think we need more real-life transparency. It's very easy to post perfect numbers or just not share any personal health metrics. It's harder but more honest to share the full picture here, especially when you have a pretty sizable audience of people listening to your content. And quite frankly, I'm less interested in looking perfect and more interested in education and shifting the needle on my health and hopefully your health, too.
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So with scan results in hand, I sent them to my buddy Dr. Thomas Daypring and I recently asked him what his initial reaction was when reviewing them. Well, I saw you had coronary atherosclerosis. Was I shocked or surprised? No, not at my age. I've seen too many people over time and it, you know, those who have risk factors sooner or later are going to show some plaque and I go back to my, you know, my good buddy and colleague is Peter Attia and he sort of did the same thing as you did, a coronary calcium at a very young age and it came back I think as a two and it shocked the heck out of him and uh, you know, so I've learned from Peter, you just never know what to expect. If you've had some risk factors over decades, those ApoB particles have dumped cholesterol in your artery wall and plaque has developed. So, can't say I was shocked. I think your 10-year risk of an event is an event meaning what we call major adverse coronary events, stroke, heart attack, bypass, angina, acute coronary syndrome is pretty low. But uh, being a sort of a longevity plus health span guy right now, you're 40, you're going to make it to 90 years old. So I would uh not want that. What you have in your arteries now to go untreated for the next even 10 years, I'd want to arrest it right now to thinking way down the road that even at age 70, I'm like, I said, just hit 79, I don't want to have a heart attack tomorrow. So whatever risk factors are there, I'm going after and we can go after risk factors a lot better now than we could when I was 40 years old where we had very few things we could do.
I was interested to know when atherosclerosis becomes cardiovascular disease by definition. While this is probably just semantics, it seems that it depends on who's asking, as explained by Dr. Dan Sofur here. Yeah, I always say it depends who's asking. So if somebody is, I'm talking, if I'm talking to a patient and they want to know if they have atherosclerotic cardiovascular disease, I say I'm not really comfortable calling it a disease, but I am comfortable saying you have atherosclerosis here, we've identified it with this imaging test. But if, for example, I need to leverage a diagnostic code in order to help them get therapeutic that is limited based upon a diagnostic code, I'm willing to use that code more liberally to help my patient. So, depends who's asking.
To date, I've spoken about these results with not only Dr. Thomas Daypring, but also cardiologists Dr. Lawrence Sperling and Dr. Martha Galati, and lipidologist Dr. Dan Sofur. All folks that are deeply experienced in preventive cardiology. The general consensus from my discussions with these folks is that most of the 61 millimeters cubed of soft plaque was likely laid down early in my life and then over the past 10 years it slowed down with the lifestyle improvements that I've made. Meaning that my commitment to a healthy plant-based diet, exercising regularly, not smoking, etc. could only have helped. But that doesn't mean that it was enough.
To understand the implications of my plaque volume, we need to talk about lifetime cholesterol exposure. We know the amount of plaque that we have in our artery walls is determined by our total cholesterol exposure over our entire life. It's similar to how the risk of lung cancer with smoking is evaluated by pack years, being the number of packs of cigarettes smoked per day by the number of years smoked. In the case of atherosclerosis, it's our level of LDL cholesterol or ApoB multiplied by the number of years at that exposure. For me, I've had 29 years of exposure at let's say an average of 125 mg per deciliter. And then the past 10 years at an average of 80 mg per deciliter. So my total exposure in LDL cholesterol in mg per deciliter multiplied by years comes to 4,425 mg years. This is a surrogate marker of cumulative cholesterol burden, which we know correlates well with total plaque laid down.
So what exactly does that mean? To help explain this, I'm putting a graph on screen and in the show notes for those that are listening from a review published in the journal of American College of Cardiology titled "Impact of Lipids on Cardiovascular Health" by Brian Ference and colleagues. If you're listening on audio, don't stress. I will do my best to explain the graph and this concept as we go. This graph shows the rate at which plaque progresses at varying levels of LDL cholesterol over time. Specifically, it shows three different levels: 200, 125, and 80 milligrams per deciliter. And it shows when you convert from asymptomatic plaque, so having plaque in the artery wall without any symptoms, to being at increased risk of symptomatic cardiovascular disease, that threshold where you go from asymptomatic plaque progression to being at increased risk of a coronary event due to reduced blood flow to the heart is 5,000 mg years. And this is actually a graph that I've had on my wall behind me for the better part of the last year. What's very evident is that the higher the LDL cholesterol, the less years it takes to go from asymptomatic plaque progression to risk of symptomatic cardiovascular disease in your life. People with an LDL cholesterol of 200, which is the red line, enter the symptomatic zone by age 20. People with an LDL cholesterol of 125, which is the blue line, enter the symptomatic zone by age 40. And people with an LDL cholesterol of 80 milligrams per deciliter enter the symptomatic zone by age 60.
So I was tracking along on the blue line, 125 milligrams per deciliter for the first three decades of my life. And then I course-corrected by shifting to a plant-based diet, begrudgingly letting go of steak, butter, cream, etc. Yes, I used to love those foods. And at that point, I got my LDL cholesterol down to 80 milligrams per deciliter. And my rate of plaque progression very likely slowed, which I've marked on the graph in yellow for you to see. If you're listening, imagine it like this. For the first 29 years of my life, I was driving towards a cliff at 125 km/h. Then in my late 20s, I hit the brakes. Not a full stop, but I slowed the vehicle down to about 80 km/h. So, while I'm still moving in the same direction and I've already covered a lot of ground, I'm now progressing toward that cliff much more slowly. Today, I'm further from the edge than I would have been had I never made a change to my lifestyle. Now, I didn't do a CT angio back then, so we can't know this for sure, but this graph and what we understand about lifetime LDL exposure strongly suggests that slowing down made a difference. And this is exactly why getting your LDL cholesterol down early in life is so important.
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If I could go back in time, I would have made lifestyle changes and considered lipid-lowering medication far sooner. An interesting question is whether or not we can confirm that I have actually slowed down plaque progression with my shift to a plant-based diet. The only way to truly understand my rate of plaque progression is to have a follow-up scan. So, we have two reference points, a baseline and then a follow-up, which may actually be on the cards. I'll share more on that towards the end of this episode.
Let's switch gears now to my latest blood test results that I measured with Function Health. This testing included over 100 biomarkers. Today in this episode, we're focusing on those that are specific to cardiovascular and metabolic health. And in an upcoming episode, I'll walk you through the other results that are important to keep an eye on.
Starting with the metabolic health markers. Firstly, fasting blood glucose, HbA1c and insulin were all within the healthy optimal range. My glucose was 87 mg per deciliter. HbA1c was 5.3% and insulin was four, indicating good insulin sensitivity, blood glucose control, and overall metabolic health.
When it came to my most recent blood lipids from a few weeks ago, I do have to admit I was a little surprised. Everything was in range except LDL cholesterol. My LDL cholesterol came back at 103 mg per deciliter. On my last test a year ago, it was 77 milligrams per deciliter. And my ApoB has gone up from 69 to 89 mg per deciliter. I'm putting this down to a recent change to my diet. As you may know, I've recently been training for a marathon. And with that, my appetite and overall calorie intake has gone up a lot. One addition has been this high protein coconut yogurt that I found, which per serve has seven grams of saturated fat. I've been averaging two serves of this per day for about the past 3 or 4 months. This shows how sensitive our lipids can be to even small dietary shifts and why blood tests matter even when you feel healthy. It's also a reminder that just because something says high protein on the packet doesn't necessarily make it healthy. And to be honest, I knew this, but it was never really something that I had tested. The effect of coconut on my personal blood lipids. Now I know. And lesson learned. Clinical trial evidence supports this with trials showing that coconut oil, which is about 82% saturated fat, raises LDL cholesterol compared to non-tropical plant-based oils, including monounsaturated fat-rich plant oils like olive oil and also polyunsaturated fat-rich plant oils like safflower oil. On the other hand, coconut oil doesn't seem to raise LDL cholesterol as much as butter. Of course, at an individual level, we're all going to respond slightly differently to each other. You may not be as sensitive as me to lauric acid, which is the predominant saturated fat in coconut yogurt. The only way that you would know this is by testing and looking at your LDL cholesterol and ApoB.
Every other blood lipid and cardiovascular disease risk marker in my results looked great. Triglycerides were low and in range at 75 mg per deciliter, which is great. And my Lp(a), which is a genetically determined blood lipid that is known to increase the risk of atherosclerosis, was very low and my hsCRP, which is a marker of inflammation, was very low at less than 0.02 mg per deciliter. In addition to these more traditional cardiovascular disease biomarkers, my omega-3 total, which includes DHA, EPA and DPA, is optimized at 7.5%. My omega-6 to 3 ratio is 4.6, which is considered in range, and my omega-6 linoleic acid is also in range. Interestingly, my arachidonic acid, which is another omega-6, was actually below the normal range. And a note was included with this result, and I quote, "Arachidonic acid levels below the reference range may reflect reduced inflammation, which can be beneficial when balanced with optimal levels of omega-3 fatty acids such as EPA." End quote. All of this I would expect for someone who supplements with DHA and EPA omega-3s and eats a diet that emphasizes healthy fats from foods like olive oil, nuts, seeds, avocado, tofu, etc.
You might be wondering, what ApoB level should I aim for to reliably halt plaque progression or potentially induce regression or reversal? Here's what doctors Thomas Daypring and Dan Sofur had to say on this. Well, my two lines of evidence which will support what I would recommend is I already mentioned the hypobeta, the genetic hypobeta. People who the day they're born have a very low apo LDL cholesterol. It remains that way throughout life. They just don't get atherosclerotic heart disease unless they're at the upper ranges of that apoB or so. So, uh, that would be one reason and make your apoB under 40 milligrams per deciliter. You know, Brian Ference is the lead author. I think it was one of the European guidelines and uh looking at Mendelian data, observational data, and all the randomized control trials. And he even showed that starting with an LDL cholesterol of 70 or 78, if you keep dropping it below there, those lines almost went down to zero as far as the event rate or so. So, it's lower is better. That is not debatable anymore. We add now the adjective lower is better and the longer it's lower is better. So, uh, I I would want your I would shoot for an ApoB. Certainly, you want to take the fifth percentile, 60, but again, your family history, you there's no harm in making your ApoB 40. There's no downside to it. The DR maybe, you know, depending on where you start, you're going to get in more and more pharmacology, and some of those could be expensive, but you could start simple and see where you get. And with a couple of generic drugs, you might be able to bring your LDL cholesterol and ApoB down to those levels. So that's where I'm going. I'm making you a hypobeta.
So I'm glad you brought up the Mendelian randomization data. It it's super interesting. So you know, in clinical medicine, we we rely so much on cardiovascular outcome trials and most of our cardiovascular outcome trials are approximately five years. Um, and in recent years they've been abbreviated by making them much larger trials so that they can get the information in three years. So you know, larger database, you can sometimes get information a lot sooner. And some of our studies maybe go as long as seven years and then they then they'll do something like an open label extension just so you can get a little bit more data than that. But most of our data comes from these very short cardiovascular outcome trials. So a Mendelian randomization trial compares to that and enables us to imagine what would happen if you had a genotypic variant that gave you a specific phenotype like an LDL cholesterol that's 10% lower than the average pop the average person in your population. But instead of imagining that as a over five years, that's, you know, you look at someone who's 50 years old with that genotype and who's had that LDL cholesterol lowering for 50 years and you compare them to a population rates of cardiovascular events and you see an outsized proportional benefit from very small LDL cholesterol lowering compared to the general population suggesting that there's compounded benefit from prolonged even small reductions in LDL cholesterol. Now, most of our cardiovascular outcome trials don't look at small reductions. They look at large reductions. You know, we like our drugs to lower LDL cholesterol by 20% at a minimum. 50% is even better. And now we have drugs that can lower LDL cholesterol by 60%. And you know, so you can get a greater short-term cardiovascular benefit and a long-term cardiovascular benefit we extrapolate as being even more pronounced because you get so much more lowering. So that that informs the lower is better and the and longer is better and then but those are cardiovascular outcome trials. If we're looking at short, you know, if we really want some other information about what's happening at the arterial level, that's where I really think the IVIS data is is really neat because you can see what's happening at the micro level using intravascular ultrasound and look at the plaque changes in a short period of time. And the data set that I think is really interesting is that Glagov remodeling study where they looked at the intervention adding evolocumab, which is a PCSK9 monoclonal antibody on top of high-intensity statin. So a high potency LDL lowering therapy on top of another high LD uh high potency LDL lowering therapy. And what you see is that when you when you get LDL cholesterol levels down to about 90 milligrams per deciliter, all you've done is about is kind of slow the progression of plaque. But in these high-risk patients, if you get it between about 60 and 90, you seem to be able to stop plaque from progressing. It really flattens out in the IVIS studies, but it's not until you get below 60 that you see some actual plaque regression at the microscopic level. You're not talking about changes in the lumen diameter, but you get these microscopic regressions. And so that might be something that we can extrapolate to your care, Simon, right? You you you don't want just to do okay. You're trying to really fix your arteries and make them as stable as possible for as long as possible. So I think targeting LDL cholesterol levels below 60 for you is a very reasonable thing to do. In if we look at ApoB goals in our treated patients at the lower end, um, the relationship is uh, at if you're using an LDL cholesterol threshold of 55, where you would do more if your LDL cholesterol was greater than 55, the real, the the, uh, number of ApoB that we would use as that threshold is 60 milligrams per deciliter. And Annmarie Navar's group did a simultaneous evaluation. They saw the same numbers and they thought, you know what, it's simpler to just say 55 and 55. Just they're so close together. It's okay to just use the same number. But for precision, we we did distinguish between them. If you're aiming for ApoB levels less than 55, I think that's very reasonable. I think that your potential genetic input into your cardiovascular risk is like a a black box. Um, in reality, I don't I don't know exactly how potent your your genes may contribute to your cardiovascular risk, but your father's story is very dramatic. And if you had seen me when you were 20 years old, knowing what I know now about atherosclerosis, not not me 20 years ago, but at knowing what I know now at about atherosclerosis, I would have said, gee, I don't have any good tool to know really what your future holds. But if I had that father, I would I would initiate pharmacotherapy on top of optimizing healthy lifestyle starting the first time you we had the conversation. And because that family history is so striking.
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In order for me to get down to this target ApoB level, closer to 20 than 55 milligrams per deciliter, I asked what pharmacologic therapy they would recommend as optimal with the assumption here being that I have access to all lipid-lowering drugs. Simon, I you know, when I sit down with my patients and talk about how to pharmacologically lower their LDL cholesterol and ApoB, I I think there are certain talking points for each of for all of them that should be the same. And uh, first thing get off the get get off the table is there are no safety issues with any of the drugs. There there are tolerability issues, but there are no safety concerns. So we we don't we can dispense with the concept of putting people in harm's way or safety concerns. And really I think the first thing to talk about is the cardiovascular outcome trial evidence. So as of 2025, there are over 30 major cardiovascular outcome trials with statin drugs, 3030 that have been completed that show not just that they lower LDL cholesterol and ApoB, but that they reduce cardiovascular events. If if you add up the cardiovascular outcome trials with all the other therapeutics, there are five, maybe if you're generous, six. So just sheer evidence, there's the evidence strongly supports the use of statins as the foundation of treatment. And then the other aspects to pay attention to are tolerability, LDL lowering potency, accessibility, which includes cost, the comfort of taking a pill versus a shot, and if you're going to take a shot, should it be every two weeks or should it be every six months? Those kinds of comfort and access issues. And And um, and you know, efficacy? You know, LDL lowering potency. So, um, it's pretty it's a pretty short list of things to pay attention to. And but statins are the foundation. Now we've come a long way since 2013 when we had zero cardiovascular outcome trials for anything other than statins and bile acid sequestrants from the 1980s. So we now you forgot Jim Finnegan in 1984 in the Helsinki Heart Trial. I did. My apologies. My apologies at leaving Jim Finnegan out. I um, I have to amend my list. So it's six cardiovascular outcome trials. I want to point out Tom that you didn't disagree with me at all. You said you disagreed with me. I I said the same thing. I think maybe the verbiage that we're using is a little different. When I'm referring to potency, I'm referring to the amount of LDL lowering per milligram of the dose. And that's why I favor atorvastatin and rosuvastatin. And I also agree with you that favor using a dose that someone feels comfortable with. I don't feel obliged to use full dose even if that's the dose that was used in the cardiovascular outcome trial that you know that we're basing our decision on. I'm very comfortable using the dose that the patient is comfortable with. And a reminder that when you double the dose, you're only getting about 6% LDL cholesterol lowering. And that that's inconsequential to the patient. Most of the LDL receptor upregulation, which is how these drugs work, occurs with the baby dose of the statin. And you get a little more LDL receptors every time you double the dose, but far less than you got with the initial dose. I thought you were saying everybody goes on a high dose statin. I miss I miss high potency. High potency. Yeah. Okay. Glad we cleared that up.
Now, whenever we talk about lowering cholesterol on this show, inevitably there's comments. But Simon, our cells need cholesterol to make vitamin D and for cell membrane fluidity, for hormone production, etc. I certainly understand why people are concerned here, but this concern is easily cleared up with a little bit of basic physiology as outlined by Dr. Thomas Daypring. Look, cholesterol is obviously an essential molecule for human life. It's in every cell membrane in our bodies and without cell membranes, no cells. Therefore, I always phrase it this way, evolution went to great power to make sure every cell in your body could de novo synthesize all the cholesterol it needs for whatever it's in its cytosol and in its cell membrane. And it even knows that above a certain threshold, cholesterol molecules are toxic because they can crystallize. It also gave every cell the ability, a tool, a membrane efflux transporter to get rid of any excess cholesterol. So cells, if you look at what we call cholesterol homeostasis, it's an imbalance. Every cell doesn't need help. Well, there might be one or two exceptions to that. Now, when I'm talking with cells, there are two types of cells in your body: brain and everything else below the brain. That's called peripheral cells. But even the brain and all the peripheral cells make all the cholesterol they need. Ergo, they don't need a delivery of cholesterol. When we measure cholesterol, we're measuring cholesterol that's circulating in the plasma lipoproteins. We're not measuring your any tissue cholesterol level or so. So, we have to extrapolate from a plasma cholesterol level. Are we injur in injuring or uh hurting a cell by depleting plasma cholesterol? And if you listen to what I just said, cells don't need a delivery of cholesterol. Then no, we're not. Basically, most of the cholesterol in plasma is within your LDL particles. And we now know their primary purpose is to bring cholesterol back to the liver and likely the small intestine. Clearance of the apoB particles. And then those organs, the uh intestine or the liver, can do other things with the cholesterol. HDLs carry the next largest amount of cholesterol in your body. And where are they going? For the most part, they're going back to the liver or the small intestine, but HDLs have the ability to deliver cholesterol to a couple of cells that might need extra cholesterol, and that would be your steroidogenic tissue. Again, for the most part, they synthesize all the cholesterol they need. They don't need a delivery. But if they do, they can upregulate something called the scavenger receptor, which delipidates cholesterol from the HDL and they get an extra supply, maybe in an urgent situation, especially the adrenal cortex where they got to start shooting that cortex. And the other tissue that can upregulate those scavenger receptors and take cholesterol from an HDL is the storage organ in the body for cholesterol, our adipocytes. Now, LDLs don't deliver cholesterol to adipocytes unless an extreme emergency. LDLs do not deliver cholesterol to steroidogenic tissue. They could, those cells could upregulate LDL receptors, but they rarely do. So the cholesterol in your plasma cannot be used as an indicator that I'm hurting a cell. Last thing I'll say is because everybody, I get tweets every day, you're shrinking your brain when you uh drop LDL cholesterol too much. Your brain starting in like the second and third trimester in utero and certainly from the day you're born synthesizes de novo all of the cholesterol it needs. It doesn't get a single molecule of cholesterol from anything carrying cholesterol in your plasma. So we've proven this in clinical trials. If I make your LDL cholesterol 15 because you're a nightmare and I want to make your ApoB or LDL cholesterol that low, I cannot hurt any cell in the body by depriving them of cholesterol.
You might be thinking, well then why the heck is cholesterol produced by the liver and shuttled into the blood within lipoproteins? Then what's the purpose of that? To answer this, let's go back to Tom. Few even modern lipidologists know this because you have to go back and start reading the 1950s data with Don Frederickson and the earlier ones and their great treatise published in 1967 in the New England Journal, a five-part series on lipoprotein and lipid transport in the plasma. They really showed that answer your question there. Essential to ship out triglycerides in the VLDL particles in the chylomicrons because that's energy for various tissues that store it or utilize it. But since no cell needs cholesterol delivery, why did the liver put cholesterol or even the intestine? The intestine sending absorbed cholesterol, but the liver making VLDL particles and it's basically to give structure and make the particles spherical. So they're larger. It's serving a structural purpose, the cholesterol in the LDL particles and even in the VLDL particles and and they send the VLDLs out. Why would they even send the LDLs out if they're not delivering cholesterol? Because Dan sort of mentioned that little tricky transfer protein, CETP. HDLs are the particles that accept unneeded cholesterol from whatever tissue is trying to get rid of cholesterol to avoid its cellular toxicity. But once the HDLs filled up with cholesterol, again, this is the genius of evolution. They said, "Hey, HDLs, just transfer your cholesterol over to the LDLs, they'll bring it back to the liver, and you will become small again. You can go back out and get more cholesterol from any cell looking to efflux it." So people don't realize when they look at an LDL cholesterol level, a substantial part of the cholesterol within the core of LDL particles was just transferred to them by HDL particles. But the LDLs were sent out with X amount of cholesterol because they're spherical particles of a certain size and it gives them structural integrity and that's why the cholesterol is in those ApoB particles. ApoB particles do not per se deliver cholesterol to tissues in an emergency. They could, any cell can upregulate an LDL receptor, but I don't think that happens much if at all. So there's complex physiology going on here and and that's why cholesterol serves a structural purpose on both the surface and in the core of LDL and other apoB particles.
So with all of that insight from Dr. Daypring and Dr. Dan Sofur, I now have a decision to make. Do I stay the course or start medication to lower my ApoB and LDL cholesterol to a level that completely stops plaque progression or potentially induces regression? All of this has certainly given me pause, a moment to reflect, a moment to gather information and make the best decision for my health going forward. And I wanted this process, this thinking aloud, the decision-making to be public because ultimately I believe that transparency, especially around how we navigate important health choices, can help others on their own health journey.
Here's where I'm currently at as I record this. At a high level, this is a powerful reminder. You can be doing all of the right things on paper. Your blood tests can look excellent and you can still be developing atherosclerosis. Heart disease is called a silent killer for a reason. It creeps up slowly, often over decades without symptoms. And sometimes the first sign is a heart attack or stroke. And our biology, which is shaped by evolution, doesn't care if we thrive into our 90s with sharp minds, healthy hearts, and strong bodies. It cares about survival and reproduction. But that's not enough for me. Like you, I imagine, I want to thrive into my 90s, mentally sharp and physically independent. Dr. Daypring often says that most of us will die with cardiovascular disease. But today, we don't have to die because of it. That's what we are talking about here. I don't think anyone really cares about plaque, the millimeters cubed of plaque that we have. We care about whether or not we have a heart attack or a stroke. That's what we're trying to get on the front foot to prevent. And prevention is something that I've taken very seriously for the past decade of my life. I'm proud of the changes that I made in my late 20s, especially shifting my diet. That certainly wasn't easy in the environment that we live in, but it worked. It dramatically lowered my cholesterol and very likely slowed the development of plaque in my arteries. That said, it's clear that I'm genetically predisposed to cardiovascular disease and
My change in diet didn't get my LDL cholesterol or my apo to a level where we see no plaque progression. That threshold appears to be around 50 milligrams per deciliter. And if I want to get there, which I do, the most effective next step is combining my current lifestyle with lipid lowering medication.
As Dr. Peter puts it, this is medicine 3.0: using modern medicine alongside lifestyle, not instead of it, to optimize for long-term health. That doesn't give me a pass to then go and eat whatever I want. Quite the opposite. The more I can adhere to a healthy dietary pattern, the lower the dose of medication I'll need. And the same dietary pattern that helps lower cholesterol also supports healthy blood pressure, glucose, inflammation, etc. So this isn't an either or, it's an and.
And when it comes to the decision that I get to make, it's not if I take lipid lowering medication, it's when. The academic curious part of me wants to wait 9 months, repeat a CT angiogram, and see what my plaque progression looks like without adding the variable of lipid-linging medications. That might confirm my hypothesis that most of my plaque was laid down during the first three decades of my life before I made these lifestyle changes. But the evidence-based risk-aware part of me says that's primarily my ego, just me trying to prove something. And in doing so, I could be wasting nine months where I could be halting progression entirely.
Even if the next scan shows no progression, the current evidence suggests that I should already be on therapy to stabilize the plaque that's there. I haven't made my mind up on this yet. One thing that I want to look into further is the radiation exposure from doing a repeat CT angio within 12 months. What are the risks there and is that worth it?
Next week, I'll share the full conversation that I had with doctors Thomas Daypring and Dan Sofa. There's even more detail in that episode than what I covered today. And in the coming weeks, I'll be sitting down with more experts to explore topics like cardiac imaging and the full spectrum of lipid lowering therapies, including statins, as well as other medicines and also neutrauticals that are often included in this discussion such as aspirin, kylic garlic extract, red yeast, rice, phytosteriles, vitamin K2, and CoQ10. I'll also be exploring studies looking at reversing atherosclerosis, be it through lifestyle changes, medicine, or a combination of the two. This is something that I've covered in my book, but it does deserve its own episode and deep dive, especially given that there's been some new evidence published since my book came out in 2021.
In case I didn't already have enough motivation to dig into this topic, I've now got a little more skin in the game. After all, this shows arguably a little more helpful and hopefully fun when the host is alive, when I'm alive. So to close this episode out to answer the question that we started with, has my plant-based diet been enough to prevent cardiovascular disease? The honest answer here is we don't know. I have a mild degree of subclinical atherosclerosis. And there are a few different possibilities here. I may have developed all of this plaque before going plant-based. I could have had more plaque and seen some regression when I changed my diet, or I may still be progressing, just more slowly than I otherwise would have. Without an earlier scan, we really can't say for certain.
But based on my current blood lipid levels, I'd guess that the plaque is still progressing, just not as fast as it would have been. In other words, switching to a plant-based diet helped slow the car down. I'm no longer speeding toward the cliff at the same pace I was, but I likely have not stopped moving forward altogether. And now I have a decision to make. Do I keep cruising slowly toward the edge for another 9 months? Or do I hit the brakes harder, combining lifestyle with medicine, and stop the car before it goes any further?
And while I'm sure some people online, many of whom haven't shared their own blood tests, let alone a CT angagram or calcium score, may twist this to suit their narrative. That's not something that I'll be giving much energy to, unless they put forward some genuine science for me to look at. Others are certainly free to speculate. I'm choosing to stick with the facts that we have at hand. If you're interested in how this unfolds, when and what lipid lowering medication I decide to take, hit subscribe and please come along for the ride. That's it for today. Thank you so much for hanging out with me. I'd love to hear your thoughts, any questions that you have, feedback, your own story, or even your own results. Drop a comment on YouTube or Spotify. I read them all and reply to as many of them as I can. and I look forward to catching you next week.
Oh, you're still here. What are you hanging around for? Well, actually, it's good that you're still here because I forgot to mention something that's really, really important. What do you call a fish wearing a bow tie? Sophisticated.