My Plaque Protocol, and Why I Started a PCSK9 Inhibitor | with Simon Hill, MSc

0:00A few weeks ago, I shared my own heart scans and the amount of regression was dramatic. In 16 and a half months, the plaque in my arteries had dropped by 48%. And the top comment on this video, how did you do this? And underneath that, person after person asking the same thing. One person said the whole episode felt like a bait and switch, that they were never going to find out how to actually reduce plaque. Fair enough. That episode, though, was about my results. This one today is how I got them, and whether that 48 % was even real. Because here's the part that might seem strange. Despite that number, I've started a prescription medication to lower my blood lipids.

0:49In this episode, I'll tell you exactly which one and why. Quick housekeeping before we get into things. This, of course, is not medical advice. It's one person's process, and your numbers belong with your doctor. If you're new here, I'm Simon Hill, physiotherapist by training, master's in nutrition science from Deakin University in Melbourne, and I've interviewed hundreds of researchers and clinicians on this show since 2018. I have a particular interest in cardiovascular disease and track this disease in my own arteries, which is what today's episode is all about. I'll go as far as saying I don't think anyone else on the internet has had their coronary arteries analyzed this many ways and then been silly enough to publish all of it.

1:34Some might even say that this is a world's first. Take that for what it's worth, of course. It's hardly a competitive field. So a quick recap in case you missed the last episode on this topic. I've had serial coronary CT angiograms or CCTAs. These scans don't just tell you whether you have blockage. They allow you to quantify how much plaque is in your arteries and what type it is. So instead of being told that you have mild, moderate or severe soft plaque, I got reports breaking it down. Soft plaque, calcified plaque, total volume, all in cubic millimeters. And just so we're clear, this isn't the plaque your dentist talks about.

2:17Different plaque, different body part. Though it would be pretty cool if we could floss our arteries. The first scan I had was in December 2024 at age 38. And then a follow-up scan 16 and a half months later in April 2026 at 39. I've since turned 40. That's a whole nother story, but happy birthday to me. Same imaging center both times. Same scanner, same protocol. at the Lundquist Institute in Los Angeles, under the guidance of Dr. Matthew Budoff, one of the world's experts on this type of imaging. Those scans, the baseline and the follow-up scan, were then analyzed by three different software platforms.

2:58On one of them, HeartFlow, my total plaque volume had dropped by about 48%. That's the number that ended up in the title of this episode. That's the number that people are asking about. But I want you to hold on to one detail. That 48 % came from one of the three platforms that read my scans. Which number I actually trust and why is something that I'll come back to later. Thinking about the results from the three providers changed how I'm treating this and also raised some rather interesting questions. Before we get to what I did between these two scans, I want to answer a different question from the comment section, because I think it's actually the more interesting one.

3:43And it speaks to the origins and the development of atherosclerosis, which is a fancy name for plaque building up in the artery wall. Someone wrote half-jokingly, how did he get plaque in the first place if all he eats is vegetables? Just to be clear, on the record, I do eat more than just vegetables. but I understand the question. If the evidence supports plant-rich diets for lowering cardiovascular risk, how did I have any plaque at all? There are three parts to this answer. The first is that I have not always eaten this way. For the first 30 years of my life, I ate a fairly standard Australian omnivorous diet.

4:22Beef, lamb, we love lamb chops in Australia, veal, chicken, milk, butter, etc. And based on the blood tests I have from my 20s, my LDL cholesterol through that period was sitting around 125 milligrams per deciliter. It wasn't until I was 30 when I shifted to a plant-based dietary pattern, swapping the meat for foods like tofu and tempeh, beans, etc. Swapping butter for olive oil. And when I did that, my LDL came down into the 70s. And this is the part that I really want you to hear. It might just be the most useful thing in this entire episode. Plark in your arteries is about cumulative exposure.

5:03It's not about what your cholesterol is today. It's about the area under the curve, how high for how long across your whole life. It's easy for us to think about cardiovascular disease as this disease that affects older people, the 50 or 60 year old man that has the heart attack or the 80 year old that has a stroke. But the road to that event was quietly being paved from very early in that person's life, sometimes from early childhood. I personally had three decades of high LDL cholesterol exposure before I changed anything. And unfortunately, plaque doesn't just reset when your diet does. And I'm not alone in having plaque at my age.

5:48A study published in the New England Journal this month, 16 ,000 adults across Denmark and Spain, none of them with known heart disease, imaged the arteries in subjects' neck, their legs, and their heart. Among men in their 30s, more than a third had plaque somewhere in their carotid arteries, in their peripheral arteries, or coronary arteries. 9 % had it in their coronary arteries. So having some atherosclerosis at my age is certainly not unusual at all. It is true that having it in the heart, specifically in the coronary arteries, is less common. But it's important to note that I was 38 at the first scan and 39 in my follow-up scan where some plaque was detected.

6:36From this same study, once you get into the 40s, the number of subjects with atherosclerosis jumps. Two-thirds had plaque somewhere and 31 % now had plaque in their coronary arteries. A lot changes between your 30s and your 40s. Now the good thing is that I found out at age 38 as opposed to finding out at 60 in an ambulance. Now coming back to our question about why I have any plaque at all if I follow a plant-based diet, The second part to my answer here is that clearly LDL cholesterol, or APOB more specifically, is not the entire story. APOB is the protein that sits on the surface of every atherogenic particle, atherogenic lipoprotein.

7:26It's essentially a count of how many cholesterol-carrying particles are circulating in your blood, and it's causal in plaque development. It's the single best lipid marker that we have. But two people can have identical ApoB and carry very different amounts of cardiovascular disease. And that difference is everything else that matters. Blood pressure, insulin resistance, inflammation, LP little a, genetics, etc. In my case, a lot of the everything else is actually favorable. My LP little a is 14, which is low. My blood pressure is good. My insulin sensitivity is great. but I do have a strong family history of cardiovascular disease.

8:12And this is where we cannot overlook genetics. In fact, I think up until the last year, I may have even underestimated the role of genetics in cardiovascular disease. It's now thought that up to 50 % of your cardiovascular risk is genetic. But this is the most important part that isn't usually down to a single gene. For most of us, it's what's known as polygenic. A signature made up of hundreds, even thousands of small genetic variants, each nudging your risk up or down a little. Each of us carries a unique version of that signature, and it could be making us more or less prone to laying down plaque as we age, independent of our cholesterol.

8:58It's one of the big reasons why two people with identical ApoB can end up with very different amounts of disease. This is something that I find fascinating and honestly under-discussed, something that I don't know enough about and want to learn more about. So I'm doing a series of genomic profiling tests with medical geneticist Dr. Robert Green for an upcoming episode. Partly out of pure curiosity and partly to have a proper conversation about where this field is at today. Because there is a harder question underneath it. Does genetic profiling actually change clinical decision-making yet? Or is it interesting and potentially very expensive information that doesn't change what you do?

9:45It's a conversation I haven't seen many people have, and I'm looking forward to it. Another reason to go and hit the subscribe button. Needless to say, there is a lot about this disease we don't fully understand. And it's entirely possible I carry a genetic susceptibility that makes my arteries more prone to developing atherosclerosis, more susceptible to these ApoB-containing lipoproteins. If you've been listening to me or some of my guests talk about the gut microbiome, you'll know that it thrives on very specific types of fiber and polyphenols and resistant starch, many of which the average person falls short on, despite the very best of intentions.

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11:14If you're a regular here, you'll recall my dad had a heart attack at 41 and his dad at 49. Now the third part of answering this question, why do I have plaque if I eat a healthy plant-based diet, is the counterfactual. And I can't test this. It's very possible that if I hadn't changed my diet at 30, I'd have considerably more plaque today. It's also possible I've been slowly regressing ever since I did make that change. I can't know. Nobody gets to run the other version of their life. you never get to see the disease you avoided. If only we all had a sliding doors movie made after our life. Now here's where this connects to everything else.

12:00My APOB without any medication sits between 70 and 80 milligrams per deciliter. That's a level which plaque regression can occur at. But the trial data suggests it's more likely and larger in magnitude when you go lower. And the study worth knowing here is Glagov. It put people with coronary artery disease on either a PCSK9 inhibitor or a placebo on top of a statin and measured the plaque in their arteries with intravascular ultrasound before and after. The more they lowered LDL, the more the plaque regressed. There was no flaw. The relationship held all the way down to 20 milligrams per deciliter.

12:44In that lowest group, 81 % showed regression. Now there are two caveats to this study and they do matter. That dose response analysis was considered post hoc, meaning that it wasn't what the trial was designed to test. And these were people with established symptomatic coronary disease, not someone who is asymptomatic like me. So granted, I am extrapolating here, but the direction of the effect is consistent with other studies and it's why I've made a decision that I'll come back to at the end of this episode. So what was I actually doing during the 16 and a half months between my scans that led to the 48 % regression headline?

13:30Specifically, what was my protocol? This is what people ask for so I'm going to be specific. Then we'll come back to the scans and results from the three different providers. Starting with nutrition, at age 30 I adopted a high fiber plant-based diet with a real emphasis on protein. I'm eating somewhere between 1.2 and 1.6 grams of protein per kilogram of body weight per day. That's higher than most people assume a plant-based eater is getting and I want to say it's deliberate. I'm training hard and I want to hold on to muscle. My favorite protein-rich plant foods are tofu, tempeh, seitan, and a plant-based protein powder.

14:15I'll usually pair one of those foods with something slightly less protein-dense like beans, chickpeas, lentils, edamame, nuts, or seeds that bumps the total protein up within the meal and also brings in more fiber. My carbohydrates are almost entirely whole foods, legumes, oats, potatoes, rice, sourdough, etc. And my fats are predominantly unsaturated. Olive oil, avocados, nuts, seeds, soy milk, other soy foods. I'd say that I naturally gravitate towards a higher fat, more moderate carb plant-based diet. I've actually found that a plant-based diet with more fat got my ApoB down the lowest and also left me feeling better than a low-fat diet.

15:09That's my nutrition. It's not complicated. It's certainly not exotic. And I want to be generous here because I think this gets tribal in a way that isn't useful and that it doesn't have to be. This dietary pattern is consistent with the overwhelming body of evidence on what a heart-healthy diet looks like that will lower one's ApoB and lower one's overall risk of cardiovascular disease. But you don't have to eat exactly like me. If you want animal foods in there, the ones with the better cardiovascular evidence are fatty fish, yogurt, cheese, and even eggs. And a high-quality Mediterranean pattern has a large body of evidence behind it.

15:53The common thread is mostly whole foods, plenty of plants and healthy fats. And it's a great thing that there is more than one way to get there. If you want to go deeper on that, I did a whole episode on dietary patterns and plaque, and that is episode 404. In that episode, I walk through the evidence for plant-based dietary patterns specifically for slowing plaque progression and possibly even reversing it. I'll link to that in the show notes. Next up is exercise, resistance training three to four times a week, about an hour each session. I play padel four to five times a week which includes a mix of matches and training although I've just had about six weeks off following a near complete rupture of my CFL ligament in my ankle.

16:41So I've been on the stationary bike much more recently. This combination of exercise puts my VO2 max at 51 and that's a proper lab test on a treadmill, not a watch estimate. VO2 max being a measure of cardiorespiratory fitness and a strong predictor of cardiovascular risk and longevity. That reading is a few years old now and I actually suspect that today my VO2 max is in the mid to high 50s. I'll get this retested later this year for a little bit of fun and report back. You can see on screen a weekly breakdown of my current training zones. 16 minutes in zone 5 per week, an hour and 40 minutes or so in zone 4 which is probably more than most people would guess and then a bit over four hours across zones 2 and 3.

17:35There's nothing fancy about this cardiovascular training. It's just consistent volume and most of it comes from playing a sport that I love, which would be my recommendation for you. Find a way of cardio that you find enjoyable so you'll do it more often. Next, we have to talk about sleep. I'm pretty good at getting eight hours a night consistently. Not perfect, but according to my wearable, 90 % of the time I do get the recommended amount of sleep. And I want to be practical here about how that happens because get eight hours as a recommendation is useless advice on its own. For me personally, I can't sleep in.

18:18I'm up and awake around six, no matter what. So the only lever that I have is the time that I go to bed. So I'm in bed before 10 and I'm fine. Later than that and the eight hours just doesn't happen. Now, if you're more of a night owl, the same logic works with a later bed and wait time. Overall, I'm very consistent with the time that I get to bed because the difference is not subtle. On eight hours, I'm clear. Under six and I get that puffy, foggy, inflamed feeling and I'm just nowhere near 100%. Now, in addition to getting to bed before 10 p.m. I will also try and avoid bright light for a few hours before bed.

19:03I try and stay away from emails and anything overly stimulating in that wind down window. I have a cool dark room and I will say I did invest deeply in a very very comfortable bed. In fact I was always jealous of how good hotel beds felt. And then I eventually realized it's a bit stupid not to recreate that at home where I sleep 95 % of the year. And finally on sleep, and I'm not paid to say this, despite 8 Sleep being a sponsor of the show, I do really believe that 8 Sleep, by temperature controlling my bed and changing that temperature throughout the night to optimize the different stages of sleep has really taken my sleep and recovery to another level.

19:53You're probably wondering about supplements, and this might be the most surprising part. Despite the hype online about natokinase and other supplements, during this entire period between my baseline scan and my follow-up, I wasn't taking any supplements targeted at my arteries. Nothing. And in fact, that was deliberate. I've done a whole episode on supplements and atherosclerosis, that is episode 425, and in that I covered aged garlic extract, natokinase, K2, omega-3s, etc. And I'll link to that in the show notes if you didn't catch it. But the point of this window between baseline and follow-up was to see how my existing lifestyle was influencing my rate of plaque progression before I added in any new variables.

20:41If I'd made a bunch of changes, changed five or more things during this period, I would have learned nothing. So to be explicit, no aged garlic extract, no berberine, no red yeast rice, no lipid lowering medication. What I was taking daily and still take is a multivitamin, creatine, one and a half grams of combined EPA and DHA omega-3s, and a prebiotic powder. If you want to learn more about those supplements, see the show notes for details. There's one more thing here that I do think is important and it's less of a protocol, more of a disposition. I try my absolute hardest not to take life too seriously.

21:26I've always leaned towards a bit of playfulness and lightness, perhaps more playful and lighter than I give on on this show because really perspective is most of the game. So when I notice I'm frustrated or I'm grumpy, which of course happens, I'm fairly quick to work out why and I will sit with it. If there's a conversation to have, I will have it. But if something is really outside of my control, I just let it go and I come back to the small pleasures, things that I can control what I'm grateful for and I want to be clear that's not avoidance I've done avoidance and I know the difference it's just being strong enough to not get stuck in the stress loops that make life harder than it needs to be most of what we stress about is noise wearing a very convincing costume.

22:22Now, that's often easier said than done, and I realize I'm in a very privileged position, so my ability to cope with stress is not going to be exactly the same as the next person's. There are ginormous inequities in the world. It's not a fair world, and it's no wonder that these inequities are strongly associated with health outcomes, including cardiovascular disease. We talk a lot on this show about important biomarkers like ApoB and blood pressure, VO2 max, etc. Here's one that most men have never measured, sperm health. Possibly the only biomarker that nobody volunteers at dinner. I did a test recently and I am pleased to report back that the boys are there in numbers and swimming well.

23:11Very well. Swim Club have shared some of their own customer 90-day results and they are striking. One man nearly tripled his total sperm count from 217 million to close to 600. Read that the way that you'd read any before and after. This is an individual customer, not a controlled trial. Not a promise, but encouraging nonetheless. What's not in doubt here is the science of the timeline. Sperm takes roughly 72 to 90 days to develop. So what you're doing now turns up in a sample a few months from now. If you're not where you'd like to be, there is a real window of opportunity to work with. That's the thinking behind Swim Club's 90-day protocol developed with Stanford urologist Dr.

23:50Michael Eisenberg, clinically studied ingredients at effective doses in one daily dose, not a generic fertility supplement. Male factors are involved in roughly half of infertility cases. So gents, it's time for us to be proactive. For listeners of the show, Swim Club is offering 25 % off your first order when you use the code THEPROOF at checkout. Head to swimclub.co forward slash the proof to learn more. Today's episode is proudly brought to you by 8sleep. When researchers line up the things that we can actually change in our lifestyles, along with diet and exercise, sleep sits near the top as the most impactful lever that you can pull.

24:33The links between sleep and heart health, brain function and metabolism are remarkably consistent. And one of the clearest factors that influences your sleep quality is temperature. Your core temperature has to fall for you to reach the deeper and very important stages of sleep. That's the mechanism Eight Sleep has been built around for years now and they've just released the sixth generation pod. The pod six is a smart mattress cover that goes over your existing bed, heating or cooling each side independently. The thermal engine reaches your set temperature about 20 % faster than previous models and the cover carries nine times the biometric sensors.

25:14Heart rate, HIV, breath rate, sleep stages etc. All carefully measured overnight with nothing to wear, nothing to charge, nothing to leave on the bathroom counter. The pod is not a medical device and should not be used as a substitute for professional medical advice, diagnosis or treatment, and individual results may vary. Use code theproof at 8sleep.com forward slash theproof for up to$200 off the pod six. That's 8sleep.com forward slash theproof. Now the part where we have a conversation about the headline, the 48 % regression. And stay with me here because this is the bit where I think many in my position would leave it out.

26:01It's also the part that I find most interesting. And if I were you and had the goal of reversing plaque, it's what I'd want someone to walk me through. I could have easily shown you one provider's result, the heart flow result that says I reversed my plaque by 48 % and just stopped there. I could have built a program off the back of that, sold you something that claims to guarantee plaque reversal. But the truth is that three platforms analyze my scans and only one of them tells that story. Shortly, you're going to see all three, including the two that don't necessarily flatter me. Because if I only showed you the good ones, I'd be doing exactly what I often criticize other people for, leaving out important information.

26:52My goal here is to help you avoid a heart attack or a stroke, full stop. that's all I care about I just couldn't mislead you and I will never withhold something that could come at the cost of your health okay so with that out of the way let's get into these three analyses same two scans at two different time points 2024 and then 2026 sent to three different companies to analyze. Qangio, clearly, and heart flow. On my most recent scan, Qangio measured 11.5 cubic millimeters of plaque in my arteries. Clearly measured 74. Heart flow measured 60. So same heart, same images, same day, and a six-fold spread between the smallest number and the largest.

27:48And if cubic millimeters means nothing to you in this context, which it certainly didn't to me, think of this in grains of rice. 11.5 cubic millimeters is roughly one grain of rice, whereas 74 cubic millimeters is roughly six grains of rice. That's the disagreement made physical. One company says there's a grain of rice in my arteries. Another says there's six. And on that, it's worth saying that's the total plaque spread across the entire coronary tree, about 60 centimeters of artery. It isn't just sitting in one lump. If it were in one lump as a grain of rice or six grains of rice, I'd have a very large and different problem here.

28:41That's the absolute amount of plaque. Then there's the change between the two scans from baseline and follow-up, which is really what I wanted to know. How was this plaque in my arteries, if at all, changing? Was it stable? Was it progressing? Was it regressing? Q-angio had me essentially flat, up about one cubic millimeter over 16 and a half months. Clearly had me up around 20 % and heart flow had me down 48%. So these three providers didn't just disagree about how much absolute plaque there is in cubic millimeters. They also disagreed about which direction it was going. And at the same time, if we zoom out a little, all three agreed on what matters most.

29:34I have a small amount of absolute plaque and none of them found rapid plaque progression, which has an actual definition behind it. In the peer-reviewed literature, rapid plaque progression means your percent atheroma volume, which is the share of your artery taken up by plaque, climbing by one percentage point or more per year. All three of these analyses came in well under that line. Now I do need to say here that I did notice something while I was going through these. The arteries themselves weren't measured as quite the size on the two scans, which means that the comparison isn't perfectly apples to apples.

30:19That's something that I'm going to dig into properly and report back on. But for now, I did run a correction recalculating each result with the artery size held fixed at whatever it was on the first scan. So the only thing changing was the plaque and it doesn't change the answer. Whichever way you cut it, none of these three go anywhere near the rapid progression threshold. Now you might be wondering though why there is some disagreement in the absolute amount of plaque between these three providers. This brings me to what I think is actually going on here. Plark on a scan like this is measured by looking at the space between the inner wall of your artery and the outer wall.

31:08Where a platform decides those two edges sit determines everything. How big it thinks your artery is and how much plaque it thinks is sitting within it. Draw those lines slightly differently and you get a different answer to both questions. And when you have as little total plaque as I do, slightly different becomes very different. Exactly why that happens is a whole episode in itself and I am going to make it. But for now, here's the single most useful thing I can tell you and it's practical. If you're going to track plaque over time like I did, pick one provider and stick with it whether that's clearly heart flow you can't use qangio because that's for research purposes only i was very lucky to get access to that but pick one provider stick with it so that your baseline and your follow-up are measured in the same way switching platforms between scans or comparing numbers from one provider to another will tell you almost nothing And this is a separate problem from scanning too soon.

32:17The interval between your scans is very important. Sticking with one provider fixes the ruler. It doesn't fix the interval. I'll come back to that at the end of this episode. So with all of that in mind, which do I trust? The Qangio results, the Clealy results, or the HeartFlow results? I asked Dr. Matthew Budoff this, the cardiologist at the Lundquist Institute in Los Angeles where my scans were performed, one of the most respected cardiac imaging researchers in the world. He'd actually written the original CTA reports for my scans himself and he'd also seen all three quantitative analyses and his answer was Qangio.

33:02Now that's one expert's view but this is someone who uses all three of these platforms in his own published work, and he's not partisan for any of them. And there's something firmer sitting behind it in a paper that he co-authored, the Miami Heart Study, published in Jack Cardiovascular Imaging earlier this year. It's actually a study that I'll come back to shortly. In their own discussion within the Miami Heart Study, the authors raise, and I'm quoting here, the potential for plaque overestimation by AI quantitative coronary tomography. They found that AI, which is what Clearlene and HeartFlow use, picked up small amounts of soft plaque in people a human reader would have called completely normal.

33:56And they say plainly here that they don't yet know which it is. Is it real disease caught early or is it the algorithm of these AI quantitative analyses over calling. But let's look at how this maps onto my three results. The two AI platforms, clearly in heart flow, came back at 74 and 60 cubic millimeters of plaque. Qangio, where a trained human being defines that artery wall, came back at 11 and a half cubic millimeters. The platform with the person in the loop reads a fraction of what the fully automated ones do. That's exactly the pattern that their own paper is warning about. So QAngio, the one that I'm anchoring to, had me going from 10.4 cubic millimeters to 11 and a half cubic millimeters over that 16 and a half period.

34:55Notice here I'm leading with the absolute number, not the percentage. At a denominator this small, a percentage is a little misleading. 10 to 11 and a half sounds like nothing because it is nothing and that's the honest way to report it. That New England Journal study that I mentioned earlier called React didn't just count who had plaque, it measured how much. And importantly, in React, they measured plaque with Qangio, the same very analysis that I'm anchoring to. Among men in their 30s who had any coronary plaque, the median was 42.6 cubic millimeters. Remember, I'm at 11.5. That's about a quarter of it.

35:41So of men my age who have plaque, I'm at the lower end. We can also look at the Miami Heart Study, which examined over 2 ,000 asymptomatic adults and built percentile curves for exactly this. Miami Heart used clearly, so if I want to know where I sit, I have to use my clearly number, not my Q-Angio one here. Remember, these tools measure the arteries slightly differently, so we need to use the same ruler on both sides or the comparison is somewhat meaningless. So here, comparing Clearly to Clearly, my follow-up number puts me around the 55th percentile for a man my age, which is just a nudge above average.

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37:50That's code Simon at im8health.com. I'm often asked for advice on building a podcast or a business. One thing that I've learned is that the people I've watched build well aren't necessarily doing more than everyone else. They're delegating better. There's a point in anything that you're growing where the constraint stops being effort and starts being expertise. You need someone who is very good at the thing you're not, and you often need them for six weeks, not forever. I've been using Upwork since 2015 legitimately when I built a customer service team out of the Philippines. They were so good I ended up flying over to the Philippines to run retreats with them in person but that's a story for another time.

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39:29No, everyone in that study was measured using the same software. So if it over calls, it over calls me and also the reference population equally. So the percentile survives. That's the whole point of comparing like with like. Now, just to throw a little curveball here, HeartFlow has its own percentile chart built from its own database. On that one, I'm not at the 55th percentile. I'm actually at the 80th, which means more plaque than 80 % of men my age. So here we have the same arteries, same scans, and a 25-point swing purely from whose reference population you stand next to. Even the percentile is somewhat platform dependent.

40:17And if you're wondering which of those three I'd stand behind, honestly, not one of them is a perfectly clean fit for myself. Miami Heart enrolled people aged 40 to 65, average age 53, so I'm right at the bottom edge of that. And the New England Journal cohort does cover men my age properly, and it used the analysis as I trust most, Q-Angio, but it gives medians, not percentile curves. And HeartFlow's chart is its own. The reference data behind it was presented at a conference last year. It's not published, so I can't see who's in it. Three reference populations and not one of them was built for a 40-year-old tracking his own arteries.

41:01That isn't a failure of any of them. It's just where this field sits right now. One thing matters enormously for how we think about this change between my baseline and my follow-up scans. Across those 16 and a half months, my ApoB sat between 70 and 80 milligrams per deciliter. Again, that was on diet and lifestyle alone. No PCSK9 inhibitor, no statin. So whatever happened between those two time points happened at roughly double the ApoB that I am now targeting. And I want you to hold onto that because it changes what the next 25 years could look like and what my goal is here. Taking QAngio here as the most accurate and reliable analysis, over this window, my lifestyle appears to have been protective, not a dramatic reversal, but stability where you would normally expect progression.

41:57Once people have plaque, it typically progresses year on year particularly if you don't intervene with medications. There's also something underneath the total amount of plaque that I think is worth discussing here. Q-Angio doesn't just measure how much plaque there is but it measures what kind and the composition of my plaque shifted between the baseline and follow-up scans. The softer more lipid-rich material dropped by about 40 % while the fibrous plaque went up and so did the small amount of dense calcium that I have. That is indicative of plaque hardening. It's the direction that you want to go because softer plaque is the kind that's more often implicated in heart attacks and stabilizing that plaque is the goal.

42:45It also means a flat total volume can be hiding a favorable change because when soft plaque calcifies, it doesn't disappear. It still takes up space. But this is where it turns into a decision. There are two things that I'm not willing to assume here. Firstly, that stability continues on its own. And secondly, that a small amount of plaque at 40 stays small at 60. As we change, our physiology changes. The physiology within the artery, that local environment shifts. Age itself is one of the biggest risk factors for cardiovascular disease and there's nothing to say that my current results will hold going forward even if I maintain the same lifestyle, which is exactly why I've decided to get more aggressive with my ApoB target.

43:37Holding the line for 16 and a half months is not the same as being able to hold it for the next 25 years. This brings me to the obvious question and what I alluded to at the start of this episode. What prescription medicine have I stacked on top of my existing lifestyle and why? The short answer is that after my second scan, I started a PCSK9 inhibitor. The goal is to get my APOB down to 40 milligrams per deciliter or lower. That's comfortably into the range where the evidence, as I mentioned earlier, says that plaque is most likely to stabilize and ideally regress. There are really three reasons for this decision.

44:19First, my APRB isn't where the guidelines say it should be. The 2026 ACC AHA dyslipidemia guideline came out in March and this is a significant document because it brings back numerical treatment goals which the 2018 version had dropped. One of the ways that you land in the group with an LDL target under 70 milligrams per deciliter is having a calcium score at or above the 75th percentile for your age and your sex. My calcium score is four and it didn't change between the two scans but four puts me above the 75th percentile which does sound dramatic until you realize that almost nobody my age has any coronary calcium at all.

45:04The 75th percentile for men in their late 30s is essentially zero. With diet alone, remember, I'm consistently sitting at an LDL cholesterol level between 70 and 80. That's a huge improvement. I was at 125 to 130 before I changed to a plant-based diet, but it's close to the target, not under it. And based on that imaging data that we went over earlier from trials like Glygov and others, it is clear to me that when the goal is to shrink plaque rather than just slowing it down lower is better so i'm aiming for an apob again around 40 so i'm following the guidelines here and getting my ldl cholesterol below 70 milligrams per deciliter and with the totality of research on this topic in mind i am encouraged and motivated to target that 40 milligrams per deciliter level or even slightly lower.

46:00This is a deliberate choice for my situation. Again, I have soft plaque, I have a small amount of calcium, a strong family history, and I really do believe the evidence that lower for longer is better to be very compelling. And remember in Gligov, the benefit kept increasing the lower the LDL went with no flaw. But again, to be clear, that is my target. This is not a recommendation. Your number, your target is a conversation with your doctor, not something to copy from me. And to be clear, the goal that I'm working towards here, it's a 25-year one. By 65, I want to have no more plaque than I have today, ideally, which will put me down around the 25th percentile for my age, meaning less plaque than about three quarters of my age match peers.

46:49It would be expected that during this time, my existing plaque would shift further towards more calcified stable plaque morphology makeup that's less vulnerable to rupture so regression of soft plaque with a simultaneous increase in calcified plaque would be expected this is what evidence-based personalized medicine looks like getting my apob to goal based on my family history my biomarkers and my clinical presentation so that's reason number one why I went with a PCSK9 inhibitor. The second is that because of my lifestyle changes, I only need one drug here. And this is the part of the conversation I think that gets missed when we are talking about medication and lowering our LDL cholesterol.

47:35Because my diet is already doing a lot of the work on my LDL and ApoB, my starting point is low. Someone else with the same target might need two drugs for example a statin plus ezetimibe if they're not prepared to make the same dietary changes that i made or if they respond differently to diet than i do i need monotherapy so one drug and on repathor alone which is a pcs k9 inhibitor i expect that to take my apob to below 40 milligrams per deciliter so the lifestyle work it didn't become irrelevant when I decided to medicate here. It's actually the reason the medication is simple. And the third reason here is that of the drugs that would reliably get me down to target one drug by itself, I had a choice between a PCSK9 inhibitor and a statin, and I chose a PCSK9 inhibitor.

48:34Now, I want to be clear up front here. Statins are first-line therapy for very good reason. They're cheap, they're among the best evidence drugs in all of medicine, and they save lives. So this isn't a knock on statins, and it isn't the right call necessarily for everyone. Some people tolerate statins perfectly well and should be on one, and some people need more than one drug to hit their target anyway, so it makes sense to have a statin with something else. For my specific situation, a few things tipped me towards a PCSK9 inhibitor and the first reason is actually adherence. A PCSK9 inhibitor is an injection once or twice a month or even twice a year whereas a statin is a daily tablet.

49:21I know myself and for sure I'll stick to the injection much more reliably and the best drug in the world really it does nothing if it sits in the cupboard. I have an alarm set in my phone and on Saturday every two weeks I get a reminder to do the injection. It takes a minute or so and then I'm done. The second is the side effect profile and again I want to be careful here because this does get misrepresented constantly in both directions online. Muscle aches are the ones that everyone's heard about. They are real with statins but they are much smaller than the internet suggests. in the blinded trials more than nine in ten of the symptoms that people report on a statin turn out to actually not be caused by the statin itself there's also a small but real increase in new onset diabetes concentrated mostly in people already at metabolic risk and a cognitive concern that's weaker still and has been reassuring every time it's been properly tested none of that is a reason to avoid statins.

50:31The benefit is not in question for the right person and nobody should stop taking a statin based on a podcast. But for a lean insulin sensitive person who likely needs one drug, those small margins, they nudged me. And if I needed a second drug in order to hit my target, truly a statin would be back on the table. So would ezetimibe and so would bempidoic acid. there's more than one way to get your APOB or your LDL cholesterol both of these to go which is great because it means we have choice as for which PCSK9 inhibitor I started on larochol and I've actually moved to repatha which is evolocomab and the reason for switching PCSK9 inhibitors is actually based on outcome data larochol has encouraging early signals but there is no completed cardiovascular outcomes trials yet showing that it lowers cardiovascular events whereas Repatha does have that.

51:31We have trials showing it lowers ABAB and LDL cholesterol and also lowers events. And coming back to my 25-year goal, Repatha is the drug that produced the Gligoff-Plark data that I mentioned earlier. So same molecule imaging data showing regression and outcome data showing a reduction in cardiovascular events. At the same time as starting the PCSK9 inhibitor, I have also begun taking 2 ,400 milligrams a day of aged garlic extract. That's not about lowering ApoB, it's actually a separate lever. There's a body of research, including imaging trials, suggesting that aged garlic extract may help slow the progression of coronary plaque and calcification.

52:16it's not in the same evidence league as the lipid lowering drugs but the signal is interesting the safety profile is reassuring and the dose used in those studies is around 2400 milligrams per day i went pretty deep on that evidence in the supplement episode that i did on reversing atherosclerosis episode 425 so i will link to that episode again in the show notes if you want to see whether it's worth considering for yourself. And yes, I can hear the objection. I've just spent five minutes telling you I deliberately changed nothing so I could see what my lifestyle was doing and now I'm starting two new things at once.

52:58And that's fair pushback. But the reason for holding everything steady was that I was running an experiment on myself during that 16 month period. I'm not anymore. I know what my lifestyle alone does over 16 months, which is what that window was for. From here, I'm treating a disease rather than measuring one. And I would rather pull all of the levers that I can than spend another five years working out which one mattered purely for academic purposes. I will rescan in five years time at age 45, then again at 50 or 55, and I'll report back along the way so you can see how things are looking for me over time.

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54:43To close, there are three things that I would like you to take from today's conversation. The first is that eating a healthy diet today doesn't mean you are immune from atherosclerosis. And it doesn't mean that your LDL and ApoB are at an optimal level. They could be, but they might not be as well. I've eaten about as well as it's possible for me to eat over the last decade. And I still have plaque. possibly because I had 30 years of higher ApoB exposure before that and because there are things about my biology like my genes that I don't control. Diet does help enormously but it's not always enough and it doesn't reset the clock on a disease process like atherosclerosis which builds up accumulates over a lifetime.

55:32How early you make lifestyle changes and your genes matters a lot. number two the most important number in this episode is not the headline it's not the 48 regression it's that all three of the analyses that i performed qangio heart flow clearly agreed on the thing that matters most my plaque burden is low and i'm not experiencing rapid progression although they did disagree on the exact change over 16 and a half months one even on the direction but they agreed it's small and those discrepancies says more about these quantitative analyses and how validated they are and how affected they are by measurement noise than it does about my personal situation and my ultimate takeaway is that you should be very skeptical of dramatic short interval scan results these tools are not perfect and if you're going to do a CT angiogram and then repeat it like I did, leave real time between the scans.

56:38In fact, the American College of Cardiology put out a statement on quantitative plaque analysis late last year. And in this statement, they suggest a minimum of two to five years between serial scans using the same scanner and the same settings both times. That's really important. If you're going to compare scans, make sure they're done at the same center using the same machine and settings. My scans were 16 and a half months apart, which is shorter than that minimum, which is part of why I'm not putting weight on that 48 % reduction that heart flow showed. The REACT paper that I mentioned earlier, which is the biggest study of its kind, looking at atherosclerosis in asymptomatic subjects, is re-scanning its participants after six to eight years.

57:27That's the sort of window over which change is actually measurable. A short interval plus a low plaque volume is how measurement noise ends up looking like a result. And here's the bigger picture, and it's the thing that I'd most like you to take away. Atherosclerosis is still the number one cause of death on the planet, and it's ubiquitous. in REACT in that New England Journal study, by their 60s, more than 9 in 10 people had atherosclerosis somewhere in their arteries. Not in their heart necessarily. For most people, the neck and the legs come first, but somewhere. So we may all end up with some plaque.

58:09That isn't really the question. The question is whether it turns out to be the thing that kills us. And with today's science, the beautiful thing is that if caught early enough, for most people, it doesn't have to be a death sentence. So have the conversation with your own cardiologist. And while we do have very effective drugs, don't overlook what lifestyle sustained over decades can achieve. This shouldn't be an either-or conversation. You can do both. You can adopt a healthy lifestyle and you can add pharmaceutical medicines where indicated. If you've had serial CT angiograms like me, especially if you've had them analyzed by more than one provider like HeartFlow and Clearly, I want to hear from you.

58:56Did you see the same disagreement between providers that I did? Let me know in the comments. and if you want the deep dive on that heart flow result specifically i did a whole episode with dr campbell rogers who is heart flow's chief medical officer i'll link to that in the show notes thanks for hanging out with me and i will see you in the next episode there you have it friends i hope you enjoyed this episode if you did and want to stay up to date with future episodes be sure to hit that subscribe button on youtube and follow on apple or spotify finally thank you for showing up and the effort that you're making to take control of your health.

59:36I look forward to hanging out with you again in the next episode.