Statins Work... But You MUST Know THIS!

How I use statins to unclog arteries. You know, you hear this kind of stuff a lot and maybe it's overdone, but I do worry about getting cancelled from what I'm about to say. You see, I'm in the middle of a big debate. You've got people saying statins are poison, that no one should ever take a statin because they cause muscle pain, they cause dementia, they cause liver problems, and even diabetes. So never take them.

Then on the other side of this debate, you've got medical systems, doctors handing out high-dose statins like they're candy, lowering LDL cholesterol at all costs without fixing the real problem. And let me repeat that last part. They're doing all this and not fixing the real problem here. This is why doctors write tens of millions of statin prescriptions every year in the United States alone. They're fueling a global market worth over $19 billion a year with Pfizer's Lipitor alone pulling in $12 billion a year. And for those of you that are in finance, this is after they've lost their patents. Before they lost their patents, it was much, much more money.

Many people see both sides of the argument and are confused. You might be confused, too. You might be stuck not knowing what to do if you're currently on statins or if you've been told to get on statins that you have to have them. That's exactly what we're going to learn in this video. I'm going to break down the benefits, the risks, and the side effects, and why my approach to statins is different so you can decide for yourself if they make sense for you.

So, let's break this down. At the end of the video, I'll tell you exactly what to do to minimize your risk if you do take statins, and I'll tell you what works even better than statins. So that matters a lot whether you're taking statins or even if you say, "Look, I just don't want to take them." At times, over half of my patients said that, and that's fine with me because I'm more focused on what works than I am on a medication.

But before we get started on that, I've got something for you. It's an ebook. It goes through my seven-step protocol. So many people that watch our show want to learn how to take care of their heart, how to decrease their risk of heart attacks and strokes, and it's for free. All you have to do is go into the link on the description, and you get our advice. It's a to-the-point guide. There are seven steps on it. It's the same process I used for myself. It's the same process I use for my patients. We'll send it to you instantly. And again, it's free.

Now, let's go back to talking about statins and when to use them. Let's start by answering a key question. You've got to know this if you're going to know the rest of it. And that is, what are statins? What do they do? How do they work? Statins are one of the most prescribed medications in the world. It's an enzyme. They block a protein in the liver. That protein makes cholesterol. I'm going to give you a geek warning. We've got a lot of geeks on the channel. They want to know the geeky terms. And this is a geeky term: HMG-CoA reductase. Don't worry about remembering the name. Just think of it as that factory switch. It's a switch your liver uses to produce cholesterol. So when that switch is blocked, your liver makes less cholesterol. And that's what most doctors are going for.

This means that the level of LDL or "quote bad cholesterol" drops in your blood. But since high LDL has been popularly linked to plaque building up in the arteries, doctors prescribe statins to bring that number down, that LDL number, that bad cholesterol. That's why statins became so popular. They lower LDL a lot. And they do it reliably and consistently. A cardiologist that's looking at a lab report and just wanting to knock your LDL down, that's a powerful easy button.

Now, let's go back and talk about a patient, though, and an example of what can happen. Let's call him John. He was excited, or he started off excited, because after starting his statin from his cardiologist, his LDL, this so-called bad cholesterol, it dropped. It was almost in half of what it was in the beginning. On paper, he and his cardiologist thought his numbers looked great, but he decided to check his arteries. He still had dangerous soft plaque. And soft plaque is a problem. That's the dangerous stuff. The stable plaque, that's not so dangerous. It really doesn't raise your risk of heart attack much more than having no plaque at all. And having no plaque at all, you're not really going to have a heart attack. So his blood test, or at least his LDL blood test, said he was safe. He was okay. But his arteries told a very different story. And that's the problem. Numbers, at least LDL numbers, can look great while the real danger is still there.

If statins only worked by lowering LDL, then everybody with low LDL would be safe. That's not what happened with it, and it's not what happens with a lot of people. It's not what we see in real life. People with low LDL can still have heart attacks and still do. And people with high LDL still sometimes don't have heart attacks. So why does this happen? Well, the real question is what's actually happening inside your artery wall.

So let's start talking for a minute about those side effects. What statins do outside of just lowering LDL? They actually have effects in the artery wall itself. In medicine, we call these side effects. Sometimes we call there's another term we use, pleiotropic. And again, sorry about the geek word. This one you might want to remember, and it might be easier to remember because there's a constellation up in the sky that uses this term. Pleiotropic comes from the Greek word "pleo" meaning many, and "tropic" meaning directions. So it's going in different directions in medicine, many different effects. Now, I mentioned you might see it in the sky, or you might know it from another area, astronomy. You may have heard of the Pleiades. It's the Seven Sisters. So again, maybe that can help you remember that if you want to. But it's not critical to remember that word, pleiotropic.

What is critical, though, is to remember that sometimes the side effects are more important than the original impact. Let's get back to the side effects of statins. First, statins help the inner lining of your arteries work better. That lining is called the endothelium or intima. You don't have to remember the name. You just have to remember that the lining is important. It's like the smooth surface inside a water slide. When that's healthy, blood flows right through without turbulence or debris. But when it's irritated, it's more like a cracked sidewall. Rough spots start to appear. Things start to catch. And over time, you start getting a buildup of plaque and scarring. Statins improve the signals that keep the lining smooth and flexible so blood can move freely.

Second, statins can make platelets less sticky. Now, you may remember platelets are those tiny little cell fragments that come together to form patches in cells or cuts. They're like little repair crews rushing to the scene. The formation of a of a bunch of platelets. When platelets start getting together, that's the very first step in forming a clot. Now, most of the time that you have clots form, that's a good thing. It's going into repair. But sometimes these clots are not what we want. Sometimes these platelets can start piling up on a plaque, an unstable plaque, and form a dangerous clot. Statins calm those platelets down, making them less likely to cause a sudden blockage, a clot.

There's another thing. Statins reduce inflammation. You remember that? Inflammation. You hear a lot about it these days, but you just don't hear too much about knowing what to do about it. And that's where we get a little bit deeper and a lot more effective in preventing heart attacks. Inflammation actually happens inside the artery wall. Every cell produces reactive byproducts. Think of them like sparks from a campfire. A few sparks are normal and they're not much of a risk. But the more sparks you get, and you get to too many sparks, you start burning holes in the tent. You can start a forest fire. Now, in your arteries, those sparks damage the lining. They oxidize cholesterol particles. Those oxidized cholesterol particles start to stick to the lining. You know where this is going. Statins dampen that spark production. They create a calmer, safer environment. So, that's another key thing to remember.

There's another thing. Number four, statins stabilize plaque structure. Unstable plaques are like potholes filled with soft, wet asphalt. You get the picture. They're fragile. They're easy to rupture. You run over it and it starts spewing hot asphalt everywhere. Stable plaques are more like concrete. They're solid. They're sealed. They're not likely to break apart and start spewing everywhere. Statins help shift plaques from fragile to stable, lowering the chance of a sudden rupture.

Now, there's one other thing I want to talk about. Number five, let's talk about arterial plaque reversal. This is probably the most important part of this video, but for that, we need to get a little bit more geeky. I'll show you the most relevant evidence. And to do that, let's go up to the studio. Here's one. It's a study published in JAMA, the Journal of the AMA, back in 2007. It looked at thousands of patients and found that when statins were used to lower LDL cholesterol enough, but at the same time nudged HDL cholesterol up a little bit, plaque inside the arteries didn't just stop growing, it actually shrank. Now, again, a lot of people say you can't shrink plaque. That never happens. We've got examples in our channel. We've got other videos where we've talked about it, but you don't have to listen to us. Go to that JAMA article.

And it's not just the hard plaque either. A review in the International Journal of Cardiology showed that statins can also affect the dangerous kind of plaque. The dangerous kind, the soft, unstable plaque. It ruptures. It sends that soft plaque out that causes a clot to form, and that's where the heart attack comes from. So even better, this effect doesn't depend entirely on how high your cholesterol is to begin with. So, even if your LDL isn't sky-high, statins can still make your arteries safer.

Here's the point that confuses a lot of people. A study in JACC, the Journal of the American College of Cardiology, showed that while statins shrink plaque, they also increase calcification. In other words, your calcium score may go up while you're on statins. Is that necessarily a bad thing? No. Again, you have to understand plaque and cardiovascular risk. Calcified plaque is stable.

Let's talk about another patient I've had. We'll call him Mike. He was 62. When his calcium score went up after starting a statin, guess what he did? He panicked. And his doctor was worried, too. Enough that he suggested, "Let's just do a stress test, and maybe we ought to start thinking about a stent." Mike thought for sure things were getting worse because the calcium was going up. But when we looked closer, what actually was happening was his soft plaque was hardening. It was stabilizing. His risk of a heart attack was lower, not higher. The score went up, but his danger, his risk went down. And that's the part that most people, even doctors, miss. What's happening is that this soft, mushy plaque is hardening into calcified, stable plaque. Think of it like patching a pothole with concrete. It may look worse on the scan, but it's much less likely to break open and cause a clot.

Not all statins perform the same way either. There was a meta-analysis. You may remember what that is. If you don't, it's the highest form of research. It's where somebody looked at every research they could find, every clinical trial that looked at this specific question. Now, this was in the American Journal of Cardiology. It compared rosuvastatin and atorvastatin, two of the most common statins. So, here are the results. Rosuvastatin did a better job at reversing plaque. And that's important because atorvastatin is often prescribed at very high doses. It's by far the most commonly prescribed statin. They were in the market first. They took that first-mover advantage, and they're still the most common statin prescription that doctors write. And that's a problem because evidence suggests that rosuvastatin may deliver more of the benefits with less of the baggage.

Here's a caveat. It's a big one. Most of the famous statin trials like ASTEROID, METEOR, and JUPITER all showed the same thing. When patients were put on very high doses of statins, plaque in the arteries could actually shrink. And that's part of the problem because these were intensive high-dose treatments. But high-dose statins come with a much higher risk of side effects. Things like muscle pain, fatigue, even an increased risk of diabetes, a significant one. And so that's why many people say, "I don't want to try the statins, or I'm going to quit. I just don't like it. I'm getting muscle pain. My doctor doesn't believe me. I'm out."

Another big problem is funding. At least a problem with those studies because most of those studies were supported by Big Pharma. So, if you don't want to take statins because of that, I respect that. I understand that decision. And as I've said many times before, and will again, there are things that are more important than statins in managing cardiovascular risk. I'm not a big fan of Big Pharma either, but I do believe some medications, at some time periods, at some dosage, can still be useful despite the business components and the money-making behind them.

So the big question is this: Do you need to max out the dosage to get the benefits? And the answer is no. That's where the newer evidence gets really exciting. Let's take a look at a study published in the American Heart Journal. It was using high-resolution MRI scans. Researchers looked not just at plaque size but at plaque composition. That's so important. What they found was that rosuvastatin, even at lower doses, dramatically reduced the inflamed, unstable, what the doctors call necrotic or dead core inside the plaques. So at a low dose, it dropped by almost 40%. At higher doses, maybe closer to 60%. So then you have to start thinking about, is that extra 20% benefit worth the higher risk of side effects and bad side effects? Meanwhile, the overall size of the plaque didn't really change that much, but the plaque itself became less dangerous. And again, this brings up the recurring point that you have to think about.

So many people, after having seen some of my plaque reversal videos, come to me and say, "I want to reverse all my plaque." And my response is, "Well, wait a minute. Do you want to reverse all your plaque, or do you want to reverse your risk?" It's unusual to reverse plaque. It's not unusual at all to reverse risk. Reversing risk is the practical goal. It's the one I recommend.

Now, let's talk about some other studies while we're talking about the geeky part here and the evidence. Take the COSMOS trial. It was in Japan. Patients started on just 2.5 mg of rosuvastatin. That's compared to some of these mid- to higher doses of 20 and even 40 milligrams a day. It's a very low dose, and most stayed well below the maximum. Even so, researchers found an average of 5% shrinkage in plaque volume after just a year to a year and a half. Now, that may not sound like a lot. In terms of arteries, though, this is huge, especially at such a small dose.

Then there's pravastatin. It's a different statin. It's the kinder, gentler statin. It's newer. It's gentler. And if you're thinking about, "Hey, I want to go on that," check with your insurance companies. It's still very expensive. It hasn't lost its patent yet. So, insurance companies are very hesitant to start paying for that unless you're having problems with other statins. But let's get back to the research, the evidence. At only 2 milligrams a day, patients had about a 10% drop in plaque volume compared to diet alone. If you're low-carb and you say, "I don't want to use any kind of medications," hopefully, this evidence helps you understand why I say, "Yep, lifestyle may be king. The most important thing. But there are times when statins can help."

Another trial called TOGETHER. It showed something even more interesting. After just one year, the pravastatin made dangerous yellow, unstable, liquid plaque turn into stable plaque. It cut that risk way down. In other words, the plaque wasn't just shrinking, it was becoming safer. Stable plaque. And again, there's another study called the Honda study, and the principal researcher was Honda, a fellow named Honda. What he showed was that once you get, you change that plaque from soft to stable or calcified plaque, the risk plummets. So this is not stuff that people are making up. This is stuff that we're seeing in the evidence from the studies that are being done.

Now, speaking of studies, let's go to another one. The SAMURAI trial. The researchers in the SAMURAI trial looked further. They looked at carotid artery thickness. You remember that's one of the tests that we've used quite a bit. Most people don't talk about it. CIMT. It's a strong predictor of heart attack risk because the arteries in the neck are the same as the arteries in the heart. This is not a plumbing issue or a local issue. If you have plaque in one area, you're going to have plaque in the other. In fact, we know the probability is 98%. Why is that? It's because this is a metabolic issue. If you have metabolic problems or some other root cause for cardiovascular inflammation, you're going to get artery problems throughout your body, not just in one area.

So, let's go back to the study itself. Patients on pravastatin not only improved their cholesterol, but many actually saw regression of the plaque or regression in artery thickness. The effect was even stronger in people without diabetes or metabolic syndrome, showing how lifestyle factors can amplify the drug's benefits. In other words, what that meant was you use your lifestyle to start taking the pre-diabetes or diabetes off the table. You get a much, much bigger impact from whatever statin you're using.

Then we have the combination therapy. A Japanese trial compared rosuvastatin alone versus rosuvastatin plus ezetimibe. Both groups improved, but the combination group saw more than four times the reduction in plaque volume, about 13% versus 3%. Now, that shows us something powerful as well. With the right low-dose combinations, you can achieve effects similar to high-dose statins but with far fewer side effects. And in fact, the review of these studies for this video is making me reconsider uses of these combinations. In the past, we've looked at them, and the evidence was more towards not so much improvement, but this was a very strong study.

But not every pleiotropic effect is automatically good. The same pathway also touches energy molecules like CoQ10. It can nudge blood sugar in the wrong direction. You remember there's more than one side effect or pleiotropic effect from statins. Muscle pain is one. You don't want that. That's not good. Getting a little bit more pre-diabetic or diabetic, that's not good. You don't want that either. But this thing about slowing down the inflammation, improving the artery walls, those are some things that we really do want.

Let's deal with the elephant in the room. Most patients who are on atorvastatin, what they used to call Lipitor, especially at higher doses, eventually do report side effects. The most common one is muscle pain. I had a patient, we'll call her Susan. She was 58. She felt like she was walking around with weights strapped to her legs after just a few weeks on atorvastatin. When we switched to a lower dose of a gentler statin, in this case, rosuvastatin, all of that actually went away. She didn't have the walking around with weights feeling anymore, and she was fine.

If you've ever Googled statin side effects, you've probably seen some scary stories. People talk about crippling muscle pain, ruined livers, even claims that statins cause dementia or cancer. I can tell you because we've done some of these reviews and we've done some information to talk about how often this appears to be a nocebo or maybe fear and concern effect versus how much it's a real effect. That really shouldn't matter to the doctor or to you. You should take what you're comfortable taking.

Let's cut through the noise and look at what the science actually says. The most common side effect by far is muscle aches, also called myalgia. Myalgia is the geek word, the medical word for muscle pain. Depending on which study you look at, it happens in somewhere between 1 and 10% of people. Now, that's real. And if you've ever felt it, you know it can be uncomfortable. For some people, even unbearable. I used to have it at a certain part in my weekly long run every week. And it, even though I do this for a living, it took me a while. It took me a while to realize, "Ah, you know what? This cramp I always get when I'm running up this hill might just be the statin I've been taking." I was able to walk it through and didn't need to stop it.

The most serious muscle problem, though, is rhabdomyolysis. Again, pardon the the geek word. "Myo" means muscle, by the way. And so what this is talking about is breakdown of muscle tissue. That's a dangerous thing. Here's the key: it's extremely rare. It's less than one in a thousand people. And when it does happen, it's usually linked to very high doses of statins, drug interactions with those statins, or other conditions like untreated thyroid problems.

Now, there is the effect of statins on the liver. They can cause mild bumps in liver enzymes. About 1% of people have that. Now, that sounds crazy, but it's almost all cases. It's not translating into real liver damage. You just need to be aware of it. In fact, they've done studies on that, too. And it's not until you get to levels of 12, even 20 times normal that you actually have danger to your liver. We can monitor that with a single blood test. And if there's an issue, you can adjust the dose, switch drugs, or even come off of it.

Here's another side effect. It also deserves attention. Diabetes risk. Some statins, especially at higher doses, can make it a little harder for your body to manage your blood sugar. The numbers work out to about one extra case of diabetes for every 200 people treated for over 5 years. Now, the bottom line is that's really small compared to the risk of heart attacks and strokes that's actually prevented by statins. Let me say that again, and I'll get a bunch of haters. You know, this is where the guys that use the high-dose statins already hate me. Now, the guys that don't use medications at all, this is where they hate me. But it's real. The problem with side effects is they're small compared to the risk of heart attacks and strokes that really are prevented by low-dose statins. It's not nothing.

Interestingly, some statins like pitavastatin don't seem to raise diabetes risk at all. That's why it's so popular, and that's why so many doctors are looking at it as a safer option. There are other claims like statins inducing cancer, dementia, mood problems, even kidney damage. The best data we have says there's just not a solid link there. I hate to say that for all the statin haters, but you've got to speak the truth, no matter which side of this issue, this debate, that you're talking to. Now, the risks keep getting studied, but so far the evidence just doesn't support them. The ones that we're talking about, dementia, I know people say, "Oh, no, dementia is a big thing for statins." Look at the evidence. It's not that good.

One thing is real, though: drug interactions. Statins are processed in the liver by the same enzyme system as a lot of other medications. If you're on multiple drugs, especially things like certain antibiotics, antifungals, or HIV medications, the risk of side effects can go up. That's why it's so important to review your full medication list with a provider.

Now, here's the bottom line. For most people, statins are very safe. The scary side effects you read about are sometimes rare, but they do happen. The key is personalization. And that's right. It's a big word, and you know what I'm talking about. The right statin at the right dose at the right time for the right person, not just start spewing high-dose statins at everybody, when every patient, when you walk in their door. That's exactly why my approach is different from the high-dose statin for everybody model.

Let me start by saying this. I don't think we can just box statins as they're all poison. You can't do that. But I also don't agree with some saying that it should be added to the water supply either. Actually, I've had patients that can't tolerate even low-dose statins. For those patients, I agree with them. They just should not take them. Statins won't save you if your lifestyle is working against you. If you're still eating processed carbs, carrying too much visceral fat, and not moving your body, no pill in the world is going to undo that damage. That's right. You remember I've mentioned it several times in this video that at the end where we're going to talk about something that's far more important than statins. And this is it. It's called lifestyle.

Here's how I look at it. Statins are a tool. And like any tool, they're only effective if you can use them the right way, in the right context, at the right dosage. The real foundation is always lifestyle. Your arteries respond to what you eat, how you move, how well you sleep, how much you eat, how much you sleep, how you handle stress. That's where the battle for plaque reversal is won or lost. And even more important, the battle for plaque danger or cardiovascular risk. It's not so much worrying about whether you reverse plaque. What you want to do is reverse that risk. Statins, when used widely, can add an extra layer of protection by reducing inflammation and stabilizing the dangerous soft plaque that leads to heart attacks. They don't replace lifestyle. They amplify it.

But here's my approach. It's different from both sides of the debate. I don't use statins as the most important part of the plan. That's lifestyle. I use a low-dose statin, not high dose, not even mid-dose statins, as a part of my regimen when it's needed. I don't use it to lower LDL. I use it if you have plaque because if you have plaque, you've already demonstrated, your body has demonstrated to you that it's starting to get cardiovascular inflammation. And no matter what the cause, most commonly it's pre-diabetes or diabetes, but for some people it's rheumatoid arthritis or psoriatic arthritis, some other things. For some people it's smoking. And it's not just diet, it's exercise, it's sleep, stress management, and all these things actually helped me as well. And I'm one of those people that actually, I was very lucky. I actually did reverse plaque in my arteries. I started taking statins when I found out that I had arterial plaque. No, not a high dose. No, not a mid dose, a very small dose. And that's exactly what I still recommend.

If you have a positive calcium score, a CIMT that shows arterial plaque, or a CT angiogram with arterial plaque, in other words, if you have clear evidence that you have plaque in your arteries, you're no longer a primary prevention patient. You're a secondary prevention patient, meaning your body has already crossed that rubicon. You've already started forming cardiovascular inflammation. You're a cardiovascular disease patient, and you need to change your management of that disease for secondary prevention. Baby aspirin and low-dose statin should become a part of what you do. If you have evidence of arterial plaque, I would recommend making changes to your lifestyle. Considering some supplements, understand what your root cause is. And if you've got plaque, I hate to say it, consider a low-dose statin, but consider the right ones. And Lipitor, atorvastatin, that's not the right one. I really only use two. I used to use some other ones like pravastatin, simvastatin. Those are not bad, but now that we have rosuvastatin 5 milligrams or pravastatin one or 2 milligrams available, that's really all I ever have to use these days. As I mentioned, I don't use atorvastatin because of the evidence that you saw that we talked about earlier. It's just not as effective. It will lower LDL, but lowering LDL is not my goal. Remember, my goal is lowering inflammation and reversing plaque, reversing cardiovascular risk. That's my goal.

I used to take my statin once a day, but the reality is most statins will actually preserve effects for several days. You can decide to take them daily or to minimize side effects, you can take them every other day. There are even some people that take them once a week. Some people mention that statins don't work because only a few people actually avoid heart attacks. Now let's get into that. It's a statistical thing. It's an epidemiological science thing. It's what we call absolute risk reduction. You see a few people in the literature talking about it. Unfortunately, the studies showing that are very short-term. However, if it is accurate, let me show you another statistic. A 2023 study showed that for every 1% of arterial plaque reversal, you get about a 25% reduction in cardiovascular risk. So, think about it. If statins can help with that 1% decrease, it's worth it.

Here's the quick hack that I promised at the beginning of the video. For my patients taking statins, I recommend a low dose, but also supplementing with CoQ10. CoQ10 is short for co-enzyme Q10. Think of it like a spark plug in your mitochondria, the little energy factories inside your cells. Without CoQ10, your cells can't turn food into usable energy effectively. So when you take statins, your cholesterol may come down, but your CoQ10 levels often crash, too. That's why some people feel drained, weak. Some people get muscle aches on statins. Supplementation with CoQ10 can put that spark plug back in the engine.

If statins are not an option for you, that's absolutely fine. You don't have to take them. Here's what I recommend in these cases. Look to see if you have inflammation. All this information about cardiovascular inflammation, it was raised by a couple really smart guys 30 years ago at Harvard, Paul Ridker and Gavin Blake. As they began to look through this, they found that it was true. Cardiovascular inflammation is a big deal. And I mentioned this earlier in the video, but one thing we didn't talk about is, is there a way other than statins to deal with this? Yes. And you see that no matter which side you see on the statin debates, people are actually understanding that yes, if you have cardiovascular inflammation, colchicine can help. What is colchicine? It used to be, it's an anti-inflammatory. It used to be one of the major medicines for gout, a simple arthritis. It's one of the oldest drugs in medicine. It's been used for centuries to treat gout. And what makes it interesting for heart disease is that it's just a very powerful anti-inflammatory, even at low doses. There were, we talked about this in one of our recent live videos. There are recent large trials like the LoDoCo2 trial or COLCOT. They show that people with heart disease who took low-dose colchicine, half a milligram a day, had fewer heart attacks. The drug doesn't lower cholesterol. It calms down the inflammation inside plaque, and that's what we use low-dose statins for. Remember that. So that low-dose colchicine makes it more stable and less likely to rupture. Although it too has some side effects. Now, let me know in the comments if you'd like a video about colchicine.

Now, more important than any supplement or medication, lifestyle, regular resistance training, high-intensity interval training, and adding this to good diet and good sleep and stress management. These are the things that you really need to focus on. Exercise, especially resistance training and high-intensity interval training, is probably, in my patients, the most neglected thing we see because working out to where you're going, that's uncomfortable for a lot of people. And working out to where you feel a burn in your legs, your thighs, that's uncomfortable, too. But those things are what really help you get your health back. They need to be a routine in your prevention program, regardless of the medications you're taking. Because there's no doubt that the most important change you can do to avoid a heart attack is improving your lifestyle first.

Speaking of which, we continue to get a lot of questions about how do you do this? We get a lot of people watching my videos wanting to say, "Hey, you know what? I'd like to DIY this, do it yourself." I don't really recommend doing it yourself when you're working on something that's as important as your life and as technical as what we've talked about. But I do respect people's desire to improve their lifestyle and to look at cardiovascular risk. We've developed our own seven-step heart attack prevention protocol. You can download it for free in the description below. In there, you will find the fundamentals to avoid a heart attack and a key pearl. Most of my patients reach out to my team because they're frustrated with the current medical system. They get pushed by their docs and their nurses and other people in the medical clinic to start a high-dose statin without even talking about root cause, the lifestyles, cardiovascular disease risk, the drivers like pre-diabetes and diabetes, metabolic disease. I went through the same problems despite following the preventive approach of the traditional medical system. I still developed arterial plaque and still had risk. You don't have to try to fix all of those problems by yourself. What you need is a team that can help guide you to make the right choices for you. I've personally trained a team of clinical advisors and nurse practitioners that can help you identify the lifestyle changes that you most need to make and that fit the best in your lifestyle. It can help support your progress and reduce your heart attack risk. Just give us a call.

Now you know how to use statins to unclog arteries, or at least how I use them and the evidence behind it. If you'd like to know more about my own arterial plaque reversal story, you see again, I'm one of those guys that actually saw reversal of plaque, watch this video right here.