The Truth About Cholesterol: Debunking the Fear Factor

In this video, the speaker discusses the misconceptions and fear surrounding cholesterol and the over-prescription of statin drugs. They argue that the focus on LDL cholesterol as the sole indicator of health is misguided and that other factors, such as inflammation and insulin resistance, play a more significant role in heart disease. The speaker explains how oxidized LDL cholesterol causes damage and leads to plaque formation, while healthy LDL cholesterol is necessary for the body. They also highlight the potential side effects of statin drugs, including muscle fatigue, liver issues, and interference with energy production in vital organs. Instead, they advocate for addressing the root causes of inflammation and insulin resistance through lifestyle changes.

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Key Insights:

  • The fear surrounding cholesterol is largely based on misconceptions.
  • Doctors often prescribe statin drugs based solely on cholesterol numbers without considering the bigger picture.
  • Statin drugs do lower cholesterol, but they primarily target the healthy, fluffy LDL particles, not the damaging oxidized ones.
  • The real causes of heart disease and plaques are inflammation, chronic low-grade inflammation, insulin resistance, and oxidative stress.
  • Small, damaged LDL particles are indicators of underlying problems, not the cause of heart disease.
  • Measuring other factors such as blood glucose, blood insulin, A1C, triglycerides, HDL, and the total cholesterol to HDL ratio is more important than just focusing on cholesterol numbers.
  • Statin drugs can have negative side effects, such as muscle fatigue, weakness, and interference with energy production in muscles, liver, and brain.
  • Making lifestyle changes, such as reducing sugar intake, is a healthier alternative to statin drugs.


Hello Health Champions. Today I want to talk about cholesterol because the way we have been understanding and dealing with cholesterol in the last 50 years is one of the greatest health disasters of all time. And there’s this huge fear factor about cholesterol. When people are changing their lifestyle and they’re getting healthier, they’re losing weight, they’re feeling better, all their health markers are improving, except one, their doctors still scare them into abandoning their healthy lifestyle and reverting to a low-fat diet because one marker, LDL cholesterol, is too high in their opinion. And this is all because we have bought into the idea, without any good evidence, that LDL cholesterol is bad cholesterol.

What I want to help you with today is to make an informed decision by understanding the true factors and what’s really going on. What we really want to get away from is the idea that if cholesterol is over 200, if your total is over 200, then you get this automatic prescription for a statin drug. Or if your LDL is over 100, that should be some magical number that now you get a statin drug.

Do statin drugs lower cholesterol? Yes, absolutely. They do, but we’re going to talk about whether that is actually a good thing, we’re going to answer what kind of cholesterol do they lower, is that something we actually want to lower. We’re going to ask about heart disease, does it actually help lower heart disease, and the answer is, there is no good evidence of that. Recent studies actually show the opposite, that higher cholesterol is associated with lower all-cause mortality and better cognitive function in your later years. Does it improve longevity? Does it help people live longer? And there is no good evidence of that either. What you do get for sure are side effects, and we’re going to talk about that as well.

So why then is there a standard prescription for a statin, even though there’s no good evidence that it actually helps? Because there is something called evidence-based medicine, and the only evidence they’re looking for is, does it lower cholesterol? Yes, absolutely. And there’s the assumption that cholesterol causes heart disease, and therefore, it must be a good thing to lower it. And that’s a false assumption. The other reason is called standard of care, that a doctor, as long as he follows the standard of care, which is to prescribe a statin if your cholesterol is over 200, you can’t get in trouble if you hurt patients as long as you follow the standard of care. The time you can get in trouble is if you step outside of the standard of care and something happens.

We want to get away from the idea of high or low cholesterol, and we want to start thinking balanced or unbalanced. Because 190 could be unhealthy and 350 could be healthy. Now this is not to say that you should ignore your cholesterol numbers. They still give you good feedback. Higher isn’t necessarily better, but higher isn’t necessarily bad either. We have to understand when to pay some attention. What are the numbers to pay attention to? We’ll go over that.

One thing we want to understand is we want to start fighting; we want to start addressing the true cause instead of the rescue attempt. So what do I mean by that? If you come to a fire, then there is probably some people from the fire department there. Most of the time that you see a traffic accident or a fire, there will be a responder, there’ll be an ambulance, there’ll be a firefighter, and there’s an association there, and that’s just like we associate cholesterol with disease, cholesterol with damage, because cholesterol always shows up at the accident site. Just like the first responders show up at the accident site. That does not imply causation. That does not make the fire department guilty of the fire. It does not make the cholesterol guilty of the damage. And if we start fighting cholesterol, we are fighting the wrong guy. That would be like setting up roadblocks for the fire department because there’s an association between fires and fire departments.

So what then is the real cause of heart disease and plaques? And the real causes are inflammation, a low-grade chronic inflammation which is associated often with insulin resistance and/or oxidative stress. All these three go hand in hand. And here’s what we want to understand, there is a strong correlation between cardiovascular disease and these three things, there’s a very weak correlation between cholesterol and cardiovascular disease. And to the extent that cholesterol is involved with cardiovascular disease, it’s to the extent that it’s associated with these three.

So what we really want to understand is when is cholesterol unbalanced, and the indicators are increased blood glucose, increased blood insulin, increased long-term glucose, called a1c, increased triglycerides, decreased HDL (high-density lipoproteins), and an increased ratio of total cholesterol to HDL. We also want to look at VLDL and we want to look at LDL size. Now one of these by itself doesn’t necessarily indicate anything, and that’s why we want to look at the bigger picture.

The first four I’ll cover very quickly because I’ve done so many videos on that. Increased glucose comes from eating sugar and processed carbs, which trigger an insulin response to combat that high blood sugar. If this goes on over time, then we get insulin resistance and our a1c starts creeping up. And once we’re insulin resistant, now this glucose is not accepted by the cells. The cells are resisting additional fuel, and if the glucose can’t get into the cells, now it gets converted into fat, which is the triglycerides that circulate in the blood.

Next, we want to look at HDL and the ratio of total cholesterol to HDL. So this person has a total cholesterol of 286, and it’s supposed to be 100-199, so that is obviously very high, so it’s marked with a flag. But this in itself does not tell us if this is good or bad. The range goes from 100 to 199, and I would be a lot more concerned if your cholesterol total was 100 than if it was 286. Then we look at his HDL cholesterol, which is generally considered protective, and we want to see this above 39. And this person has 46, but is that high enough? It’s above that threshold, but is it enough to kind of offset the total cholesterol. So now we look at the total cholesterol to HDL ratio, and now we want to have zero to five. Again, a lot of these ranges are kind of ridiculous because there is no way a living human could get to zero. Zero or one is not a good number because then you would have virtually no cholesterol in your body, and that is an essential nutrient. But this person has 6.2, so that’s above the range, and what does that mean? And this is on most standard blood work, so this is not anything unknown or out there. It says please note you have half the average risk of heart disease if your ratio is about three and a half, and you have average risk of heart disease if your ratio is about five, and this is from men, it’s a little different for women, but you get the idea. So based on this marker, this person’s estimated heart disease risk is 1.3 times, 30% higher than average. So that’s not great, and this is based on one marker that I use. I’d like to see this ratio in the three to three and a half range.

Next marker is called VLDL, very-low-density lipoprotein, also known as remnant cholesterol. And the range is between 5 and 40, and this person is 16. So what does that mean? This marker is very often overlooked, but it’s a great tool to look at to see where you are on your insulin resistance journey. The way you get this is you take the total and you subtract the other two. So it’s just what’s left over, you subtract LDL and HDL, and you’re left with VLDL. And I like to see this number between 15 and 20. So this number of 16 is actually really, really good. To say that it should be anywhere between 5 and 40 is a little bit ridiculous because your body is not indifferent to if the number is eight times as high as the low number.

So what is this thing, the VLDL cholesterol? It’s a carrier. The purpose is to deliver dietary fat to the cells, to the tissues. So this has some triglycerides, and it has some cholesterol, it has a lot more triglycerides which are light, and this is why it’s called very-low density. And the purpose is to deliver the fat to the tissues, and when it’s successful, then it quickly offloads these triglycerides and the cells take them in, and now this VLDL becomes an LDL, a healthy normal fluffy LDL. But if you’re insulin resistant, then the tissues resist the delivery of these nutrients, of this fat. And therefore, if it’s unsuccessful in delivering, then it’s going to linger, it’s going to stick around in the bloodstream for a long time, and the levels go up, so when we measure them, they are much higher. So if you have a value of 35 or 40, then you’re quite insulin resistant because your tissues are resisting the delivery of fuel.

Now let’s talk about the really important stuff that hardly anyone gets. Ninety-nine percent of people prescribing statins have no idea of what I’m gonna tell you. We said that the liver packages nutrients into certain vehicles for delivery, and one of those is the VLDL, and if all goes well, this quickly is converted into a normal healthy fluffy LDL. And then what happens is your liver wants to recycle this LDL. It wants to keep it going, so it has receptors, and if this LDL is normal, then this system works like a revolving door. Very, very quickly does the liver reabsorb it, repackage it, and put it out again, and it does this with VLDLs, with LDLs, with HDLs, with all the different types of cholesterol. They are always appropriate, whether they’re high or low, they’re appropriate for what’s going on in the body.

But what happens if you introduce some oxidative stress and some low-grade chronic inflammation and some glycation? If you get some sugars stuck on these LDLs, now they become damaged, and when they’re damaged or oxidized, now they shrink. And this is why we’re talking about the size of the LDL, and the bad LDL is the damaged LDL. But again, it’s not the LDL that’s bad, it’s small, and therefore it indicates that you have had some oxidative stress and some inflammation and glycation. These are the real problems. The small LDL is just an indicator of those problems.

And here’s one of the first big keys to understand. This healthy LDL fits into the revolving door, but this oxidized LDL does not, when it’s small and damaged, now this receptor doesn’t recognize it. It doesn’t fit into the system. The liver cannot reabsorb this LDL. And therefore, the numbers of small damaged LDLs start building up. And what was it that caused the oxidative stress, the inflammation, and the glycation? It is sugar, insulin resistance, food allergies, stress, and the list goes on and on. All those things associated with chronic disease.

So now listen up very carefully. Here is the real cause of atherosclerotic plaques. This oxidized LDL can do some damage. It damages the intima, which is the inside lining of the blood vessel. If you notice this yellow plaque, it’s not actually inside the lumen of the blood vessel. That there are different layers of the blood vessel, and the inside layer is the intima, and then you have various different layers. So what this oxidized LDL does, it damages the inside layer and makes the gaps grow bigger, and now this oxidized LDL, which is tiny, can slip through the crack and start getting into the wrong place. And now there’s something called a macrophage that starts following this bad guy in through that crack. And a macrophage is something that eats something. That’s a white blood cell, sometimes it’s called a phagocyte, it goes by many different names, but it’s basically, we’re going to call it Pac-Man, and this Pac-Man, its job is to go after and gobble up this LDL. Because the liver receptors cannot recycle it as a healthy cell, this oxidized LDL is now treated as a foreign intruder. It’s not part of the friendly guys in your body anymore. And the only way to get rid of it is through your immune system. So it’s treated like a virus or a bacteria or a fungus or something we need to get rid of. And when Mr. Pac-Man has gobbled it up, now it encloses this, and it becomes a foam cell. So it sort of protects the environment from this damaging cell, but it becomes another problem in the process because these foam cells now become the plaque.

So to really drive home the importance of looking at the big picture and the sizes, let’s look at a couple of real live examples. We did one test on January 25th, and we did another one on April 5th, that’s a little over two months, 70 days. We started off with a total cholesterol of 297, which was flagged as high, and 70 days later, it is still high, but it’s a couple of points higher at 299. We look at LDL cholesterol, which is traditionally considered bad, and that was 225, and the later test was still 225. So this guy was a patient who had been doing some changes in his lifestyle, going doing a low-carb, high-fat diet, and let me tell you, his medical doctor was not impressed. He was asked very sternly or told to get on a statin drug, they said, „Look, it’s not getting better.“

So then we ordered an NMR profile, we had this on both occasions, which is where you measure the particle count, which takes into account the size of these particles. And now it starts looking even worse because we want this number to be under a thousand, and it is 3448. And now you may have noticed that this has my name on it as the ordering physician, so you’re wondering why am I bragging about this case, it just doesn’t look too hot. I mean, this guy is in trouble, right? Well, once we look at the next step, we look at the change, we see that his LDL particle count went down from 3,400 to 2,900. We had a change, a reduction in 455. A 15% reduction in the number of cells, but more importantly, what kind of cells, which cells were reduced. So now we look at the small LDL count, and that went from 1653 to 1227. So what we see here is crucial, almost all of the reduction was the small damaging oxidized LDL particles, the ones that caused the plaquing and the damage. And on this test, we also get an average size of the LDLs, and we want this to be over 20.5. So this guy started off in January at 20.9. So even though his numbers didn’t look too impressive, they were probably much, much better than they were six months or a year earlier. We just don’t have any data on that. And then we look at what happened in these 70 days, and it climbed. The size average increased from 20.9 to 21.3. And that may not look like a huge change, but let’s look at it one more way. LDL particles can be called small pattern or large pattern, and we see that on the first test, this person was already into the large pattern size, and 70 days later, he was further in. It doesn’t look like a whole lot, but now let’s look at this. They also give you what’s called an insulin resistance score, and in January, he was in the 57th percentile. That means there were still 57 percent of the population that were healthier than he was in this regard, but 70 days later, he was in the 33rd percentile, and he had made tremendous progress because what this means in only 70 days, he had passed 84 million Americans in terms of health. And this is why it’s so important to look at the big picture because if you only looked at the milligrams of total cholesterol and LDL, it looked like he was making no progress, but when we start understanding the big picture and we actually measure, now we’re more interested in the direction he’s going, are we making progress, and can we monitor that continued progress.

So what would be the pros and cons of a statin drug? We know they lower cholesterol, but now let’s understand what type of cholesterol they actually lower. So what does a statin drug do? It increases the number of receptors to reabsorb LDL particles. That would seem like a good thing, right? Well, the thing is that these healthy fluffy LDL particles, they fit into these receptors like we talked about. So if we take a statin, then we will see these numbers of LDL particles go down. We’re going to see a dramatic decrease of these fluffy LDL particles. But we also said, if you remember, that these small ones, they are not recognized by these receptors, so the statin drug will decrease total cholesterol, but it will only reduce the cholesterol that we want. It will not reduce the cholesterol that we’re trying to get rid of, the damaging cholesterol, there is no change. These damaged, oxidized LDLs can only go down if your immune system is working. And as we saw in the previous example, your body has a chance to do that if you reduce the level of oxidation so that there is less oxidized damage.

Now one point we could say in favor of the statin would be that if we reduce the LDL particles, then there is less total LDL out there to be oxidized, but the better idea obviously is to reduce the actual root cause, which is the oxidation, the insulin resistance, and the inflammatory damage.

So let’s talk about why these statin drugs do some damage as well. The first question is – why does the liver upregulate the receptor sites for LDL when we introduce a statin? Is that a good thing or a bad thing? Well, the statin blocks an enzyme called HMG-CoA Reductase, and don’t memorize the name, it’s totally not important. But when we block that, then we’re stopping a process. The body made that enzyme for a reason, it wanted to accomplish something, now we block it, then the end product of this pathway can’t happen either, and farnesyl pp was supposed to become cholesterol and CoQ-10. So these are two very precious substances, the body doesn’t make unnecessary things. It wants these things for a reason, so the reason that the liver upregulates these receptor sites is that when we block the production of cholesterol, of an essential nutrient, then the liver perceives a lack of cholesterol. It wanted that cholesterol. Cholesterol is very expensive to produce, everything in the body is expensive to produce. So when we block the production, so there’s less of it, the liver senses a lack, so now it kind of gets desperate and tries to reabsorb as much of that cholesterol as possible. But again, remember, it can only reabsorb the normal, healthy LDL, the stuff we actually want to get rid of is not affected. The other precious nutrient, CoQ-10, is involved with 95% of all the energy production in the body. So when you block the pathway, you reduce CoQ-10, you reduce the overall energy production in the body as well. Which tissues would be the hardest hits? It’s the body parts and tissues that use the most energy normally. So muscles use a lot of energy because you have to move around. So statin drugs cause muscle fatigue, muscle pathology, and weakness. And if you recall, one really important muscle is called the heart, and we take the statin drugs because we’re afraid that the cholesterol will block the artery and shut off the oxygen delivery for energy production, but now we take a drug that actually shuts off the energy production and the delivery to the heart. So now the heart has to work harder, and we often get heart pathology like cardiomegaly and things like that. Another very hard-working organ is the liver, so first we interfere with the production of cholesterol, so it has to try even harder to make and reabsorb cholesterol, and then we block the energy production to that. And then there’s one more place that uses more energy than any other, and that is your brain. It’s two percent of your body weight, uses 20% of all the energy in your body. So let’s take some statins, so we block the energy production to that as well.

So you could take statin drugs and you can interfere with all of this, or you could just stop eating sugar and get healthy. If you enjoyed this video, you should really take a look at that one next if you want to understand how the body works and truly master your health. Thanks for watching.