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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 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 actually , 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 to 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 department. , 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 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 a 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. 99% 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 VLDL's with LDL's with HDL's. , 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 LDL's 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 it'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 LDL , starts 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 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 LDL's 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 stat , 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 LDL 's 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 up regulate 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 , up regulates 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 sense is 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 a 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
