Dr. Boz [Annette Bosworth, MD] - Why I Don't Prescribe Statins For High LDL Cholesterol

This is your bad cholesterol. This is your bad cholesterol. One will kill you; the other one is part of a healthy metabolism. If you're taking a statin, which one does it lower? Let's take on this topic of cholesterol.

First of all, when you go to the doctor to get your cholesterol checked, you're actually not checking your cholesterol. You're checking lipoproteins. These are the carrying units that carry around the fatty substances, like this fella, found inside the lipoproteins. Your blood is water soluble, and if fat floated around in it, it would cause a clot. You can't do that, so we have to measure these lipoproteins.

This one is a chylomicron. It comes out of the liver and is the biggest and fluffiest one. But notice what's here: these are what we are talking about on your lab reports. This is a VLDL, much smaller than a chylomicron, and this one is smaller yet, because it's gotten rid of more of its fuel. It's called an IDL. Finally, here's the bad boy called an LDL, a bad cholesterol, a low-density lipoprotein. But we have two of them, one that's fluffy and one that's a bullet. Notice that both of these have lots of cholesterol components in them, but one of them is much smaller and more deadly.

Let me further explain the difference between how you get from a fluffy LDL to a bullet LDL. Let's talk about this cycle and begin with a healthy patient. Here is a perfect, pristine liver, and it has packaged the fat into chylomicrons. These last a hot minute in our system and are quickly converted into IDLs by getting rid of a bunch of triglycerides. These are nutrients for ourselves and our body. These VLDLs offload the triglycerides, some of that fatty nutrient, to our cells, and they get smaller. That smaller version is an IDL. Notice how the cholesterol is more concentrated at every step. The next packaging is the LDL, better known as the bad cholesterol. These lipoproteins are the smallest, and they have the least amount of triglycerides and the most amount of cholesterol left in them. They get recycled back into your liver. They're going to get repackaged and put back into the chylomicrons. This is what healthy looks like: your liver packages up the nutrients, the good stuff, the fat, and it delivers it throughout the body, and then it recycles to do it all over again. That's normal.

This is not normal. Not normal starts with high insulin. Notice our liver does not look so healthy anymore, and those chylomicrons are going to do what they do. They're going to get rid of a bunch of triglycerides and transition into the IDLs and LDLs. Those VLDLs are going to try to get rid of that commodity. They've got triglycerides, but the cells are kind of full; they've got the energy they need, so it takes them a little longer to get rid of it. But now the IDL does come about, and as they get rid of those triglycerides and transition into this smaller version of the lipoprotein, the IDL is a final resting point for the LDL, that bad cholesterol. Now we have a problem: insulin is preventing the recycling of going back into the liver. If you look, that liver is pretty full of fat, and it's trying to do a job it's already struggling with.

This is a close-up of your blood vessel and the little lining of the blood vessel. These are healthy cells, which are pretty boring. The LDL cholesterol comes in and goes into the liver, and there's not much to see here. But when its lunch shows up, it starts to deteriorate the lining of the inside of your blood vessels, and some gnarly things start to happen.

Let me show you a liver that lives with normal insulin and with elevated insulin. During a state of elevated insulin, your liver fills up with a bunch of stored glucose called glycogen. Once those storage bins are all filled, a layer of fat storage begins. These are triglycerides, and that storage bin then quickly fills up as well. The liver starts to change. It gets harder, it gets filled jam-packed with fat, and that hardening of the liver is cirrhosis. Today, most people with cirrhosis of the liver don't have liver cancer or even alcoholism; they have cirrhosis from too much fat in their liver, and that's from high insulin.

So let's dive back into that blood vessel and see what happens in a state of high insulin. First, we begin without the protective layer that's naturally found on the inner lining of your blood vessels. As the LDL cholesterol comes in and tries to get into the liver but many times can't, these very small, dense, bullet-like LDLs slip between the cells and are now in the arterial wall. This is not good. They're looking for a parking spot. They've run out of parking spots in the liver, and they happen to fit in this secret compartment in the lining of your arteries. Your body is going to try to protect itself. First, it changes the LDL particle; it oxidizes it. This signals the white blood cell system to come in and attack it, because it doesn't belong there. The body is trying to clean up and get it out of there. As it does this to one particle, that's no big deal. But as LDL particles in the small, dense, bullet-like version dip into this hiding spot, they recruit more and more and more of your immune system's attention, and eventually you've got a mess.

This is where your small, dense, bullet-like LDLs are ending up: as oxidized LDL. If you've worried about having a heart attack as you eat a bunch of fatty foods, wondering whether it ends up in your artery, this is not the process. This fatty, gooey substance came from the inability to recycle that good, fluffy LDL cholesterol in the liver. And if it pops, if this leaks into your blood system, it does cause a heart attack.

So if you're taking a statin in hopes that you lower your LDL cholesterol, your bad cholesterol, you're going to lower the LDL cholesterol floating around in the lipoproteins in circulation, not the ones stuck in the arterial wall. Those will cause a heart attack. Here we have your low-density lipoproteins filled with cholesterol. This one is fluffy, this one is your bullet. This one does not cause a heart attack; this one does. This one is increased by eating saturated fats. This one is increased by eating carbs. This one is lowered by a statin, and this one is not.

If you're a physician who has been seeing patients for the last 30 years trying to prevent a heart attack, you've written for statins hoping to prevent that heart attack. But you might be interested to know that in some studies you would have to treat 50 patients for two years, taking a statin every day, to prevent one heart attack. In other studies, over 200 patients were needed to treat in order to prevent one heart attack.

If you're taking a statin and you're trying to prevent a heart attack, do not stop your statin by watching a YouTube video. Talk to your doctor. If you're trying to prevent that gooey stuff living in your arterial wall from exiting and causing a heart attack, you need to lower the inflammation. In other words, you need to decrease the insulin. If you've got enough of that goo around your system, it means your insulin probably isn't listening to you; it's resistant. Fixing insulin resistance is not child's play. You need to know the rules. Check out this video, and I will teach you them.