Dr. Boz [Annette Bosworth, MD] - Statins... what keto doctors don't tell you

The transcript is in English. Here is the cleaned, readable version of the transcript.

My total cholesterol is too high, and most doctors would prescribe me a statin. If you watch this channel, you know that statins are not at the top of my prescribing list, but I haven't told you the whole story. Let's begin by stating that statins are not evil. They do lower cholesterol, and that is one of the risk factors for heart disease, the number one killer in America. I do not think you should put statins in the water, but when you look at people with the risks for heart disease and you're trying to reduce risks, cholesterol medicines like statins can improve that risk profile.

You've also probably heard me say that we need cholesterol. Cholesterol is what makes our fat-based hormones. It's what's found in every cell with a nucleus, because if you want those cells to talk, they use cholesterol to do that, and it's so important that any cell with a nucleus can make cholesterol. When you were a baby in development, making brain cells and all these important processes that require cholesterol, what was your total cholesterol? It was not 270 like mine. It was 50. How well your cells can make cholesterol inside them to use them does not depend on the transport of moving cholesterol around. Years of elevated cholesterol, yes, they have an increased risk factor for heart disease, and that's why statins come to the table at all.

That being said, I don't want to take a statin. If they're good for lowering cholesterol, and high cholesterol leads to heart disease, and lowering it doesn't hurt you, why are they bad? Well, they do have side effects of muscle pain. Thousands of patients have taught me that their brains do not work as well when on them, and it does calcify their arteries. Although that can be helpful in a select number of patients where they're about to have a heart attack, I'm not sure I'd do that to everybody. Let's take a closer look. Teaching about cholesterol can be very confusing, so stick with me.

Let's start by looking at a lipid panel. This will tell us what your total cholesterol is, what the triglycerides are, what your HDL is, and then finally this bad cholesterol called LDL. What we're really looking for is who has the bullets, whose LDL cholesterol is going to kill them. When you look at cholesterol traveling around our blood from one location to the next, it actually travels in lipoproteins, or these spheres or balls filled with triglycerides and cholesterol. These are called lipoproteins, and on the outside of those lipoproteins we have these markers, either APO B or APO A. This tag on the outside tells the cell what's on the inside. It was years into seeing patients before I actually learned that the LDL cholesterol, that terrible bullet, was a calculation, and that the math is messed up.

Here's an example. In a lipid panel, we take several of these spheres, these lipoproteins, and we pulverize them. We take all of the cholesterol and put it in one section. We take the triglycerides and put them in a different section, and then we take the markers from the outside, and actually we hardly look at those. That total cholesterol comes from all of the lipoproteins that are in that blood sample, and the triglycerides also come from all the lipoproteins. This may not sound like a big deal, but hang with me as we look at the smorgasbord of lipoproteins. Again, the one we really care about isn't just LDL cholesterol. It's the LDL cholesterol that acts like a bullet. Let's see how we find that.

For starters, right after you eat, your body packages triglycerides and cholesterol into the largest of the lipoproteins, called a chylomicron. But you don't draw your cholesterol level right after you eat. You fast for at least 12 hours. When I look at the size of these monstrous balls of fat floating around your blood, well, they're gone after about an hour. In fact, if I see any of these 12 hours into your fast, I call a major problem is happening. Those chylomicrons deliver most of the triglycerides, and that sphere goes from 500 nanometers down to around 50, so a massive drop in size. We now have labeled these, strangely enough, very low density lipoproteins, VLDLs, and these are in circulation for 2 to 6 hours. These also get rid of triglycerides by delivering them to any cell that's hungry for energy. By the end of their life cycle, we've reduced their size, and we're now several hours into the life cycle of this lipoprotein. Again, we drop off a bunch of those triglycerides, and now we have the bad cholesterol, yes, that LDL cholesterol, the bad one. Notice how there's hardly any triglycerides left. There are a bunch of cholesterol left, but we call it bad because suddenly these cholesterol are terrible. The LDL cholesterol actually can last up to days in circulation. We call it the residency time: how long does it live in circulation? When we look at all of these cholesterols lined up together, again we are looking for this special bullet. So do I have them? Let's take a closer look.

Let's start out 12 hours after I've eaten a meal, and they give out their cholesterol and triglycerides, but mostly triglycerides, to any cell that's hungry. So it's been several hours after I've eaten, and there are a few VLDLs in circulation. We are now going to watch the lifespan of what happens in my body. Take notice of how gorgeous that liver is. There's no excess sugar or fat. As I deliver triglycerides to the cells that need it, those particles get smaller, and we start to change their label from VLDLs to IDLs. But also notice how many of them are recycling back into my liver. As the size of those particles decreases, we change their label from VLDL to IDL, standing for intermediate-density lipoprotein, before we graduate to an LDL particle. It's at the end of that route, where the particle has given away all of the triglycerides it can, and anybody that did need cholesterol got it, but now its job is done. Let's tuck it back in the liver. If we look deep inside that liver, there are these catcher mitts, or receptors, that will take these particles and sweep them out of circulation, take them out of the residence of our bloodstream, and put them back in the liver where we recycle and start over again. This healthy chemistry set is constantly sweeping out the lipoproteins and emptying the blood.

So is this LDL bad in me? Well, part of that depends on how quickly I bounce down these different sizes of lipoproteins, distributing out the triglycerides, and then recycling proteins back into my liver as quickly as they are no longer needed. The number of bullets in my bloodstream will depend on how long it has been a resident in my bloodstream.

Let's compare this to someone whose insulin is high, and they come and say, "Doc, I don't want to be on one of those statins. I want to use the ketogenic diet to lower my risk of a heart attack." Except her story isn't like mine. Her insulin has been high for years, and the first thing that did was store a bunch of sugar in her liver. When all of those storage spots were filled, she packaged them into glycogen, no problem, easy to get rid of those if you need to. But she didn't get rid of them. She stored even more energy and turned triglycerides into fat globules in her liver. Now she not only has high triglycerides in circulation, she has a bunch of fat found in her liver. That high sugar, that high triglycerides, that fatty liver, and high insulin are all markers of where her metabolism is and how we might want to reverse it. Her risk of heart disease goes up with each of those markers, as well as her age, high blood pressure, tobacco, and a few other risk factors.

So let's take a look at that VLDL inside our patient. Her VLDL starts out about the same size as mine. As she dishes off those triglycerides, she creates smaller lipoproteins but also leaves a bunch of them in her rearview mirror. There are lots of VLDLs that did not get recycled back into her liver. As she proceeds down the cycle of decreasing the size of her lipoproteins, that LDL particle doesn't recycle back up into the liver as fast as it should. It hangs out in circulation, having a long residency time, and becomes that purple bullet.

Let's dive back into her liver and see how these lipoproteins are processed. There are those catcher mitts again, waiting for those lipoproteins to be recycled out of the bloodstream and into her liver. Except in this case, there are not very many of them. The liver is full. It doesn't need any more of those inside it. It's stuffed to the brim already. As those bad cholesterols run into the liver, the number of catcher mitts, or receptors, is pretty small. In addition, that high insulin state that caused all this melted away or destroyed the slime layer that protects those particles from exiting the circulation. As these LDL particles look for a new home, they wiggle their way out of circulation and into the wall of your artery. Those lipoproteins do not belong there, and your immune system attacks, saying, "Get the heck out of here." A few lipoproteins outside the circulation and inside your artery wall, and your immune system will keep up, no problem. But when thousands and thousands and millions of them exit the artery and hang out in this artery wall, it creates this pimple that will explode into your bloodstream, causing the heart attack. It's in cases like this that if I calcify this, like a statin would, it can actually protect you from the popping pimple. But that's not all that statins do. Statins increase the number of these receptors, which decline because your liver is full, and statins restore the number of catcher mitts. So these LDL cholesterol and other lipoproteins can recycle and get out of your bloodstream without heading into your arterial wall.

So here we are, where we started. My total cholesterol is above 276. My triglycerides are 88, and my good cholesterol is 107. My bad cholesterol is 155. So why aren't I on a statin? For starters, here are the risk factors for heart disease, and I don't have any of these. Let's get a little more specific. Let's look at my Framingham risk factor as a 51-year-old female with elevated total cholesterol, no history of smoking, normal blood pressure, and an HDL cholesterol that's pretty high. My total risk of heart disease over the next 10 years is less than 1%. So if I were to present to me asking if I should take a statin, the answer would be no. I fast every week, I work to keep my body weight down, my blood sugar is low, and I push my mitochondria to be the best health they can be.

When patients present saying, "I don't want to take a statin, and I'm kind of keto," well, the risk is real and high in those cases. There's a lot of benefit for reducing the number of lipoproteins in circulation. I hope you don't have to use a statin, but if you're looking for a way to do that, you do need to be consistently keto. I have people near and dear to me, patients, friends, family members, who say, "I don't want to be on that statin. Teach me how to live without it." But they come with a history that's filled with cancer and radiation, high cholesterol numbers, uric acid, and diabetes, and a history of lots of medical problems that have landed them with a really high risk of heart disease. Some have already had a heart attack. This is where I strictly remind them: YouTube is not the place for you to get medical advice. It is a place for you to come and get educated, and I'm really trying to do that with an honest assessment of what statins do and why they are so heavily prescribed, and then return the responsibility back to you. Understand the science, go to your doctor with this conversation, and if you don't want to take a statin, then be like me and control several of these things. Is your hemoglobin A1c as low as you can get it? Is your uric acid controlled? Do you have an ideal body weight? And are you growing the heartiest crop of mitochondria possible? If you want to talk cholesterol with me, the first thing you have to do is control this number. Check out this video before we ever talk cholesterol.