They Lied About High LDL — 27 Years Proof with Dr. David Diamond

Dr. David Diamond, thank you for joining us. Why have doctors and researchers been lying to us for the last 40 years about LDL using relative risk tricks to push statins that barely work?

Well, first of all, thanks so much, Ken, for inviting me to be on your your podcast. It's always a pleasure to speak with you. You know, I have just have so much admiration for you as an MD. you're not just following guidelines, you're actually reading the literature, you're listening to people such as me and and others, MDs and other researchers. So, um it's just such an honor to be here and share what I've learned.

Thank you.

Um it's a little strong your question because it implies every doctor is lying to us and I don't believe that's true. When my doctor recommended that I go on a statin, and that's because I have very high cholesterol going back 26 years ago, uh I didn't think he was lying to me. The real question is why do doctors follow the guidelines very sheeplike? Why is it that they don't do the research for themselves to see that it's really not justified first of all to lower your LDL, especially if you can work toward being healthy? Um, and as you really say in your question, the actual benefit of statins is just so minuscule that people aren't aware that they're so ineffective. And yes, you mentioned relative risk and I actually do have a a slide later on that we can either cover right away or if you want to go right to it um or we can lead up to it because what I think is important is understanding the science and and it it may be and I know you wanted to get right to the point but I I don't think your listeners know many of them know who I am but many may not know who I am. I mean, the question is, why should they care about anything I say?

I put it right in there. I'm a PhD. I'm not an MD. I didn't go to medical school. I'm not a cardiologist. So, why should anyone listen to me? And if you don't mind, I just think briefly.

No, I think that's an excellent idea. I do want you to tell people how long you've been researching this. And you know, basically, we're going to get into the slides momentarily and show what you found through your years of research, but I also I want you because you're almost 70 now.

That's right.

And I want you to after you've given us your bonafites, I want you to really let us know at age 69, what how many years have you had documented high LDL cholesterol? How many strokes and heart attacks have you had? Uh what are what's your daily you know regimen look like? Are you are you crippled and disabled or are you out there are you out there running around enjoying your best life?

Okay. Um so just briefly um 1978 I had planned on going to medical school um but I took a course on neuroscience walked into a neuroscience lab and decided neuroscience was going to be my life. And for the past 46 years, I've been a neuroscience neuroscientist. And so my PhD is in biology, which is an area that I absolutely love. Uh along the way, I've received millions of dollars in funding for my research on primarily PTSD and Alzheimer's disease. I retired as a career scientist at the VA. And so I've published about 150 papers in medical journals on neuroscience um both papers, reviews, articles. Um and so you know I've been very successful as a neuroscientist and understand I'm not a contrarian by nature. Anyone who knows my neuroscience research, my neuroscience colleagues have no idea of the controversy that I've been involved in. Um so we've got the one part of me that's a neuroscientist 26 years ago. actually 27 now, 1999. I had a blood test taken because I wanted to get some life insurance and they put me at the high one of the highest risk. I was near risk for a smoker because actually I had astronomically high triglycerides and extremely low HDL. A ratio that was about 25, which for anyone that knows that's some seriously bad ratio. You don't want your ratio to be more than two or 3 to one. and mine was 25. And in fact, what happens when your triglycerides are that high, mine were between 700 and a thousand.

When they're that high, they don't even give you your LDL because it's calculated based on relatively low triglycerides. So, my first concern 1999 was um I've got and triglycerides are dangerous. Um I got dangerously high triglycerides. My doctor did want me to go on a statin. I understand I was a I'm a neuroscientist, not a heart disease researcher. So, I just learned took a look at it. Yeah, that was extremely bad. Um, and all my adult life, I had believed I had the impression that eating meat was bad for you. Eating bread will be good for you. So, I pat myself on the back because I'd eat bread, but, you know, not have any butter on the bread. That got me learning about the science and I decided rather than take any medication, I needed to learn why I had triglycerides. Bottom line is I learned that it was because I had a very high carbohydrate diet. Got my carbs down. Although I do have a genetic anomaly that results in relatively high triggs. It's not normal to have them at a thousand.

Um, and I have a relatively low carb diet. Not probably not ketogenic. I do drink some exogenous ketones. So, my carbs are between 50 and 100 grams a day and my triglycerides are now much lower. My ratio is much better. Um, but once I got my triglycerides down, then I had an additional problem. Then they could actually look at my LDL. This is now after about six years and it was alarmingly high. My total cholesterol was 300. My LDL is about 200. And it's been there for about the last 20 years. And when you ask uh all right, what have I done about it? Um I've done nothing. No statins, no medication, no change in lifestyle.

Let me ask you this, doctor. Did did lowering your carbohydrate intake from whatever it was when your triglycerides were over 700, did lowering your uh daily carbohydrate intake to under 100 grams a day roughly, did that fix the triglyceride issue?

Well, it dramatically improved my triglyceride issue. So, I'm routinely about 150 now on my triglycerides. My HDL range is about about 50. So, I've got my ratio down from 25 to three or so.

Beautiful.

And and really, I'm an anomaly because that's still a high ratio, but I have no other risk factors. Um, so weight, blood pressure, you name it. um inflammation. I have no other risk factors. So, in a sense, I'm like the lean mass hyperresponders, but with just a a high triglyceride HDL ratio. Um, you ask how many strokes and heart attacks. Listen, I don't want to be like the guy who was actually on TV decades ago who said, "I'm going to live to 100." And he had a heart attack during the commercial and he died. So, I don't want to be the guy that says, "Nothing bad can happen to me." So, we just talk about the past. Um, I've been very healthy. I've been able to lose weight. I was heavier. I I was never obese or diabetic, but I was a good bit heavier 26 years ago. I've been able to get down to a good weight. I now work out five days a week. Um, and I I feel great. Yeah, I'm almost Oh my god, almost 70 years old. Um, and so yeah, I'm doing I'm doing really well. Uh, no heart attacks, no strokes, no problems, no chest pain, nothing.

So, ju just to be clear, we're we're about to jump into the all the research that Dr. Diamond's been doing, folks, but he's had documented high total cholesterol and high LDL cholesterol for over 20 years, well over 20 years. No heart attacks, no strokes, feels amazing at 69 years of age. I understand you're still an active boxer and quite quite active and quite vigorous and obviously very vigorous mentally.

Yeah. Well, thank you. Um, yes, I'm a I'm a professor here at the University of South Florida. Uh, I I do personal training. I like boxing a couple days a week and play raetball a few days a week. You know, I go two hours playing raetball and an hour of boxing. And so, I I think that's that's really helping to keep me young and and understand um my doctor's given up on recommending statins for me. Um, so, you know, I've had the same doctor for 20 years and he's followed my progress. But I tell you something, it's interesting. I know so many MDs that a segment are like you. So curious um and a segment that have absolutely no curiosity. I mean, here it is. My my doctor I he knows that I'm a scientist. He knows that I've been able to lower my triglycerides and and yet he's never asked for any of my publications. I have a neighbor who is an MD on a statin and I had a good talk with him about cholesterol and statins and and frankly and that was 10 years ago and he hasn't followed up on it all and he's not interested. The doctors I believe are not lying. Okay. When a doctor recommends a statin, the doctor is being obedient. And I actually teach a course at USF to premed students called medical controversies. And I just love being able to influence them now before they're getting to medical school because I tell them you've got to be you got to be curious. You got to learn and you got to understand the guidelines are tainted by financial conflict of interest.

Beautiful.

So when doctors are told that when LDL is above a certain level, you therefore prescribe statins, um they just sheepishly just follow the guidelines. Now, in their defense, which I think is weak, in their defense, doctors take a chance when they don't follow standard of care.

A doctor feels, and I I've heard this, what happens if I don't recommend a statin to someone with high cholesterol and that person has a heart attack? I'll potentially be subject of litigation. I could lose my license. So, this is the world in which we live in. Now, who are the people who are lying? I'm not going to name names because I don't want to get in trouble. Um, but the people at the top are the ones that are lying. The people at the American Heart Association, which is very well financed by industry. Understand the American Heart Association takes in almost a billion dollars with a B each year from sponsorship, much of it from the food and the drug industry.

Yep.

And it's amazing how they're clearly deceptive. They don't follow the literature. They basically follow the hand that feeds them. And understand also it's the food industry that benefits by demonizing cholesterol. I mean you got Cheerios, okay, which basically tastes like cardboard. And you get people to eat Cheerios and the only way you can eat Cheerios is you got to put sugar on it because it tastes so bad. And and what do they have in the front of their box? Cheerios. Good for your heart. And it's in their commercials. I'm eating Cheerios because I want to live to see my grandchild. And so you've got herbs and you've got garlic and you got supplements all based on the idea that LDL is harmful. And so this is an industry that's absolutely dependent on LDL being harmful. Let's also talk about vegetarianism. This is the only diet that's been shown reliably to lower LDL. Aside from LDL, there's absolutely no benefit to being a vegetarian. And so the vegetarians will look for every opportunity to demonize LDL. So you got a financial conflict of interest. You've got philosophy. You got people have a philosophy that being a vegan is healthy. Look at how it lowers LDL. I hear this all the time. And yet you've never they've never been able to show actually fewer coronary events in those who are vegetarian compared to omnivores. So there is clear deception at the top. Um, and then there is simply people following guidelines at the lower levels. You've also got, it's remarkable. I'm on Twitter, which is X, and I see people who aren't MDs, and they'll so vigorously say, how can you say that LDL is not harmful? And these are just regular people who have been convinced by their doctor to say you've got to lower your LDL. So, it's a it's multiple levels. And what I'd also like to get into at some point today is we've also got our allies. There are people in the low carb sort of camp that I think have also either not they've either demonized LDL, express great concern over LDL or they've ignored the literature that says that high LDL for a low carb dieter is not harmful. So we're in a sense we're fighting. It's David versus multiple Goliaths in this camp in this battle.

Yep. I totally agree. Now, you've done some research on a condition called hyperc cholesterolimeia, which is a genetic condition that gives people extraordinarily high total cholesterol and LDL cholesterol levels. But, and so the average person and the average doctor would think, well, these people are doomed. They're going to have a heart attack very early in life. There's no way they'll live to be 69 years old and still boxing like you. But uh you we're going to pull up your slides and we're going to go over some of this stuff. Actually, when you look at the hyper cholesterolimeia data, that's not what you find, is it?

Yeah. So, as a scientist, basically what I do is publish papers. I evaluate the literature. I publish papers. And so, I and I I want to say I I don't do this myself. I have worked with cardiologists, physicians, PhDs, non-PhDs, and we publish this work. This isn't just me coming on to your podcast and saying, "Well, this is my opinion." I've actually looked at the literature, and it's actually the primary medical literature that's being completely ignored by the cardiologist, by the American Heart Association. And I do have one slide because you wouldn't allow me to show 50 slides. So, so I'm giving you one slide that right here summarizes

um one paper that I think really epitomizes what people should know about hyper cholesterolmia and it's called familial hyper cholesterolmia because this is a genetic anomaly in which the cholesterol the LDL cholesterol does not bind very well to the LDL receptor and as a result you actually have extremely high LDL. So the LDL depending on whether you have hetererozygous or homozygous, it'll be double or triple or quadruple what is considered healthy. So these people can have total cholesterol of three, four or 500. And Brown and Goldstein actually studied this decades ago and did find actually that subset of people died young. And if you've got both anomalous genes, it actually does appear to be deadly and these people die very young. And that is basically the view that you get from medical school. Now there are so many papers that have been published that show that overall people with hyper cholesterolmia have a normal lifespan that they live to be 80 years of age. And the question is how is that possible? So this is a slide that I've shown in quite a few talks and it's not done by an LDL denier. Understand this is research that was actually done by people who are recommending that people with ILDL go on a statin.

And this was published in the Journal of the American Heart Associations journal. Correct.

Right. The Journal of the American Heart Association. This is real science. This isn't stuff that I've made up. This isn't my opinion. This is real hard data. And this one slide I think is really important. So what this is showing is the age specific rate of death. So the first bar in the far left is 0 to 19. So this is the rate of death for people with hyper cholesterolimeia who are from birth to 19 years of age. And then you see along as you move the decades, what is the rate of death of people with familial hyper cholesterolmia? And that 1.0 is the rate of death for the general population at that age.

Okay, let me interrupt, doc. We've got a we're actually videoing this live in front of the PhD community. So, if you guys are watching this on YouTube, our PhD community members actually have the opportunity to ask the leading metabolic health leaders questions. And so, Rad Brown says, "What does the SMR in this slide stand for, Dr. Diamond?" So, answer that and then continue. I'm sorry for the interruption.

Okay, sure. No problem. I'm really glad to get the questions. So that was what I was just saying is the SMR stands for standard mortality rate and so that is the mortality rate for individuals at that age. So the far bar to the left 0 to 19 1.0 is the rate of death for people in the general population who are 0 to 19 years of age. And understand almost nobody dies in the first 19 years of life. So it's an extremely low rate of death for that age range. This is actually important because you notice that those bars are above 1.0. This actually means that people with FH, the hyper cholesterolimeia, have a higher rate of death in the first 39 years of life. Two things about this are important. The first is there's no asterisk there, which means that increase is not statistically significant. So there's a subset, but it actually is important. There's a subset of people who are born with extremely high cholesterol that do die in the first 39 years of life. That's why the bars are above 1.0. But it's such a small subset that it's not statistically significant, which means the vast majority of people with hyper cholesterolmia are not dying in the first 39 years of life. So you got a small uptick and that subset is important and I will return to that. I'm not trivializing it. It is important. Now this is the most interesting part. Look at what's happening starting at 40 years of age. The people with FH that sensor familial hyper cholesterolmia. These are people who are living their lives with extremely high cholesterol. You've now gone down to 1.0 at 40 to 59. Starting at 60, you're going below 1.0, which means beginning at 60 years of age, these people are dying at a lower rate than the general population. And in fact, the people in their 70s with extremely high cholesterol are lowering have a lower rate of death, a 40% lower rate of death. And that was shown in the paper. And that's why in fact I copied and pasted. The only significant difference is this is from the authors not from me is that people in their 70s had a significantly lower rate of death. And this isn't compared. Sometimes people will talk about reverse causation in which people with extremely low cholesterol tend to be very sick. And so they have a very high rate of death. We're talking about comparing people in the general population to people that have FH. And so the people who have are in their 70s who have lived their lives with high cholesterol are less likely to die than the general population. And the authors didn't do statistics, but it appears to me if they did that if they simply started at 60 and gone beyond, you would find people over 60 have a lower rate of death compared to the general population. Now, why is that? Is this a strange finding? No. This has been shown repeatedly that people with extremely high cholesterol are actually healthier than the general population. And what are these people actually dying of? So in my talks I show that they have a normal rate of cardiovascular disease. The LDL has no influence on cardiovascular disease death. They have half the rate of death from cancer as well as death from infectious disease. And why is that? Because LDL is a part of our immune system. When we have a bacteria or a viral invasion, any bacteria, a pathogen, the LDL attacks that pathogen, a pathogen being bacteria or a virus, it's the LDL that actually helps us to survive an infection. And in fact, people that have the highest LDL are much less likely to develop sepsis, which is this massive infection and response by the immune system. The immune system works better when we have high cholesterol compared to lower cholesterol. So that helps us to understand why it is elderly people with high LDL are so healthy. We published a paper. I I have to again I want to acknowledge the people I've worked with. We published a paper reviewing the literature on extremely high LDL in elderly people and what you find is there was not a single paper that showed a higher rate of mortality in elderly people with high LDL compared to middle or lower LDL. So I just want to hammer away at this.

Yeah. The LDL in the elderly is not unhealthy. So this makes no sense.

Yeah. And it actually this is the reason

you

years back uh after I saw your first presentation with that slide, I started calling LDL cholesterol the other good cholesterol.

That's that's right. And I have to say it's been 15 years since my first presentation and uh it's been a few years since our our last time we've chatted here online. And uh I'm really glad to be able to sort of update what I've learned in the last few years as well. So I want to get across this idea that high LDL is not unhealthy. That in fact quite the opposite. Having high LDL is actually healthy. Now let's get to let's get to why is it a subset of the people with hyper cholesterolmia die young?

Is that the next slide?

That is in in the next slide. So these are people with hyper cholesterolmia and they're and this is a standard thing. If you got hyper cholesterolimeia you put everybody on a stat. This I think is a shame but this is happens worldwide. So these are people who have hyper cholesterolmia the genetic kind and they're all put on a statin. That's why their levels of LDL are not outrageous. So they're at about 150 which is high. Um but it's actually brought down by the statin. And so in this graph again which I have taken generally the American College of Cardiology this is a medical journal data in the medical journal shows their LDL on the statin between those that have heart disease now and those that don't. And you see that basically it's identical. They're both at around 150. The red are the people that have heart disease. The blue are those that don't have the heart disease. And you see the LDL is about the same. So what is the difference? The difference is the most important measure that there is and that's coronary calcium. that coronary calcium is able to predict who will have the heart disease and who will die in the next 10 years of heart disease versus those who don't. And so you see in blue, it's actually in red are those that don't have the heart disease. Those in blue have the heart disease. And so CAC is in the middle and their coronary calcium is relatively high. And so their coronary calcium is about 230 in blue. Whereas those that have no heart disease, that's the red, it's zero. And as the authors have, nearly half of those that had no detectable coronary calcium had a lifetime of significantly high LDL. And this is why coronary calcium has been downplayed by the American Heart Association and by cardiologists because it is a far superior measure of who has heart disease and who doesn't. So there was one important difference between the two groups and that's fasting glucose. So you see the group that has the heart disease in blue on the far right has significantly higher fasting glucose in the range borderline diabetic whereas those that don't have the heart disease they have low coronary calcium their fasting glucose is below 100. So this is such an important measure that is ignored by those who want to promote the idea that LDL causes the heart disease. This is an example of how people who live a lifetime of high LDL don't have the heart disease, but if they have high fasting glucose, then they're much more likely then to develop the heart disease. And I I think I agree with you that the hyperglycemia and the uh usually accompanying hyperinsulinemia is probably the primary driver for a coronary uh vascular coronary artery disease. Now having studied the CAC score in depth, having had multiple conversations with Dr. Agiston, uh Dr. Noritchitz, Dave Felman, and others. I I am coming to suspect, and I could be completely wrong about this. This is just a hypothesis, the CAC that you've got listed in the with the blue uh blue column. I'm coming to wonder if it is the actual CAC score that matters or and I I think it does matter, but is the CAC score actually what it's actually giving us is it's a proxy marker for the level of soft plaque and inflamed plaque in the average patient because we know that if you take a a statin, it's going to tend to increase your CAC because it's it's effectively turning the soft plaque and hard plaque. And we know that the the calcified plaque is a much more stable scesscent plaque than a soft plaque or an inflamed soft plaque. And so you you can feel free to disagree with me on this, but I'm I'm wondering is the CAC just a rough proxy marker for soft plaque that because if you have calcified plaque, you're probably going to have some soft plaque as well. And is is could it be that that's the actual danger that's being reflected in these CAC scores? Does that make sense?

No plaque is good plaque. So, uh I with you and the CAC the coronary calcium doesn't tell you about soft plaque and that could be measured separately. But I understand something. Um it's so well established that coronary calcium is the best marker independent of age. You can be 40 with um coronary calcium of 200 which is shows that you're more likely to have a heart attack in the next 10 years. You can be 80 with zero coronary calcium which means you're not going to have a heart attack or stroke. Uh and it's so well established the link of coronary calcium to heart disease and I mean real events and mortality

Yep.

that the field was faced with a problem when it came out that it's so clear that statins increase coronary calcium you could imagine the problem that the American Heart Association American College of Cardiology and the cardiologists are faced with. What are we going to do with given that statins increase coronary calcium? Well, let's call it stabilizing calcium that it's a good thing, right?

That statins increase coronary calcium.

This is absolutely amazing to me that they can turn something that is harmful into being beneficial. So, increased coronary calcium is bad unless the statin does it, which is ridiculous. So yes, you've got soft black which you don't want to minimize its importance, but I think you want to maximize the importance of that coronary calcium score. Now you got a coronary calcium score that's greater than zero. I think it's important to think about it. You know, mine is greater than zero, but not terribly high. Um, and I think it's important and mine is stabilized, and having stable coronary calcium is the best thing you can do. you don't want it rising over time. It means there's something wrong think with your diet or lifestyle. Um, so while I agree with you that the soft plaque is important, I I don't agree that the hard plaque, the coronary calcium is less important than the soft plaque because, you know, the cardiologists like to say, well, the soft plaque is the one that you're going to develop a thrombus and you're going to therefore have a heart attack. The best evidence is that it's the coronary calcium that will tell you with almost absolute certainty if someone is going to have a coronary event in the next 10 years independent of age. So sure, if you've got soft plaque and coronary calcium, you got to do something about it. Um, but taking a statin is not going to help. And you know, they've had such trivial minuscule changes in in plaque magnitude with statin use. and they'll talk about how it reduces plaque. Um, and they'll take a fraction of a millimeter and talk about the benefits of statins. Um, but essentially there really are no benefits of statins when it comes to changing plaque size um or really making a dramatic change in uh in coronary events.

Excellent.

Now, let's um Oh, I'm sorry. Did you want to

go ahead? Yeah. No, go ahead.

So, let's get to though. Why is it a subset of people with FH and that's in this slide? Because this is a really important slide. U what is it that actually kills you? What causes coronary events? Yes, I've got high blood sugar in here. Blood glucose is up off to the right diabetes. But there are so many other factors that contribute to coronary events. And you can see as you go around this you'll see infection which is not blood sugar infection, smoking, stress, inflammation. There is a common element to all of these risk factors for heart disease. And that common element is the production of clots and then interfering with the ability to break up the clots which is called fibbronolysis. And so we get back to the people with hyper cholesterolimeia. This is not a disease of high cholesterol. This is a disease of hypercoagulation. The people that have the genetic anomaly that causes them to have high cholesterol. These people also have highly reactive platelets. Platelets are the cells that produce clots. When we get stressed, that adrenaline will activate our platelets. And quite literally, when you get stressed, when you get angry, you produce clots. Um, I actually find it's very helpful because I lecture about stress and I remind people when you're stressed, when you're angry, you are literally making clots. And then we've got a system as well that breaks up those clots. The people with FH have extreme reaction to all these factors. They have an extreme ability to have their platelets sensitive to all these factors. So when they have high blood sugar, they're not going to have the normal amount of clots. They're going to have far more clots produced. If they have an infection, they have far greater clots produced. Whenever they have adrenaline released those platelets are 20 times more sensitive than a person without FH. So the subset of people in the first 40 years of life that have high blood sugar that have inflammation that have an infection that are smoking that have uh hypertension these are the people that are going to die young and it's not because of their LDL cholesterol it's because of the excessive clotting.

So we really should not call this group of people with this genetic defect familial hyper cholesterolimeia. The actual meaningful title would be familial hypercoagulability.

I I think they they should be called that now. And these studies are out there. The thing is they've been largely ignored. You go back 50 years ago. People were studying the platelets of people with FH and they were studying in a dish. should put their platelets in a dish and you add some adrenaline and you see the extreme sensitivity of their platelets to adrenaline and that's been ignored when people are talking about FH. Now the extreme form which you actually find with lean mass hyperresponders is the people who have the double gene a gene from each parent to produce hyper cholesterolmia. These people have extremely high cholesterol like 600 or or more LDL of like 400 and these people do die young. I mean that is now fortunately it is extremely rare. It's considered to be like one out of every five million people have the double gene. But what is also being ignored is that these people have extremely high clotting factors more than just hyper cholesterolmia. So they had some of the highest levels of fibbrronogen which is a protein that triggers clotting. And we actually published this um in our review that this work was shown decades ago that the people with the extremely high cholesterol who die young these people have extremely high fibbrinogen. Now, that has been completely ignored and it's really a shame because it's only one paper that I found published about 50 years ago, but it's been ignored. And

I have to tell you what is so terribly disappointing to me is the lean mass hyper respponders, which Dave Feldman has done such a nice job in characterizing these people to show that their plaque is unrelated to their LDL. What they should have measured was their clotting factors because it's a mystery and it was left a mystery in their publications and in the movie Cholesterol Code. It was left unressed as to why it is these people aren't having heart attacks. And you see Nick Norwitz, who I have great admiration for because of all he's accomplished, but when he says, "I should be dead," because he compares himself to people with extremely high LDL, he's either being disingenuous or he's ignoring the literature that I have shared with him because the people with homozygous FH have been shown to have and the ones they die young to have extremely high clotting factors.

Yes.

So the real question that's been ignored are the clotting factors.

And let me be very clear here. I think that there's probably some overlap between people with homozygous familial hyper cholesterolimeia and the lean mass hyperresponder community. But just because you're a lean mass hyperresponder does not mean uh contrary to what many a doctor has told their patients that does not mean you have familial hyper cholesterolimeia. Correct.

So yeah this is real important. The people who are the lean mass hyperresponders we should actually be defining it better. These are people that start off with relatively normal cholesterol and what's considered safe normal LDL levels. And these are people for whatever reason, often it's because they have an illness of some kind of affliction and they choose to go on the ketogenic diet. And what you find is a dramatic increase in their cholesterol. So you can go from a total cholesterol of 200 up to 500. And your LDL can go from 100 up to 300. And so doctors are alarmed when they see someone's cholesterol go up. And so you have someone who is ketogenic, who is incredibly healthy. Every marker is ideal except for their high LDLC. And so they're completely different. They are not like FH at all because these are people because of a genetic anomaly have high cholesterol from birth. The people that are called lean mass hyper respponders have high cholesterol solely because of a ketogenic diet. Now, what's really important and really has not been addressed, it's so terribly disappointing to me that this wasn't addressed in the movie The Cholesterol Code. This has not been addressed by Nick Noritz when he says he should be dead because of his high cholesterol. Frankly, it bothers me for him to say that because he's well aware of the literature. I've certainly shared the literature with him. My colleagues, I have a dozen colleagues who have published on this. We published a paper on coagulation being so far superior to cholesterol. And so we've shared that paper with him. We've shared actually two papers. And so what we need to know is why is a subset of the lean mass hyperresponders have black? Um and so what's critical and and let me take a step back. I have so much admiration for Nick Norwood, first of all, for a paper he published in 2020 analyzing his own cholesterol. And this actually leads us to the next slide because he showed in a in an elegant study the importance of the quality of the LDL. in his own LDL which is extremely high he wrote an elegant paper so scholarly emphasizing it's the quality of your LDL not the total LDL and so that's covered in this slide in a healthy metabolically healthy person so we're talking about someone that doesn't have high blood sugar doesn't have hypertension doesn't have high triglycerides the LDL that is produced First the VLDLDL produced by the liver that ultimately becomes LDL that LDL is called large buoyant LDL and that's has just to do with the structure of the LDL that LDL has been shown repeatedly to be unrelated to heart disease. You can have extremely high large buoyant LDL and it's unrelated to heart disease. Now for those people who have very high triglycerides, high blood sugar or diabetic, the structure of the LDL is different. It's called small dense LDL. As you can see here, um you got the small dense on the right, the large buoyant on the left. Small dense LDL, I think, is what carries the connection of LDL to heart disease. Because when you've got the high blood sugar, then you have a greater prevalence of the small dense LDL. And so small dense LDL never exists by itself. It exists in a metabolically damaged environment. It exists in a person that is overweight, that has high blood pressure, has high blood sugar, and has small dense LDL. that person will have more heart disease than the person that is metabolically healthy. And what is so frustrating for me is that Nick Noritz published a paper and reviewed the literature on this in 2020 and he has clearly very low small dense LDL which explains why he's not dead. It explains why he has no plaque. He has a metabolically healthy environment. He has low small dense LDL. And so crucial is you want to have that great balance. Low small dense LDL high. But you don't want to take a drug to reduce your small dense LDL. What you want to do is like I did get your triglycerides down, get your blood sugar down.

So am I hearing you correctly? Are you saying that when somebody adopt who's previously eating a high carb diet like the standard American diet or even the American Diabetes Association diet or the American Heart Association's DASH diet which are all very very high in carbohydrates, you're saying when somebody adopts a low carb keto or carnivore diet, all of which are going to be much lower in carbohydrates that they can actually shift their numbers of large buoyant LD to you.

Yeah. In fact, if we go to the next slide, um I can substantiate what we've been talking about.

Okay.

So, this is work again, you know, published in a medical journal in which you are looking at the people who have a dominance of small dense LDL versus significantly lower small dense LDL. what does their physiology look like? And so in red, what you've got are the people that have high small dense LDL. And you see their triglycerides are high over 200. Those that have low small dense LDL in blue, their triglycerides are nice and low below 100. Now we look at their overall health by looking at metabolic syndrome. So how's their HDL and their blood pressure and their their weight and their blood sugar? And that's metabolic syndrome. The people who have the high small dense LDL, over 70% of them are diagnosed with metabolic syndrome. The people that have less small dense LDL, only about 20% have metabolic syndrome. So again, this is from the general population. You're not looking at people on a ketogenic diet. You're just looking at the general population.

Yep.

You can see this distinction. So we start off by emphasizing the small dense LDL does not exist by itself. It is a consequence of having a damaged metabolism. But now let's look at the next slide. Oh, and what I unfortunately you have to go to my talk u because you had me cut out so many slides.

Yes.

In the previous slide, the people who had the high small dense LDL also had significantly more heart attacks and strokes. And so obviously the people with metabolic syndrome are going to have more heart attacks and strokes. And one indicator is the small dense LDL. So what I say to people don't fear the small dense LDL. Fear the high blood sugar and the high triglycerides and low HDL.

Yeah.

Now we're actually looking at heart attacks. This is another study. So here we're looking at people that have relatively it's not low LDL, but we're looking at people that have LDL below 170 versus those that have really high LDL over 170.

Yep.

And we're looking at that ratio. Aside from coronary calcium, this second ratio tells us the most about whether or not someone will have a heart attack or not. And that's the ratio of triglyceride, that's TG, to HDL. And realize HDL rises when your blood sugar drops. Okay? And so as and as you exercise, exercise and low blood sugar raises HDL, lowers the triglyceride. So when you've got a triglyceride to HDL ratio less than 1.7, you have a relatively low rate of heart attacks. And that's the blue showing that those people with LDL below 170 had about a 4% of them had heart disease. And the people that have a high ratio, the one that I was so concerned about, and I'm still concerned about it, those that have a ratio greater than 3.1, you got three times as many heart attacks, heart disease, say 12%. But now, let's look at those with high LDLC.

It's the same. Those that have high LDL over 170 have no difference in their incidence of heart attacks. you see the LDLC is irrelevant.

So, let me just So, for those of you watching this, if you'll look down at the bottom of this slide, the the left hand side of the slide, it says less than 170. That would be their LDLC number. And the right two columns of blue and red would be an LDL cholesterol of greater than 170. And again, let me repeat what you said earlier. These are not your numbers. This is not something you made up on your PowerPoint uh spreadsheet. This is from an article from the Archives of Internal Medicine.

Correct.

You know, this is published 25 years ago and it's the kind of thing that people know. This is not hidden, but it's the kind of thing that everyone should know, the patient should know. You know, when you go into a doctor and your LDLC is over 170, what is the knee-jerk reaction? Well, you need to go on a statin.

Sure.

What they really need to look closely at is your triglyceride to HDL ratio.

Yes.

And if that ratio is low, then you're damn healthy.

If it's high, you need to get healthy. And I see every day

I see every day on Twitter now ex uh prominent cardiologist completely dismissing the triglyceride to HDL ratio and saying that if you're if you're focusing on anything except LDLC and or apo if you're even talking about triglyceride to HDL ratio you're misleading people. You're harming people. you you don't know what you're talking about.

Now, one reason why cardiologists are dismissing triglyceride HDL is because there have been drugs that have been developed. We have a very drugoriented medical care system.

Correct.

There have been drugs that have been able to raise HDL.

Yep.

And they're not only ineffective at reducing coronary events, they can actually potentially cause harm.

Yeah. They're dangerous. And so this is the way our medical system thinks. Well, if you can't improve health by giving a drug to raise HDL, then HDL doesn't matter,

right?

And what they're not thinking about, and frankly, what I I love about you, Ken, because you do think about this, is if you change your lifestyle, then your ratio changes. Your triglycerides come down, your HCL goes up naturally. Now, that's not easy, frankly. You do have to say no to the sugar and to the carbs. You need to actually get off the couch and do some exercising.

Yes.

It's a lot easier to take a drug than it is to actually change your lifestyle, but that's I mean, you think it's easy for me to say no to all the carbs that I'm not eating. I love ice cream and pizza and, you know, high sugar foods, but I want to get my triglyceride HCL ratio as low as possible without medication.

Yes.

Because the medication doesn't work.

That's right. Exactly. And the the one that they were studying that would actually raise your HDL cholesterol actually caused an increase in mortality. So they

studies people actually died.

Yeah. They quit studying that very very quickly and then focused all of their efforts on lowering the LDLC and now the APO. Now, one of the

one of the things when I I watched your first presentation all those years ago, you were talking about relative risk versus absolute risk. And one of the preeminent studies that's still cited to this day is the Jupiter study. And uh in that study they completely minimized absolute risk. All they wanted to talk about was relative risk. And then when all the Lipur ads started coming out they would they would show oh look you can decrease your risk by 35 40%. But what they were talking about is relative risk. And I think you you said this earlier, but I want to reiterate you're the average doctor that somebody watching this would that would go they would go see that doctor. That doctor is a follower. That doctor is not a leader. That doctor is just has read the Jupiter trial, has read the other studies and it's just following the leader.

They had they don't think about this. They don't research this. They just say, "Whoop, this is what it said. I saw that Lipur ad. I saw the new patha ad. This is what it says. Therefore, that's how I'm going to practice medicine."

But I believe, as you do, that people at the top, the the the in the boardrooms of the far pharmaceutical companies, in the boardroom of the American Heart Association, I think they do know that they're being being duplicitous. I think they do know they're they're misleading people. They either just don't care or the money is too good.

Uh, is our next slide coming up? Is that the Jupiter trial? Well, to finish off nuclear, but to finish off, you did ask me about diet.

>> Yes, improving >> markers. So this is from one of my papers.

>> Um, so the next slide before we leave >> yes >> uh small dents. Um, I, this is, you know, and again, I don't do this myself. I've had some great collaborators. In this case, I wrote this paper with Jeff Volik and Blair O'Neal, who's a cardiologist, and we, we summarized diet effects on cardiovascular risk factors. So you asked me, well, with a low carb diet, improve the risk factors? And absolutely, the answer is yes. And so I've got an arrow here pointed to the large buoyant LDL, but you can see this huge increase in large buoyant LDL in those people on a low carb diet. And the HDL also goes up. And what's important, all these markers going down is good, such as weight, insulin, uh, triglycerides. And right here, the small dense LDL drops significantly compared to a low-fat diet. So here, this is where we reviewed all the biomarkers related to cardiovascular disease, and they all move in the right direction. And and overall, there's very little change in LDLC.

Um, so, you know, that kind of brings this to the conclusion that really, you want to take your health in your own hands. Take charge of your health. Cut back on the carbs, and it'll improve every marker. And, you know, people now, they'll dismiss LDLC. What happens is LDLC, they say, "Well, it doesn't really matter. It's the particle count. It's APOB, >> right? >> And we, we published a paper on this as well, which we're going to get to at the end." Understand something. Apo B is simply the particle count. And what's a substantial part of that particle count? The small dense LDL. So, as the small dense LDL goes up, you can have more particles. And you can have bo large buoyant LDL, small dense LDL. You're really talking about the particles. So when a person is really unhealthy, they can have a dominance of the small dense LDL, not small dense APO B. But this is what the cardiologist, the American Heart Association claims to the particle count compared to the LDLC.

So now, and you've introduced it. Let's get to Jupiter.

>> Yes. So, I think we got that little symbol blocking. I don't know if everybody >> Oh, hang on. Let me I think I can take that out. Uh, where is that? I can't find it. Where is that?

>> So, that's 54% underneath that symbol.

>> Go ahead. I'll I'll try to remove it. What does it say under there that I've completely blocked?

>> Um, so I've lowered my risk of a heart attack by 54%.

And understand something. And there are surveys that show this. Doctors think they've had the medical education, so they understand risk, but they really don't. Um, studies have shown, and we're going to talk about relative risk versus absolute risk. When you give doctors the relative risk figure for lowering cholesterol, they're more than twice as likely to prescribe medication than when you give them the absolute risk value. So doctors, with all due respect, not to you, Ken, to other doctors, are not aware of their ignorance.

>> Exactly. I didn't see that 54%. And so they say you're lowering your risk dramatically by taking Crestor.

>> Yes.

>> And they stop there. So now, where does that 50 54%? Okay. Your listeners have got to be impressed by that because listen, you're lowering your risk for having a heart attack by 54%. You got to feel good about that. Therefore, you want to take Crestor.

>> Yep.

>> So now, let's look at this the summary of the study in the next slide.

>> Okay. And but first, let me say to everybody watching this, there's something about doctors. And I'm saying this as a as a doctor. I've been practicing for almost 24 years. Doctors are not special. They're not demigods. They're not all knowing. They are just dudes and chicks. And so when you have that, when you understand that, yeah, they are just as susceptible to the marketing from big pharma as patients are. So the the commercials on television or on YouTube videos, they put the same kind of advertisements in the medical journals or they show them to the doctors, and the doctor sees 54% and the doctor stops thinking right then. They don't think, well, yes, but is that relative or absolute li risk? No doctor thinks that because they're just dudes and chicks just like you. They're just like, oh, 54%, dude, that's a big deal. Okay, I'm going to prescribe that drug.

Now, next chart. So here you're seeing the principal investigator, the one that ran Jupiter, Paul Ritker, is summarizing what Jupiter found. And these numbers are huge. In only 1.9 years, you have a 44% reduction in all events. And we take the biggest one, 54% of myioardial infarction, which is a heart attack, reduction in stroke, reduction in mortality. So this is how it is presented to the medical community. The findings of Jupiter. Understand, he is intentionally showing you only what's called the relative risk. He is not showing you what we are going to talk about, the absolute risk. So this is deceptive, and people have published editorials over the decades saying what he is doing here is wrong. It is deceptive. It is intentional to promote the use of Crestor okay by physicians and also for people to acquiesce and to take Crestor.

So what I do is I look at all these these studies and I share with the community. I share actually at cardiology meetings, I share at the meetings, and I cover, well, what did Jupiter actually find? By the way, and I'm not covering it here. That trial was supposed to go five years. They stopped it at 1.9 years. Now, the question is, why did they stop it? Because so many people were developing diabetes. There was a significant increase in new onset diabetes in the Jupiter trial. And, you know, it's interesting. They dismissed it. They said it was just a matter of chance, but it was statistically significant.

Now, let's go to the next slide where I'm actually showing you what they found. So, it really would be comical, okay, if this to me weren't such a tragedy.

>> Yes.

>> You're looking at here at the percent of people that did not have a heart attack. And so, I've drawn that dashed line at 99%. And both values are greater than 99%. This means that over 99% of the people in the Jupiter study did not have a heart attack. And as you look at that, the the red are the people that had are given Crestor, and the blue are the percent of people that did not have a heart attack, even a placebo. And I defy anyone to show me a 54% difference between the red and the blue bars. And I, I just, when I show this, you know, people, it's like children that are sort of first learning there's no Santa Claus, okay? It's like their mouths are open.

Okay, next slide. I'll show you how they came up with 54%. So they had almost 18,000 people in this study in order to show an effect, and only 31 people out of 8901 had a heart attack given Crestor. Only 68 out of 8901 had a heart attack given the placebo. So less than 1% had a heart attack. 0.35% on Crestor and 0.76% on placebo had a heart attack. So one way to look at this is you go to your doctor and you got high cholesterol. You say to your doctor, "What's the likelihood I'm going to have a heart attack if I don't take the Crestor?" Well, your doctor should say, you have like a 99.2% 2% chance of not having a heart attack if you do nothing.

>> Right?

>> Okay. So, where does the 54% come from? Well, you take the 0.76 and you subtract 0.35, you get 0.41, and 0.41 is 54% of 0.76. Do you see the games that these people play? I mean, this should be criminal. This should be the headlines on the news at what they have been able to do. And as a result, this got Jupiter got FDA approval. This was published in 2009, and it's the Jupiter trial that got FDA approval and has now sold billions in revenue for the company.

>> Yep.

>> Producing almost no benefit whatsoever. So this is deception of the highest form to me.

>> And at what level >> relative risk again emphasizing relative risk is the ratio >> between the two absolute risk differences. Absolute risk is the arithmetic difference between those who treated versus those who are untreated. And arithmetic or the absolute risk is really what you want to ask your doctor about >> because that's what applies to the individual patient.

>> Correct. Absolutely. When your doctor says you should go on Crestor, and the reason why often people go on Crestor is because they're on Lipur and they have brain fog, and so they get brain fog and say, "We'll put you on Crestor," which, by the way, the reason there's brain fog with Lipur is that Lipur can get in the brain. And we published a paper. I have to admit >> we tried and tried and tried. It's very difficult to publish papers on this topic, but we finally found a journal that would allow us to publish it to show that cognitive impairment is more common in a drug like Lipur than Crestor.

>> Yes.

>> Because Lipur can get in the brain.

>> Yes.

>> And it interferes with the brain's ability to make memories, to produce new cells.

>> So that's why they'll often put people from Lipur onto Crestor because Crestor can't get in the brain, but still, it has almost no benefit for your heart. So now, when we go to the next slide, what the ad should say is that I've lowered my risk of a heart attack by 0.41%. And then how many people would want to take that drug?

>> And how many doctors would want to prescribe that drug?

>> And, you know, it's not just Crestor. You've heard me talk before about Livore, in which Livore has a 1% difference in in benefit, which they've inflated to be a 33% difference. And that's what the doctors see. And it's virtually every trial with statins has shown almost no benefit, which is then inflated using the relative risk to impress the doctors and to use in the ads.

So at what level, Dr. Diamond, do you think that the uh dishonesty, where where does that at what level do the PhDs and MDs know we're tricking people? We're making billions of dollars. Do is this do you think this is common knowledge at the American Heart Association that this kind of foolishness is going on?

>> It it can't not be common knowledge. They have to be aware of it. And and what they're doing is, it's gone to the next level. And so because there is such a trivial effect of LDL lowering, and they always blame it, that 1%, they always blame on residual LDL effects. And that has promoted the idea that we need more drugs, we need different kinds of drugs to lower LDL almost to zero.

>> And so that's why you've got this new generation of drugs.

>> Yes, >> which the PCSK9 inhibiting drugs are one example. And and another thing that is beyond bizarre, beyond belief >> is to modify people's DNA >> and that's coming >> a lifetime of lower LDL.

>> Yep. There's actually a a new there's actually a new treatment in trials right now that will alter your DNA to make you a permanent have permanently lower LDL cholesterol.

>> And really, what it does is it interferes with an enzyme called PCSK9, which is involved in moderating LDL receptors. And so when you have more LDL receptors, they're going to bind to the LDL in the blood and bring it into a cell. So you're going to end up with an abnormally high level of cholesterol inside the liver cells, which ultimately, I think you're going to find is is unhealthy.

>> Drugs really have had trivial effects. Talking about one or two percent benefit. Now, potentially, again, the statins um reduce inflammation, they reduce clotting, and that's why there's a very small benefit, that 1% or so um, and they potentially, they can also reduce a small dense LDL. And so this is actually why you have a very small benefit of the statins, and potentially the PCSK9 inhibitors will have an extremely small benefit. Um, but certainly, it's not going to be the 30 to 50% that's advertised.

So, we've we've talked about this small benefit, and this is where people will say to me, well, still, it's better than nothing. I'm still helping my patients by giving them a statin. And even though maybe it's not 50%, but 1%'s better than nothing, right? Which takes us to the next slide.

>> Let me pull that up. So this is what I get from physicians when I lecture to cardiologists. And so without going in great detail, and this is included in my papers and in my presentations, the adverse effects are extremely well described. They're in the medical literature. There are dozens of papers showing adverse effects of the statins. This is why half of all people on statins want to stop taking it within a year. Even though the doctor will say, "Well, sure, you've got muscle problems. You've got brain pro brain fog." Well, what's better? Muscle problems, your inability to exercise, or do you want a heart attack? This is what doctors tell people.

>> Absolutely.

>> And the the increase in diabetes has been trivialized, but it is real. It is substantial. There's a very nice study that came out of Scandinavia funded by the government, which showed that um spontaneous development of diabetes in people occurred in about 5% of those on placebo and about 10% of those on a statin. So when we're talking about doubling, that's a substantial number of people that are developing diabetes as a result of being on a statin.

>> Yep. And there are so many papers, but we don't have time. But I do want to cover one paper in the next slide, which I think is so incredibly important. So here, and this paper was published over a decade ago. You have people that went to their doctor and they're complaining about memory problems. They are diagnosed with dementia. These are 75-year-old men and women. Go to their doctor. They have memory problems. These people are all taken off of their statins after a month. Their cognition improved. They no longer have dementia. And the critical manipulation is that now all these people are put back on their statin, and a dementia returned. This has been minimized by the American Heart Association. That's minimized by most cardiologists, and they say, "Even if you have a cognitive problem, we'll just switch you to another statin, which will cause you muscle problems."

>> Right?

>> You know, we have an epidemic of Alzheimer's disease in this country and in this world. And we have a high percentage of elderly Americans that are on statins, and we don't know what percentage of those people on the statins have a functioning brain which is being impaired by the statin. We just don't know because this is a study in which has no methodological flaws, and no one has followed up on it. And this is the kind of study that needs to be done on people diagnosed with dementia who are also on on a statin.

So you think that if we took a population of say, a thousand people who've been diagnosed with dementia of some severity who are also taking a statin, and you stop the statin therapy for all 1,000 of those participants, you think there would be a meaningful reduction in their dementia score?

>> There's no way to answer that question scientifically. It's an unknown.

>> Right. What's your hypothesis would be?

>> My hypothesis would be, particularly those that are on a statin that can gain access to the brain, they get through the what's called the blood brain barrier, >> like Lipur and >> Zokor. My hypothesis would be that we would find that a substantial percentage of those people, their dementia would resolve, that their cognition would improve. And that's such a simple study. Um, and so I would really like to see that done. But, you know, I actually wanted to do a study like that at University of South Florida, and they're unwilling to have people taken off of their statin, if only for a month. I am very pleased that I do have work going on with people at University of Cincinnati who actually are going to take people off of their statin and see how it affects them a month or two later.

>> Excellent. So I am working with some really great MDs in my research. So the next slide, I think, is incredibly important as we sort of bring this to a close. You know, you listen to some of these leaders, lipidologists like Tom Daypring.

>> Yes.

>> And Tom Daypring talks about LDL particles like they're cannonballs. Literally says that that they hit the artery wall and at a certain concentration, basically break through the artery wall and accumulate inside the artery. Um, and this is like a standard textbook view of how plaques develop. The LDL particles find their way into the artery wall. Macrofase, white blood cell, engulfs the LDL, and then ultimately, it becomes plaque. It's such a simple story, and it makes no sense. Again, getting back to the people with hypercholesterolemia being so damn healthy when they're old, >> right? >> All it takes is high LDL cholesterol to kill you, then people with FH shouldn't live beyond 20 or 30 years.

>> So clearly, this this model is wrong, and yet it's being taught in medical schools. So let's go the next slide. I think it's crucial to help us understand. So there's something called the glyicoalix.

>> Yes.

>> And the glyicoalix is almost entirely ignored.

>> Yep.

>> By most cardiologists.

>> And I've been yelling about the glyicoalix for at least a decade. Uh, and I, I actually have a Google uh reminder for me. Anytime there's a new paper published that contains the word glyicoalix, I get a a Google notification on my Gmail. And let me just tell you, it's s very, very seldom that I get a notification because even though I think it's one of the most important things in cardiovascular arterial health, nobody at the upper echelon of research seems to be interested in it whatsoever.

>> Well, I wouldn't say nobody.

>> Almost nobody.

>> But it, you are right. It's the people in power are ignoring glyicoalics entirely. So what are we talking about with the glyicoalics? So in the bottom of this slide is a picture, an electron microscope picture of a real glyicoalix. It's a um, an artery, and that furry looking thing is the glyicoalix. And so these are glycoproteins that line our blood vessels.

>> Trying to make it where we can see it better, but that that's as good as we can get. See the bottom? Everybody watching this, look at the bottom right-hand black and white photo. It looks like the hair on top of somebody's head. Go ahead, doctor.

>> Right. It looks like a bad hair day.

>> Yes. Um, and so understand this is a layer of protection that is on lines all of our blood vessels.

>> Yes.

>> And as I have in the diagram, and this is actually from a paper which I find interesting, um, a paper from a strongly pro-statin group, John Castelline, very strongly pro-statin, and yet they also publish good good findings. This is a review of theirs. So when you have a healthy glyicoalix, which happens when you have low blood sugar, low blood pressure, >> y >> um >> the LDL doesn't simply find its way through, >> right? >> LDL doesn't pass through the glyicoalix.

>> And let me let me add one thing from an animal biology perspective, an evolutionary biology perspective. The glyicoalix is ubiquitous across every species of mammal. Now, just from a biologist standpoint, anytime something is conserved like that, meaning that every species of mammal on planet earth, if we have looked at a cross-section of their uh arterial wall at a microscopic level, they have that bad hair day that you see in that bottom right-hand picture. There is no mammal on planet earth that does not have a glyicoalix, which means that it is very, very important, or there would be examples in the biological literature where that didn't exist. I'm sorry to interrupt. Go ahead.

>> Oh, great point. Thank you, Ken. The problem with the glyicoalix is it's a very delicate membrane. It gets stripped off when you have high blood sugar and high blood pressure.

>> Yes. And and I want to emphasize this cartoon figure on the right is not mine. I don't make this stuff up, >> right? >> This comes from a strongly pro-statin group, and they're basically presenting really good science here. So it's not entirely ignored. Now, it happens this paper, I don't, unfortunately, I put the year. I think this paper is about 20 years old. So I don't know if John Casteline would really want to continue since he's strongly prostatin, >> right? >> But um on the right, what they're showing is the glyicoalix gets stripped away, and you then have a an endothelium which really is not designed to be protected against high blood sugar and high blood pressure, and it gets damaged.

>> And let me let me add this doctor. As a a medical doctor who went to medical school, I've went back and I've pulled all of my pathofizz books, all of my physiology books. None of them. I cannot find a single example in my medical school education that when they show a cross-section of a cardiac, a coronary artery or any other artery, not a single one of them shows that glyicoalix. That's super super important because so the average doctor, and I'm I I you not. If you ask the average doctor, including the average board-certified cardiologist, what is the glyicoalix and why is it important to coronary artery health, they will have literally no idea what you're talking about. And so if they were not taught in medical school and they were not taught in residency, >> then it's not important. That's how the average doctor looks at this. Does that does that make sense? Tell me in the comments, viewers, does that make sense? And so also, this is another great question because I've I've researched the glyicoalix enough to know that you can damage it. It can go from looking like that picture on the bottom right, the black and white picture, which is a very healthy glyicoalix. You can have one bowl of Cheerios that you talked about earlier, and it will immediately within minutes to hours damage the glyicoalix, presenting a denuded endothelium, which should not it should always have that hairy covering. That's what protects it. But when you eat when you eat that bowl of Cheerios, or even worse, that bowl of Lucky Charms, you damage that glyicoalix. And then we've got a great question from one of our PhD community members, and you can just include this in your answer. He says, "Can a damaged glyicoalix be healed or reformed?" And I know the answer, but I want you to I want you to include the answer in your uh overall answer. Go ahead. Sorry for the interruption.

>> Well, it's actually it's an interesting question. I always like to think about the literature when I come up with an answer. Presumably, we have this great we have this great ability to heal. And so I've got to believe, even though I I have not seen a study on this, I've got to believe that the glyicoalics can recover. It it must because if you had um the thing about heart disease developing over decades means that you denude, you strip away the glyicoalix, you have damage, glyicoalix recovers, you once again have high blood sugar, it's damaged, it recovers. So I think there there can be little doubt that the system must be designed so that the glyicoalics can recover. Would you agree, Ken?

>> I totally agree. But I also agree with your implication that it's very odd and very concerning that there's I can't find a study that shows, oh, you eat a bowl of Cheerios, it damages your glyicoalix, and then you stop eating the Cheerios for a few weeks and have bacon and eggs, your glyicoalix completely recovers and regrows, which I think is what we would find.

>> Yeah.

>> But no one's done that research.

>> Yeah. Now, I don't have a slide for this, but I do have it in various presentations I've given. It is it is possible to measure the glyicoalix in a living person, which sounds surprising, but the glyicoalix, as you said, is on every blood vessel. >> And they do it by taking samples from the underside of the tongue, the little tiny blood vessels. >> And they actually, it's sort of like a camera >> that is put under the tongue because you got some nice large blood vessels. And people have actually measured the glyicoalics in middle-aged people, and you can actually measure the stripping away of the glyicoalics in people. And there's a beautiful study out um, it's really too bad, maybe we'll we'll include it somehow in the show notes.

>> I'll put it in the show notes for sure. Send me the link.

>> So you've got you've got people who have their glyicoalics measured in midlife, and they're followed, I believe, for about five, six years. Those people who had high cholesterol had no relation to the events. So LDL was unrelated to the events. Those people who had diabetes had events, uncontrolled type 2 diabetes. Those with hypertension had events. All the conventional really important risk factors. But the biggest association between events and the measure came from those who had a stripped away glyicoalix. Those who had a denuded glyicoalix had more events than those who had a healthy glyicoalix. And so um, I think that's the kind of study we clearly need more of. We need to know, well, the people with diabetes must have chronically denuted glyicoalics. Of course, >> get that blood sugar down, it enables glyicoalics to recover.

>> I love that. I and I think that's so important. And again, I think every viewer watching this should ask themselves the question that sounds super important and relevant. Why isn't there more research on that? And I think that uh, what Dr. David Diamond and I have implied it through this entire video as far as what people at the top of the AHA and the and the kind of the cardiovascular research community. I think they're well aware of what we're saying here, and I think they choose not to study the glyicoalix uh for certain financial reasons.

>> Absolutely. There's no drug to improve the health of the glyicoalix, and again, our medical system is just so drug-oriented. um, they mention diet and lifestyle, and then they move on to medication.

>> Yeah.

>> So we're bringing this to a close with a paper I published in the next slide um, which really had a title that >> oh, actually, this I guess this is a slide. So your small I think what's important, I don't need have feel any need to defend LDL. Um, I don't say that LDL is entirely beneficial or neutral. I think the the small dense LDL is damaged LDL. >> And it's involved potentially in inflammation. Uh, I think it it gets engulfed by the white blood cells. It gets brought into the artery wall. So I think it actually becomes part of the problem. um, the high triglycerides, high blood pressure, and the high glucose, it all contributes, I think, to the damage. And then when you get a wound, when your artery wall is damaged, it is really just like any other wound. And so, you're going to have platelets that are going to accumulate there. You're going to have a wound, you're going to have clots. And so, it is like any other wound, which then repeats over and over over the decades. And so, you lose that glyicoalix, you then get a tear. It is really so much like a wound of the skin. Yes. And the repairing of that tear over and over over the years ultimately chokes off the artery.

>> So let's bring this to a close with the next slide. Um, and we had the provocative title, which I was so pleased to work with Ben Dickman and Dr. Paul Mason. To some great colleagues. >> And uh, you know, it's it's and here are some of the the conclusions we covered in a lot of what we've covered today, Ken. Statin therapy is not warranted for basically a metabolically healthy person. And, you know, this was not just an LDL denier. We had 250 references. This is a massive review. To me, this is the most comprehensive review of cholesterol and cardiovascular health that you'll find anywhere, frankly. And I was greatly helped with Ben and Paul for this paper. So, I really think if you want to see why it is we're saying people should not go on a statin if they have high LDL on a low carb diet, they should look at this paper.

Now, again, though, what is frustrating to me is, of course, the American Heart Association will dismiss this paper, and of course, cardiologists will dismiss this paper.

>> Sure.

>> But I've been frustrated now over the last few years with the lean mass hyperresponder analysis. I've been frustrated that this perspective has not been incorporated to give the lean mass hyperresponders a sense that having high LDL in a metabolically healthy person, there's no evidence of harm. And I watched Cholesterol Code, which is a beautiful movie as far as showing the great benefits of ketogenic diet, but it leaves people with high LDL still being a cause of heart disease. It leaves people still worried about their high LDL. And you have one person who added carbs back to her diet.

>> Yeah.

>> Because she had high LDL.

>> Correct.

>> Her doctor, I'm not going to mention his name, but I've talked to him. He added carbs back to her diet to lower her LDL, and she then had a remission of her psychiatric disorder. And this paper I think is so important to tell people that in a metabolically healthy person, you're going to have the dominance of the large buoyant LDL, less small dense LDL. You're even going to be more healthy if you have high LDL than someone who has low LDL. And this is laid out in this paper, which we published actually already now it's four years ago. Maybe I think we need to do an update on this paper.

Um, so really, again, getting back to FH, what kills you is excess clotting. So you want to keep your stress down, your blood sugar, your blood pressure down, because those clots are what's going to cause you to have a premature death.

>> And the next slide is really a tribute to all the people who I've helped. Uh, I've I've been helped by. Um, you know, Sir Isaac Newton said he saw further because he stood on the shoulders of giants.

>> Yes.

>> And and I I feel so much um appreciation for those who have come before me, some who are no longer alive, and those I work with now, the dozens people. And I sort of want to give recognition to Uffy Rabinskov, who I think was one of the leaders and has been saying this for decades.

>> Yes.

>> Not to fear cholesterol. And the others I've worked with. So, the title one fat and cholesterol don't cause heart attacks and statins are not the solution. Lipid lunacy, um, the ketogenic bible, I have a a chapter in there um in Tim No's Bible on cardiovascular disease. And um, there's just so many people that I really appreciate. And I just want to put in the last thing to express my frustration because you got influencers who have such a powerful effect on people. And one of those influencers who I have such great admiration for, and I hate to say it, but what's frustrating me is how Nick Noritz has not acknowledged anyone that has come before him. He's fully aware of the books that I've shown of the decades of research. You know, you go back to John Utkin decades ago battling against Anel Keys. You can say it's the sugar that's killing us.

>> Yes.

>> Keys said it was the fat and the cholesterol.

>> These people need to be acknowledged. And it's not just me.

>> It's Malcolm Kendrick, Loopy Ravenskov, so many other people who came before us, and they have they benefited me, they benefited you. Um, and what frustrates me is that these people are not being acknowledged. The basically, the the pioneers who have stood up against the American Heart Association, American College of Cardiology. These people I think really need to be acknowledged as to the the history in which for decades people have been saying LDL does not cause heart disease.

>> I totally agree. And I I have nothing but uh thanks and reverence for all of the MDs, PhDs, DOS who've come before me uh who opened my eyes. I mean, you know, back in 2003, 2004, I was that ignorant doctor who was prescribing everybody Zokor, Lipur at the highest dose I possibly could because I thought I was doing a good job as a family doctor. And thanks to all of those kind of mavericks who've gone before me, I can now stand confidently and tell people that is not going to benefit you at all.

>> Uh, let me let me ask you a one final question for people who've watched this. You mentioned earlier fibbrinogen. Are there any other coagulation studies that you would recommend versus an an LDL? Even for people with familial hyper cholesterolimeia, even for lean mass hyper respponders, what coagulation studies would you recommend that they check?

>> So we we published two reviews on coagulation studies, and the literature is actually massive, and it goes back 50, 60 years.

>> Yes.

>> Um, you got not only you got fibro fibbrin, you got factor age. Not only do you have excess clotting factors, there are also genetic anomalies in which some people overproduce the clotting factor called prothroin. Um, and you can actually see if you can have have these clotting factors measured.

>> Yes.

>> So the the first thing is to understand the clotting factors themselves are benign. They're sitting there waiting to help you if you need to make clots. Um, the thing to realize is evolution has prepared us to make clots even in the absence of a wound. When we are afraid, our bodies, our physiology thinks we're about to get killed.

>> Yep.

>> If we get angry, our body is preparing to be wounded. And the way it does that is by making clots and activating our immune system. So we need to understand those clots can happen anytime you've got stress, you've got anger, as well as when you've got high blood sugar. So the first thing to do is to minimize those risk factors that trigger the clots. The second is, it's worth a blood test to look at your fibbr baseline fibbrronogen levels, factor a, proth thrombin, potentially look at a genetic test if you especially if you have FH, because that does increase your risk.

>> Um, so I'll share with you the papers that we wrote, the reviews.

>> Yes. And >> everybody watching this, check the show notes. I'm gonna put all the citations that we've talked about. Uh, Dr. Diamond is going to send me a comprehensive list. They're all going to be in the show notes. And also, uh, if you have a doctor who's currently a a statin believer, you can screenshot any of the slides that were in this video and print those out. Take to your doctor and you can print out the studies in the show notes. Take to your doctor and say, "Yeah, but what about the glyicoalics?" "Yeah, but what about my fibbrronogen? What about my >> what about my insulin?" You know, doctors don't want to test insulin. They're satisfied with A1C. Get a fasting insulin. Please get >> fasting insulin.

>> Yes, >> Dr. Diamond. This has been amazing as always. Uh, our last video got over a million views. I think this is probably going to do even better than that as time goes on. Uh, I'm happy to help you with your furthering your research in any way I possibly can, both as being a mouthpiece or otherwise. Thank you so much for the work you're doing and thanks for the time you spent today educating us about this very important topic.

>> Thank you, Ken. I mean, I think you're fantastic. I appreciate having the air time.

>> Thank you very much. and