Why LDL is Not Enough: The Tests Your Doctor is Missing to Assess Your Risk of Heart Disease | Know Your Numbers

Dr. Mark Hyman:
Coming up on this week’s episode of the Doctor’s Farmacy, primarily today, the major root cause aside from some of these inherited genetic lipid disorders for heart disease, and that’s insulin resistance, prediabetes and diabetes. And this requires a more nuanced, personalized diet and lifestyle treatment.
Welcome to Doctor’s Farmacy. I’m Dr. Mark Hyman, and this is a place for conversations that matter. And today we’re diving into our special episode in my podcast series called Know Your Numbers designed to help you understand how your body works, what your own lab and biological data mean through lens of systems biology and functional medicine, which is the science of creating health. And today we’re taking a deep dive into the numbers that matter to assess and track your risk of cardiovascular disease. Now, it’s way more than just knowing and treating your LDL cholesterol with a statin, which is primarily what most conventional doctors do, and I need you to listen up because this is important. Why? Well, heart disease is the number one cause of death in the world. It’s known as the silent killer and often remains undetected with no signs or symptoms until an event strikes making it one of the most challenging public health prices of our time.
I mean, the first symptom of heart disease for 50% of people who have it is sudden death. You don’t want that. Now, during my 10 years in the emergency room, I witnessed the limitations of our modern healthcare system over and over again. I had patients who arrived in the hospital in their most dire and vulnerable states in the middle of a crisis, and these experiences led me to ask, and that’s so obvious question, which is what could have been done to prevent them from ending up in the emergency room? A simple question, but nobody seemed to be asking at the time. Now, this question highlights a real gap in conventional medicine, this narrow one size fits all approach that focuses on treating diseases with and cardiovascular disease, with statins and stents and surgery and impersonalized advice. So lower your cholesterol intake or eat less fat and exercise more and so forth.
In fact, the truth is that this is a very complicated disease with many variables, many factors that influence it and most of them are not being examined or looked at. And now for the first time, we actually have the tools, the ability, the understanding, the science to look at this and it’s way more than you’re getting on your typical cholesterol panel you get at your annual doctor’s visit. In fact, that should never be done in my opinion. It should never be done. I’m going to explain to you exactly what should be done and why you should do it and what it means. And this is going to be a long one, so I want you to buckle up and hold on, relax, sit back in the chair or get on your treadmill and just listen to this podcast because I think it’s going to be important for you to understand the nuances around treating cardiovascular disease rather than just the one size fits all.
Cholesterol is high, take a statin, good luck. And that’s not really what we need to be doing. Now the current approach to heart disease is really outdated. It’s been proven effective for preventing disease progression and mortality on a national global scale. We’re seeing increasing rates of heart disease. Maybe a few less people are dying from it because we’re better at treating it aggressively at the end stages with stents and bypasses and technology and advanced medication, but that’s not really what we should be doing. And we were told for a long time that essentially it was our saturated fat consumption that was causing heart disease. Now this is called the diet heart Hypothesis, which basically focused on cholesterol as a primary culprit. And because saturated fat raises LDL cholesterol, it was assumed that heart disease was the result of saturated fat. But now thanks to systems-based medicine were and many more studies that have followed on from this original data that we’ll talk about in the fifties, sixties and seventies.
We now understand that this is much more complex and it’s a lot more nuance into how our lipids are managed by our environment and how our biology works and the inner workings of our physiology when it comes to heart disease. So functional medicine is a powerful paradigm shift in medicine. It basically adopts a proactive approach. It looks at root causes of heart disease by recognizing both the diet and lifestyle factors, but also looking at advanced diagnostics and lab testing and imaging and AI enhanced angiograms that never were available before until really recently that provide a way more comprehensive, way more nuance and personalized assessment and the ability to customize and personalize treatment. And maybe you’ll need medication or maybe you won’t, and we’re going to talk about that, but you probably can get it way ahead of this game and prevent this condition. In fact, I remember in medical school learning about William Ser and back in the 19 hundreds he wrote the first textbook of internal medicine.
I actually have it. It’s really quite good. I mean, they updated it obviously, but he would call all the other doctors, all the residents, all the medical schools to the ward of a hospital. When someone came in with a heart attack, it was such a rare condition. It was so rare that it was sort of alarming that we’d see it and then they would rush to evaluate this, see this patient, examine this patient. It was like someone coming in with syphilis today. I’ve never seen syphilis in my life, but if there was a syphilis patient, I’d want to run to the bedside to see it. But then it was common because they have antibiotics. But same thing with heart disease, then it didn’t really exist until this century at the levels that we see it. So we’re going to deeply dive into a more systems-based thinking approach, a functional medicine approach to why we need to look at your risk differently, what you need to know to prevent it and what you need to do even to reverse cardiovascular disease.
Now, part of the problem is that most of us don’t get the right tests, and for too long, healthcare is required you to go to your doctor to assess your own blood tests and biology and rely only on your doctor to guide you. But we’re way past that medicine. Now you can be the CEO of your own health, right? We’re entering an era where each of us can access, understand our own biological data and really take ownership of our health fully. Now, let’s know your numbers series in general, we’re going to help you understand key lab tests that you need to track your health. It’ll look at critical tests. Traditional medicine often ignores and doesn’t measure. You’ll learn how to interpret your own lab test. The true optimal range is not what the standard reference range is for normal, which is basically the average in a population.
If we’re a sick and overweight population, then the normal is skewed to what’s not optimal. In other words, if you’re coming to America and you’re a martian, you see, oh, it’s normal to be overweight because 75% of people are overweight. That’s the bell curve in two standard deviations, but that’s not actually optimal. You’re also going to learn how to optimize your health based on your own personal medical history and biological data. You’re learn when it’s important actually to see the doctor to get further testing and treatment, and we’ll talk about that. In a perfect world, this and I’d have the chance to see millions of patients, but the truth is I’m just one doc and over 30 years I’ve seen millions of biomarkers and tens of thousands of patients. I’ve come to understand that so much is being missed by conventional healthcare. We often wait until we have symptoms or diseases and then get tested, but the transition from wellness to illness can often be detected decades before any symptom or diagnosis.
I want people to have access to their own health data and the ability to engage in self-care and lifestyle practices that can optimize and reverse the trajectory of chronic diseases that now affect six in 10 Americans and accounts for over $4 trillion in healthcare costs. I met my friends is why I recently co-founded a company called Function Health where I’m the chief medical Officer. Now, function is a revolutionary new way to understand and manage your health through lab testing that you’re not often getting through our healthcare system. All the results are delivered in an easy to use dashboard that tracks your numbers over time and gives you actionable insights for every biomarker. We’re building function to democratize much of what I do to give you the keys to your health and put control of your health firmly back in your hands. So now let’s get started with this episode of know your numbers, talking about why the heck we should care about heart disease, what we need to know about it and what we need to do to treat it, and how we can avoid dying of a heart attack or some other cardiovascular disease.
Now, why should we care about this? Well, every 33 seconds, every 33 seconds, somebody in America dies from cardiovascular disease. Every 40 seconds, someone in the US has a heart attack. Now, over 50% of people, like I said, who had die or suffer from a heart attack have no symptoms prior to the event. In other words, they’re fine and then boom, they get a heart attack. So the first symptom is often a heart attack or a sudden death and 70% of heart attack victims are now considered low risk by methods that we now use for assessing heart disease. This is not my opinion. This is from the Journal of the American College of Cardiology. So I want to share with you that every single statistic, everything I’m citing today, all will be in the show notes. All the references are there. You can dig it on your own.
But I want you to know this is not just Dr. Hyman’s. This is actually based on conventional peer-reviewed medical research that is not being translated into clinical practice, and this is why we’re doing this today. Now, what’s also really surprising everybody is that people who are young, 25 to 44 are having heart attacks at an increasing rate. It’s rising about 2% a year every year for the last 10 years. This is from the American Journal of Cardiology. So why does conventional medicine miss the boat here? Well, cardiologists practice siloed medicine. All they think about is the heart and they don’t connect cardiovascular disease to the meta framework of your human biology. And typical doctors just run a lipid panel. It’s total cholesterol, L-D-L-H-D-L, triglycerides, and this is essentially just measuring the weight of your cholesterol. It doesn’t measure the quality of the cholesterol, the number of particles.
We’re going to get into why that’s important, but it’s an antiquated test that should be deleted off of every lab order prescription. It should never be done anymore. And yet it’s done in 99% of the cases of screening for cholesterol, and it’s completely inadequate to look at what’s really going on. It’s like trying to use an X-ray instead of three tests that MRI to look at something we have now the capacity to have a much more sophisticated look at what’s happening. So the reference ranges now again, as I mentioned, are set based on what’s normal and normal is not really meaning normal. It means what is two standard deviations from the mean. In other words, if you take a population and you kind of cut out the 2% at the top end 2% at the bottom end, that group in the middle is considered normal.
Now, if the population is sick, it’s skewed to be sick. It’s skewed to be abnormal. Like I said, with obesity, it’s normal to be obese or overweight in America, it doesn’t mean we should all be able to rate and obese just because that’s normal. So the average population in America is pretty unhealthy. We now say conservatively, this is really conservative according to the CDC that 50% of Americans either have diabetes or pre-diabetes and another data, 93% of the population, actually 93.2 have been found to either have some elevated cholesterol, elevated blood sugar, elevated blood pressure, have had a heart attack or stroke or overweight. This means they’re metabolic and healthy. That’s nuts. 90, I mean, 6.8% of us are healthy, which is crazy, but we’re seeing this in our testing at function health. We’re seeing 95% of people with abnormal lipid particle number 89% with abnormal small LDL.
We’re going to talk about what that means, but this is stuff that’s missed on the nutritional panel. I literally did a review of a panel the other day with a friend who did the function help test, and his cholesterol was on 1 48. It looked perfect. His hhl triglycerides were normal. LDL was normal. We looked at his particle number and he had extremely high lipid particles. He had poor quality particles, he had too many small particles. These are the things that cause risk. And he tended to eat more carbohydrates, have a little extra belly fat. And so even though he was healthy exercise, you wouldn’t expect that he had issues. He was someone I would be concerned at high risk. It’ll be completely missed by a traditional cholesterol panel. Now here’s the deal. In addition to diabetes, about 25% of US adults have what we call fatty liver disease or nafl D.
Now, why is this important? Because it also is a big risk factor for heart disease and 700,000 people die every year of heart disease in the United States alone, it’s one in five deaths in America, and probably half of adults over 40 may have a hidden heart condition. They just don’t know it, and they’re not being tested and it’s not showing up on their cholesterol panel. And the problem today is that most of our cholesterol treatment, most of our prevention for heart disease is based on a very simple idea that high LDL causes heart attacks, that the treatment for preventing heart attacks or for preventing a second heart attack if you had one, is too lower LDL as much as possible. And this is done with intensive statin therapy like Lipitor or Crestor and so forth, or maybe even other drugs, and exclusively focuses on LDL cholesterol as the main biomarker to lower.
Now this is interesting because when we reviewed the data, this was published in the American Heart Journal in 2009, the study of 136,000 patients who were admitted to the hospital with heart attacks, 75% of them had a normal normal LDL cholesterol, including almost half of the people had a LDL cholesterol under a hundred milligram per deciliter was considered normal, was even more concerning is that 17% had an LDL cholesterol in the optimal range of under 70. Under 70 is amazing. If you get under 70, cardiologists love it. They do a high five and they think they’re doing a great job, but almost one in five of those people with perfect LDL had heart attacks. Well, how does that make sense? Well, here’s the kicker. Almost all of those patients of the 136,000 patients who had heart attacks, had high triglycerides and low HDL. And why is that important?
Because those indicate that you have some degree of insulin resistance or prediabetes. So high triglycerides, low HDL is far more predictive of your risk of heart attacks than looking at your LDL, but there’s no easy drug to take to fix those, so we just treat what we can. It’s like the guy who was dropped his keys on the street. His friend comes by and sees him looking under a lamppost and he goes, Hey, what you doing? He says, well, I’m looking for my keys. Said, where’d you drop? Well, I dropped him down the road. He says, why are you looking here? He said, well, the light’s better here, which is exactly what we do, right? Light’s better here. It’s easy to check LDL. That’s what we look at. That’s unfortunate. In another study, a prospective study of 29,000 women after 19 years, those who had LDL under 70 had an over twofold risk of hemorrhagic stroke.
That’s a 217% increased risk of stroke. Now, when you look at a statin, we think, oh, it’s a blockbuster drug. It lowers your risk of heart disease by 30%. This is concerning because when you see LDL very low, it may mean something else and there may be association. It may not be causal, but it’s something you’re paying attention to. Also, we kind of jump in to do diagnostics sort of after the fact. If you’ve had a heart attack, if you have chest pain, if you have something acute, then we’ll give you an angiogram. Only if you have suspected heart disease, not as a preventive. And now there’s newer technologies where you don’t have to stick big needles up your groin and put you on sort of basically conscious sedation and get you in the hospital and do this whole long procedure that’s risky, where you shoot dye in the arteries from the groin.
That’s the old fashioned way. There’s a new way using CT scanners, high resolution CT scanners that are interpreted with artificial intelligence that essentially allows you to an angiogram that’s actually better at seeing what’s going on than an old fashioned angiogram, which we used to do. So medicine keeps evolving, but practice doesn’t, right? Science is growing and changing and we’re learning, and unfortunately your doctors aren’t using this science. Now, ask yourself if you had heart disease, who’s had a AI interpreted CTE angiogram? Probably nobody, maybe a couple of people. So what do we do normally to treat cholesterol? Well, it’s statin. Statin statins. This is I think the number one selling class of drugs in the world. It’s a multi-billion dollar industry, and it’s not that great a drug, actually, if you look at it, it can help prevent second heart attacks. It can help stabilize plaque.
It may reduce inflammation. It has benefits by inhibiting nitric oxide syn, so it activates anti-inflammatory pathway. So there’s benefits to it, but I just want to be clear, it may not be because of the cholesterol lowering, and I’m going to talk to you about this paradox of people who may have high cholesterol in LDL but don’t have heart attacks because it depends on what’s happening in the rest of their biology. And what statins do is target an enzyme called H MG COA reductase, which inhibits the synthesis of cholesterol, and that leads to also increased LDL receptors in the liver and decreased LDL and also lowers something called A OB, which we’ll talk about. But it has side effects, and these are not side effects. These are effects that we don’t like. We call side effects of drugs, side effects because we don’t like them, but they’re actually part of the mechanism of action.
HG coa reductase also is involved in this synthesis of co-enzyme Q 10, an incredibly important mitochondrial cofactor for creating energy in the body. So what happens when you can’t create energy in the body? If you, for example, run up a mountain and your legs are sore and you’ve got painful muscles and sore muscles, why does that happen? Because you run out of energy and your body starts producing lactic acid because you can’t produce energy to keep up with the exercise, then you get soreness. Well, that’s the same thing that happens with statins. You get muscle pain and muscle soreness. We’re going to talk about the prevalence of that in a minute, and it’s common far more common than you think. It also injures the mitochondria. And so I’ve seen studies looking at muscle biopsies, even in asymptomatic, people who don’t have muscle soreness, don’t have elevated muscle enzymes called CCB K.
They have mitochondrial damage at some cellular level that can be detected on a mitochondrial assessment through biopsy muscle biopsy. So even if you’re not symptomatic, this may have effects. It also seems to reduce your response to exercise. That was a 12 week trial where they gave a high dose statin or no drug or placebo drug. I mean, they put people through a training program, and again, in 12 weeks, the people not on the statin had an improvement in every biomarker of fitness and parameter of fitness, whereas the people on the statin, it blunted their response and they actually had very little improvement in their overall fitness. So it has a significant effect on mitochondrial function, which I think is important because it’s the key to longevity and aging. So I really worry about this. Also, we know that it increases the risk of diabetes and insulin resistance and it causes higher levels of insulin.
It also may cause liver damage in all day liver function, and in some people it may cause brain fog because it actually affects the neurological function of the brain because literally cholesterol is what most of your brain is made up. So now that’s not to say that most people don’t tolerate it pretty well. They do, but I worry about some of these underlying effects. Some of ’em we can feel, some of ’em we can’t. Also, it doesn’t lower important biomarkers like LPLA. It doesn’t really have a big impact on triglycerides. It doesn’t raise HDL significantly. Some stats may have an impact and it leads to reabsorption of cholesterol in your gut, so you’re kind of in a little bit of a loop. And so this whole concern about muscle function is really important in mitochondrial function. This was reviewed in the expert reviews, clinical pharmacology, and it does a number of different things that increases calcium in the muscle cells.
It can cause switching or cramping. It inhibits a synthesis of vitamin K two, which is really important in something called matrix GLA protein. It’s something that protects the arteries from calcification. So vitamin K twos are incredibly important for heart health and bone health and statins inhibit that. It also inhibits a synthesis of selenium containing proteins, which are really important, like glutathione peroxidase, which is one of the most important antioxidant enzymes in your body. It leads to mitochondrial injury as we talked about. Now, this would all be fine if the payoff was great, right? Well, what’s the payoff of taking statins? Well, there’s a method of assessing the efficacy of a drug in medicine called the number needed to treat. Now, in other words, how many people do I have to treat for five years for one person to benefit benefit? So for example, if you have a bladder infection or strep throat and you take an antibiotic, pretty much maybe 90 plus percent of the time, if you pick the right antibiotic, it’ll work or maybe even more.
I mean, sometimes there’s resistance and you need to switch antibiotics or look at antibiotic resistance, but basically the number needed to treat is like one or two, right? You don’t need to treat that many people to have a benefit. It essentially works on everybody. For statins, it’s not like that. Now, there’s two ways we use statins. One is we call primary prevention, meaning we only are using it to prevent a heart attack in the future in someone who has risk factors. In other words, high cholesterol. So what do we know about that? Well, it does not prevent any deaths period. Second, you have to treat 217 people for one people not to get a non-fatal mi. In other words, 216 people get treated with a statin for five years and have no benefit, but the one person does. You have to treat 313 people for one person not to get a non-fatal stroke.
Not such a great drug. On the other hand, about one in 21 people had muscle damage and one in 204 got diabetes. So it’s not a great drug for primary prevention. This is from really well researched data around number needed to treat for these diseases. Now, what about if you’ve had a heart attack? How does it work? Is it better? Well, yeah, it seems to be better if you’ve already had a heart attack, getting a statin might not be a bad idea, although there may be other approaches that are better. But essentially one in 83 people were helped by saving their life. In other words, you had to treat 83 people with statins for five years to save one life. About 39 people had to be treated to prevent another non-fatal heart attack. So a little bit better. You had to treat 38 people that didn’t benefit and wouldn’t prevent a second heart attack, but one out of 39 would.
Now one in 25 were helped in preventing stroke. So still not a great drug, right? Imagine if you had to treat 125 people for one person to benefit from an antibiotic for a bladder infection, it’d be a pretty crappy drug. And here’s this kicker. One in 50 people were harmed who took statins. So they developed diabetes for example. They had muscle injury, one in 10 had muscle damage. So this is a lot to think about because these drugs don’t really work that well. They have some benefit, there’s significant side effects and a lot of people are harmed in the process. So what’s the balance of what you should do? It’s really individualized. I’m not saying never use statins. I’m not saying they’re all bad. I’m not saying we shouldn’t have this part of our toolkit in medicine, but the fact that most cardiologists see your LL cholesterol, it’s all elevated.
They give you a statin or most primary care doctors see elevated cholesterol. They give you a statin, is just antiquated medicine. And let’s get into Y in a minute. Now, there’s some other drugs that are used and that are more coming around which are interesting, and I am not opposed to using medication, but one of ’em is called PC KS nine inhibitor. Now, this is a new class of drugs. It’s an injectable. It’s kind of expensive, but it doesn’t have the same side effects, and it helps by improving the LDL receptor population on your cells that clear your blood of cholesterol because PCSK nine actually degrades LDL receptors. But if you inhibit PCSK nine, it actually means you have more LDL receptors and then the LDL will be cleared from your blood, and A OB will be cleared from your blood. So they’re very effective.
It also may reduce something called lipoprotein little a, which we’re going to talk about. There’s very few drugs that do that. It’s a genetic issue and it increases your risk significantly of heart disease. And this was published in the Journal of the American College of Cardiology. There’s other drugs that help block cholesterol absorption like Zetia, and this drug is known to be effective in people are hyper ABS absorbers, and we’re going to talk about that, and I’m sure your doctor never checked your absorption of cholesterol, your production of cholesterol. There’s tests that actually do that. We’re going to talk about why we need to do those. The Zia treatment can be very effective in a subclass of people who are hyper absorbers. So it’s really about personalizing the treatment in the drugs. There are other drugs that are used in the management of cardiovascular disease such as beta blockers, ACE inhibitors, diuretics, anticoagulants, aspirin.
And these are used typically when someone’s already had a heart attack and or has high blood pressure or some of their other issue. So the problem with our current approach is it’s sort of a one size fits all high LDL statin C later, good luck. And as we just talked about, it’s not as simple as that. There are many other factors and you’re going to be surprised at how many factors are you have to consider and why most conventional lab testing just misses it. Most doctors checkups miss it and why you need a deeper panel, and that’s really part of why we created functional health to get you the right test, to be properly informed about what’s going on in your body. So when you look at someone to assess their risk, you need to look at all their risk factors, their diet, their lifestyle, sleep, exercise, their genetics, their age, their sex, metabolic factors like glucose, insulin, A1C, inflammation markers, oxidative stress markers, cholesterol absorption markers.
I mean the list goes on. We’re going to go through all of them, and we really need a full proper lipid panel, which is a 21st century panel and it’s called lipoprotein fractionation. It’s a bunch of gobbledygook words, but essentially what it means is we’re looking at your total cholesterol profile in a much deeper way, not only looking at the weight, in other words, because cholesterol is measured weight, your total cholesterol or LDL is milligrams per deciliter. How many milligrams of weight of this cholesterol is in a deciliter of your blood or a 10th of a liter of your blood? Kind of meaningless because you want to know the quality of that cholesterol. If it’s extremely high quality, if it’s low risk cholesterol, it could be very elevated, then you don’t have a problem. So we need to look at how we track all these different particle numbers and particle sizes and cholesterol quality.
We’re going to go through all of that today. So buckle up your sheets. Like I said, it’s going to be an in-depth view of everything you wanted to know, probably more about your risk of heart disease and how to deal with it. There’s also many, many other biomarkers besides just cholesterol. We need to look at as a holistic view to see what your overall risk is, including your glucose metabolism, levels of inflammation, oxidative stress, cholesterol absorption, many, many other factors. Now, functional medicine takes a very different look as systems medicine thinking is very different, and we look at not only your numbers, we call the total cholesterol triglycerides, H-T-L-D-L, which is typical. We look at that as well. But we look at not just the total cholesterol number we call LDLC or LDL cholesterol. We look at LDLP, which is LDL particle number and HDLP and other similar markers.
So we want to know what’s going on with lipoprotein fractionation, and that’s the goal. It should be the gold standard. There should be no other cholesterol tests that you get, period. Unfortunately, it’s less than 1% of all the cholesterol tests done in the United States. Now, I’ve been doing this for 25 years. It was first discovered over 40 years ago by Dr. Ron Kraus, who’s been on my podcast. We’ll link to that in the show notes. This is just a brilliant scientist who first discovered this and he really changed his whole thinking about cholesterol based on understanding the quality of the cholesterol. And this looks at the size, the density, and the number of the cholesterol particles of LDL and of HDL and of triglyceride or BLDL particles. And there’s basically two methods that are used to look at this. One is called NMR, nuclear Magnetic Resonance.
Literally they put your cholesterol under an MRI machine, a little mini MRI machine that they can look at like A MRI machine looks at stuff, super high resolution and see what’s going on. And there’s another one called Cardio iq, which is a lipoprotein fractionation that’s also known as the ion mobility test. They both are equivalent and are pretty good one. Different labs do different tests. So Quest will do the cardio IQ and LabCorp will do the NMR. There’s also other things you need to look at that are really important and two biomarkers that almost never get checked when you’re looking at your cardiac risk. Probably the most important is APO lipoprotein B. And I bet you never heard of that before or maybe you did, but if you did, you probably dunno what it is and most doctors have no clue how to think about it.
But APO lipoprotein B is kind of a surrogate marker for all the crappy types of cholesterol in your blood. So the higher the apo B, the higher risk, it’s one of the most predictive numbers that you can get to assess your risk of cardiovascular disease. And it’s also something you want to target in treatment, and we’ll talk about what those target numbers are. Also, we want to know something called lipoprotein little A or LP little a LP little A is a biomarker that is highly implicated in cardiovascular disease, is primarily genetically determined and is very difficult to lower, although it can be particularly with the PCSK nine inhibitors and other potential treatments like plasmapheresis. Some supplements can be very helpful and it’s important if you can’t lower it, you have to remove all the other risks. So that doesn’t become a problem if it’s in the context of an overall healthy metabolic state and elderly lipid profile, it’s not really a significant issue.
Also, we have to kind of look at the reference ranges, right? So again, we talked about Americans being obese and overweight. It’s normal to be that in America, just as with cholesterol, we need to know what’s optimal numbers. What you get on your lab panel may not be optimal. The total cholesterol that we say was optimal was like two 50. Now it’s 200. It used to be LDL of I think one 30 and now it’s 100. It used to be triglycerides of over one 50 or a problem, but it probably should be under a hundred. We’re constantly changing the metrics. Diabetes used to be blood sugar one 40, now it’s 1 26. And we’re constantly adjusting the numbers down because we see the risk increases with each increasing number. We need to look at all the risk factors, and I look at a lot of stuff and it is stuff that you can do on a regular lab panel.
It’s not that much. You look at all these biomarkers and you get a really comprehensive profile. Not only do you need to look at all the lipid and lipoprotein fractionation and a OB and lipoprotein A, but you need to look at your metabolic health. And this involves measuring insulin, glucose, hemoglobin A1C. And also sometimes I do a glucose tolerance test because sometimes you can’t always tell by a fasting insulin or fasting glucose because the body keeps those numbers pretty low until late in the game. And I’ve had patients, for example, have perfect blood sugar numbers, but their insulin levels were off the chart. And so you have to kind of look not just at your A1C as your measured metabolic health, which is your average blood sugar over six weeks, not just your glucose insulin, but sometimes a full blown glucose tolerance test. But measuring not just glucose insulin as well at one and two hours and fasting.
We also look at levels of inflammation because they’re highly important in determining your risk because without inflammation, this is worked done by Paul Ker at Harvard. It doesn’t seem to matter where your LDL cholesterol is. If there’s no inflammation in your body, there’s no heart disease most of the time. So the key here is that inflammation damages the lipid particles, causes oxidative damage, and it’s these oxidized or rancid fat particles that end up in your arteries and cause plaque. So we also measure oxidized LDL because we can measure oxidized rancid cholesterol in your blood. We measure something called F two isop tine, another marker of oxidative stress. We measure other markers of inflammation like high sensitivity crp, ppla two, mala peroxidase. And these are all, again in the show notes. Don’t worry about the names. We’re having all this sitting. So those are really important.
We also want to look at your liver because associated with metabolic disease is high levels of fatty liver, and this is a big contributor to heart disease. We need the liver function test. Kidney disease can be affected by diabetes, insulin resistance, hypertension. We want to know what’s going on there that really affects your risk. We look at small levels of protein in the urine called microalbumin. We look at kidney function. We also look at uric acid, something that is related to insulin resistance. The higher the uric acid, the more inflammation and more injury you have, the more mitochondrial damage you have something easy to treat with diet. We also get hormones because hormones are affected your estrogen progesterone to some degree. But if you’re high levels, high levels of insulin, you’re going to make more estrogen as a man, as a woman, you’re going to have more risk of cancer.
But what also happens is in a men, your testosterone levels drop, you lose muscle, you lose sex drive, you lose all sorts of benefits that you need from elevated testosterone. And I literally just read a paper that came out this week that was polished in frontiers of endocrinology called Correlation Between Visceral Fat Metabolism score, meaning how much belly fat you have and erectile dysfunction. And this was a cross-sectional study from NHANES over three years looking at 3,600 people and man actually and found that the bigger your belly, the more erectile dysfunction you have. So just keep that in mind guys. When you’re looking at the next cake or donut or sugary thing you’re thinking of eating, you might not want to do that. So those are some of the blood tests we look at. Now, there are other tests that might be important too. We’ll get to those in a minute. But what’s really fun now is that we have extremely safe, very low risk, high resolution imaging studies using artificial intelligence to map out exactly what’s going on in your heart.
We’ve kind of moved through an era and just kind of give you the history a little bit, but I want to tell you where we’re going to end up, which is this incredible new test. It’s really the interpretation of an old test through AI called the CT angiogram that revolutionizes everything. We are thinking about how we need to look at heart disease, and this is, I think should be a baseline for everybody, probably at 40, another 50. And if you have heart disease, you can do it more frequently as you’re looking at treatment and reversal. So we used initially a coronary angiogram, and we only did, some people had heart attacks or chest pain or having an abnormal stress test. So it was kind of like a late stage test and using IBD, putting it through big catheters in the groin to look at blockages and plaque.
Actually, it’s not even that great a test because it kind of misses things. If you have concentric plaque, meaning the plaque is even all the way around and narrow, you can’t actually tell that there’s a narrowing, like an uneven narrowing. So that’s not even that effective. And they improved that by using intravascular ultrasound. So like a mini mini ultrasound machine that goes end of a catheter that looks at inside the arteries and can actually tell how thick the wall is and how much plaque. So that was good, but again, that’s a little bit invasive, not really want to do that. That’s something I would just go do for fun. Then we developed this thing called a CT, coronary artery calcium score or cac, and this measures calcified plaque. Now, calcium goes with his inflammation, and the calcium on these arteries gives you a proxy of the fact that there’s been some atherosclerosis or hardening of the arteries.
Literally hardening of the arteries is what this means. It’s calcified arteries. The problem is calcified plaque is old plaque, that’s stable plaque. So it’s not really, we call vulnerable plaque or soft plaque, which is the at-risk plaque. That’s going to break up and give you a heart attack. So you can have a high calcium score, but it does correlate to some degree with your risk, but it’s not that perfect. And we’ll talk about why even for example, if, and we’ll get into some of this interesting data about comparing calcium scores and LDL and what that means and how we can determine risk. But now we have a new scan that came around a number of years, so called the CT angiogram, and this is using a conventional CT scanner with dye. It then looks at your coronary arteries using a very high resolution CT scanner.
Again, great improvement. So instead of having to go through your groin, you can do a CT angiogram much safer, much easier to do, much quicker, and it’s improvement. That’s great. But the next generation where we are now, and this is again, it takes 20 years sometimes for things to go from science to practice. And this is one of those things just like lipoprotein fractionation has been around for 40 years and it’s less than 1% of all tests done. Same thing with this test. You probably have never had it. You probably never heard about it, but it is the gold standard to today for how you should evaluate your risk. And I believe how you should determine whether or not you need drug therapy or not. And I’ll just tell you a quick story after I explain this, but basically what this test does is it uses a normal CT coronary angiogram or A-C-C-T-A we call, and it takes that information and uses, and I’ll explain this test a little more later.
It uses extremely large amounts of data and analytics to assess the plaque in the arteries. Is it calcified plaque? Is it noncalcified plaque? What’s the difference? Is it inflamed plaque? Is it non-inflamed plaque? So much more important. So someone can have a zero calcium score, but tons of soft plaque and you’d miss it on a coronary calcium score. So this is really, really the gold standard anchorage, everybody to check it out. It’s called clearly C-L-E-E-R-Y. You go to clearly health.com, find one in your area. I don’t have any financial relation with the company. I just think it’s the gold standard. And this is based on, not on my opinion, but it’s based on the literature. So we’ll get deep into that in a minute. And then there’s other tests you can use to look at your vascular health, like your carotid artery scan. I think that’s important to look at a carotid intermediate thickness, which is basically the thickness of your carotid arteries walls, and if there’s plaque or anything in there, that’s a simple ultrasound test.
Okay, so do all that. There may be other things you need to do because I had to do this because I have a really bad history of heart disease in my family. I actually did this clearly scan. I surprisingly saw some plaque and I was like, how is this possible? I’ve been eating healthy my whole life. I’ve exercised like crazy. I obviously have stress, but who doesn’t? I may be part of it. I don’t smoke. I don’t have diabetes, I don’t have blood pressure. I take my vitamins. It just didn’t make sense to me. And I remembered that my family has extremely bad history of heart disease. My grandfather’s family, almost all his brothers and sisters had heart attacks and bypasses in their fifties. This is early heart disease. He delayed it a little bit. He was a laborer, he was deaf, and he basically worked for the New York Times. He had to throw the newspapers on the truck all day for decades. He was super fit, used to do handstands. I mean headstands at 80 years old. It was very impressive.
And he walked every night after dinner, which is great. He used to feed the cats in New York and the neighborhood in Queens. He would just bring scraps of food and feed all the Allie cats. So he had more exercise and made it better help. But I actually did my lipid genetics and now we’re able to do genetics in a way that we’ve never done before. It’s not like one gene that’s the problem. It’s a whole collection of genes that affect your risk and they’re some protective and some not protective. There’s a company called GB Insights. Again, no financial relationship, but they look at a wide array of risk genes for cardiovascular disease. For example, I always seem to tend to run high triglycerides. I just never knew why, because I don’t eat a lot of carbohydrates, but I have a OE C3 gene. I also have other genes that increase my cholesterol absorption.
So I absorb way more cholesterol from my bile. I excreted from my liver, it goes through my bile into my stool, but instead of pooping it out, I reabsorb it. So I didn’t know that. I also have this phenomena called being a lean mass hyper responder where certain people, if they have a lot of saturated fat, will have a dramatic increase in their LDL particle number in their LDL small particles. And it’s very strange because these people typically are thin, healthy fit, kind of like me. They have a high HDL, they have low triglycerides, but their LDLs are really high, their particle number really high. And these lean mass hyper responds, see dramatic elevations in LDL cholesterol after ketogenic diets. It’s high in saturated fat. I saw this in one of my patients. I had a patient, for example, who was overweight woman and very metabolically and healthy.
She had insulin resistance, and she was like, I really got to deal with this. I want to lose weight. I can’t lose weight. I why don’t we try ketogenic diet? Essentially put her on butter and coconut oil. 70% of her diet is fat. And not only did her cholesterol drop a hundred points, her triglycerides drop 200 points, her HGO go up 30 points, which is almost something you never see. And everything normalized on her lipid panel. Her blood sugar normalized, insulin normalized. She lost 20 pounds. Everything was great. And another guy in his mid fifties who was like a biker, would bike 50 miles a day, super fit, super lean. He’s like, I want to do a ketogenic diet. I heard it was good for you. I was like, I don’t know if it’s good for you, but if you want to try it, let’s try it, but let’s track what’s going on.
And it turned out he did the opposite. So eating the same type of food. His LVL went up through the roof, his particle number went through the roof, his small particles went up, everything went fluey. And I was like, oh. So there’s a lot of genetic variations sometimes getting your genetics. It’s important, determining exactly how to precisely affect you. There are actually even genes that look at statin intolerance. I, for example, have a gene that causes statin intolerance, meaning I can tell in advance if a statin’s going to cause me more problem because of muscle damage. Another test that we do that’s really important in addition to the lipid genetics when we need, which can look at different kinds of familial hypercholesterolemia, but there’s a lot of variations there. I don’t have the typical kind, but I have another kind and there’s just a lot of variations, but we’re learning more and more about how to customize and personalize treatment.
Another test I do that’s really important is called the cholesterol absorption and production test. It’s called Cholesterol Balance by Boston Heart Lab. And it’s a really, really good test, and it helps me create more precise treatment. For example, I’m a hyper absorber. So when I check my test, I absorb a lot of cholesterol that was excreted from my bile into my gut. I reabsorbed it. So by taking a cholesterol blocker or extra fiber like Zetia or extra fiber, I am actually able to really dramatically lower my cholesterol simply by preventing that absorption. It also tells you if you’re a high producer, so you might need something to help inhibit production or some other drug. So it really helps in personalizing treatment. So you got to identify the root cause. This isn’t a one size fits all. It’s not like LDL high statin. See you later.
That’s kind of what medicine does. It’s ridiculous. It’s not current science. It’s not what we should be doing. It’s not how medicine should be practiced. Unfortunately, doctors are busy. They hear from drug companies, they do their best. They try to learn. They’re in, they’re in the matrix, you know what I mean? Took the pill. I don’t know. Were made hooked up to the thing. They’re in the, you know what I mean? They made the matrix. They don’t see they’re in the matrix, and this is a problem. So turns out that there’s a number of things that are really important is the root cause. And we’re going to talk about what I think is primarily today, the major root cause, aside from some of these inherited genetic lipid disorders for heart disease, and that’s insulin resistance, pre-diabetes and diabetes. And this requires a more nuanced, personalized diet and lifestyle treatment.
So now I’m going to go into it. So get up, take a drink, put this on pause, go to the bathroom. I want to talk about all the numbers in detail. So we give a high level. We’re going to get into a deep, deep analysis now, but I promise we’re going to get to the take homes, which is what you should do, what you should eat, how to know what to do when, and how to navigate this whole process. So first of all, what is cholesterol? Why does it matter? Well, cholesterol is a waxy fat like substance. It’s critical for human biology. It’s not like it’s bad. Cholesterol is not bad, right? It’s obtained from food. It’s primarily produced in the liver. What you get from food is insignificant. I mean, if you have a cholesterol of 200, it means you have 200 milligrams per deciliter, meaning you have five liters of blood, you have enormous amounts of cholesterol.
Well, I don’t know what the math, 200 times 10, that’s 2000 times five. That’s 10,000 milligrams of cholesterol floating around in your blood. And if you take an egg or have some cholesterol rich food, that may be a couple hundred milligrams of cholesterol. Turns out it’s really not significant for most people. So I think people have come to understand, and the dietary godliness reflected this, that we should not be worrying about dietary cholesterol, but it’s important to understand what cholesterol is. It’s a fat, so it’s not soluble in water, and it has to be bound to a protein. This is called a lipoprotein. So LDL is low density lipoprotein, HDL is high density lipoprotein. It’s just how cholesterol is transported in the body, kind of bound to proteins so that it can kind of move through the fluid of your blood, which is like water, right?
Then it’s transported all over to do whatever its things. Now, it has so many functions in the body, thousands of functions. It’s part of every cell membrane. You have 37 trillion cells. Every single one of those cells requires it to have the proper amount of cholesterol. It’s critical for nerve sheath covering. So basically every covering of your nerve that is important for the transmission of nerve singles is made up of cholesterol. 25% of all the cholesterol in your body is in your brain. Cholesterol is also the building of blocks for hormones like estrogen, progesterone, testosterone, cortisol. So I mean, people see an extremely low fat, low cholesterol diets. They have very often low testosterone in other hormones. It’s also important for bile production to help you digest your food and absorb your food. It’s important for vitamin D production. So when your sun hits your skin, it combines with cholesterol to make vitamin D, which is involved in thousands of biochemical reactions in your body.
It’s critical for immunity, for mental health, for bone health, muscle function. I mean, just the list goes on and on. And I encourage the list of my vitamin D Know your numbers podcast. How do we end up with this hypothesis that saturated fat causes L-D-L-L-D-L causes heart attacks. So the key to heart attacks was to lower LDL and cut out saturated fat. That’s basically what we’ve been told. So this was based on a epidemiological study, which essentially does not prove cause and effect. So it’s correlation, not causation. And I wrote a lot about this in my book, eat Fat, get Thin. So if you want a deeper dive into the science of this, have a look at this book effect, then it’ll unpack this in great detail. I can’t go into that many detail, is be an eight hour podcast. I’m not going to do that.
But the seven country studies basically showed that saturated fat seem to be linked to LDL. Cholesterol seemed wheeling to heart disease, and there were many design flaws, a lot of bias, lots of conflicts of interest. In fact, when you actually looked at the study, it was sugar and starch that were the biggest drivers, and they didn’t account for that. And many of the original researchers on this study actually subsequently, including Ansel Keys, repudiated the findings of the study. So they kind of went back on what they originally had thought because the evidence kept mounting that they were wrong and they acknowledged it. So Ancel Keys was the father of this ended up kind of turning around on this and actually realizing that it wasn’t the issue. So the guidelines from this that we were all told was to minimize saturated fat, to reduce dietary cholesterol, to eat more vegetable oils and lower cholesterol.
So vegetables do lower cholesterol, but it’s not necessarily protective. One study that was done by the NIH, it was a large study that was a Minnesota coronary experiments, some other studies that were related to that, that actually did an interventional trial. Now, it’s very hard to do dietary interventional trials because people eat what they want unless you give them the meals. Who knows then if they eat it and then maybe they eat something else, have ice cream at night. You don’t know. This was a group of people who were inmates at a mental institution, 9,000 people. They separated ’em into two groups, half got corn oil, which is an Omega six vegetable oil, and the other group got butter and saturated fat. And guess what? The LDL dropped in the Cornal group, but heart attacks went up dramatically. Now, I wrote about this in my book too, but this is a really important study because it’s one of the few interventional trials we have that it looks head to head at vegetable oil versus saturated fat.
And even though the LDL went down, the risk went up. And for every amount that the LDL went down, the risk of RT attacks went up and up. So it was kind of a linear relationship and a very impressive study. They actually didn’t publish a study for 30 or 40 years. It didn’t believe it. And they basically had it buried in a garage or a basement somewhere. And NIH researcher knew about this study and he found the son of the guy who was the researcher, and he said, Hey, do you have any data on this? Oh yeah, my dad died, but he left this huge box of stuff in the basement. Why don’t you come and check it out? And that’s actually how they figured it out. So our concerns around saturated fat I think are a bit misguided. It’s heterogeneous how we respond. As I mentioned, for example, I don’t do as well with saturated fat, whereas other people do incredibly well and it fixes their cholesterol.
So there’s really inconsistent overall evidence. We need to understand the overall food pattern. If you’re eating a lot of saturated fat with sugar and starch, that’s a problem. That’s a problem, which is basically how we eat it, right? It’s like you have your burgers, fries, and a coke, and that’s not a good thing. So we have your bread and butter. That’s not good. You’ve got saturated fat on carbohydrates, you have ice cream, which is fat, saturated fat and sugar. So those are bad. Never eat saturated fat with carbohydrates in that way that are refined in starchy eating and sugary because that’s a bad news problem and I have no argument with that. But if you’re eating an overall healthy diet and you’d have low starch and sugar and low ultra processed foods and you’re eating fat not as big of an issue. Now, 22, sorry, 2020 Cochrane database systematic review.
Now, Cochrane database you should know is an independent group of scientists have no industry ties, no industry funding, no conflicts of interest. It’s kind of the purest, pure, pure of science. They do big reviews of all the data and they’re not funded by a drug company. They’re not funded by statin makers, they’re not funded by some vegetable oil company. They’re independent. And they found that reducing dietary saturated fat had no effect on heart attacks, including total mortality, cardiovascular disease, mortality or coronary heart disease mortality, fatal heart attacks, non-fatal heart attacks, or other coronary heart disease events. In other words, it didn’t prevent any deaths or any heart serious heart attacks or anything bad. So I think we have to kind of take a step back and look at should we be considering this as a problem or not? And again, I wrote a lot about this in e effect.
Then you can learn more about some of the data and there’s always more data emerging. I wrote that number of years ago, but it’s still the issue now. Again, it’s heterogeneous. So that doesn’t mean saturate fat’s good for everybody. Just find out if it’s good for you or not by measuring your labs and checking it periodically. Dietary cholesterol, which was the boogeyman for a long time, don’t eat eggs, don’t eat lobster, don’t eat shrimp. Again, there was no evidence to support that. And in 2015, the US dietary guidelines said dietary cholesterol is no longer a nutrient concern. So eat your eggs, don’t worry about it. So what actually causes heart attacks if it’s not dietary cholesterol, if it’s probably not saturated fat for most people, what is it? Surprise. It’s insulin resistance. It’s what I’ve been talking about in writing about for over 20 years.
And this is a really interesting study that sort of caught my attention a long time ago called the Uro Heart Survey. It was A1 10 centers, 25 countries, over 4,000 patients who had a heart attack. And what they found was when they did glucose tolerance tests and they measured their A1C and tracked their metabolic health, that 67% or two thirds of those patients had either diabetes or pre-diabetes. For example, 31% of them had full-blown type two diabetes. 61% had pre-diabetes based on a glucose tolerance test. This is crazy, right? So if you think about it, two thirds of the people that walk in emerge with a heart attack of their sugar and starch in their diet, not their saturated fat. And now insulin resistance is present anywhere between 50 to 88% of those with abnormal cholesterol. And it’s the type of cholesterol that’s bad. And I want you to listen up here.
This is a really important point. The type of cholesterol that’s bad, all those abnormal particles, too many particles, small particles, we’re going to talk about those in a minute. All of those are caused by insulin resistance. So sugar and starch is what actually screws up your cholesterol and causes the atherogenic cholesterol. It’s called atherogenic dyslipidemia. It’s literally got a medical term for it and it’s meaning the type of cholesterol that causes heart attacks. And it’s a pattern of high triglycerides, low HDL, high LDL particles, small particles. And we know that. We know this. People with diabetes are two to four times as likely to develop heart disease. This is from data from John Hopkins, and that’s a 200 to 400% increase in the risk of heart attacks. If we see a drug like statin that lowers the risk by 30%, we go, wow, Yahoo Blockbuster drug.
But it’s kind of almost insignificant. So what causes insulin resistance? It’s our standard American diet. Start sugar, ultra processed food, lack of whole foods, phytochemicals fiber, lack of healthy fats, all this stuff we’ve been talking about forever. Sugar in your diet drives insulin to be high. That causes insulin resistance, that leads to inflammation. And this mechanism is very well mapped out. Paper publishing cardiovascular, diabetologist talked a lot about this, but essentially you get inflammation when you have insulin resistance because the fat around your belly, which insulin stores is like an inflammation factory, it spews on inflammation. That inflammation basically causes oxidation like rancid fat. It oxidize your cholesterol, it causes dysfunction in your blood vessels, we call endothelial dysfunction. It causes plaque formation. So starch and sugar have the most adverse effects on your lipid profile. It alters lipid metabolism. My head causing this atherogenic dyslipidemia it cause you small dense LDL, high triglycerides, low HDL, actually small HDL large triglycerides, which is not good and it drives inflammation and oxidative stress.
So really important to understand the underlying mechanisms, not saturated fat, starch and sugar total cholesterol. Let’s talk about that. Why does it matter? What is it? Well, it’s the total number of everything of your L-D-L-H-D-L triglyceride or V-L-D-L-I-L-D-L, all these cholesterol particles. It’s the total number and it’s used to assess cardiovascular risk, but it’s kind of irrelevant if your cholesterol is two 50, which sounds high, but your LDL is 90, well, it may be that everything else is okay. So you’ve got to look at this in context. I’ve seen women with cholesterols of 300, but their HDL is a hundred. They triglycerides are low, they have no small particles, they have free particles, they have all large light fluffy particles, they have no heart disease and they’re in their seventies and eighties. And I see this often and I actually asked Peter Libby, who’s wrote the quote textbook on cardiology at Harvard, he’s the head of cardiovascular medicine there.
He said, yeah, no, I wouldn’t treat these people. There’s no data that show that we should treat these people even though their numbers look bad, they’re not bad. So you have to really look at the whole context of everything and look at the particles, not just this total cholesterol number. The optimal range we say is probably less than 180, normal is less than a hundred, but it really depends, right? If you have a lot of large fluffy particles, your LDL might be high, but or your total cholesterol might be high, but it may not be an issue. So you have to look at the whole profile. But if the total cholesterols can price of these little small dense particles, then you’re in trouble. How about triglycerides? What is that? Well, it’s the most common type of storage fat in your body. It stores excess calories from food.
It’s caused by excess carbs and starch and sugar which are in the body. And initially it some of that stored glycogen. You get about 2,500 calories of glucose in the form of glycogen stored in your muscle. So once that’s done, where does it go? Well then all of it’s converted to triglycerides in the liver, in the fat cells, it’s called lipogenesis and you get high triglycerides. So it’s either stored in the liver for later use and you get again fatty liver like fo gra. How do they get fo gra, which is this fancy French thing where you get it actually means fatty liver and french FO liver and GRA means fat. It’s basically fatty liver. They get it by force feeding ducks with corn, basically starch. They don’t give ’em fat, they get a fat in liver. And then the body uses it as it needs it for energy.
When glucose is low, that kind of causes lipolysis, which is when you fast or you do long-term aerobic exercise. So it’s really important to kind of understand that triglycerides are important but they’re not something you should be taking for granted and they’re something you should seriously focus on in your lab test. Now the conventional range is one zero, which I dunno how you get zero zero to 1 49. Nobody has a triglycerides of zero. You need some triglycerides. So the reference ranges are all cocked anyway, but the optimum probably range is less than 70. And you should have smaller triglyceride particles, not the big large ones. Even though large LDL and HHL are good, large triglycerides are not. And we can see this on the test that we do. If it’s over a hundred, you start to worry a little bit over one 50. That’s very concerning to me.
And that over 300 is really severe, requires aggressive treatment and sometimes even medication. But it’s treated really by treating the underlying issue, which is insulin resistance. When you look at people who have this high biomarker, if you have high triglycerides that increase your risk of heart attacks by in cardiovascular disease by 32% men and 76% in women, it also drives fatty liver or actually hepatitis from fatty liver. We call that nafld or non-alcoholic fatty liver disease or nash, non-alcoholic steatohepatitis meaning hepatitis from fatty liver from sugar and starch. And this is a big problem. I mean in the end, this was not something we ever saw before. Now a hundred million Americans have this and guess what? 8 million kids have this, 10% of kids and now their kids as young as 15 years old needing liver transplants from chucking down soda. And it’s the fructose, particularly in the soda that drives the increase in fatty liver.
So high fructose corn syrup, fructose added sugar, all that driving this. And you’ll see sometimes elevated liver function tests, A-L-T-A-T-G-G-T, you might need to a liver ultrasound. So they called the fibro scan to see what the fibrosis is because it eventually causes a scarring and cirrhosis just like alcoholic liver disease. And you can also look at liver fat based on MRI. So I had my liver MRI done as a whole body scan and my liver fat was less than 2%. Now shouldn’t be more than 2%. So when you have high liver fat, that’s a problem. What about H-D-L-H-D-L Cholesterol is important. It’s known as the good cholesterol, that whole good and bad cholesterol. If you hear that, if someone’s saying that it means they don’t understand lipid biology and you should just talk to somebody else about it. But it is protective in many ways, but it depends on the quality of it.
It is an antioxidant lip particle, it’s anti-inflammatory activity. It helps in reverse cholesterol transport, meaning it absorbs cholesterol in the blood, it brings it back to the liver, clears it from your blood so it’s really good. So it helps you excrete excess cholesterol in the bile and then you poop it out. If you have high levels, it seems to be lower risk of heart disease and low levels are associated with a higher risk of heart disease, generally high HL. It’s a good thing, but it’s all kind of more nuanced than that. Remember a guy from Quest Labs once came to give a talk when I was at Canyon Ranch and he was like, I wanted to know what was causing longevity. So I looked at all these people, death certificates of people, and I went and found their death certificates and I correlate with other labs because they had thousands and thousands and hundreds of bottom millions of people’s lab tests and they found that the higher the HDL, the longer people lived.
Now it’s not as simple as that, but it’s not a bad biomarker, but we need to know the quality and the size of the cholesterol particles and particularly HDL. So HDL can be small, dense and dangerous or it can be light, fluffy and protective. And you want the light, large fluffy cholesterol, HDL particles, which is the HDL two particles. Now we can fractionate HDL. So it’s not just whether it’s large or small, it’s actually we can fractionate the subtypes of HDL. Again, this is very sophisticated lipid analysis, but you kind of need to know what you’re dealing with. It’s like you don’t want to drive with your blinders on. You want to see what you’re doing before you start any treatment. So you can have HDL two, which is protective, but HDL three is small, dense and has high risk of heart attacks and strokes, so not good.
So conventional medicine says anything over 40 for a man is good, 50 for a woman is good, probably optimum ranges are over 60. But again, it tells you nothing about the quality. You want to know about the large fluffy protective ones. You want more HDL two particles. You don’t want the small dense, less protective particles and you can have the same exact number of HDL, but it can be completely different in terms of its risk depending on the quality of it and the treatment is different. Now the main thing here again is that sugar and starch cause the HD L to be more HDL three more dangerous. There are a number of reasons for low HD L that we talked about is primarily in insulin resistance. Our high starch and sugar diet, pre-diabetes type two diabetes being obese belly fat, low omega fat levels, smoking will do it, not exercising will do it.
So smoking drops, HDL and no exercise. And when you have these small dysfunctional all the HDL, you get more inflammation and so forth. Now there are some genetic conditions that cause this. It’s called familial combined hyperlipidemia. It’s not because of what you’re eating, it can be a genetic thing, so that may require different treatment. What about LDL? That’s what everybody’s talking about. Everybody’s focused on what is it? Why does it matter? Well, it delivers cholesterol to the tissues, basically important for brain function, for nerve function, for cell membrane integrity, for hormone production. It’s quote known as the bad cholesterol, but it’s not bad or good. It just has functions and if it’s the wrong kind it’s not good. But here’s the problem. As I mentioned, LDL alone is just an incomplete measure of your cardiovascular risk. You really want to look at the overall pattern and a new study in 2023, it was published in circulation.
It was the Western Denmark heart registry study and now this is a study of 23,000 symptomatic patients who are evaluated for coronary artery calcification. We talked about that before basically with a hard plaque and they found that high LDL was only associated with cardiovascular events like a heart attack if you had a high calcium score. But if your calcium score was zero and you had a high LDL, there was no association with LDL. As I mentioned before, calcium that we measure on this test is put down by inflammation and inflammation is what causes heart disease. And the revolution in cardiology was that we began to understand that heart disease was not a plumbing problem of fat buildup in your arteries. It was an inflammation problem and inflammation was what was driving the problem. And what’s driving the inflammation is our inflammatory diet and particularly starch and sugar and environmental toxins and our microbiome, and this is more complicated but a lot of stuff.
But essentially this is a remarkable study which they found even if your LDL is high, if you didn’t have calcium in your heart, you didn’t have any risk of heart attacks. But they also found in this study that smoking diabetes and low HDL independent of the coronary calcium score were biomarkers for high risk of cardiovascular events. So in other words, if you smoked they have diabetes or had low HDL and aside from the smoking, these are really all caused by star sugar. It’s a problem even if you have a zero calcium score. Why? Because you can get soft plaque. So this is really important. Now when is LDLA problem? Well, if you have high amounts of LDL particles, we call LDLP. And if you have high amounts of small LDL, you have high amounts of A OB, which essentially is all the dangerous cholesterol particles in your blood.
These get essentially deposited in your arterial walls when those walls are damaged, say a one cell thin lining of your arteries when those arteries are injured because of oxidative stress and inflammation from our diet, from insulin resistance, from stress, from smoking, alcohol, high blood pressure and environmental toxins like heavy metals, the microbiome particles like lipopolysaccharides and bad bugs in your gut, latent infections, sleep deprivation, aging, which is an inflammatory process or various genetic factors, you end up getting cholesterol deposits in your artery. And when you get endothelial damage happening, when you get this high LDL and A OB, you get lower levels of something called nitric oxide synthase. You have lower nitric oxide in your blood, which is important for both the dilation of your arteries as well as reducing inflammation in your arteries. You get more oxidative stress and then the LDL particles that are inflamed and oxidized get stuck in the arterial wall they glom on with platelets.
These macrophages which are white blood cells kind of basically like Pacman ingest LDL particles, they go inside the wall, they create a foam cell essentially the base of the plaque and that’s called atherosclerosis, which is what we’re all dying and then it’s inflamed and the inflammation is what makes the plaque vulnerable to rupture. It’s like a pimple, think of it like a pimple and you can pop the pimple. When you pop the pimple because of some injury or stress, then platelets glom onto the pimple to repair it. You get a blood clot, boom, you get a heart attack, that’s what happens. Or you get a stroke, same thing. Now what should your LDL be? Probably typically less than a hundred optimal less than 70. But again, it’s just so much more nuanced than that. You’ve got to look at the cholesterol particle number. I don’t care what the total LVL or total cholesterol is.
I want to know what the quality is because I’ve seen people, for example, with extremely low cholesterol with extremely high particles and people with extremely high cholesterol with very low particles and very large particles. So it really depends on the quality of the cholesterol. What about a OB? Now, eight OB is really important because it plays a crucial role in cholesterol metabolism and it basically transports lipids to cells and tissues. It’s associated with lipoproteins and caries cholesterol and triglycerides and it’s a major structural protein in LDL particles. So each LDL particle typically carries one A OB molecule. So in a way it’s kind of a poor man’s assessment of your lipid particle number and quality. So if you have a lot of LDL particles, your A OB is much higher and that tracks with more risk. So it’s kind a surrogate marker for all the lipoprotein fractionation, but it’s so cheap now you need to see the whole thing and a OB is quite problematic because it correlates with these small dangerous dense L DL particles.
This was well described in the archives of physiology and biochemistry. Of all the biomarkers that you can track, A OB is associated with the highest risk of atheros and heart attacks. In other words, of all the cholesterol biomarkers, the one that is the most important to track to see a risk is not LDL or HDL or triglycerides. It’s A POB. And guess what folks? That’s something your doctor almost never checks. Go to function health.com. You can sign up, get on the wait list or if you want to skip the wait list, you can use my code young forever. But essentially you got to know this number. High numbers of small LDL, which is indicated by hypo OB, they bind LDL where they can be clear from the blood but there’s not enough LDL receptors to clear all the LDL particles. It basically leaves these particles in circulation.
Then you get high risk of damage from inflammation and conversion to oxidized LDL. Now oxidation impacts their chemical structure. It prevents ’em from binding the L receptors clear from the blood. So it’s basically this rancid fat in your blood. That’s the problem and inflammation. So if we can cut down inflammation, cut down rancidity by eating a whole foods anti-inflammatory diet with lots of antioxidants, we can prevent a lot of this. And when these oxidized lipids occur, they become foam cells because they’re taken up by the white blood cells called macrophages. They damage the lining of your blood vessels, they accelerate inflammation, you get the soft plaque, then it ruptures like a pimple and boom you got a heart attack or stroke. Now the normal reference range in conventional medicine is 20 to 90 and the risk increases most over 120, but probably the optimal range is 40 to 70.
Now people who have heart attacks or have plaque on a scan like the clearly scan, you probably want to drive that number down to less than 50. Now if it’s lower than 30, it may be problematic when you have too low cholesterol, but if your LDL is high and your A OB is low, your risk of heart attack is low. Lemme say that again. If your LDL is high, which is the thing your doctor would measures, but your A OB is low, which she doesn’t measure or she doesn’t measure, you really have very low risk of heart attacks. If your LDL is normal or low and your A OB is high, your risk is high. In other words, if you have a low LDL, remember this study where people have all these low LDLs and they had heart attacks 70%, they had a high A OB because they had high triglycerides, low HDL and insulin resistance.
So that’s really important. Most cholesterol panels just measure LDL cholesterol, which is why this nuance of risk assessment is so important and why we need to look at the full picture and not get a false sense of security by just looking at one or other numbers. And you have to look at all the relevant lipid biomarkers and all the metabolic markers and all the imaging tests to really figure out what’s right for you. I don’t want to take a drug for the rest of my life, let’s say I know exactly what’s happening. Alright everybody, so now let’s get into the real meat of the topic, which is the cholesterol panel you should all be having that you’re probably not having. In fact 99% of you are not having, which is called lipoprotein fractionation. Doesn’t really matter what it’s called, but essentially it’s a measurement of the quality and type of cholesterol particles you have.
It’s the gold standard for measuring your lipid numbers. It really should not be anything else that you’re looking at When you measure cholesterol, the typical plan you get at your doctor, your annual checkup is just inadequate, grossly inadequate to assess your cardiovascular risk. And it’s like the dark ages. It’s basically trying to figure out what’s going on in your heart with a stethoscope instead of doing a full-blown MRI or CT angiogram or whatever, you just can’t tell what’s going on. So it’s the gold standard. It uses two different technologies, MRI technology called NMR or an ION mobility test called Cardio IQ. One is done by LabCorp, one by Quest both pretty equivalent. It measures the quality of the size and the number of your cholesterol particles, which is important and not just the weight. As I said, the weight is a milligrams per deciliter and it’s like if you put for example 10 beach balls or a hundred golf balls, it could be the same weight, but they’re very different in their quality of the type of particles.
So you can’t really tell what’s going on by just looking at the LDL number or total cholesterol number. And this is a really important topic and I talked about this twice before in my podcast with Dr. Ron Krauss, who’s led the research to develop lipoprotein fractionation and has shown that the size, the density and the number of particles are better predictors of heart risk than your traditional lipid panel tests. Now, small dense LDL cholesterol particles are the worst actors. They have a greater tendency to damage the lining of your arteries to become oxidized and to trigger the development of plaque and they’re highly correlated with A OB. So you can use your A OB if your doctor doesn’t want to check your lipoprotein fractionation, although they should. All this stuff, the whole lipoprotein fractionation, your insulin, your metabolic factors, all the other risk factors we’re going to talk about today.
There’s also small, but there’s medium sized too. So medium and small are basically the problems. If you have, most people have a combination of small, medium and large, but you really want the more large and you don’t want the small and the medium and VLDL or very large LDL is also a eye marker that’s important and if it’s large and fluffy, that’s not good. You want the small aero triglyceride particles are related to your triglyceride particles. This gives you insight into the types and numbers of cholesterol particles. Like I said, you could have a hundred LDL on your blood test and it could just be a few large luffy buoyant LDL particles that are protective or you could have the hundreds of small dangerous dense LDL particles. So you can’t really tell just by looking at your LDL for example, if you have an LDL one 50 but no small particles and under a thousand overall particles, your risk is low.
But if your LDL 70 sounds good, and I saw like this the other day, her total cholesterol was like one 10 or LDL was like 50, but she was a vegan and she had extremely high numbers of small LDL particles. She had very low HDL, she had very small HDL, she had very small LDL and she was at considerable risk for heart attacks since she was 30 years old. And this is partly because she was eating a healthy vegan diet but was predominantly eating a lot of starch and carbohydrates. So the same LDL number on your regular panel can a profoundly different impact on your risk and also require very different kinds of approaches to treatment. Let’s look at the reference ranges. Your LDLP, which is different than the LDLC. The LDLC is your regular cholesterol panel. LDLP is the particle number should be less than a thousand. If it’s over a thousand your risk goes up. If you have high LDL and many small particles and all LDL particles, you probably have insulin resistance or pre-diabetes or diabetes. And abnormal lipids like this are typically caused by starch and sugar, not fat. This whole panel of atherogenic dyslipidemia is caused by starch and sugar, not fat small LDL should be zero to a hundred LDL.
Small DL depending on the lab can be under 500, under 600. But I’ve seen many patients who have undetectable small and other patients who have thousands of small LDL particles. So probably the lower the better LDL medium, similar reference ranges, we’re doing the show notes, but optimal levels are probably less than two 15. What about HDL particles? Well, we want to look at those too, not just LDL particles. And this measures how many large HDL particles are circulating in your blood and it’s good to have a lot of these large fluffy HDL particles and you can measure, as I mentioned, fractionation even of the HDL particles. So you can see, oh gee, well I seem to have a lot of HDL, but it may not be the good kind. So these help remove excess cholesterol from your blood. They reduce your risk of heart disease as the number goes up in general, but you really want to look at the overall particle number and it should be over 6,700. This is sort of the particle number. It’s less than that and like I said, this vegan for example, she had very, very low good HDL particles, which is not what you want. We also look at another marker LDL pattern. It’s instead of a surrogate way of looking at the overall picture, you can get pattern A or B. A is basically good, B is bad. B reflects more of the atherogenic lipid particles, the small HDL, the small LDL, the high triglycerides and so forth.
But you got to interpret it in terms of all the other biomarkers that we talked about. The full lipoprotein fractionation, A OB, lp, little A-H-S-C-R-P, the inflammation level insulin, blood sugar, A1C, uric acid, liver function, all this stuff. We want to look at not just one thing, pattern B as I said, sort of as a risk marker. Now there may be rare genetic causes, but generally it’s the result of a high starched sugar diet and this young vegan woman, she had a pattern B, even though like I said, her total cholesterol was like one 20, her LDL was super low, her HL was low, triglycerides weren’t too bad, but she had a really significant atherogenic risk profile at 31 years old. Now it’s a helpful marker for those who have a family history of heart disease for people taking cholesterol medication. So it can be a really good marker, but I don’t use it that much.
I think it’s just part of the overall picture. The next thing you should know about is something called lipoprotein little. A lipoprotein little A really matters. It carries cholesterol similar to LDL, it has an additional protein called apro lipoprotein A. It’s synthesized in the liver and its function is not fully understood, but it’s believed to play a role in wound healing and tissue repair. It’s structurally similar to something called plasminogen, which is involved in the breakdown of clots and it can compete with this plasminogen sometimes to actually hinder breakdown of clots, which means you have a higher risk of blood clots in your arteries, which translates as a heart attack or stroke. It is a predisposing factor to heart disease and atherosclerosis it higher levels of LPA or coordinating with higher calcium scores. It can deposit in the artery walls, it can undergo oxidation more readily than LDL and it can contributes to the same type of these foam cells which are not great and it’s involved in causing worse endothelial dysfunction, damage to your blood vessel lining.
It’s pretty much inherited for the most part. There’s A LPA gene which encodes a OA essentially, and there’s a lot of genetic variability and it influences your level. So for example, I have almost none of this. I see the patients with extremely high levels of this, and so it’s important. Certain ethnicities have more risks of Sub-Saharan folks, African-American populations. Sometimes diet and lifestyle plays a role, but it’s a risk for at a high level for heart disease, heart attack, stroke, aortic bowel stenosis independent of your LDL. So it’s important. It seems to me if you’re a man, it’s a worse problem than if you’re a woman and it seems to be if you have high overall cholesterol, bad cholesterol pattern like we talked about and you have ILPA, it’s also bad. So if you can lower your overall risk by lowering all the other bad biomarkers that we just talked about, the LPA doesn’t necessarily cause as much problem, but it is also linked to fibrosis of the heart and scarring in your heart, enlargement of your left atrium dysfunction.
So there’s a lot of things that we’re still learning about there. There’s various risks, there’s various cutup points. What’s the reference range? The lab I think is still trying to figure this out, but seems to be if your level’s between 30 and 50, you have about a 60% high risk of calcium on your scans. If your level’s over 50, it’s over 2.3 times risk of having heart disease. This is from a journal of atherosclerosis. It was over 20 in other studies and cholesterol, a review published in cholesterol journal in 2012 showed that it had a twofold increased risk of heart disease. Now about 25% of the population has a problem with this. Generally the lower the better. Under 20 is better, but we’re still learning a lot about it. And again, there’s not a lot of good drugs that can lower this PCSK nine inhibitors may plasmapheresis may certain supplements may help lower it.
Generally lowering your other factors is the key to lowering your overall risk. Then there’s something called non HDL cholesterol that we measure. Essentially it’s all forms of cholesterol. They’re not HDL, so it’s sort of another amalgamated number and it seems to be a better predictor of your risk of heart attacks than LDL or total cholesterol. It’s basically taking your total cholesterol as subtracting HDL and that number is your non HDL cholesterol and includes the L-D-L-I-L-D-L-L-D-L-L-P-A and something called chylomicron. So we won’t get too much into that. But basically if you have high non HDL cholesterol and what we call atherogenic dyslipidemia caused by insulin resistance and poor metabolic health, it’s all connected, right? So diet high in starchy sugar will typically cause high non HTL cholesterol. So what should you be at? Well, typically commissional lab ranges say less than 130, probably optimal is under a hundred and basically it’s a reflection of the fact that you have more small dense LDL more triglycerides, lower HDL and so forth.
So it predicts your risk of heart disease basically. There’s a few other things you want to know when you look at your profile is you want to look at this pattern that we call atherogenic dyslipidemia. I’ve mentioned it a few times, but essentially it’s the overall pattern that matters, not any one number, right? So the atherogenic dyslipidemia is caused by Sargent sugar, predominantly prediabetes diabetes. You have many, many small LDL particles. You have small HDL particles, you have high triglycerides, you have low HDL, and it’s all connected to this issue of poor metabolic health caused by ultra process diet and starch and sugar and sedentary lifestyle and so on. There are other factors, genetics, environmental toxins and things that can affect this, but that’s primarily the reason the microbiome and so forth. Higher blood triglycerides gives you a sort of a discordance between LDL cholesterol and LDL particle number and A OB.
So in other words, you can use triglycerides as a sort of a surrogate indicator to see if you should actually trust your LDL cholesterol number. In other words, you can have a low LDL cholesterol like your regular lab test that you get from your doctor, but if you have high triglycerides, it usually means that you have a lot of small dense LDL particles, even if the quote number of LDLC is normal on your regular lab test. So that’s why you want to look at LDL particle number and A OB, so very, very important. The other number you should pay attention to is the triglyceride to HDL ratio. This is on your typical cholesterol panel. It should be easy to measure and the ratio should be one to one if it’s greater than two. In other words, if your triglycerides are, let’s say a hundred and your HDL is 50, then your risk of in insulin resistance goes up if your ratio is higher.
In other words, if your HDL is 30 and your triglycerides are 50, that’s a ratio of five to one highly predictive of heart disease, insulin resistance, prediabetes, and how do you fix it? You lower starch and sugar refine carbohydrates to exercise. Exercise is one of the few things that can actually improve HDL and normalized triglycerides. So what are symptoms that you might get if you have all this stuff? Well, typically you’re going to look down and see belly fat. Belly fat is the cause of all this abnormal cholesterol typically, and it doesn’t have to be a lot. You just kind of have to have a little pooch basically. It can be a little bit, and the best way to determine this is a DEXA scan, that’s a body composition scan. We’re going to do another podcast to talk a lot about body composition, but essentially it’s measurement of where the fat is in your body and it’s in your belly and it’s that organ fat that’s the dangerous inflamed fat that causes heart disease.
And you might have other symptoms, you might have carb cravings, you might get low blood sugar because of blood sugar swings and insulin. In severe cases, obviously you’ll get symptoms of a heart attack, shortness of breath, chest pain, so forth. But most time it’s as asymptomatic. You might see other things like with insulin resistance. You might get acne, you might have low sex drive, you might have fatty liver, you might have a lot of other things that affect you. Now, what are the root causes of all these abnormal ranges in general? Well, it’s really, as I said, I feel like a broken record. I feel like I’ve been saying this over and over, but the world hasn’t figured this out yet. It’s in some resistance from eating a diet this high in starch and sugar. It’s eating a diet that’s high in ultra processed food.
It’s 60% of our diet, 152 pounds of sugar per person, 133 pounds of flour per person a year. This is what’s causing the problem that leads inflammation, that leads to oxidative stress, that leads to damage to your arteries and the whole cascade. Now, saturated fat may be a problem in some populations, so I’m not saying the saturated fat is good for everybody, but in general, the data show that it’s not a big risk factor particularly, particularly people who have atherogenic dyslipidemia, particularly people who have pre-diabetes and diabetes, saturated fat actually may be helpful for them. And so you have to look at your response to the diet. You can’t rely on a study. You have to look at your own biology, and that’s why function health is so great. You can do a test, you can change your lifestyle and diet. You can repeat the test and see what works for you because when you come to it, at the end of the day, it’s all about what’s happening in your own biology, not what’s happening for the general population.
Also, other things play a role. Genetics play a role like a family history of heart attack, cholesterol issues my family had that you’re a lean mass hyper responder. That’s me. I’ve got some variations of inherited genetic disorder that I have high absorption, and we can kind of customize our approach based on this. Age plays a role as we age, we become more in some resistant, we get loose muscle. We don’t exercise as much. We need to kind of tune up our biology a little bit better. Stress can trigger in insulin resistance, alcohol, obviously sedentary lifestyle. Smoking obviously is bad for you will cause heart disease because it causes more inflammation, oxidative stress, but not through the mechanism of insulin resistance, but it’ll cause low HDL and other things. And certain medications can mess things up like beta blockers, corticosteroids, birth control pills, certain diuretics. Now, there may be reasons why your lipid numbers are low.
We can go into that, but cancer, well, obviously you can cause all lower cholesterol, vegan diet, genetics, malnutrition, malabsorption, hyperthyroidism when your metabolism is so fast. Injury illness, high doses of certain drugs like statins or PCSK nine inhibitors. So having low cholesterol is generally a sign of poor health in general. And we see this also. There are many conditions associated with problems that are above range, like high blood pressure, diabetes, obesity, menopause, PCOS, but these are all related to some degree to this problem in insulin resistance. And certain autoimmune diseases also seem to screw things up. Thyroid issues screw things up. So if you have a low thyroid, if you have autoimmune disease, you’re more likely to have a heart issue. So now we’re going to dive into additional diagnostic tests that need to be done that are beyond blood tests. They’re imaging tests that we use in medicine to help identify the health of your blood vessels and your arteries and in no particular order.
The first is a crowded ultrasound. This is something that’s this easy screening test noninvasive. Use an ultrasound over your carotid artery to see if there’s plaque thickening of the wall and any blockages, and that can be very helpful in determining your risk. And it’s an easy thing to, and it can be done in an outpatient setting in a non-invasive, painless way. The next thing is what we call a CT coronary angiogram, which is specialized test that uses iodine dye into the vein. That helps look at your arteries while you’re getting image with a CT scanner, it detects blockages and narrowing the arteries. It can be very helpful. It’s obviously more invasive than an ultrasound, but you get a little bit of radiation exposure and there’s contrast ice, so there is some risk, but very low. The next is what we’ll call a CT coronary calcium score, CCAC.
And this is just measuring calcium in the walls of the arteries. Now it could be old plaque, calcified plaque, stable plaque. You don’t know if there’s vulnerable plaque, but it gives you a rough idea if you’ve had heart disease and if it’s there at all, it’s not invasive. It doesn’t require any dyes or any other exams that a CT scan. It does give you a little bit of exposure to radiation less than a CT angiogram, but it does not measure soft plaque. The gold standard, I believe today in 2024 is something called an AI enabled coronary CT angiogram. And the company that does this work is called clearly and it’s redefining cardiovascular care by helping doctors identify at-risk patients that provide the most effective preventive and precision healthcare and heart care. I had a patient, for example, with a 63-year-old man who had horrible cholesterol numbers, but he was otherwise healthy.
He exercised, he ate well, he didn’t smoke, he didn’t drink, he had normal blood pressure, no diabetes. I’m thinking God, based on his numbers, he had small particles. He had high lip approach A and high B, and it was like, I thought it was going to be a disaster. And we did his CT angiogram with the AI interpretation and his arteries were perfectly clean. So what that taught me was that you can’t just rely on the blood test. Those are risk factors. They’re not the actual disease, right? It’s like pointing something but not the thing itself. So it points to potential risk if you have small particles, if you have all the things we’ve just been talking about. But it actually doesn’t tell you if you have the actual disease, which is clogged up arteries and plaque in your arteries and soft plaque. And so this is the first test that allows us to do that.
We found, for example, in his case, he didn’t need statins, he didn’t need any drugs, he didn’t need any treatment. He was fine and he was probably not going to get any issues. He was already in the mid sixties and by then you usually have plaque. I think it was really an eyeopener for me. This is a company clearly health that uses FDA cleared machine using learning algorithms for non-invasive analysis of plaque and stenosis before the symptoms occur. So I that you should never prescribe any drug or treatment if you have someone who’s got risk factors without knowing this information. It’s kind of like flying blind. And what it looks at is a 3D model of your coronary arteries and it looks at where the blockages are. And in kind of plaque you have, is it noncalcified soft plaque we call low density noncalcified soft plaque.
This is dangerous. This is high risk. This is likely to rupture. So this is not picked up on any other kind of imaging. It also looks at noncalcified plaque. That may be scar tissue. It also looks at calcified plaque less likely to rupture. Now this approach is grounded in a lot of science. So over 10 million images, 40,000 people over 15 years in multicenter landmark clinical trials. And it shows that it has accuracy that’s better than the current clinical gold standard, which is an angiogram, even like one you do invasively. It reduces lots of costly and invasive diagnostic procedures and it’s reduced the need for invasive coronary angiograms by 86%, meaning where you’d have to stick a catheter up the groin. So really important. And it also looks at the phenotyping of the arteries, meaning you look vessel by vessel, how each vessel is, whether it’s a right or left coronary artery, left inter descending, right, circumflex all the different arteries.
You get this basically staging system. It’s based on all this AI data that is based on your plaque volume and the degree of stenosis and the quality of the plaque, and basically gives you a sense of where you’re at, zero to three. If you’re a three, you’re bad, zero, you’re great. So basically can help you look at treatment over time. And I’ve had patients who’ve reversed plaque based on using this data and aggressive management of the risk factors. So it allows you to create personalized diagnosis and treatment and it’s really amazing. So I think it’s revolutionized cardiology. There are a number of other tests we’ve talked about that are important, getting a full metabolic assessment before you decide on any treatment. We’ve already mentioned a lot of these, the lipoprotein fractionation, A OB, lipoprotein A, the clearly heart scan. Those are sort of bare minimum.
But we also want to look at inflammatory assessment with CRP and myop oxidase, L-P-P-L-A, we’ve talked about this. Look at oxidative stress measures. Look at metabolic biomarkers like insulin, glucose, A1C, vitamin D levels, uric acid, every kidney function, urine protein levels, sex hormones, magnesium levels, important cardiovascular health, Omega-3 fat levels, cholesterol balance testing, looking at absorption or production of cholesterol from Boston, heart diagnostics, choral ultrasound. All this is to say that we need a comprehensive picture. Just relying on LDL alone is really outdated. It’s bad medicine and we should not be doing it. We need a full picture to know what’s going on to manage your cardiovascular risk. So what do you do? How do we treat this? What do we do? Well, everybody’s different. And this is the whole point of this conversation is that it’s about personalized medicine. It’s personalized therapy based on understanding your biomarkers, your risk factors, your genetics, your scans, and everybody needs to be treated differently.
For example, some people, like I said, respond to a ketogenic diet and improve all the cardiovascular biomarkers like people who are diabetic often do, or people who are thin and fit, they don’t do so great on high saturated fat diets. They’re lean mass hyper responders. So it’s about personalizing things. The other thing is you want to focus on fixing insulin resistance. This is the biggest driver of cardiovascular disease. Like I said, two thirds of people who walk in the emergency room with a heart attack have this at least. And I think we’ve talked a lot about how to address insulin resistance and blood sugar issues. On the podcast. I’ve written many books about it, the Blood Sugar Solution, the 10 Day Detox Diet and many others. But you want to track your numbers. So you want to do your test, you want to make the changes, you want to follow it every three to six months to see what’s going on.
And you can do that with function health. It allows you the ability to actually make changes to your life and then see what happens as a result. There’s a number of foods that you want to get rid of, things that we just know are not good for you that are going to promote heart disease. And this applies to everybody and is I think universal regardless of age, race, or your risk of heart disease. First, ultra processed food, which is really science projects made by the food industry to kind of addict you and are deconstructed things from raw materials that bear no resembles to the original structure or form or molecular shape. And so this creates all kinds of weird signals in the body and it’s essentially all the stuff we are eating in America. It’s 60% of our diet. It’s 67% of kids’ diet. For every 10% of this food you eat, your risk of death goes up by 14%.
So it’s all the packaged, processed foods, pretty much everything on the grocery store shelves except for fruit, vegetables and the dairy products, eggs and the animal products. So essentially it’s stay out of the middle aisle, you rid of all the lasagna, pizza, ravioli, mac and cheese and chocolates. It looks like food, but it ain’t food. The next is trans fat, hydrogenate fat. This is in lots of things shortening margarine. It’s supposed to be out of the food supply, but it’s still there. Just look for the word hydrogenated. Never eat it. Sugar starts and sweeteners. Look, everybody likes sugar. We all like sugar. We’re programmed like sugar, a little bit fine here and there, but not in the pharmacologic doses. Were having it. So get rid of all the refined flour, sugar, all the different kinds of sugar, high fructose corn syrup, artificial sweeteners, cane juice, whatever you call it, brown rice syrup, it’s still sugar.
You want to dramatically reduce this a little bit. Occasionally is fine, but it should not be in your diet on a daily basis. Sugar sweetened beverages for sure don’t eat. Those are biggest drivers of insulin resistance. Also, fruit juice, although it has some minocin, maybe a little fiber generally is bad news. You wouldn’t eat 10 apples, but you could drink 10 apples and there’s none of the fiber or the matrix there that slows the absorption. So you want to stay away from that. Also, non-dairy creamers bad for you. They’re hydrogen oils. Usually they make them smooth and thick, but they’re really bad for you make goods. Of course, they occasionally want something that’s fun, but be careful with that stuff. It’s dangerous. Fried foods, definitely an occasional French fry’s not going to kill you, but it’s basically the daily or weekly habit of eating fried foods that drives up a lot of inflammatory products.
Dairy products can be okay, but I think you want to make sure you’re eating more sheep and goat and not factory farmed cows or other products. Fast food, I don’t have to say that’s bad. You all know it. I think there’s like 30 ingredients in a chicken nugget and only one of ’em is chicken. Who knows what the rest are. Refined oils definitely not a good idea for most people. All these soybean oils, sunflower canola, corn oil, saffer oil, grape seed oil, peanut oil. And this is, again, this is controversial and I think there are many people have different opinions than this, but if you look at the data, there’s a systematic review and meta-analysis of randomized controlled trials. They use a technique called Mendelian randomization, which is a much more accurate way of analyzing data and determining the real risk. And they found that higher levels of omega sixes in your diet had a higher risk of heart attacks.
Large artery strokes, higher blood sugar, higher cholesterol, LDL higher HDL, decreased triglycerides and a lower total cholesterol. So in this study, they found that people who had higher intakes of omega sixes had a higher risk of cardiovascular events, heart attacks, strokes, they had higher fasting blood glucose, they had worse cholesterol profiles even though potentially LDL went down. There were other things that kind of went off. And it may indicate that there are lots of small dense LDL particles, but it also oxidizes the LDL. So you get higher levels of arachidonic acid, lots of prostaglandins, leukotrienes. These are cytokines that drive up inflammation that cause oxidation. And as we talked about, it’s the oxidizer or rancid fat. That’s the issue. Saturated fat is a more complicated story. For those who are sensitive and had genetic and cardiovascular risk factors. It may be an issue. See what happens.
Try it. See what you can find when you repeat your test, but check. So sometimes butter and fatty meats are fine, but generally I would say you want a test, not guess. What should you be eating? Well, you want a diet that’s low glycemic, and that means lots of low glycemic, non-starchy veggies, all the colorful veggies. You want lots of low glycemic, non-starchy fruit. You have blueberries, blackberries, raspberries. You want to have starchy veggies, but not huge amounts, right? Sweet potatoes, yams, parsnips, butternut squash, acorn beet, those are fine. They’re not going to kill you, but you don’t want to be like eating the majority of your diet as that whole grains can be fine, but you don’t want to be eating a ton of grains if you’re insulin resistant. Beans also can be fine. Stick with the lower glycemic beans, red lentils, green lentils, black lentils are fine.
But again, it depends on you and what your metabolism is. And some people, for example, insulin resistance have trouble with that. Focus on color. Phytochemical richness, a lot of diversity. Focus on anti-inflammatory spices, turmeric, oregano, rosemary cloves and so forth. Protein is also important. You want to make sure you have high quality protein, grass-fed or generally raised bison, elk, venison, pasture raised eggs, past raised poultry, non GMO, soy, Tempe, tofu, all that’s fine. Grass finished beef is also fine. Ideally regenerative. And I like force of nature, which is a great company and get all the regenerative meat you want. Omega-3 is really important for your heart. So you want to have small little fish. Herring, ancho. Macro sardines, which contain E-P-A-D-H-A salmon can be okay, but you want small salmon. Vital choice makes good varieties. Lots of nuts and seeds, walnuts, flax seeds, chia seeds, hemp seeds, all have good omega threes.
But plant-based kind, which you want to make sure you’re also getting the animal-based kind probiotics are great for your gut. Sheep and goat yogurt, kimchi, sauerkraut, all the microbiome stuff is really important for regulating your blood sugar. And then blood sugar regulating foods really important. They’re foods that actually helps you control your blood sugar. Bitter melon, which is a Chinese food, I like it. People don’t like it. It’s kind of bitter. It’s what they call it, bitter melon, but it actually has effects on your blood sugar, Fenig, Greek spice, ginger, cinnamon, turmeric, all help. Fat’s really important. You need good fats. Olive oil, avocados, nuts and seeds, macadamia nuts, all the nuts, cashews, almonds, pecans, walnuts, hazelnuts, Brazil nuts, pistachios, all the seeds, chia, hemp, flax, pumpkin, sesame, all important. And what they found in a big European study, randomized controlled trial of people who had olive oil and or nuts, handful of nuts compared to a low fat diet.
They all did better with the olive oil and the nuts. So it is shown to reduce the risk of heart attacks as much, for example, as statins. So saturated fat, as I mentioned, can be okay in the absence of starch and sugar like coconut oil, ghee, grassfed butter. But if you’re a hyper responder like me, you probably want to stay away from it. What else can you do to lower your blood sugar and help improve everything? Well, I think first thing you want to do is to figure out when you’re eating what, right? So you want protein and fat and veggies before carbs. That slows the absorption, blunts the effect. So if you have your sweet potato at the end of your meal versus at the beginning, you’re going to do better. Start the day with protein and fat, right? It can be a protein shake, it can be avocados and eggs and olive oil and tomatoes.
But stick it away from the carbs and sugar for breakfast. Also, don’t eat bread with every meal. Alcohol, refined carbs before you eat the protein, veggies, or fat, as I mentioned, when you go out to dinner, they know is going to make you eat more. So they give you the wine and the bread basket and the drinks at the beginning. Eat your veggies and your protein and fat first. And also when you eat, you eat that way, you’re going to have a better blood sugar. Certain other things can help. Time restricted eating, leaving 12 hours between dinner and breakfast, maybe even 14, avoiding three hours before bed. Also important, it improves blood sugar control, improves insulin sensitivity, helps your A1C come down your insulin, calm down, your glucose come down in a five week randomized trial time-restricted eating. Basically they ate between 8:00 AM and 2:00 PM in pre-diabetic men and improved their insulin sensitivity.
Their beta cells, which make insulin, their blood pressure, oxidative stress, all got better. This was in cell metabolism and the results were not just due to weight loss, actually it was controlled feeding. So the food intake was matched with controls. So it’s really talked about the benefits of eating within your circadian rhythm. And insulin sensitivity is typically better earlier in the day. And this may even help your cholesterol too. So studies have shown that in frontiers and current atherosclerosis reports that you get improved in triglycerides and LDL. It’s kind of variable. What about lifestyle? Well, lifestyle plays a huge role. Obviously exercise is the best medicine. So we know that exercise increases. HDL improves the beneficial functions of HDL improves the large fluffy types of HDL Subfractions. It actually helps to have the HL work better and transport cholesterol better. So it improves HDL in every way and there’s no good drugs that do that.
Also, walking, you can just start with walking. I mean, if you do a thousand steps a day, your all cause mortality goes down by 15%. If you do 4,000 steps a day, your cardiovascular mortality goes down by 16%. If you do 10,000 steps a day, your cardiovascular mortality goes down by 77%. So 10,000, you probably reached the limit, but that’s an easy thing to do. Aerobic exercise also, as I mentioned, increases HDL lowers triglycerides, improves the ratio and basically about 150 minutes a week of moderate intensity to figure exercise. Basically 30 minutes five times a week. Not that hard. Just take a hard brisk walk. And then there’s HIT training, which also works, which is high intensity interval training, maybe one to two times a week with short bursts of really intense activity like running with walking. So you can do 30 minutes, sorry, 30 seconds to 45 seconds of a sprint or all out effort on a treadmill or a bike, and then one minute of slow walking, jogging, and then do it again.
And you do that for 30 minutes and you do that a couple times a week and you’ll see improvements overall in your cardiovascular profile with lower triglycerides. Higher HDL improved on LDL, non HDL cholesterol too. Strength training also works two to three days a week, helps a lot. And it can be something that improves your overall cholesterol profile. As I mentioned, you can use squats, lunges, pushups, bend pressures, biceps, tricep, dips, shoulder press, leg press, all the heavy lifting makes a big difference. Obviously don’t smoke. Smoking is really bad for your cholesterol and for your heart risk. People who smokers have lower HDL, they have higher LDL and of course dramatically increased their risk of heart attacks and e-cigarettes are no better. Stress, stress, big factor. There’s been quite a few studies on this actually. Stress increases. Sympathetic nervous system tone that increases platelet stickiness because you’re running from a tiger, you cut yourself, you want to be able to clot your blood.
So you have increased platelet stickiness, you get increased oxidative stress, you have more insulin resistance. When you increase cortisol, you get more likely to have diabetes and so forth. So it leads to damage to your blood vessels, to restriction of your blood vessels, to blood clots or heart attacks. We all know that stress can kill people. So meditation, this is an NIH funded to study in circulation, took 201 African-American subjects who were randomized to either TM or AL meditation or a health education group who had heart disease. And they found that over five years the meditation group had a 48% reduction in cardiovascular events, almost a 50% reduction in heart attack, stroke, and mortality than the control group. That’s amazing just by sitting on your butt, meditating for 20 minutes a day. And those practicing regularly had a 66% reduced risk. Some people didn’t do it every day.
And they also know to reduce blood pressure and reduce psychological stress, and it basically helps enhance all medical treatments. What about alcohol? It’s good for your heart, right? Sorry. Nope, we thought it was, but it turns out it’s not. Ideally none. No more than one drink a few times a week at max. But the studies show that alcohol consumption is heart healthy are based on these population studies that have something called healthy user bias. Meaning the people who drank tend to have other healthful habits. They drank red wine. The bottle was good for them, they exercised more, they ate better, so forth. No amount of alcohol is protected against heart disease risk. This is a 2022 study of 370,000 people from the UK Biobank published in jama. No amount of alcohol was protected and all levels were associated with increased risk of heart disease. So one drink a day increases the risk of hypertension by 30% and heart disease by 70%, even in moderate drinkers, it can increase.
For every one drink a day increase, you get a 70% increase in high blood pressure, 80% risk of heart disease. If you drink a lot like 25 drinks a week, your risk of heart disease goes up by 470%. And these Mendelian randomization to control for confounding things. So really important to take note of this, alcohol affects your cholesterol badly, basically lowers your HDL worsens insulin resistance makes you have more small particles, increases triglycerides, causes fatty liver, all this stuff you don’t want. So it increases high blood pressure, heart failure, atrial fib, strokes, I mean it’s just bad news. So if you had a drink a day, which doesn’t seem like a lot, it increased your risk of stroke by 14% of heart failure by 9% of fatal high blood pressure disease by 24% and on and on. So I think the bottom line is if you want to be healthy, drinking’s not part of that plan.
What about supplements? Supplements can be helpful and I use them as part of my overall care. Omega fats fiber. I use plant sterile. Sometimes I use a product called arterial cell, HP that helps to affect the quality of the inflammation, the artery vitamin D, sometimes you can use probiotics for help. Blood sugar support like akkermansia, berberine, lipoic acid, various nutrients, B vitamins, all help with blood sugar regulation and insulin resistance and cardiac health. So the key is you want to get tested properly, you want to implement the changes that we talked about. You want to recheck and see what’s going on every three to six months, which you can do through function health. You want to get advanced testing, the clearly scan done as a baseline and then depending on what’s going on yearly, if you’re aggressively treating things or maybe every five years if you’re good or more.
And if you’re not getting better on the basic lifestyle things, and some people respond dramatically to lifestyle that people don’t, you might need to use medication. So if you have high A-O-E-A-O-B and triglyceride levels and lots of lipid particles and you have a genetic disease, sort of a cocktail of genes that makes you more likely to have cholesterol problems, you might want to look at some of these new therapies. Statins can be helpful for some select patients. But again, I think they’re overused and over promising and under delivering. As we talked about some of the new therapies like PCSK nine inhibitors, they target cholesterol related pathways that could really improve things. And I think I’m a bit bullish on that for now. Cholesterol blockers like Zia can be helpful. There are new drugs coming down the market called CTP drugs, which may be helpful. We still don’t know about side effects, so you have to look at the whole picture, but it’s really about personalization.
It’s about finding the right approach for you diagnostically treatment wise. And most of the time people I think don’t need medication, but sometimes they do. So I think if we look at what’s going on in this country, we’re seeing an epidemic of heart disease. We need to get serious about this and it’s really about improving our overall metabolic health. So that was a long one. I’m sorry guys, but it’s the number one killer. I had to go through this. You’re getting all kinds of information, probably not the most clear information. I just wanted to give you a lowdown on what the science was about, how to assess and test for your cardiovascular risk and what to do about it if you find you have risk. So that’s really it for today’s Know your Numbers episode. I hope this laid the groundwork for understanding your cardiovascular risk and what you can do for prevention treatment that will helpfully decrease your risk of having a cardiovascular event so you can live a long healthy life.
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This podcast is separate from my clinical practice at the UltraWellness Center, my work at Cleveland Clinic and Function Health, where I’m the Chief medical Officer. This podcast represents my opinions and my guest opinions. Neither myself nor the podcast endorses the views or statements of my guests. This podcast is for educational purposes only. It’s not a substitute for professional care by a doctor or other qualified medical professional. This podcast is provided on the understanding that it does not constitute medical or other professional advice or services. If you’re looking for help in your journey, seek out a qualified medical practitioner. Now, if you’re looking for a functional medicine practitioner, you can visit ifm.org and search their find a practitioner database. It’s important that you have someone in your corner who is trained, who’s a licensed healthcare practitioner, and can help you make changes, especially when it comes to your health. Keeping this podcast free is part of my mission to bring practical ways of improving health to the general public. And in keeping with that theme, I’d like to express the gratitude to those sponsors that made today’s podcast possible.