Giovanni Campanile – The heart of anti aging

Introduction:

Well, thank you everybody for coming. My name is Giovanni Campanile. I’m a cardiologist and this is my partner Scott Berliner, who’s a compound pharmacist. And we run a practice called CorAeon, which is a heart centered anti aging practice. Scott’s an expert in supplements and hormones and in nutrition. So we work together to really do what’s best for the patient in a very practical way. This talk is going to be a an overview of lipidology cardiology in the sense of coronary artery disease because when we talk about heart disease we’re talking about coronary artery disease and atherosclerosis. So I want to show you what that means. You know, how we evaluate it and how we treat it.

Let me add that we started out with 180 slides. We actually could be doing this for a week or more, and maybe it’ll evolve into it. We touch on every aspect of cardiovascular health, which if you improve every aspect of cardiovascular health, you’re going to live longer and you’re going to live better. And our focus is on health span, you know, shortening the sick days at the end of your life and extending the quality days of the rest of your life.

So Corian means heart age in Latin. And that’s because we feel that the heart, you know as a cardiologist is the Canary in the in the mine, in the coal mine. If the heart goes, then everything else goes. And luckily, the same risk factors for heart disease apply to cancer and arthritis and other other entities that affect health span.

We have a big focus on inflammation, as everybody here probably already is focused on. But I think we also now we’re looking at mitochondrial dysfunction as another contributor to aging and to cardiovascular health.

So what’s happened over the years is that life expectancy is dramatically increased and this has led to what we what we call age-related diseases and and the the price we pay for living longer are these age-related diseases. So we need to focus more on prevention and reversal of disease. This is a new concept. I was the Director of the reversal of heart disease program with Dean Ornish program for the East Coast and we have good data showing that we can reverse disease and we have patients that we follow regularly that we see reversal of disease.

Risk Factors for Heart Disease:

So cardiovascular disease is by far the biggest cause of death worldwide. About 20 million people die of heart attacks in the Western world. And the reason is that there are a lot of risk factors for heart disease and and elevated lipids and we all know about the traditional risk factors but it’s more the non traditional risk factors that are maybe as important or more important. For instance stress, low estrogen levels, we see this in our practice, toxins in the environment, all these things lead to these high lipid levels that we have in the western world. So the way we get lipids in our body, the the abnormality is that our lipid levels are way too high. And if you take anything away from this talk, remember APOB, APOA, one capital A1, which is a good thing and APO small lipoprotein small A, which is a bad thing. Those three factors are the main factors we focus in on. And the way we get this elevated lipids in our system is either through the liver producing it, the endogenous pathway, exogenous pathways is what we eat or also what comes from the liver and then recirculates through the gut. And then there’s a reverse cholesterol transport system and that’s the capital A1, which I’ll show you how meaningful that is. So again, Apob, there’s four big risk factors. APO lipoprotein B is the most causative factor that we look at in the lipoprotein molecules that we measure in the blood. And there’s four big factors that causes the heart disease and that’s APO, BS #1, insulin resistance, hypertension, smoking and all the data. You know, a lot of people sometimes question the cholesterol hypothesis, but all the data really points in One Direction. The epidemiological data, the clinical trials and more importantly the Mendelian randomization trials, those are newer trials that really point to the fact that these, this factor, this APOB factor is is not only a marker, a biomarker, but it’s also causative. So we really need to reduce it LP little A, which is confusing because LP big A is A is a good thing, the higher the better. LP little A is a genetic factor and it causes atherosclerosis, blood clots and calcification of the aortic valve. So it’s a very big factor when we look at these biomarkers.

The LP little A particles are very atherogenic, so it increases a person’s risk dramatically and that increases our aggressiveness in treating the person when we see that. So this is schematic of an artery. So our normal vessel, you can see on the inside where the white is, there’s a monolayer of cells called endothelial cells and the artery looks normal. And then as APO B starts accumulating in the vessel wall, you go down and you get diffuse intimal thickening deposition and then foamy streak formation. Now what’s interesting about this is that the foamy streak form A, you know, the atherosclerosis starts in utero and then progresses over 20 years in the Vietnam War. They did autopsy studies on unfortunate GIS in American and they already had all of them had some fatty streaking at age 18 to 20. Well, the Vietnamese boys who had a different lifestyle had nothing. And then this, this process progresses over the next 40 years. Where you see it on this slide, the where it says thrombosis. Thrombosis is when a plaque becomes complex, ruptures and becomes in a blood clot forms and you get a heart attack. And that process takes another 40 years because the average age for a heart attack is about age 65. So this is a lifelong process and the longer we have APOB and problems in the blood, the longer the more risk we have. But this also goes true for the longer we take care of this. The longer we we bring down the APOB, the better it is for the patient.

Evaluating and Measuring Risk:

So Falk is a major researcher on atherosclerosis and he says atherosclerosis is a multifocal, smoldering, immuno inflammatory disease of medium sized and large arteries fueled by lipids. So you need the lipids and the inflammation to make this happen. This is an unfortunate person that’s a pathology slide. The white part is a is a heart attack and this patient didn’t survive this heart attack. And one of the key things to understand is that up to 50% of the first sign of a heart attack in men is cardiac 7 death and it’s higher in women. It’s up to 69% in studies in women. So this is something we need to prevent because it can be a lethal disease for the first time we know anything about it.

The important part of this is that the vascular endothelium is very important. The vascular and ethelium we we know that certain foods like L arginine rich foods increase nitric oxide and Scott and I use this quite therapeutically. When we tell patients to eat things like beets and arugula and almonds, these are very high in L arginine and we see the the nitric oxide increase and this then goes into the smooth muscle of the arteries to make them more flexible. If your artery is not flexible, then it becomes diseased and we measure things like ADMA and SDMA which are biomarkers of this process of of the endothelial dysfunction. So some of the nitric oxide supplements, we’re used to using arginine for many, many years. I’ve always had some questions about using high doses of arginine because of the issue around viral replication. So we’ve been looking at other things like citrulline lately we’ve been using potassium nitrate also for sugar sensitive patients. There are beet crystals that are around that will do the same contribution to increase nitric oxide without the sugar. This shows on the left side the normal tensive artery and on the right side the hypertensive, and these nitric oxide supplements can increase the flexibility of the arteries and the endothelial lining. So we used to think that the first thing that happens is endothelial dysfunction, but we now know there’s something even before the endothelial dysfunction. But this is more information. This shows the arginine and arginines that were converts into onethene then into citrulline and then eventually it gets into the system is nitric oxide. So having increases in your arugula rich foods is, in our world the first thing that we should do, because we always focus on diet first.

Other biomarkers that we look at are the new One of the newer biomarkers is TMAO or trimethylamine and oxide and we know this comes from a diet. You know, if you consume, if one consumes too much dairy, red meat and choline in general, you get increases of carnitine, betane, choline and then this through a process in the liver increases this substance called TMAO, which is a independent risk factor for coronary disease. And you know, we can measure this as a biomarker.

I found some studies that Lactobacillus remnosis GG, lowest TMAO and also having optimal vitamin D levels can lower TMAO For many of you that are using adrenal support supplements, Many of them contain phosphatidylcholine and phosphatidylcholine will raise TMAO. Whether that increase from phosphatidylcholine is deleterious or not, I don’t think we know that yet because TMAO is definitely linked as a risk factor. So this is the newer information we have about the inner lining of the arteries. It’s called the glycocalyx. The glycocalyx is a hairy like structure. You can only really see it on electron microscopy and it’s very, very important to protect the endothelial layer of the cells. It’s a it’s a mechanical sensing cells. It’s selective permeability and it and it protects the spaces between the cells. So you probably all have heard of leaky gut. There’s also leaky arteries and this is how a leaky artery begins is by the glycocalyx becoming disruptive. So we have newer ways of checking glycocalyx. There’s a a mechanism called Glyco check. It’s a it’s a company that makes this machine and by looking underneath the tongue with sublingual microscopy, we can actually see the flow of red blood cells and the the rheology or the flow of these red cells should be uniform And if they get disrupted, if there’s a disrupted glycocalyx, we can see this and then treatments that we have to treat this, we can see it get better or not get better. So these are some of the products that are on the market. The glycocalyx Pro has been renamed to regenovasc. I believe they’re basically chondroitin, glucosamine and then Alteracel is Ramnam sulfate. We’re not sure exactly how much Alteracel it takes to increase or improve the glycocalyx. But many of our patients also have arthritis. So we use substances like chondroitin and glucosamine sulfate that are combined in certain supplements that work not only for joints but also work for the arteries. So this is a what’s called a Neiman pic receptor. We all have some of this, some of us more than others. It’s a it’s a receptor that the the top part of this picture, it resides inside the lumen of your gut and the RET and the other inside the lumen of the epithelial cells of the gut. And this, depending on how many of these you have, will dictate how much you absorb cholesterol and saturated fats. So this is maybe why some people respond better to low saturated fat diets than others because if you have more of these neeman pic receptors, you’re going to hang on to more of the saturated fat. This may go back to a time when you know it was protected for starvation. You know we have great genes for starvation. We don’t have great genes for overabundance and let that may be one of the reasons why in the western world we have so much heart disease. So you may have heard of these newer drugs for cholesterol called PCSK 9 inhibitors. The way this was discovered, which is fascinating. Helen Hobbs in the early 2000s discovered a group of people that had a mutation in the PCSK 9 gene with less PCSK 9. What PCSK 9 does is it it attaches itself to the LDL receptor. And So what happens is you don’t eliminate LDL or bad cholesterol and so it accumulates in your body. So the longer this LDL stays in your body, the worse it is for your risk for heart disease. So in this group of people that had this good genetic aberration, these patients had normally we see LDLS of greater than 100 in an average American, but in these patients it’s 20 very low and they had not one of them had any heart disease and also not one of them had any other disease that you may some people talk about low LDL cholesterol associated with some other heart disease, but there was no association like cancer, diabetes and dementia. And there’s a corollary group of people that had hyper functioning gene and these people have what we call familial hyperlipidemia, very high atherosclerosis risk, a very high risk of heart attacks and need for bypass surgery and this sort of thing. So the the new drugs which are very effective are called PCSK 9 inhibitors, it’s an antibody to the PCSK 9 molecule. So the LDL receptors actually increase in quantity and you get much better elimination of cholesterol from the body or LDL cholesterol. It’s a real game changer in our world of cardiovascular health. Unfortunately, the insurance companies are very resistant about paying for it, and of course you have to fail on a statin or have other risk factors before they’ll approve it. But super effective, we’ve had patients that we’ve put on and have shown reversal of disease with these drugs. So it’s a very effective drug. Now newer technology that’s coming out, there’s a mRNA technology, which is an infusion of a a PCs canine inhibitor that you get infused twice a year. So you get 2 infusions and your LDL cholesterol stays down very low for the whole year. And then even newer technology which has been shown in animals to be very effective is CRISPR technology where you get one, one treatment for your life and your LDL cholesterol never comes back. But we we you know that’s not FDA approved yet, but it’s looks very promising. They did an initial CRISPR with sickle cell anemia patients and it actually cured it. So the future looks great for CRISPR. Yeah. What will happen for heart patients is that if you have a heart attack or if you have bypass surgery during your hospitalization, you’ll get this one CRISPR infusion. And then the rest of your life, your your cholesterol will always be low. If it’s safe, you know what could go wrong with genetic editing, right? So, you know, right now we, you know, we’re integrative. So we like to use lifestyle, we like to use supplements, but we do use medicines or and statins when they’re effective. There’s you know, statins have a really bad name if you Google them or especially in the integrated world and they do have side effects, but they’re not as bad as some people make them out to be. About 7% of patients on statins will have problems with myopathy or muscle aches and then you can get transaminase elevations, the we call them liver function tests, but actually what they are AST and ALT, they’re really a measure of inflammation in the liver. So they can’t cause inflammation in the liver and then they can cause in my mind even more importantly elevation of blood sugar and in about 0.4% of patients you get actual type 2 diabetes. So you have to be very careful when you give statins to patients. But in the most for most patients they work well. There’s now data from children that were put on statins. They have familiar hyperlipidemia age 6 and now we have 35 year data, very low side effect or risk profile. But you know, we try not to use these medicines if we can get away with it. But in patients that have serious bulky disease in places in their arteries that can actually kill them, you know, we do, we do use them. Just like every drug, it’s always about the benefit versus the risk. What we know about statins is there’s over 500 positive studies on statins, so I think a lot of the stigma should really go away, especially among us, among functional people. It’s not that we don’t try diet first, exercise, all of the above. But if it’s familial and it’s genetic, you know, sometimes the none of the natural supplements are as potent as these high intensity statins. And we talk about effects on the mitochondria, but there’s no real convincing data showing that it actually affects the mitochondria in a bad way. Although we use things like coenzyme Q10 at high dosages on all the patients that we end up putting on statins and. And then the other issue is that, you know, cholesterol is essential for life. You can’t live without cholesterol. Cholesterol is important for the cell membrane, for steroid hormone production, for our brains. But there’s no, there’s no big correlation between what we measure in the blood and in those areas where cholesterol is vitally needed. So that’s somewhat of a myth, you know, because a small, only a very small percentage of the total body cholesterol is in the blood. So even if we were to get it to zero, it wouldn’t affect those other areas because those other areas can make their own cholesterol, Our cell walls can make them, our steroid hormones can make them, our brains can make them. So you know, again, APO bees or LDL cholesterol, the typical average in an American is about 100 In. In babies who are producing an enormous amount of brain cholesterol, it’s it’s 20. And in modern hunter gatherer societies where they have a great lifestyle, they don’t have the stress that we have in Western countries also in that same range. And then there’s something called statin play atrophy which is good benefits of statins like they’re anti-inflammatory, they help the endothelium, they they reduce levels of C reactive protein because the inflammation. So, and some people feel that one of this is a more important reason why these medicines are good for your risk of heart attacks than the lowering of cholesterol itself. So everybody probably here knows about red yeast rice contains tiny bits of lovastatin or the prescription was mevacor originally and it’s safe. But sorry, but when recommending red yeast rice you have to be very careful. There is a contaminant in it called citronin. Most of the companies that I work with and that you probably work with test for citronin and either purify it and get rid of it or they don’t use it. So the, yeah, so in all of the studies and this is a great reason for using one of the medical grade companies that we’re used to working with, only one out of 37 did not have citronin in it. So the range is from 200 to 4800 milligrams a day. We tend to not go higher than 3600 milligrams, usually split the dose. You know with statins, you take them once at night. But with these things, since you make roughly 60% of your cholesterol at night and 40% during the day, I usually split the dose morning and evening. However, they’re not nearly as potent as any of the statins. So there’s a lot of reasons why we still using red yeast rice. A lot of it has to do with people that still hold that statin stigma. That or their risk is very low, but not low enough that we’re not willing to leave it alone. And we do have several patients who have actually done quite well on red yeast rice. You know, you’ll see when we go through the particles and the different things that we measure. So we do have biomarkers to be able to judge. Plus there’s the Drucebo effect, the placebo, the nocebo. I don’t know what other Ebos we’re going to have, but there’ll be more. So as Giovanni mentioned, we do treat almost every patient get some kind of Co Q10 Ubiquinol is roughly 3 times as well absorbed as ubiquinone. And the more recent studies actually show that ubiquinol and the ribose, one of the slides that we eliminated the two together, actually reduced the symptoms of heart failure and actually preserved an increased ejection fraction. This happens to be my blood work and what’s missing before March of 2022 was I was on red yeast rice at 3600 milligrams a day. It lowered my cholesterol from 266 and you could see it went down to 192. But if you look at the HDL levels, the LDL levels, it didn’t touch any of those adequately. In June of 2022 is when I actually went on a statin three days a week by the way, not a lot. And you could see that my LDL went from one O 7 to 53. More important, my APOB went from 105 down to 62. Now the only thing that really didn’t change was my CRP. I’m going to talk about this later, but what I introduced at that time, since my CRP was always way too high, was SPMS, Specialized Pro resolving mediators. And then you could see in the August lab that my CRP came down. Now my other levels went up, but what I didn’t tell you was I had sciatica for four months leading up to the August blood work and the lack of exercise, cardiovascular exercise has probably had a huge impact. You could see my particle number went slowly from 826. We like it under 1000 up to 14189. But if you look back, you’ll see that the red yeast rice really didn’t have a huge impact on that. So I think if your risk is high enough, I’m not sure red yeast rice is the way to go. We also look at bergamot, which is a very interesting product. We think that the bergamot fruit and its constituents actually lowered cholesterol by inhibiting the cholesterol synthesis and absorption. So we do use quite a bit of it. We actually use the Sicilian version because that’s where Bergamot is the best, not to mention their Sicilian. We wrote a book. My wife is a physician and we wrote a book together about the Mediterranean diet in Sicily from Sicily called the Sicilian Secret Diet Plan.

Advanced Testing and AI in Cardiology

So this is a picture of Pearl Harbor and and the reason why I show this picture is that you know if nothing was around the corner, if everything was stable and beautiful, we wouldn’t need to do any kind of testing. If if we had, if at Pearl Harbor, if they knew something was around the corner, you know, they would take all kinds of actions to prevent death and prevent destruction. And this is what we do in our world. We do testing with the idea of measuring what’s coming around the corner. This is why we do things like advanced lipid testing. And this is important because if you look at the slide, there’s about 10 to 50,000 heart attacks that are missed. Even these are patients that actually go to the emergency room with symptoms and they’re missed. So it’s, you know, heart attacks or heart disease can be very atypical in its presentation, especially in women. And so it’s missed frequently because of these. Atypical, if you come in with crushing chest pain and your EKG is abnormal, it’s obvious. But if you come in with just shortness of breath or you come in with abdominal pain or you come in with some some other issue, you know, it could be very difficult sometimes to make that diagnosis. You know, I had a patient that came in with severe wrist pain, and they were going to do an X-ray of his wrist because they thought he broke his wrist. But they were going to do an EKG on the patient next to him. And the technician made a mistake and did an EKG on this patient and he was having a heart attack. So it was, you know, so it’s going to be very atypical, the presentation. So what’s really fascinating, this is artificial intelligence electrocardiograms. And these are, there’s information in electrocardiograms that as cardiologists we can’t read. We can’t even see it. But if you feed these electrocardiograms into a database, the computer can figure things out that you know, we can’t figure out. You know, this is artificial intelligence. And what what they did here is they they put in Ekgs on patients that died at age 30, died at age 40, died at age 50 and then the EKG can be read by a computer and you can tell, you know, your biological age much better than any other biological age measure we have. So it’s a fascinating way. You know, we have the EKG is a measure of the electromagnetic field that’s coming out of our heart, like our electromagnetic field is now communicating with each other. So that that electromagnetic field is very powerful. This is another study looking at artificial intelligence and atrial fibrillation. Atrial fibrillation is a is an abnormal heartbeat from the top part of the heart and the the big risk with atrial fibrillation is can cause strokes. So you really want to know if someone’s going to develop atrial fibrillation and with artificial intelligence it can predict better than any other risk method we have of someone who’s going to develop atrial fibrillation in the near future. And this is very important because then we can start monitoring that patient and see when they actually develop atrial fibrillation and treat them appropriately. We’ll probably see a lot more of AI in medicine, and I hope that we do. It really is the future for us.

Personalizing CV Risk with Advanced Biomarkers

So the reason why we even use advanced lipid panels is because they’re more predictive of future events. You know, the old good and bad cholesterol is not as good as the newer markers we have. So we use there’s different types of these advanced lipid panels. There’s LabCorp, has NMR, then there’s Berkeley, and then there’s Cleveland. We tend to use Boston Heart because I trained up in Boston and I know the person who started the company and it’s a very high quality company, but any of these companies are good. But the reason again that we use this is because the prediction of the future is much better with these advanced markers. So this shows you, if you look at the top graphs of all ’cause mortality and myocardial infarction or heart attacks, APOB is much better than our other markers like LDL or non HDL cholesterol. So if you really want to assess someone’s risk, you really need to know some of these advanced markers. And then the other benefit of this is again, Boston Heart. It tells us where the cholesterol’s coming from. It tells us with certain markers if the cholesterol is being made from the liver or if it’s you’re being absorbed like I showed you earlier with those neeman pic receptors in the gut, are you hyper absorbing from the gut? And this is important because it tells you what you need to do, how you treat it. If someone is producing a lot of cholesterol, then you really need to affect the production of the cholesterol. If they’re absorbing a lot of cholesterol, then you need to affect the absorption. So this is how we personalize what we do with our with our patients and this is an example, production markers being elevated with this mostrol and lathosterol. And this is the other important thing about measuring these is that in a very, very small subset of patients that you put on a medicine, they actually stop producing cholesterol to in a major way like this. Monsterol is a good indicator of that. If the if someone, if you put someone on a statin on a medicine and their does mostral level goes down, you need to take them off then because that’s that those patients will develop dementia especially if they’re APO E 3, E 4. You know the E 4 gene is a very big factor with that. So if someone’s E4 their does mostral levels go down, then you really have to switch your therapy. And leathosterol is a measure of peripheral cholesterol production, like steroid hormones mostly. So we almost never see that happen, but it can’t happen. Another risk assessment is polygenic risk score. You know there’s we used to look at genes like 1 gene causing one disease. Now we’re looking at polygenic risk or analysis which is our hundreds and thousands of genes or or snips that congregate to increase one’s risk. So we can see with polygenic risk scores, this is not only for this is for CAD or coronary artery disease, but we we measure this for atrial fibrillation, for hyperlipidemia, for a APO lipoprotein, small A for a lot of different factors. The polygenic risk analysis is now becoming more and more part of the risk assessment and again if you see someone’s risk is high then you start monitoring them a little bit closer. And again this is the APO A1. You know before I mentioned the small A which is bad, this is the APO A1 capital A which is very good. And the things, if we see this low, then we recommend things like lifestyle change, you know, like exercise or decreasing carbohydrates in the diet and for every milligram increase in this APOA One, there’s a 26% reduction in CBD risk. So this is a major factor for CBD risk or CBD stands for cardiovascular disease risk reduction? It’s a very unique marker that Boston Heart gives us the ability to look at the activity, how good is the HDL? You know, we have patients with HDL of 100, but we don’t know just based on the number, how protective those HDLS are. So with Boston Heart providing this map, you could see the A1 particles being very large. We have a good feeling that the patient’s HDLS are going to be protective. Now, the other thing that’s important about this is that we used to think HDL cholesterol, the higher the better. That turns out not to be true. If your HDL cholesterol is above 80, it may not be. It may be dysfunctional and may cause disease and not protect you from disease. So we need to know that and this is, this is one of the ways to know that because if this A1 particle on the APOA one is nice and big and then it, then it is protective. And so this is you know, this is how to show you. You know one of the things we look at is the APOB, APOA one ratio and we divide APOB which is a bad thing B for bed and A1 and the lower that number the lower your risk. And so if you look at the very back column, that’s the highest risk, that’s patients that have a very high APOBA one ratio. And then if and and in the front the the lowest risk are the people that have the lowest ratio. And you know again this goes back to a time when you know it was an energy production genetic thing that protected us from starvation and many animals don’t have apobe. This is a somewhat of a unique thing for humans and and we know that it’s not only a biomarker but it’s causative. So it means that we need to get it down whatever way we can because it’s like any other risk factor, you know, like it can cause disease. Now another way we have of determining risk is endothelial function and we know that you know you’re the better your endothelial function the less risk you have and evaluating the endothelial function in addition to other risk factors can increase your risk prediction by greater than 25%, which is a major additional risk factor. So and then we know we can with this is actually the endopath system where we can measure endothelial function, give some treatments like exercise, diet, sauna or whatever treatment we think is appropriate and then remeasure the endothelial function and see if it’s improved. And that lowers your risk once the endothelial function is improved. And this is another and by the way this is a very practical thing we’re showing you here.

Carotid Interim Media Thickness (CIMT)

Scott and I had these slides up in with our patients as we go through we actually use all these tools to see our patients. This is what’s called CIMT, that’s carotid interim media thickness analysis and it’s very helpful because first of all it’s ultrasound, so you can do it over and over again. And secondly the atherosclerosis begins in this in these layers and you we can see very, early in patients that have the beginning of disease or if we’re treating someone we can see the disease get better or reverse and and we get a you know a a print out an arterial age because it’s normalized for patients of the same age. So we get an arterial age for the patient, which is very important. How patients don’t like it, Yeah, arterial age is usually higher when we first work with them. We’ve had many patients that we followed over time that we’ve seen the seen the CIMT come down, which is great. So that’s really proof that lifestyle, diet, exercise all really work. So diet and obesity is also very much associated with a lot of diseases as you all know this, but it’s very much associated with atherosclerosis and also associated with elevated insulin and insulin resistance, which is a major risk factor for coronary disease. And what we’re more interested in is not in the adipose tissue we see, we’re interested in this visceral adipose tissue, which is very highly inflammatory and this is the tissue that’s around the arteries, around the organs. And this is really what causes problems in terms of both heart disease risk and cancer risk. And we use, we have an in body 770, which is a very sophisticated way of looking at the body composition. And what we’re very interested in here is that top right panel where it says visceral fat area, that’s the amount of visceral fat the patient has. So we want to see that come down to more normal areas because we know that when that happens the risk goes down. And we also look at percent body fat, we look at muscle mass because sarcopenia is a very important thing that we want to avoid. Sarcopenia is the loss of muscle mass. So when someone tries to lose weight or they get it getting older, they get sarcopenia. Muscles is a carbohydrate sink, so we really do not want anyone to lose muscle mass if at all possible. So we follow this very closely. We really like this machine. It does 30 tests, six on five different body parts. It also gives us phase angle, which is the reason this particular model is the most expensive. Phase angle has multiple studies on it for cell health, so it gives us hints about whether their nutrition is actually adequate. Fish, oil, multivitamins, things like that actually can improve phase angle in patients that have those deficiencies. Also, it gives us the basal metabolic rate. Nutritionists really don’t like focusing on calories as much as they do on diet, but it does help us get an idea about how much how many calories a person should be eating per day in order to not just maintain, but also to prevent the loss of muscle, which we now know. Protein is a huge part. We measure, we weigh almost every patient that we see, and we’re we right now we’re using 1.6g of protein per kilo of body weight. It’s more than any other study prior to recent times which use .6 to 1.2. So we do think that you need more protein now than was previously described. Yeah, and as people get older, they tend to eat less protein and this phenomenon of sarcopenia is a big deal. So we want to really prevent that. The two ways to do that is by eating enough protein it’s got and also exercising properly type the proper type of weight training.

Now the other way to do this is DEXA scans. DEXA scans are very useful, you know, because you can look at their bone health, but also you can see where the visceral fat area is, You know you can see where in the body this doesn’t tell you where it is, it tells you just the total amount. But we find this to be super useful. There’s no radiation involved and iwe do it serially in all our patients. So the Holy Grail of cardiology, I used to be an interventional cardiologist. I’m a reformed interventional cardiologist. I used to put a lot of stents in and what we really want to know is, is the plaque in your arteries vulnerable? That means is it about is? Does it have the risk of rupturing and causing a heart attack and causing sudden death? And there are a lot of ways that have been researched to look at this. When I was in the cardiac Cath lab, we used to use intravascular ultrasound and we could get an idea for plaque was vulnerable, but that obviously an invasive test the important thing about. Plaque is that you know we do use calcium scores, but you have to keep in mind that a plaque is only 8% calcium. The rest of the plaque is non calcified. So if you do a calcium score you don’t see the rest of that plaque. So that’s the part that’s important because it’s the non calcified plaque that ruptures and gives you a heart attack. This is a calcium score. And again, we need to know more than this. You know, this is useful. It’s less expensive than the newer technology, but it’s not as informative. This is a new technology where artificial intelligence called clearly it’s a CAT scan with contrast with artificial intelligence over read. And it’s really been transformative for what we do, you know, preventive cardiology because we can now see the plaque. We can see where the plaque is and we can see the nature of the plaque, whether it’s inflamed or not inflamed. If you look at the where it says low density non calcified plaque in red, that’s a very, very dangerous plaque because that can rupture and that caused a heart attack. If it’s just yellow then that’s non calcified plaque that’s not inflamed and then blue is calcified plaque and calcified plaque is actually stable as long as it’s not obstructing the artery. We really don’t need to do much about that. And so this, this is how we decide how to treat patients is based on study on testing like this because if someone and that’s why this kind of test is good either way, if it’s low risk, we don’t have to be very aggressive. If it’s high risk then we have to be a little bit more aggressive. So that’s when we start using statins or bepodoic acid or PCs canine inhibitors. Now this is an actual patient of ours and who had a calcium who had a clearly test in 2021, then again in 2024. And this is a great example of how a plaque can change but actually be stable. The calcium score if you look at the very bottom went up from 164 to 213, but the low density plaque went away so that this patient in reversal of the dangerous inflamed plaque and the total plaque volume didn’t change appreciably and the total non calcified plaque went down significantly. So this shows a transformation of the plaque into a more stable pattern and which is what we want, you know, we want that plaque and now we can see if we’re if our treatments are moving the patient in the right direction. The blue is stable, so it’s not a high risk for the patient, but we see the reversal of the yellow, the non calcified plaque. So using whatever tools are necessary based on everything that we do with testing, we can actually reverse a lot of this heart disease. It’s such a valuable tool even though it’s not covered on insurance, it’s so worth doing. It’s not we our plan is to do it every two years to follow our patients, but we have patients that are willing and want to do it yearly also just because it’s so descriptive of what’s actually going on and it’s also descriptive of the things that they’ve done to make changes, whether it be medications or lifestyle changes. Yeah, we just had a patient, we were talking about it yesterday. She is in her mid 40s, perfect shape, exercises every day, eats perfectly. But she has a lot of coronary disease genetically and she had a lot of this yellow and with the treatments it went down dramatically, almost completely away. So you know, you can really get, this is the way we see if someone’s getting reversal of disease. This woman that he’s mentioning, I found her many years ago. Her cholesterol was 330, I believe on red yeast rice. I got it down under 200, but it wasn’t until we switched to to medication that we really saw the reversal of disease. So with 330, you would think her risk was high and we all did think so. But actually she’s in great shape now. It’s amazing to see and clearly it’s the only thing that really could show us that so.

Lifestyle and Dietary Approaches

I’m a functional cardiologist. I get patients come from all over, they say I don’t want to be on a statin. First thing they say to me I don’t want to be on a statin. But sometimes you have to be on a medicine. And for instance this patient if she wasn’t on a medicine, she would never had reversal disease. So you know you don’t want to die of heart disease without being on A and say, you know I’m not on a statin. I mean if you have to be on something it’s it’s better than getting the the deleterious effects of this very lethal disease. So another thing that we look at is heart rate variability. There’s an imperceptible timing difference between each heartbeat. This is called heart rate variability. And we should not have metronomic heartbeats that are exactly the same time. The more there’s a little difference between each heartbeat, the better. And this is a this is a measure of our autonomic nervous system. And so the better our autonomic nervous system, the better the heart rate variability. And now we have wearables that we can measure this with. And this gets better with certain lifestyle changes like exercise, diet, connection with others. Like I said, our electromagnetic field is now together. And you know with the heart disease reversal program, the Dean Ornish program that I was directed over, we looked at each piece, diet, exercise, stress reduction and then connection with others. And if you take out any one part of that, you don’t get the reversal that you would get. So the connection with other people is very important. And then we’re using newer wearable technology like continuous blood sugar monitoring, which has been very helpful for us because again insulin resistance is a big part of heart disease. And by using things like continuous glucose monitoring we can you may be aware of this, but it it, you know there’s glucotypes. My wife and I both did this for a while and things she ate didn’t affect her and think it would affect me in a much worse way and vice versa. So we learned about things that are very bad for our our blood sugar, and that in turn effects particle numbers and and and particle sizes. It’s a great tool for patients because they really learn about food and how it affects them. A lot of people have questions about wine. Does it raise their blood sugar? About alcohol in general, so this is really a great tool for people to really understand what these carbohydrates especially alcohol and simple carbs really can do to your blood sugar. And you know we’re multi focal in terms of our approach to cardiovascular disease because our goal is to extend health span. So this is schematic of an artery and as an artery that yellow the plaque gets worse. We see inflammatory markers come out that we can measure in the blood. So we know by some well done randomized controlled trials like the Cantos trial that by reducing inflammation you reduce overall cardiovascular risk. And when we talk about cardiovascular risk, again we’re talking about heart attacks and death. So these are big risks and if you lower the inflammation by any means this is this was using a pharmaceutical agent to lower the inflammation, we know that it’s as important or maybe even more important than lowering lipids to lowering the inflammation. Diet is also very important and diet can affect inflammatory markers in a good or bad way depending on what kind of diet you’re on. This was a study looking at a Egg Mcmuffin study where a patient was given Egg Mcmuffin and then nuclear factor Kappa B was measured. Nuclear factor Kappa B is a very deleterious inflammatory marker. And what’s interesting about this, if you look at the graph below, you know the the NF Kappa B stayed raised for hours after the ingestion of the of this high fat meal. And so, you know, we can tolerate this sort of thing. You know, if you eat one of these once a month, you know your body’s going to talk. But if you’re someone who eats one of these or two of these every day, then you’re going to have a continuous increase of this NF Kappa B and where there’s a lot of other inflammatory markers also that get affected by this. So inflammation, cancer risk, heart disease risk all go up. So nutrition is very much associated with this. You know we talk about diets and you know basically you know a prudent diet or a Mediterranean style diet is very, very good for them. Gut microbiome, you know this is what it has phytochemicals in it. It’s high in fiber. It’s high in omega-3 fatty acids. And and if the bottom line is that it affects the gut microbiome in an excellent way and if we have a good gut, gut microbiome, everything else follows suit. You know, I, a lot of my patients, they come in to see me and I ask them a lot about their gut and they’re wondering why a cardiologist would do this. And that’s because of this because the the gut is very much associated with heart disease. You know and again in a Western diet where, you know, very high in fats, you know the gut microbiome, the the you get dysbiosis, leaky gut, it’s it’s, you know, it leads to problems. Triglycerides is a proxy for insulin resistance. So we measure triglycerides. It’s a way of measuring insulin resistance. So diets, diet studies are generally not good diet, not good studies, but there are some good randomized controlled trials that have looked at good diets like a Mediterranean diet. One of the very first one was the Leon France diet heart study and this actually looked at people that have already had a heart attack and they put them on a Mediterranean style diet compared to American Heart, not even a bad diet, American Heart Association diet, significant decrease in cardiovascular risk. Now what’s interesting about this study is that they enrolled patients well into their 80s and even in their 80s. You’re genetically able to modify to improve. And then the other big trial was the Predimet trial, and this was done in Spain. There’s a Mediterranean diet in a country that already eats somewhat of a Mediterranean diet. And all they did was added olive oil and nuts. They made sure they ate those things and they reduced their cardiovascular risk significantly. So the Mediterranean diet has been shown over this is a meta analysis of randomized controlled trials in terms of inflammation. So inflammation in all the trials went down. Cancer risk also goes down South. One of the the nice things about what we look at for risk factors for heart disease, they’re the same risk factors for dementia and for cancer and cognitive function, again across the board improvement and chronic diseases like CBD, mortality, type 2 diabetes all improved. So this is a study, it’s called the lifestyle change study. This is not any any treatment. It was just taking patients and putting them on a diet, exercise, stress reduction. And this showed in the top a reduction, a significant reduction of the blockage in the coronary artery. And then on the bottom panel, that’s a what’s called a PET scan and we can see the blood flow to the heart muscle. And on the left, we see that the blood flow is very bad and then there’s a 300% improvement. And this is after just a few months on this lifestyle change trial. And these patients also showed increases in their telomere lengths. Telomeres are those caps on the end of DNA. The longer the telomere, the longer your DNA lives. So it’s a indication of DNA health and the telomere length after five years increased dramatically. So this is this is a test called Omega Check that Quest bought from the Cleveland Clinic. A guy named Bill Harris invented this test. The average American has a Omega check of around 4%. A lot of Asian cultures have between 8:00 and 11:00 percent and there’s a drop in all ’cause mortality by five years just by getting your Omega check up. Of course it’s a reflection of diet fish and fish oil. So here’s the effect of fish oil on cardiovascular disease. It’s anti-inflammatory anti. You can check all those pathways. It increases nitric oxide production. There’s zero downside, but this examines it. This looks at the dose of the fish oil and the response at 1g per day. There was no benefit or all in this vital. There’s another study. It was 1g of fish oil with vitamin D How interesting. That vitamin D had an impact and there was a 28% risk reduction in MIS. And then if you look down a little further, there’s a study called the Reduce IT study that showed that 4G per day there was a 12% risk reduction in cardiovascular events. And then if you look down further to the lower part of the slide with an omega-3 with an Omega check greater than 4%, all of those things below it improve 14% risk reduction of all causes of death for taking fish oil. I think that’s pretty easy to do. And one of the things about these studies like fish oil and vitamin D studies, you have to read them carefully. Sometimes they only go by the doses given, not by the blood level. Like you have to really look at the omega-3 fatty acid index or the vitamin D level in these studies. Russia, you know, you’re not really, you really don’t know what’s happening in the patient. So a lot of negative studies about these are because they don’t do it that way. And we try to optimize those levels in our patients. So we follow these continuously. You could see all the different advantages including reducing the telomere attrition, which essentially is our goal in extending health span. So there used to be the simple 7 smoking, healthy diet, weight, cholesterol, blood pressure, blood glucose and physical activity as a risks for heart disease. It just became 8. Sleep is a risk factor for heart disease. And we know that’s, you know, the we now know because of the glymphatic system where the brain detoxifies only during deep sleep, that you have to get a certain amount of good sleep for that to happen. Otherwise you get total body stress. It’s not just the brain. I mean, dementia actually goes up, Alzheimer’s disease goes up, but heart disease also goes up. So sleep is very fundamental. So good sleep hygiene is something we teach our patients over and over again and we like incremental changes. If they’re sleeping six hours and then they get 6 1/2 hours, that’s a that’s a major step in the right direction. And then exercise, you get most a lot of bang for your buck and exercise. So the exercise effects many, many things in your body including the heart. Heart cells actually increase, muscles increase the brain, BDNF brain derived neurotropic factor goes up in the in the bone marrow improves. Exercise is very, very much associated with risk reduction and we recommend patients to do a variety of different exercises including weight training, some kind of stretching or yoga, and then zone 2 training, which is getting your heart rate up to a certain level. It’s usually 180 minus your age for 30 to 45 minutes and then alternating that with high Intensity interval training because high intensity interval training has been shown metabolically to be excellent for the heart and all these other factors in the body. We also find that the High Intensity Interval Training can lower visceral fat, so we try to have every patient incorporate it. Of course, a lot of our patients are a little too lazy to be exercising five days a week, but we still promote it and we get fairly good outcome.

Emerging Therapeutic Options:

So semaglutide, you’ve probably even heard about this is the weight loss medicine and it’s up till these medicines, these Glucagon like peptide 1 receptor agonists before they came out, we really didn’t have any safe drugs for weight loss. These are actually very safe and this study is actually very interesting and it was published in the New England Journal Medicine that this is in Patients with pre-existing cardiovascular disease were overweight but they did not have diabetes, had improved cardiovascular outcomes using these drugs. There is some data showing that there’s a possibility of muscle loss with semaglutide. So you know, it has to be a select population, but in patients that have obesity and cannot lose weight any other way before they go to bariatric surgery, this is a great, great choice. So berberine is one of our favorite herbs. And as an integrated pharmacist, I’m very concerned with the absorption of a lot of the substances that we’re recommending. It turns out that the phytosome of berberine is absorbed 10 times as well as the straight herb. So that’s pretty much what we’re using right now and it’s been shown that it actually can reduce oxidative stress, LDL’s, triglycerides, insulin resistance and even improving mood. The dose is usually we start with 500 milligrams twice a day at the beginning of two meals. And berberine has also been shown to be a natural PCSK 9 inhibitor. In some patients, it can attach to the PCSK 9 molecule and have the same effects as the PCSK 9 inhibitor. These are some of the benefits that Berberine has. I’m not going to go into detail. I think we’re running out of time, but NATO kinase is something that we’ve been using more and more, especially in patients with elevated LP. Little a the standard is the NSKSD strain. It’s NATO that’s been fermented with Bacillus subtilis and the NATO kinase. That result is standardized right now in Fibrin units or FUS. The standard 100 milligrams is 2000 FUS. This particular study that was really significant actually used 10,800 units of NATO kinase or roughly 5 capsules a day. And this is a study that looked at niacin. A lot of people ask me can I use niacin? Niacin does lower cholesterol, but this is a good example of what you use to lower cholesterol makes a difference. And niacin has never been shown to reduce outcomes. So we don’t like using things that don’t reduce outcomes. You know, we don’t really care about the cholesterol. We care about outcomes, you know, whether you’re going to get a heart attack or whether you’re going to get something like that. So it’s never been really been shown, although if we’re LP little a nice and does lower it, we still don’t know if lowering LP little A makes a difference or not. So the jury’s out. Also, often when you get to the dose high enough that it is effective, it does come up. It does affect the liver. So this is cereolimus or rapamycin is a fascinating molecule. It was discovered on Easter Island and it’s it’s a anti proliferative agent and as a interventional cardiologist I use this quite a bit because when you talk about stents you may have heard of drug coded stents. The coding on that stent is rapamycin and rapamycin has been shown to be anti remodeling. So it helps in patients with heart failure to increase cardiac cells. It may also be one of the most promising treatments for longevity. Of course, because it hasn’t some immunosuppressant nature. The dosing has really come into question and I don’t think we have a clear idea about what that means.

And. Photo biomodulation is a new area where by using red light therapy, and this is usually used intranasally because the aeration of the face is so great, it affects the mitochondria and stem cells and this has also been studied with heart failure patients to increase heart cells. So the heart failure improves sauna. We’re big fans of sauna, you know, saw. There’s a lot of data from Finland. The Finnish doctors have studied this quite extensively. And sauna decreases inflammation. It’s an antioxidant, it decreases blood pressure, it actually decreases cholesterol and increases endothelial function. We find this to be very effective. There’s a if you use sauna 3 * a week decreases your cardiovascular risk by about 3040%. Also, if you combine it with exercise, it actually enhances the benefit of exercise. Yeah, biomarkers of exercise like heat shock proteins go up with with sauna. Cryotherapy also is very helpful. You know it reduces inflammatory markers, bad cholesterol and markers of plaque instability. So it’s a it’s a good thing to do in conjunction with the sauna and then hyperbaric oxygen is also an evolving therapy that is akin to in the Cath lab we used to use pre ischemic preconditioning meaning that we we caused a little bit blockage and then opened it and that would improve blood flow and blood function. This sort of does the same thing, it helps angiogenesis, it reduces inflammation, it reduces cellular senescence. So it’s an up and coming treatment for patients. And then Walter Longo is a we you probably have heard of him. He’s the guy who developed Prolong. He’s somebody we interviewed for our podcast and he’s very knowledgeable about fasting and fasting. He studied it probably better than anyone and it and there’s time restricted eating, intermittent fasting and then his fasting mimicking diet, all of these whatever you choose to do helps ATP production, mitochondrial function, it helps cellular senescence, it helps heart function, it helps improve natural D non alcoholic fatty liver disease. So it’s a very effective way. I’ve used this in patients therapeutically and found to be very effective. He wrote the book The Longevity Diet, by the way. And then you know now we’re using a lot of wearables and this is very helpful in cardiology. For instance, the Cardia 6 lead cardio device is a wearable or patients can transmit to me their rhythm if they’re having palpitations and also things like blood pressure. Scott has an aura ring. He measures his sleeping quality with this and then some. This is an evolving area of in in cardiology, so so cardiovascular disease is a multifaceted problem which requires A multifaceted and multidisciplinary approach.

So this is a book I wrote with my wife. She’s a physician and it’s about the Mediterranean diet from Sicily. We have several different practices and Scott, you know his compound pharmacy, his life science pharmacy. A couple of things that we couldn’t fit in the slides. Estrogen today can be extremely helpful for women and men actually for heart disease as well as testosterone. Estrogen is cardioprotective, testosterone is vasculoprotective. We’re also interested in mitoquinone, a new kind of Co Q10. We’re looking at Urolithin A as a new molecule for mitochondrial dysfunction. So there’s new stuff coming all the time. There’s just not enough hours in the day to do everything that we want to do, and certainly not enough hours in this day to include everything that we would have liked to relay to you about this.

Questions:

Combining Repatha with Supplements

And thank you for coming. If you have any questions, you know, we’ll be happy. Yes. Yeah. OK, and I think one of the important things is, as you were stating, my dad used to say too is the more tools you have in the toolbox, the better. Start off conservatively. Nobody has any problems. We look at it. You start with red yeast, rice. You try to do the statin drugs when you did that, when you’re treating those things and then look at the symptoms, if it’s bothering the patient, then you try something else to see what works for you. But I I think the question we have, I mean, I was very fortunate. I had a heart attack, but I did all the right stuff. I exercised, They had stress. They had a double bypass. I mean, luckily I was in a great, a great place where they well stint they went, they did it within 15 minutes. I was in a great place. They corrected everything. All my blood work was normal, which was bizarre. So I think the eight boy may have been off, but there was no indications. And then I have a fabulous cardiologist that put me on to I already exercise, I diet, I do all those things. And then he tried to put me on a statin. Drugs have familial elevated levels, which you may not know if you don’t have any symptoms, which there were none. And now he’s got my own Repatha, which have lowered all my levels. It’s increased my energy levels. So there’s none of the side effects to that. So moving forward from that, I mean, I think we can put ourselves into each of those pictures because you don’t know what you have. Sometimes you may be perfectly fine in the next thing you know you don’t know.

My question is with the Repatha that you’re on, can you and I don’t know enough about the Repatha, but can you add in like the glycocalyx? Is this still good to do the Kilcoenzim Q10? I’m still exercising and eating well, but is there something you recommend with the Repatha? I don’t see any side effects to anything I can find in the literature. So in your opinion, how does, how do we fit that into the studies that you may or may not be aware of?

Well, we, we feel very strongly about mitochondrial function, and mitochondrial function can be disrupted by a number of things. And maybe even with Repatha, we don’t know. We don’t have good ways of measuring mitochondrial function, but we have new ways of treating it. You know, with urolithin, A methylene blue. And there’s some peptides out there that are controversial, but they work. But the most important thing is that we need to have ways of measuring mitochondrial function. One way that we’ve used up to this point is exercise. If you could do a certain amount of exercise in a certain amount of time, that’s an indication that your mitochondria is probably working well. But now there’s other technologies coming out where we actually can measure mitochondrial function, which would help determine what you need. Also, what’s the harm in taking something that we know will improve the glycocalyx or some form of ubiquinol? Ubiquinol, you know, of Co Q10, which we know from tons of studies, is going to aid your mitochondria. It’s going to aid the heart, which has a concentration of mitochondria.

Yeah, Scott mentioned the D ribose that we use in heart failure patients. D ribose is a is a is a special sugar molecule that’s preferentially used by the heart muscle cells and the mitochondria. And it’s been shown studies to improve heart failure. It was originally under the name Corvolin, and Dr. Teitelbaum actually studied it for fibromyalgia, which is energy, basically. Yes, Sir.

Lowering Lipoprotein(a) Levels

In some patients the question was is PCs, can I lower LP little A and in some cases it does. The unusual thing about LP little A, we know it’s a major risk factor. We don’t know yet if we lower it, if it makes a difference in outcomes. So even if it lowers the way we use LP Little A is that the highest level you’ve ever had in your life. You’ve had high risk for LP Little A. So we’re more aggressive with the APOB. So let’s say you have average coronary plaque and you have APOB somewhat elevated and the LP Little A is not elevated, then we can get your APOB maybe down to 60. But if you have LP Little A elevated, we want that APOB to be at 40. It’s just directs us at how aggressive we are.

Statins for Primary Prevention in Women

Hi, sorry this two-part question about statins. So one is about primary prevention of women. I’m still not aware of any study that shows that taking statins for primary prevention of women, it’s not like the same data that we have a robust data for men. I asked this because I’m a woman and #2 the cognitive effects of statins. Now I have tried several different statins and you know my my family doctor and cardiologist are getting fed up with me. I get depressed and I get anxious and maybe that’s because I was treated during my perimenopause with an SSRI. But you you both said there’s not very much data that there’s I’ll effects to statin, but honestly, like, I take my blood pressure medication no problem. It’s not that I’m phobic, I’m a doctor about the medication. I just get these side effects. So I don’t know if there’s any studies revealing that in women who haven’t had heart disease. What like what would you recommend at statin? Yeah.

This is why the newer technology and assessing risk like clearly is super helpful. You know if you have a clearly and we hadn’t, we have a few patients that have completely normal, normal, clear. They have no plaque whatsoever. You don’t have to be as aggressive as that as venting A statin, but the statin the a lot of people think that statins cause dementia. The reality is the meta analysis that have looked at this, there’s less dementia in patients on statins versus patients off statins. That’s because statins help vascular dementia, which is the more common form of dementia. So you know it’s A and I and I believe you this is, you know, you do get side effects. You know we have plenty of patients with side effects that we have to take off. But the the good news is we have other great drugs. You know, bepadoic acid that works only in the liver, doesn’t have the muscular effects and PCSK 9 inhibitors, they’re great. The only downside is they’re costly. The cost. OK. Thank you. You know Zetia,

Statin Risks and Considerations

That’s another option. Yeah, yeah. Well, P, you know, APOE is a gene for Alzheimer’s, basically. It’s also a gene for cardiovascular disease. If you have normal E2E3 or E3E3, your risk is average. And you don’t have that added risk. If you’re at E4E 3E4, then you have a 25% increased risk of dementia and Alzheimer’s disease. And if you’re E4E4 then you even have a greater risk. So in those patients, if they’re put on statins, you have to be very careful because if their desmostral levels go down, then their dementia risk goes up. If their desmostral levels don’t go down, there’s no data showing that there’s an increased risk. And again, by lowering lipids you decrease dementia risk. So you know there’s a E3E4 is a risk for dementia without the vascular component, but the vascular component is very important. So by decreasing the vascular component, you know you decrease risk. But in those patients, I tend not to use statins, I just don’t use them. You know, I use we have plenty of other things we can use that are great. There’s you know like we said bepodoic acid, there’s PCs, canine and then there’s Zetia Ezetamide which is you know helps those Neeman PIC receptors very effective when used in combination with bepodoic acid.

Optimal Omega-3 Levels

I have two questions. The first one is, is quick omega-3 index. The reports that we get say like you’re in the Green Zone if you’re over a 3.2, but what percent do you aim for? Percent of Omega-3? Could you repeat that? She said that what percentage do we aim for in the omega-3 fatty acid index? We aim, the higher the better. You know, in certain Asian cultures, like in Japan, where they have an omega-3 fatty acid index of 10%, their cardiovascular risk is very low. Because of that, It all ’cause mortality goes down in the United States since people don’t eat fish. You know, the average omega-3 fatty acid index is about 4%. And if you get your omega-3, some studies have shown if you get the omega-3 from 4% to 10, you add five years of quality to your life. So it’s a very important factor. Let me also add that we also don’t just look at the omega-3 index. We look at the actual EPA and DHA. And let me just add one thing about that. You know there’s a organization called IFOS International Fish Oil Standard. So if you have question about your fish oil, Ifos actually checks those products for rancidity and for labeling accuracy. In other words, is the EPADHA stated what’s really in the product? So really good products will usually have something on the bottle which shows Ifos, Ifos.

HDL Levels

Thank you so much. This was incredibly informative. I have two quick questions. Can you talk a little bit about HDL’s being too high and if they’re, you know, over 100 or you know what then do we do? Do we take out healthier fats like extra virgin oil or? Well, the HDL, again, we used to think when we only measured good and bad cholesterol, HDL being the good and LDL being the bad, that the higher the better on the HDL. And generally that may be true. But now we’re not. We know that if it’s too high, like over 80, then it could be dysfunctional. And what that means is, you know if you look at this, if you remember the slide I showed you how cholesterol gets into our body either it’s made endogenously, it comes exogenously. And then there’s another balancing the reverse cholesterol transport, that reverse cholesterol transport is defective in patients that have defective HDL cholesterol. So you you don’t get the cholesterol the, the time it stays in your system goes up and and that increases your risk. So in in patients like that what we do is we do things that help the HDL cholesterol. When Scott showed his numbers when he stopped exercising because of his back, his HDL went down and his HDL size went down and that’s a great example of how exercise is, is very important and and and diet is also very important. Carbohydrates seem to be more associated with HDL sizes and quality than other parts of the diet. So you know those two things. Might also be a time for you to do that Boston Heart. You don’t have to do the whole panel so you can just figure out what the cholesterol balance is and that would help you adjust your diet too. Right.

Dietary Approaches for Hyper-Absorbers

Yeah. And that leads me to any recommendations for someone who is a hyper or super absorber intestinally rather than the liver, You know, in taking it endogenously. When we when I used to run the Ornish rehearsal heart disease program, we’d put patients on a 10% fat vegetarian diet, right? And for most people, that lowered their cholesterol. But in some people it didn’t do anything and those are usually people that don’t have a lot of receptors in their: then they’re in their gut and so, but if they do have hyper absorption then we reduce their saturated fat intake. You know the the tropical oils, you know, those are the worst, you know. But also, you know, there’s a misconception about a lot of our patients eat a lot of poultry, a lot of chicken like every day. You know, the chicken is a saturated fat, you know, but a little bit less than red meat. But you know if you’re a hyper absorber and you’re eating high quantities of these things, then it, it can accumulate, you know, through your gut. And so you know we make dietary changes and and if that doesn’t work then those are patients that do well on things that block that absorption like ezetimide. Like. Citrus also Ezetia. Zetia is a drug that’s used for that, or ezetimide. It’s also called. Also, we used to use a lot more plant steel rolls for for blocking the absorption of cholesterol. Now we’re suspicious that even though it does block the absorption that it may increase plaque. So we’ve really backed off from plant steel rolls unless we have no other option.

Omega-3s, Magnesium and Atrial Fibrillation

Thank you. I just want to say I’m really happy to see Scott looking well and being part of this team and I’m looking you up as a cardiologist because you’re in New Jersey and accessible. But this is an amazing, amazing presentation. My question is on atrial fibrillation and what do we know about omega-3 helping? Is there some data on magnesium being beneficial? You know, with the electrolytes? Anything you can share with us? That’s one thing that omega-3 that you have to be careful with you take 2 high omega-3 is there is some data showing that it can cause atrial fibrillation. So. How high? Well, if you get the omega-3 level, you know in in patients that have atrial fibrillation, I usually don’t aim for 10%, I aim for you know 5% or 6% that kind of thing. So you don’t get it overly high that it may induce atrial fibrillation. For some reason it does that and we don’t know why that is. We did have 4G A. Day 4G a day would still be good to give a patient. I’m sorry. Would 4G a day still be good? Well, I think you you go by the omega-3 fatty acid index, you know we we use anywhere from 1G to you know 6G you know, depending on the omega-3 fatty acid because absorption is also part of the issue. Yeah, we tend to use some Omega threes that have better absorption also in Terra coded so it stops some of the gastrointestinal symptoms. But there were a bunch of slides we had to eliminate about magnesium. We we are big fans. We measure every patient’s magnesium RBC, not just serum magnesium and we tend to use a lot of magnesium L3 and eight recent studies show that it does cross the blood brain barrier and increase cognition. But we also use magnesium glycinate because when the body splits the magnesium from glycine, the glycine is very calming. It helps with sleep. But I don’t think that we really have really good data. That magnesium really has a huge impact on a fib. You agree? Yeah, there’s not good data, but you know it. It does have some. Amount of data. There’s some small data. Yeah, there is, there’s some, but there’s no no convincing data but we use it quite a bit. So it’s we we like getting our our patients RBC magnesium levels to a high level. You know I I’ve had a lot of patients that have you know other arrhythmias like SVT and that sort of thing. Magnesium is very helpful for that. So we we combine what we do. You know, there’s all different types of magnesiums. Magnesium taurate is good for these kind of arrhythmias, you know. And then there’s now three and eight that’s good for cognitive function. I mean, we use all different types of magnesiums, right? And we only citrate at the laxative, though we don’t use it for its magnesium properties. And yoga and stuff like that is the data that it does help with atrial fibrillation using the breath. I mean, there’s some of that stuff. How do you recommend it for your patients? Yes, absolutely. Yeah, there’s good data about that all. Right. Good. Thank you.

Cardiovascular Risk Factors

Yes. Can you speak to other risk factors that I think are important but that we’re not really mentioned small density LDL, oxidized LDL and homocysteine? Yeah, well, first of all, APOB encompasses all that. That’s why APOB is such a good marker because it encompasses large and small LDL cholesterol. So everything that’s what we call atherogenic dyslipidemic is, is under that APOB umbrella. That’s why we’ve we find Apob to be the the best overall in terms we you know if you have small LDL cholesterol your Apob goes up because the more particles you have the more Apob. So it’s it correlates and homocysteine, yes, we we measure though that on every single patient. Homocysteine’s in the methionine pathway and it’s related to MTHFR genetic abnormality and it increases cardiovascular risk, increases dementia, it’s another measure of endothelial function. So where you you know there’s no good way to measure what you give for those patients. It’s trial and error, but we use methylated B vitamins as first line therapy. Yeah, we checked every patient for the MTHFR. We’re a little bit more aggressive with the C677T especially if it’s homozygous. But even if it’s the A 1298 and we see home the homocysteine elevated, we will still methylate those patients. We use either a methylated B, sometimes we’ll use trimethyl glycine, sometimes we’ll combine them. You know, we’re very aggressive because homeless elevated homocysteine is representative of risk.

Second last question, is there a Dean Ornish clinic that’s still around? Well, they they there are some, they’re not, there’s not many. But for you know through insurance that’s the problem. If you want to do it through insurance, you have to have an event like you have to have a heart attack, a stent bypass surgery and now he has a virtual program which is excellent. You know they send you food, they they virtually connect with you. So it’s a it’s a very good program. It’s Dean ornish.com and we’ll. Yeah, yeah. On deanornish.com. Yeah. Thanks.

Balancing Protein Needs and TMAO Risks

I’ll be quick. I’m wondering on the DMAO piece of the puzzle, kind of balancing that with especially recent recommendations and focus on maintaining muscle mass and like these recommendations for huge amounts of protein. Do you preference recommendations for plant based proteins or like plant based protein powders? Knowing that you know dairy and meat and even fish can raise DMAO or does it all come out in the wash in a Mediterranean diet? Well, you know, that’s a great question by the way. It’s TMAL is a big risk factor and it’s very much related to diet. You know, you can get a lot of protein from from plant based sources. You know, we went to a talk this morning and for per calorie you get more protein from plants than you get from from animal protein. But you know a Mediterranean diet or a prudent diet is an omnivore diet. You know, you eat poultry, you eat some meat, you eat fish and and eggs, you know, so you you can get plenty of protein. There’s and and we like Scott mentioned earlier, we like the 1.6g of protein per kilogram of body weight. So for a typical woman like your size, you know that would be about up 90 grams of protein a day. It’s difficult sometimes to get that. So we do use protein powders and we like things that have L leucine, high doses of L leucine because L leucine really stimulates muscle growth more than any other amino acid. So you know we use whey protein. Certain fish like cod and halibut are very high in LLC. So there’s very good ways to eat a, you know, a good healthy diet and still get all the protein you need. The problem with the planned protein powders is the leucine content per average serving is under 2000 milligrams and we think that you need 3000 milligrams. The average serving of whey or egg protein is 3000 or close to 3000 milligrams a day. Leucine is stimulates muscle synthesis. So that’s one of the things that we really try to impress on our patients, especially they’re all aging like we are. That’s helpful. So it sounds like you’re sort of not hyper concerned about those levels of protein intake at least in terms of the inflammatory effects? Of more protein is better than less. Yeah, The quality of the protein is really what we focus in on. You know, we don’t want you to eat. We don’t want patients to eat a lot of you know, especially the, you know, the animal saturated fats some but not a lot, you know, because you know those are related to cancer, heart disease and you know, so we we really don’t promote that. Thank you. Thank you very much. That’s really good, good talk.

Nutritional CVD Risk Reduction

Can I ask one? Yeah, two things. One is that do you use any restriction on eggs if the cholesterol level is high and then the risk is high? Yeah. Usually what I what we recommend is 4 to 6 yolks a week for preferably, you know and a whites all you want for protein and so a whites ad libitum and for yolk because we think the, you know, eggs are perfect proteins and there’s a lot of good things in yolks like choline and that sort of thing. Good for the cell membrane but in excess quantities it may not be the best thing. You know the data about eggs goes back and forth. There’s a lot of things like dairy and eggs where the data goes back and forth. So we try to take a more balanced approach to these kind of recommendations. And then one more is that what is the name of the test? You know what what what measures? You know the plaque formation that the angio. Clearly, yeah, yeah, that’s clearly. And it’s clearly health.com if you want to look it up CLEERLY healthoneword.com. Yeah. OK. Thank you. Yeah. Well, oh sure. If a patient chooses to be vegan. We don’t. We don’t dissuade. I mean there’s there’s ways to be vegan and eat a healthy diet. We don’t promote that as our primary diet, but you can be vegan and and still be. Usually when you’re vegan though, you have to supplement, you know, you have to supplement, you know, B vitamins and and that sort of thing. But I mean. You have to be a smart vegan to make sure you’re getting all the right nutrition, yeah.

Well, thank you very much. This was our pleasure. All right.

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