DANIEL CHONG, ND - Nutrition and the Prevention of Cardiovascular Disease

dr daniel chong is a licensed naturopathic practitioner in portland oregon and he's been practicing since 2000 where he focuses on healthy aging of the brain and body as well as risk assessment prevention and drug-free treatment strategies for cardiovascular disease and diabetes he also maintains an active virtual practice via the internet for group and individual coaching in cardiovascular disease prevention in addition to his degree in naturopathic medicine dr chong has completed certificate training in cardio metabolic medicine with doctors mark houston and joel kong at the academy of anti-aging medicine he is also a contributing editor in cardiology for the natural medicine journal and a clinical consultant for the boston heart diagnostic labs you can learn more about him at drdanielchong.com please join me in welcoming dr chong thank you ginger and also wanted to say thank you to peter and everybody else involved in setting up this conference this is awesome it's so great to look out and see so many people out here thank you all for coming as well i actually wanted to start with the show of hands can you show me how many people out there are medical practitioners wow all right um what about other healthcare practitioners if you don't consider yourself medical okay great and how many people in whatever practice you do see a lot of people with cardiovascular disease either actually having it or trying to work on preventing it good okay good because we're going to dive pretty deep uh into into that topic so hopefully you guys appreciate it so once again thanks for coming i just wanna you probably already heard i have some disclosures i'm a clinical uh consultant presenter for boston heart diagnostics laboratory and a contributing editor for the natural medicine journal so i like quotes and i feel like this one is is particularly good for today's talk dr albert sin giorgi is the person who originally discovered the molecule vitamin c and as you're going to hear later on in the talk that is going to be a big focus of what i'm talking about today but i do also like what he has to say here innovation is seeing what everyone has seen and thinking what nobody has thought and i think that applies really well to cardiovascular disease so if i were to say you know what is the cause of cardiovascular disease especially maybe to a room full of more conventionally trained and conventionally minded practitioners most people would probably still say ldl or cholesterol or something along those lines so we're very used to hearing that that idea as that you know that is the cause of cardiovascular disease that's the target of treatment etc and so what we're going to try to do today is is see what we've all you know consider what we always see with cardiovascular disease and what we consider to be the cause but think about it in a way that nobody or very few people have thought about before and why you know why would we want to do this if if we're so if we have such a good understanding of cardiovascular disease and why it happens why do we want to talk about this well when you look at these statistics you'll see if you don't know already that there's still a lot of work to be done so still to this day one in approximately three people are dying of cardiovascular disease and now that's worldwide now and i know with a lot of your backgrounds you're probably familiar with you know these traditional cultures of people who ate a more plant-based diet and had much lower rates of cardiovascular disease or these other people who lived in more traditional cultures like in africa etc who had very low levels of cardiovascular disease that's all disappearing now as people become more and more westernized so it used to be one in three people in the united states or westernized world were dying of cardiovascular disease but now that's more worldwide as everybody adapts our sub-optimal diet i've probably been talking for i don't know five minutes and there's been a heart attack every 40 seconds approximately during that time so this the statistics of cardiovascular disease and heart attacks are dismal and yet the last figure i've seen for cholesterol lowering drugs especially statins in terms of sales is 35 billion dollars annually apparently it's maybe going down a little bit it did it did just come off patent it's up to you to decide whether or not that has anything to do with it but the point point being if you're selling 35 billion dollars worth of statin drugs or cholesterol lowering drugs each year that's a lot of people taking that drug and yet every 40 seconds somebody's still having a heart attack and one in three people are still dying of cardiovascular disease so i wonder you know why that is how can that be if we've if we've honed in on and we've figured out what the cause of cardiovascular disease is and we're pretty certain about it and we have a drug that does a really good job of treating it i.e lowering the cholesterol levels the ldl levels et cetera why are we still seeing such dismal statistics in spite of apparently a lot of people taking it that is the big question uh to try to answer with this lecture so one of the reasons and perhaps the primary reason why that may be is this general law and medicine epidemics will tend to persist as long as the genuine cause of the disease is not understood so that can be applied to all kinds of different chronic health issues etc obviously we're not talking about acute things and accidents and that type of thing but when somebody's dying of a chronic disease or there's a lot of people dying of a chronic disease the point being if you're not identifying the cause of the problem in all likelihood that's going to continue and i feel that that's very much the case with cardiovascular disease and as it relates to cholesterol and that type of thing so just a brief overview of what we're going to talk about today we're going to go over the sort of conventional understanding of the cardiovascular disease process and then from that i'm going to help raise some questions to you for about about that conventional viewpoint and and discuss how there's certain questions that when you use the conventional viewpoint you cannot answer certain questions about cardiovascular disease and why it happens and also there are certain facts about cardiovascular disease that will explore that when if indeed they are true which they are that doesn't really fit in with the conventional viewpoint of cardiovascular disease as well and then we'll discuss some emerging concepts in the world specifically of nutrition that do help explain and answer those questions that the conventional viewpoint cannot answer and also help to verify and clarify those facts to be actually true and that will help us build this new potential viewpoint or hypothesis about cardiovascular disease and why it's really happening with the primary goal of them really understanding the cause of the condition and then allowing all of you to go out there and focus on the cause of the condition and really start helping people beyond what's being done so far and why i will go over some studies and things that help develop these or validate these concepts as we go along so this is a busy slide but it's it's the conventional viewpoint essentially of of the cardiovascular disease process this is kind of like how most people are going to agree is the way cardiovascular disease develops so we start off here with genetic tendencies or family history genetic tendencies plus risk factors and again in the conventional viewpoint the potent you know perhaps the biggest risk factor is high cholesterol high ldl so when you have an ongoing combination of enough genetic tendencies plus enough risk factors there's obviously other ones smoking obesity diabetes etc whatever they are if we group them into risk factors and we combine them with any type of genetic tendency over time that will eventually lead to what's called endothelial dysfunction which is sort of like the start starting point for the eventual development of plaque so it's it's what happened what's happening in the arteries prior to plaque like the anatomical change in the arteries that that leads to plaque and so the point being vulnerability or genetic tendencies plus enough risk risk factors plus enough time will create endothelial dysfunction and and certainly high ldl is a contributor to that as well over time with endothelial dysfunction in place for a long enough period of time you will start to get a penetration of ldl particles into the vascular wall and i do make a point of making sure we're clear on the particle idea the particle is what's the actual um chemical structure that's carrying the cholesterol around that's what's getting stuck into the wall of the artery the majority of the time and creating problems so if that happens on an ongoing basis and enough there's enough of that happening day in and day out you start to see a collection of that and an immune response by the body to that to those particles being stuck they become oxidized and they turn into what is viewed by the body as foreign particles that need to be removed and that's what incites the immune response by the body and creates things like foam cells fatty streaking and eventual plaque formation if over time that continues and there's no nothing done none of you people have treated this person and they continue to get worse you'll start to see an advancing plaque that becomes more and more vulnerable to rupture the the cap over top of it thins out it gets inflamed and as blood flow is rushing by especially if it's turbulent blood flow you can get a rupture of that plaque eventually and that will then then lead to a thrombosis and then a heart attack and so this is this is basically you know the the this sort of steps that take place to get to a heart attack and the most people out there there are a few people who have heart attacks for other reasons but this is the vast majority of people and so this is again the the basic process that we understand and really as far as i would know nobody's going to argue against this this is well understood well well accepted viewpoint of how cardiovascular disease begins and again the main issue is this high ldl and that's the main thing that's being treated with statin drugs this is also the viewpoint of the conventional medical center you know the conventional medical viewpoint the process that i just described is considered basically to be harmful fatalistic in the sense that it does lead to killing a lot of people and the main point being it serves no biological purpose it's just it's like oops all this cholesterol is floating around in the bloodstream it got stuck in the wall of the ax the wall of the arteries by accident and stayed there and then this process happened that then ended up killing the person for no reason and i don't know about most of you but as a naturopathic doctor i'm very trusting in the the the wisdom of the body and i think i don't really consider almost any circumstance where the body is not doing something on purpose with reason it might still end up you know causing the death or demise of the body but there has to be a reason behind it and that's a big part of what we're talking about here but again in the conventional viewpoint we don't really think that way we think that this is just a a fatalistic process that that just happens almost by accident and that's we're gonna we're gonna kind of try to rework that today and see if we can think about it in a different way that makes a lot more sense so i think it's important to focus a little bit on ldl because it's such a big component of the conventional viewpoint in terms of focusing on how to treat people obviously with statins and getting getting the ldl as low as possible in my in my opinion we should question whether or not ldl is a cause of the problem or just a component of the problem it's clearly you can't have plaque without cholesterol getting you know deposited into the wall of the artery it's clearly a part of the process but the question is whether or not it is a cause because if we can prove that it's not really the cause and we can find another cause that's more makes more sense and actually is more involving the physiological process is going on then we can identify how to better treat the condition and get rid of this epidemic so if we look at this graph this is from a study of over 130 000 patients hospitalized between 2000 and 2006 with coronary artery disease so these are people that not only have plaque in their arteries has gotten serious enough that they've been hospitalized for it whether or not it's for a heart attack or chest pain or whatever so each of these people were upon upon admit being admitted into the hospital they had their ldl levels checked and what you can see is on the bottom here this is their ldl levels this is the percentage of patients that have those levels and when you treat somebody medically for cardiovascular disease and you're using a statin or a cholesterol lowering drug you're trying to and especially if they have high risk or they're a pretty serious case you're trying to get cholesterol level at the very least below 100 even to 70 sometimes but as you can see the majority of patients that were actually hospitalized in this study of 130 000 people had what would be considered normal cholesterol so that raises a big question if if if we're focusing just on ldl and we're trying to get it down and we get it down and these people still end up in the hospital are we treating the cause of the problem it doesn't seem like that so that's that's why i'm asking this question that's why i really want people to start thinking about that because it's such an accepted viewpoint that there's very little you know real consideration for statistics like that sorry so does that make sense pretty clear good yeah i mean it's it's it's very obvious there's even right here this is like 110 120 it's that's not going to get people very excited it's only when you start getting up into this range that people get you know doctors are really trying to get a higher dose of the drug or whatever but we're down here and people are still getting hospitalized the majority of the time so more about this idea like i said ldl is clearly involved you cannot get a development of plaque without penetration into the wall of the artery with ldl or a related lipoprotein so we can't ever deny that it's or another way to think about it i don't if if i can have somebody's cholesterol levels or ldl levels come down naturally with the treatment that i'm doing i'm happy about that i always give patients this analogy of when we're talking about trying to prevent plaque developing if you imagine a chain-link fence and then you imagine a bucket of golf balls okay and you're taking the golf balls and you're throwing them at the chain-link fence and the golf balls are essentially the ldl particles obviously some of them are going to get through and sorry the chain-link fence is the wall of the artery so we're trying to keep any golf balls from getting through that chain-link fence obviously the golf balls are small enough typically that some of them are going to get through but you you would also imagine that the higher the number of golf balls that you have to begin with the higher your probability is that some of them are going to get through right does that make sense so we're trying to i don't want to dismiss the idea that ldl is important it's still a very important thing to focus on the idea is more what else is going on and what else can we focus on to give ourselves a better chance of helping more people and we're going to get again deep into that as we go along here but the point being ldl is clearly involved we don't want to deny that we also know that statins are clearly good at lowering cholesterol and most people the more you give the lower it gets and yet we saw that the statistics that we're talking about we know that statins don't work i wouldn't say they work really well if does any is everybody familiar with the term nnt or number needed to treat anybody okay good so basically for anybody that doesn't know that's a that's a term used to when we're when we're when we're having a drug tested for the first time and we're trying to clarify how effective it is the nnt tells you basically how effective the drug is and it basically talks about how many people need to take that drug in order for one person to get the desired result of that drug right so an nnt of one would be the best that you could possibly have right because if if you have an nnt of one that means every single person that takes that drug gets the desired result okay when we're talking about statins the the research depending on whether or not it was funded by the pharmaceutical industry the nnt for statins is somewhere between about 50 and 100. so and a good drug is really considered like in the teens if you ever if you have an nnt in the teens that's a pretty good drug so that's not a very effective drug although if your goal is to have every single adult in the united states take that drug then one out of every 50 or 100 of that is actually still pretty effective but my point is i think we can do better but the point is you know so statins clearly lower cholesterol and yet they don't seem to work that well so that's already a disconnect the other thing to point out that i think is really interesting is some of the research that i've looked at has shown that statins when they do work well tend to work best when that person is also having issues with inflammation going on most people are probably familiar with chronic inflammation crp as a as a you know contributing factor to chronic disease but it's it's very important to recognize that if somebody has high ldl or high cholesterol and they don't have high inflammation they don't tend to get the same benefit from statin drugs as they do if if they have both if they have inflammation and high ldl so again that would suggest something else must be going on here than just this standard got to treat the high cholesterol the other thing to point out is statins do not prevent i just kind of went over that but statins do not prevent events cardiovascular events nearly as well as they lower cholesterol so those are a lot of things to consider about about ldl and i'm hoping it's getting you guys to ask the question of why why how can that be how can ldl be involved how can it how can statins clearly lower cholesterol and yet they don't seem to work that well there must be something else going on with this theory about why cardiovascular disease develops just in case we got some more questions to consider i alluded to this before at the beginning we're going to go over some questions that are very difficult to answer from via the conventional viewpoint so number one why do we get infarctions of the heart but we rarely get them in other organs or tissues so has ever has anybody ever heard of a an earlobe attack or uh um you know whatever a pinky pinky toe attack it doesn't happen you don't tend to get or even like a liver attack or a spleen attack or a liver infarction or something like that you if you think about it you don't really hear about attacks of any organ other than the heart or infarctions very commonly of any other organ other than the heart that's an important thing to consider when we're trying to get at this cause of the problem we're going to go into that more in a moment here the next question that we're going to consider is why do we get atherosclerosis i.e plaque developing in the arteries but we don't get vanil sclerosis meaning plaque developing in the veins so if you think about it anybody that draws blood or sends people out to get their blood drawn and have their cholesterol tested where is that blood coming from the veins or the arteries veins so you're you're taking a blood sample out of a vein that's super high in cholesterol and yet have you ever thought about the fact that why if if just having high cholesterol floating around in the vascular system is the cause of the problem why don't we get any plaque in the veins it's that's where it's floating around in the veins as well not just the arteries so that's an important point to consider and again a point that the conventional viewpoint that cholesterol is the cause of the problem can't answer that last question that we're going to go over is why don't other animals with high cholesterol get heart attacks we're going to go deep into that one as well so let's talk a little bit more about the first one why do we get infarctions of the heart but rarely of other organs or tissues if you look at this this diagram you know the the primary areas you're getting plaque development are in the arteries right around the heart and the arteries feeding the neck you know the carotid arteries and the circle of willis here in the brain and then oftentimes wherever there's a bifurcation or a division in the artery so if you think about it what's what you don't typically see is like plaque developing in the you know long portion of your arm or in certain parts of your feet or whatever and the reason for that is that there's a very important thing to consider that is to do with the turbulence of the blood flow so the most turbulent area of the whole arterial system is going to be right around the heart because as soon as that heart beats some of that blood is being shunted very sort of sharply back directly into the the arteries that feed the heart another area with a lot of blood turbulent blood flow is the carotid arteries this because again when the heart beats it shoots right up there as well and that carotid artery bifurcates into an internal and external portion of the of the artery and right where that bifurcates is also a very common place to get plaque and yet if we go back to the idea well high cholesterol causes cardiovascular disease we would expect to see plaque development everywhere if you think about a plumbing system in a house that's got a lot of sludge in it you're not going to just find sludge at certain points in the in the pipes you're going to find it collecting on the walls of the of you know the pipes all throughout the house and that's because in that situation the primary cause of sludge collection or sorry you know the sludge collecting on the wall on the walls of the pipe is how much sludge is in the system this is a very different situation going on here and we have to be able to explain this if we want to get at the cause of the problem and and more thoroughly treat people so second question why do we get atherosclerosis but not venous sclerosis like i said i kind of went into this already you draw blood from the veins there's as much cholesterol floating around in the veins as there is in the arteries and yet we essentially don't see plaque almost ever develop in veins and obviously we see lots of plaque developing in the arteries so that has if you're trying to be thorough that has to be answered if you're trying to say that you have a an explanation or uh you know you've found the cause of the problem that should be an answerable question with whatever theory that you're going by and why don't these guys get heart attacks okay so this is obviously a bear i believe it's a grizzly bear and what we know is that throughout a year depending on the season etc a grizzly bear's total cholesterol levels will vary between three and 600 on average so obviously if anybody came into your office and they had a total cholesterol of 600 you would be surprised to be seeing them if they were an adult and still alive and you would be you know trying to take some pretty urgent uh action with those people and yet bears walking around all year long with at least a level of 300 which again would be considered quite high they don't ever get cardiovascular disease all the research that's been done they cannot find a bear in the wild that has plaque in their arteries and that is an important thing to consider so right then and there you could just stop right there and say well there's got to be other things going on it can't just be high cholesterol that's causing the problem even when with other animals that they've studied in the wild if they they occasionally will find these cardiovascular disease like lesions in their arterial system but the the more detailed research into into that has discovered that in all likelihood those lesions are due to parasitic infections and not high cholesterol not anything to do with why we get lesions as human beings also important to consider most research animals including rodents and rabbits they have to actually you know these are the ones that are being used most commonly in these research studies and being given plaque so on and so forth to test drugs etc in order to do to get them to get plaque in the first place they have to genetically alter these animals to make them get more human-like cardiovascular disease and even when they do so they basically they genetically alter them and make them more susceptible to the deposition of plaque etc and even when they do that they still have a hard time giving them plaque they have to actually feed them from what i've read the equival the equivalent of approximately 30 egg like we're talking about mice here they have to feed them approximately 30 egg yolks a day to get them to get plaque even when they're genetically altered and made vulnerable to cardiovascular disease and it's important to remember that you know some people out there that are humans could just look at an egg and they probably get a little bit of a plaque in their arteries so what's going on there why is there such a difference that's that's an important question that we're going to answer so here we are we've got some unconsidered facts at least hopefully many of you haven't considered them before we've got some unconsidered questions we have evidence of still severe morbidity and mortality happening worldwide and a massive economic burden not just from the drugs that we buy that people buy but also obviously the surgeries happening etc when we add those together i think it's time to recognize another hypothesis that might be a little bit more getting at the cause of the problem so this is the hypothesis that we're going to talk about today atherosclerosis is a necessary physiological repair process so it's purposeful the body does it for a reason and we're going to go into the reasons and you'll see that when we do go into these reasons it it basically explains everything number one and it gives you a much clearer idea of how you want to go about treating this condition more thoroughly so i'm calling this the wrath and pauling view of the cardiovascular disease process before we go into it i just want to point out matthias rath is a medical doctor and researcher and linus pauling how many people know who linus pauling is all right good they are they are the people who originally came up with this um this whole process i'm going to go a little bit more into detail about them in a moment but i just want to sort of say thank you to them and and like that's why i wanted to call it that because they are the people that came up with this this whole idea so real quick if we go back this is our basic viewpoint this is what most people are operating on you know many people are just saying look at ldl give us dating hope you do okay but this is a more detailed look at the the basic conventional process just to remind you got genetic factors risk factors endothelial dysfunction the ldl particles get in the wall of the artery we get plaque thrombosis heart attack okay now we're going to think about it in a different way the primary initiating step is right here nutritional inadequacy we're going to go into various nutrients in particular later but the point being when a person has nutritional inadequacy and it's of certain nutrients they become vulnerable to that endothelial dysfunction they also the collagen which most of you are probably familiar with collagen it's the primary component of artery walls that make them strong pliable resilient to that turbulent blood flow that we were talking about earlier so the poorer your nutrition and especially vitamin c which we're going to talk about later the weaker your collagen is when you make it in your in your artery walls also if you have other deficiencies that we'll talk about you can get vascular smooth muscle dysfunction which becomes very important in the process of atherosclerosis as well but again none of these happen if you don't have that first if this happens for long enough you get an increased vulnerability to structural damage in the artery wall and then the hemodynamic forces or this turbulent blood flow that we were talking about as l as well as various types of vascular stressors like high blood sugar smoking etc they expose the vulnerable areas this is a very important point if we think back to this little picture remember these vulnerable areas that the places how we're trying to explain why we only get plaque in certain areas well it's because you have to have a combination of vulnerability and weakness in the wall of the artery plus turbulent blood flow so turbulent blood flow is here turbulent blood flow is here turbulent blood flow is not so much here or in the earlobes or the pinky toes like we talked about so oops sorry so again nutritional inadequacy leads to this this uh dysfunction here and weak collagen that makes you vulnerable to structural damage and then when you have these different areas in the body that have high turbulence high hemodynamic forces and vascular stresses that's where we get an exposure of the of the of this inadequacy that's where the wall starts to get damaged it's also true to note that before you ever get plaque developing in an art in an artery on a microscopic level you will see cracks crevices and damage to the wall of the artery anywhere that you eventually get plaque and that's what's happening right here so if you sprain your ankle what happens to your ankle swells it gets red swollen etc so this is just damage happening in the wall of the artery and what's the natural human body response to damage a mobilization of an inflammatory inflammatory repair process and specifically in this case to prevent hemorrhage and death so if you think about it if you have an artery wall that's very vulnerable to damage and you have turbulent blood flow that's causing this constant damage like waves crashing into a cliff wall that's eroding if you have no means of repairing that and the process is just continuing on and on what's going to eventually happen to that wall it's going to rip open that's where you die very quickly right so of course your body and it's you know unen you know never-ending effort to stay alive as long as possible and hopefully contribute to a passing on of its genetics by propagating the species the body will come up with ways to do the best it can with the cards that's being dealt and that's essentially what's happening with atherosclerosis as this goes on long enough in an effort to prevent that ripping open and hemorrhaging and death the body will start to send these fat and nutrient transporters into the wall what would be another word for these fat and nutrient transporters ldl you know lipoprotein particles these are all cargo ships carrying substances various places in the body including into damaged areas of the vascular wall and you get immune activation and inflammation etc just like you would with any other injury anywhere in the body unfortunately if the person keeps doing whatever they're doing to create that damage in the first place which dr esselstyn at the end of the day is going to hammer on it will continue the process will continue it has to it's just natural you'll start to get this this repair happening now the goal of the body is to repair it in a way that the plaque once it forms gets stabilized so you know if you think about plaque that's been calcified it's harder it's it's less vulnerable to rupture the thicker the fibrous cap is over the plaque the less vulnerable it is to rupture that's basically like the body going okay we've got a damaged area let's fix it it's nice and stable cool it's good we can just leave it alone because the blood will still flow on past that but for various reasons as the way people live et cetera their ongoing nutritional inadequacy that doesn't always happen and this continues to be like this smoldering inflamed massive you know effort that your body's trying to do to repair but it's still vulnerable and then when you have these hemodynamic forces especially if you have high blood pressure or something like that or somebody gets really stressed out on a monday morning the turbulence goes up that vulnerable plaque ruptures and then you get a heart attack but the point is this whole process that we're talking about does serve a biological purpose it is not random and it is not meant to be fatalistic it's actually the opposite it's meant to keep the body as alive as long as humanly possible so this notion of atherosclerosis as a repair process answers the first two questions very well why do we get infarctions of the heart but rarely of other organs because that's where the arteries around the heart that's where the turbulence and the blood flow is highest in the whole body so it's it's it's it's not random it's not by chance it's very it makes a lot of sense if you think about everything we just talked about why do we get arterial or atherosclerosis that's meant to be but not venous sclerosis it has a lot to do with turbulence and blood pressure where is the turbulence highest obviously in the arterial system there's this massive pump that's shoving blood through it you know every with every heartbeat in the venous system it's more of a passive slow uh blood flow that's not so turbulent so of course if if we're going by the hypothesis that we're talking about you're not going to see the same type of development of plaque in the veins as you would in the arteries some examples of this idea of repair that we have already we have identified through research so increased ldl and other lipoproteins like i was alluding to before actually bring repair nutrients to the area everybody knows that cholesterol is a crucial uh component of the body it's it's crucial for cell membrane integrity it's crucial for repair in various ways we can't live without it we just don't need tons of it but the point is if you're trying to do repair somewhere you're going to want to bring a little bit of cholesterol to that area potentially and there's other nutrients that take rides on lipoproteins as well all of which are technically involved in repair and we know that because we see the same nutrients etc being deposited any other place that you get damaged sprained ankles etc most people are familiar with fibrinogen high fibrinogen levels are also a known risk factor for cardiovascular disease well they're a known risk factor for plaque development because they're serving a purpose when you get elevated fibrinogen you're helping to for to form micro clots in those damaged parts of the wall that's that slow the and stop the bleeding from happening slow and stop any potential for hemorrhage so again normally you're a doctor you run lab work you see a high fibrinogen level you go oh gosh that person's at increased risk for a stroke or a heart attack let's put them on a blood thinner or something like that there's no thought about why that's there and if there was we might treat that person in a different way that's actually getting at the cause of the problem because no blood thinner is getting at the cause of the problem it's treating the result of the problem and then we also know that calcification of plaque is is purposeful as well it's meant hopefully to stabilize the situation and allow that to continue so most of you probably know that when you do like a stress test you're not typically going to get symptoms like chest pain or dysfunction of the heart etc unless the plaque the blockage is quite significant some research shows like over 70 percent so a 50 percent blocked artery if it's really stable doesn't cause the person any symptoms at all and that's purposeful it's by the body it's like okay this is the best we can do we just want to keep blood flowing through here so we're going to make this plaque cover that that area of damage stabilize it and let the blood keep passing through and the lack of symptoms that you get the lack of any chest pain etc shows that it's sufficient amount of blood flow that's going through there and the body's essentially solved the problem at least for the time being this is an interesting thought i'm not going to really go too deep into this i i spoke with actually one of dr rath's main researchers about this idea that they're actually starting to investigate everybody knows diabetes causes high blood sugar they are starting to theorize that the body may when when the body identifies there's that there's an increased risk for this damage happening to the walls of the artery partially due to poorly formed or weak collagen they are starting to theorize that the body may actually be allowing for some of that blood sugar level to remain high as a backup way to create cross-linking in the collagen itself so if if the body so in other words if the body can't build the healthy collagen in the first place it it has an adaptive mechanism to try to help strengthen that in some way shape or form and it's all because blood flowing through arteries is so important you obviously are going to die very quickly if you have a massive hemorrhage so it's an interesting thought i'm not really going to go too much more into it because i haven't seen much research on it but it's it goes right along with this whole idea that the body is doing the best it can as it's going along so and number three again we talked about number three why don't animals get heart attacks and this theory helps to answer that and this is where we're gonna we're kind of introduce the main part of the rest of the lecture and so the reason based on the theory that we're talking about the reason why animals other animals other than humans don't get heart attacks is because of a lack of susceptibility so i showed you already in that process the first thing that happens is nutritional inadequacy that is what creates susceptibility to a great extent certainly genetics play a role as well but nutritional inadequacy is crucial for for this idea of susceptibility so huma humans have especially high susceptibility because we lack this enzyme right here is that does anybody know what l goolono lactone oxidase is other than dr mars who knows in this anybody that is the enzyme sort of the rate limiting step for manufacturing vitamin c in your liver human beings all human beings that we know of have a have a genetic mutation that keeps them from being able to produce this enzyme interestingly enough they did apparently at one point many millions of years ago pre-humans did have the ability to manufacture this enzyme and that allowed them just like many other animals to manufacture vitamin c in their own bodies in their own livers it's basically as far as i understand there's less than 10 species of animals on the planet the entire planet that cannot manufacture vitamin c the vast vast vast majority of them all make their own vitamin c right in their livers including those grizzly bears so if we consider the fact that vitamin c is crucial for collagen production and also for the maintenance of endothelial function we could definitely conclude that if we have a lack of vitamin c we're going to have vulnerability to collagen poor weak collagen production just like i was talking about and endothelial dysfunction just like i was talking about so the point being most animals make all the vitamin c they need every day they will make whatever they need and they are not going because of that fact they're not going to be vulnerable to weak collagen production they're not going to be vulnerable to poor endothelial dysfunction both of which are precursors to the development of plaque so even if you're a grizzly bear walking around with total cholesterol of 600 and it's you know banging into the wall of the arteries if your arteries are super solid strong and impervious to damage to a great extent you're not going to get plaque developing like you would if you didn't have that in the first place that makes sense hope so okay interestingly enough we're all familiar with the uh most of us are probably familiar with the idea of guinea pigs like the classic lab animal i know we don't like to talk about lab animals for in general but it's important to make a point here guinea pigs are this classic uh lab animal that used to be used much more than they are now probably because it's uh too expensive to use guinea pigs but the interesting thing is they were once considered the best animal model for cardiovascular disease research interestingly enough they are one of the ten species that i mentioned that also cannot make vitamin c in their bodies just like human beings so what do you know they happen to be really easy to create plaque in just like humans are so that's an interesting point and so remember like i said some human beings barely have they they don't even you know have to do have to have very many risk factors and they get serious cardiovascular disease and those other animals we talked about have to be almost forced to get cardiovascular disease well though the ones that have to be genetically altered and made vulnerable etc all of those animals make vitamin c in their bodies so it makes perfect sense when you think about it from this perspective they are very very resistant and resilient to the to the development of plaque because of that fact and that is what um matthias rath who was again dr pauling's main researcher back in the late 80s he learned about that information along with some other information i'm about to tell you and started to create this hypothesis of maybe the whole starting point is nutritional inadequacy so this is an interesting study i'm sorry if you can't read it very well i will read it for you what they did in this research study is they took mice and they genetically altered them so that they could not make that enzyme we were just talking about l-gulano lactone oxidase so they essentially turned them into humans in the sense that they also could not make vitamin c in their livers anymore and then all they did is they messed around with the level of vitamin c in their diets and watched what happened the main things i want to point out is what one thing that they saw very clearly as plasma ascorbic acid or vitamin c decreased i.e they gave them less and less in their diet there was a small but significant increase in total cholesterol and decrease in hdl so if you think through that for a second hdl's one of hdl's primary jobs is to reverse the process of plaque formation right but if the body is all of a sudden stuck with a situation where it has to form plaque in order to stay alive it's going to lower hdl to decrease it what it's trying to do and it's going to raise total cholesterol and ldl all in an effort to try to develop plaque like literally on purpose the other thing to think about are to to point out in this study so they basically conclude marginal vitamin c deficiency affects the vascular integrity of the mice unable to synthesize ascorbic acid with potentially profound effects on the pathogenesis of vascular diseases so this is an early study there has been some more exciting things done in this regard but i wanted to point this one out first this is some of the earliest stuff that they did starting to mess around with vitamin c production in particular in 1990 again that's dr pauling dr rath they they published their some of their first papers on this on this theory on this idea that we're talking about and then a lot one of their primary ideas is basically that atherosclerosis is an early form of scurvy so everybody knows what scurvy is when we think about people dying of scurvy we think about what they bleed out they hemorrhage their blood vessels literally disintegrate and they they bleed out which makes perfect sense if they can't make collagen and have strong blood vessels what many people don't realize is that if you have what you'd call latent or sort of sub-acute scurvy that have that goes on for a long period of time so the person's getting not enough vitamin c but a little the primary symptomatic response to that is rampant atherosclerosis so if you think about that if somebody has low consistently low level scurvy going on they get really severe atherosclerosis which fits exactly with what we're talking about their body loses its primary way to keep it is blood vessels strong and healthy and so it does a backup mechanism all over the place to try to prevent hemorrhage if the if the scurvy is too severe then then they will die very quickly because they can't even the effort to make this plaque is insufficient and they start to hemorrhage and they die dr pauling and rath also focused specifically or to a great extent on lipoprotein a who knows what lipoprotein a is oh my gosh not enough people you guys all have to start testing lipoprotein a little they actually just a a couple of weeks ago i believe insurance companies are now starting to pay for lipoprotein a and hopefully after you hear what i say you're going to want to check it on everybody but they believe that lipoprotein a was an actual adaptation to the loss of the ability to make vitamin c that happened millions of years ago so what we know is the only animals that make lipoprotein a are human beings and other primates no other animals on the planet manufacture that molecule which is what's interesting to note is that human beings and other primates are the only long-lived animals on the planet who can't make vitamin c in their bodies so they dr rath especially theorized that lipoprotein a production was an adaptation to the loss of the ability to make vitamin c and when you in a moment you'll see why it was such an important adaptation but basically their idea is that atherosclerosis is an early form of scurvy and lipoprotein a is a repair molecule that functions as a backup to repairing damage caused by the deficiency of vitamin c and weakened connective tissue in the vascular wall one little note i will say it's not just lipoprotein a all the other cholesterol-related molecules would fall into this type of description as well now that we know what we know these are some early drawings that dr rath did to try to give you a visual for this idea so this was a basically the title of the study if you can't read it solution to the puzzle of human cardiovascular disease its primary cause is ascorbate deficiency leading to the deposition of lipoprotein a other lipoproteins like ldl and fibrinogen in the vascular wall so this is a schematic of what it would look like if you have optimal ascorbate concentrations in your body you get just a little bit of these guys floating around no damage to the vas to the endothelium no damage to the vascular wall in general if you have a score bait deficiency they would hypothesize if if it was in a vessel like we were talking about with normal or mild hemodynamic stress or turbulence you're going to get a little bit of damage but not severe damage it's only in this area where you have the combination of ascorbate deficiency as well as increased hemodynamic forces that you start to get plaque development like that and you know encroaching on the on the lumen so that was what he drew in 1991 um i have my theories as to why it didn't like take off from there but this was 1991 but lucky for us even though dr pauling died dr rath has continued his work and we'll see some of that in a little bit here so just a little bit more about lp little a because i think it's fascinating you can look at your phones right now if this is a little too much detail it's it's really a unique repair molecule that is the the really the the primary reason for its existence whereas when we think about it from a conventional viewpoint people look at lp little a as the nastiest of all the cholesterol-related molecules or the most atherogenic and so they're you know trying desperately drug companies are trying desperately to figure out a way to shove it down but when we think about it from the perspective that we're talking about you can call it both a highly atherogenic molecule and a really good repair molecule and mean the same thing if you if you understand what i'm saying it means you're still following me which is be good but basically there's some unique attributes it is essentially an ldl molecule with an extra protein structure around it called apolipo protein small a and this whole combination of structures and molecules etc create some very interesting attributes it's very sticky it binds to things like fibrin and collagen and connective tissue components as well as endothelial cells so it's made to go and find breaks in the walls of arteries and stick to them it also completes with plasminogen long story short by doing so it reduces the process of fibrinolysis so fibrinolysis would be a breaking down of clots forming if you're trying to fix something in the wall of the artery partially by making clots there you don't want plasminogen coming along and breaking that up it's like you're breaking up it's like you're trying to build a house and somebody's coming and pulling the planks of wood off that you just nailed into place so lp little a has a unique property of of competing with plasminogen and keeping that from happening it also does not bind well to ldl receptor sites in the liver and therefore it is not taken up out of circulation very easily and that's why again the drug companies are beating their heads trying to figure out a way to lower this molecule because it is very difficult to get it to go down much more difficult than standard ldl molecules and the reason is that one of the reasons is that it does not bind very well to these receptors in the liver that would pull it out of circulation and again as i mentioned only humans and other primates naturally manufacture it so this is sort of like the seminal study of dr rath here's the dr rath research institute this was in 2015. in this study they went a step further than the one i showed you before where they knocked out the ability to make vitamin c in this study they took mice and they knocked out the ability to make vitamin c in all of them and then they gave a portion of them the ability to manufacture lipoprotein little a or lp little a and then once again they varied the levels of vitamin c in their diets step back and watch to see what happened okay so some amazing things were figured out and and proven really so to me the hypothesis that we've been talking about is now actually being proven based on this work here so some of the findings that they did in this research study on this side we have a cross-section magnified cross-section of a arterial wall with the endothelium and a group of the mice who again had their vitamin c production knocked out and no capacity to make lp little a and they were given no vitamin c this is what their their blood vessel walls look like this is all smooth muscle getting all into the whole thickness of the of the wall here the endothelium as you can see is all disrupted and broken this is the everything is exactly the same except these mice were given vitamin c in their diets so again both sides had their vitamin c capacity production capacity knocked out the right side was given vitamin c the left side was not look at the difference which one looks more vulnerable to damage from turbulent blood flow this one that's all nice and lined up and strong looking and the smooth muscle is all lined up here or this mess the left side the left side okay this is also from that study this is a little bit i'm just going to explain what this is so basically let's just talk about this section here this is um days of uh life essentially and this is um like how much were originally alive at the start of the pro the study so this color group here were mice that had their vitamin c production not knocked out and they were not given the ability to make lp little a this group here also had their vitamin c levels knocked out but they were given the genetic ability to make lipoprotein little a and what we can see is the ant the mice that had no ability to make vitamin c and really poor ability to um sort of adapt to that did not live very long if they were given the lp little a even though it eventually killed they eventually died they lived quite a bit longer so this is another this is like a visual representation of how lp little a was an adaptation to try to survive as long as possible and we all know you know the primary goal of nature is to propagate the species right so if you have a situation going on where you're vulnerable to this disease and you can adapt in a way to live long enough to make a few babies and help them grow that's good nature's like cool that worked perfectly it doesn't care if you then die of a heart attack when you're 60 because in all likelihood you made some babies already so it's like it's working it's it's doing the best as it can and that's the whole idea that we're seeing here this is just male mice female mice same thing seen in both cases no lp little a they can make lp little a so it's very clear one more here um again sorry a busy slide but this is basically lp little a levels in the blood with varying levels of vitamin c in the diet so this is females and males so what we see is that when they don't get vitamin c in their diet they have higher lp little a levels than when they do just like that other study that showed if you take out vitamin c cholesterol levels go up well lp little a levels go up as well as soon as you give them vitamin c they go down so it's just further proof of what's going on here with this process one last one about the study um if we imagine this is like a cross-section of an artery and blood flowing that way so creating turbulence going that way in this group here this is the cross-section of an artery from a mouse that had very little again had their vitamin c production capacity taken out they were they were made to make lp little a but they were given very low levels of vitamin c or no vitamin c in their diet this is a plaque that has ruptured all this brown area is lp little a doing its best to try to stabilize this damaged area it didn't work because the plaque still ruptured but this is the body doing its best in this case it's every all conditions are exactly the same except they were given a full dose of vitamin c in their diets you see no brown anywhere meaning no lp little a deposited anywhere on the wall of the artery because the body didn't have any need to try to fix anything and certainly you don't see any plaque sorry one more just to drive this point home really really hard um again no vitamin c normal vitamin c lp little a levels in the blood high and low lots of plaque lots of plaque no plaque anywhere all the smooth muscles in the right area the endothelium is intact and looking good the endothelium is all disrupted here plaque everywhere smooth muscle everywhere this is what a plaque looks like but the only difference was vitamin c on this side no vitamin c on that side everything else the same so to sort of summarize that study the idea is that vitamin c deficiency leads to an increased vulnerability in the damage of the artery wall lp little a binds mostly to damaged areas of the artery the artery walls thicken wherever the lp little a is deposited providing structural this is the key structural reinforcement against scorputic hemorrhaging or low or hemorrhaging due to low vitamin c or ascorbic acid in chronic subclinical vitamin c deficiency this continual repair process creates various types of large plaques in the artery even without administering any experimental diet so that sounds a lot more like a human right we're talking about even in those mice that they make vulnerable to plaque in some of these other research studies they still have to feed them a heavily atherogenic diet these are mice also that were changed in the way we just talked about they didn't even have to feed them an atherogenic diet like 30 egg yolks a day type of idea just normal amounts and they still got plaque just like humans do so it's important to stop here because you know if you believe everything i'm saying you're sitting here going well vitamin c must be the absolute cure-all for cardiovascular disease and yet when we look at the research we find some troubling findings that would call into question everything that i'm talking about so this was a recent review in the cochrane database looking at various vitamin c studies and their conclusion was that currently there's no evidence to suggest that vitamin c supplementation reduces the risk of cardiovascular disease so should i just leave now or should we talk about why that might be there's a lot of reasons to potentially explain that we'll go over but at the same time i did want to point out other very well done research this was a large meta-analysis of randomized controlled trials so good quality studies on vitamin c supplementation and we clearly see that it improves endothelial dysfunction and if you remember what i said you cannot get plaque without endothelial dysfunction happening first it has to be involved to some degree in helping prevent plaque deposition this one showed that vitamin c inhibits hdl oxidation and preserves its antioxidant activity so in other words vitamin c makes hdl work better so again we know that we want to have good hdl levels to try to prevent cardiovascular disease so you see some evidence that shows that vitamin c doesn't work and some some evidence that shows it should work and then all the other stuff i just said before that so what's going on here to me there's three potential explanations to to explain these different findings number one we have yet to replicate the wrath study in humans and i don't think we ever will so don't hold your breath but that would clearly give us a much clearer study a lot of the studies that they looked at in the cochrane review were not very well done studies nowhere near replicating to the degree of specificity that this study did so until we get a study in humans that's that specific and that detailed i wouldn't necessarily expect to see such clear evidence number two there's also in any of these studies that are being done there's what i call a lack of capacity to control for confounders related to what other animals make so what i mean by that is if you look they've studied for example goats okay an average sized goat does anybody know how much an average goat weighs louder louder what okay so like a a half human okay size wise goats are really good at making vitamin c and the research that they've done has shown they sort of study goats under optimal living conditions and they still make somewhere between three and four thousand milligrams of vitamin c in a 24-hour period in their bodies they are also not very vulnerable to cardiovascular disease just like the bear just like the bears were talking about even gorillas in the wild who don't make vitamin c just like we don't they don't find cardiovascular disease in those animals almost ever either and they've they've analyzed the average diet of an adult gorilla in the wild and they eat through their plant food etc approximately 2 000 milligrams of vitamin c a day so that's important to to recognize when we're when we're talking about these studies that are being done many of which are being the the human beings are being given 500 milligrams a day to me the research on goats and other animals that can make vitamin c and even on gorillas etc would suggest that we need higher amounts that are being given in the studies that have been done that don't show any effect there's also an important point to make about the varying half-life of vitamin c in the body so as far as i understand it in terms of nutritional molecules vitamin c has the widest potential half-life in the human body of any nutrient so in other words if everybody's familiar with the idea of a half-life it's like how long it takes for half of it to disappear or be used up depending on what is going on with that person in terms of um stress levels etc they may the the half-life of the body may vary between somewhere between three hours and three weeks so that's a huge half-life which you you know and again some of these people in these studies are going to be stressed sick et cetera they're they're using up vitamin c and much different rates so you're going to get a lot of sort of mixed mixed results in that type of situation the third thing to explain what i'm talking about is is it possible that human beings are adapted to synergism and when i thought about this question that is what made me think of this question this this slide here so that's dr esselstyn there dr campbell both of whom are big proponents of food so all the studies that they've reviewed in that cochrane database just use vitamin c supplementation so what about the idea of this holism versus reductionism can we do better than just taking vitamin c this is a study done real quick where they looked at people eating a mediterranean type of diet that was particularly high in vitamin c containing foods and compared that to people eating a more standard diet who were given a similar amount of vitamin c via oral supplementation long story short neither acute intra-arterial nor sustained administration of oral vitamin c improves artery function in healthy older adults like a diet rich in vitamin c does so if you give the same amount of vitamin c and food it seems to help your blood vessels more than supplementation would one more study to just quickly review this looked at they gave a group of people vitamin c straight and then another group of people vitamin c plus a citrus extract and they found that ascorbate and the citric extract was found to be more bioavailable than ascorbate alone so in other words if you give vitamin c with a food that naturally contains it and all the components that that comes along with you absorb it better again those things were not done in those studies that showed that vitamin c doesn't help cardiovascular disease so i'm going to go quick through this these are just you can look at your notes here foods vegetables high in vitamin c so in other words if you want to start using high vitamin c foods with your patients more some of these i'm sure look familiar fruits high in vitamin c particularly some of these are not as consumed as often but should be considered in people who who might need more vitamin c if there are if there are any carnivores in the audience i don't want to leave you out if you want to eat vitamin c in your food you got to eat raw liver raw fish eggs raw adrenal glands and raw eyeballs so again i'm going to go quick past this one these are some other nutrients that have to be considered if we're trying to thoroughly address this whole hypothesis these are all nutrients that are involved in various aspects of blood vessel production or blood vessel function that's going to make a person less vulnerable to the development of atherosclerosis there's a number of nutrients as you can see here i'm not going to go over each one but what do you think is the food group that naturally contains all of them fruits and vegetables when to consider supplementation because it still should be considered in some situations obviously if you have a non-compliant patient who's not willing to eat that you're probably going to get some benefit by giving them vitamin c as we've seen from the mice studies if they have severe cardiovascular disease in my opinion you should double up on your chances and also you know feed them the optimal diet that dr esselstyn might suggest plus vitamin c it's not going to harm you and it might help you low quality food options so so processed food etc post surgery even post cardiovascular disease surgery those people should all at least temporarily be given supplementation and certainly if you have infections and also what i forgot to put here is chronic stress i don't know if anybody out there has stress on an ongoing basis but if you do it might up your levels of vitamin c requirement beyond which you can satisfy with food so to quickly summarize current theories of cardiovascular disease process cannot explain certain facets of the pathophysiology of that disease this lack of understanding and subsequent focus away from the causative factors contributes to the severe morbidity mortality and economic burden that we see humans and other animals who cannot make vitamin c have a particular vulnerability to cardiovascular disease and that vulnerability may be compounded by additional nutrient deficiencies which should also be considered this vulnerability may in fact be a purposeful it i don't even i'm not going to say may it is a purposeful backup protective mechanism designed to delay death as long as possible that is a theory that explains everything that we're talking about so providing sufficient nutritional support via an optimized diet high in various supportive nutrients along with damage control so no smoking all the things you know about may render that whole process unnecessary another way to say that it may make cardiovascular disease a thing of the past so thank you very much you

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Length: 72min 9sec (4329 seconds)

Published: Tue May 11 2021