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Heart Attacks & Strophanthus- Webinar from April 9th, 2025

• Dr. Tom Cowan

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SPEAKER_01

Hey, welcome everybody. Today is another Wednesday webinar. Let's see, April 9th, 2025. I think I got that right. And thanks everybody for joining me as always. And yeah. Okay, so today, um what what I'm the main event, so to speak, is going to be talking about heart attacks and Strephanthus. So one might ask why am I doing this? Because we've had a number of webinars on exactly this subject. And the reason I decided to do it this week, mostly, besides the fact that it has been a while since we've looked at this subject, was I was sent an email by a fellow named Whelan de Busmann. I'm not sure if that's how to say his name. He's a German either dentist or a pharmacist, I'm not sure. And he he probably knows as much or more about Strephanthus as anybody alive. And he keeps a very clear website on all things to do with Strephanthus and the research and how to get it and people's stories and everything. And he sent me an updated res uh updated uh link, I guess, to his website. And in there was a link to uh what used to be the heartattacknew.com website, which was the best website that I had ever encountered and had a huge impact on my thinking about this, this being heart attacks and strepanthus. But for some reason, about five years ago, the website disappeared. And even though I had uh still could find the video, which I'm going to show you, uh, there was no way to find the website, and all the valuable information was on that was on there. Now, when I got this email, there was a link to it, and it took me to something called the Internet Wayback Machine, I guess. And there was the website, and there you could find the video and all the content. And I thought, uh, because I don't know if this is going to be lost or whether it's going to be scrubbed from the internet or how people are going to find it. But I but it seemed to me important to uh go through the website, what I think are the most important features, and show the video again and his uh information on Strephanthus so that it really becomes in the public record in somewhere that's easy to access and easy to find. And that's really the purpose of this webinar, as well as a few words about my story with heart attacks and maybe with Strephanthus. So that that's the intention here. Um, to basically uh put the Knut Sroca is the doctor's name. He's a medical doctor, was I think an internist in Germany. He probably knew more and wrote more about what really causes heart attacks and the use of Strephanthus for the prevention and treatment of heart attacks and congestive heart failure, and probably published more and knew more about this subject than anybody. And I don't know what happened to him in the last five years. I don't even know if he's still alive, I assume so. But um, so I thought I would take this opportunity to get his work out there accessible to the public, and we'll put a link to where you can find the web the website, and that was it. So before I do that, uh, because I think this is also relevant and to not only this conversation or this presentation today, but it seems to be very relevant to everything we've been talking about for the last five years, including about virology and about uh DNA and about contagion and hormones and and on and on and on. Uh, and the the this that I'm talking about comes from a book called Science at the Crossroads by a guy named Herbert Dingle, and it's also called A Rational Scrutiny of the Clock Paradox in Einstein's Relativity. Now, let me just give you the background of this short paragraph that I'm going to read, which is the important point. So, Herbert Dingle was one of the most prominent physicists of the 20th century, most prestigious, most, you know, published, I guess. And in particular, he was an expert on Einstein's relativity theory, and even gave lectures about it, talked about it. I think he had something to do with talking at Einstein's funeral. And so uh there was no doubt that he was as expert as you could get on Einstein's relativity theory. And then at some point in his career, I think you could say to his surprise, he discovered this, or maybe he didn't discover it, but he uh investigated this paradox called the clock paradox, which he then claimed disproved Einstein's special relativity theory without any doubt. And he then wrote about it and he published some papers about it, uh, and he asked every physicist and every scientist and every mathematician who had any interest in the subject to explain to him how his reasoning was flawed or an experiment, if possible, to show that his experiment was or his reasoning was incorrect. He didn't do an experiment, he was just a reasoning exercise that showed that Einstein's uh special theory of relativity could not possibly be true. And to his shock and amazement, nobody took up the challenge. In other words, nobody tried to uh refute what he said or give him any proof or explain to him where his reasoning or logic was incorrect, they just ignored it. And he went to the Royal Academy of Sciences in Britain, and he went to Nature that had published a number of his other papers, and they wouldn't hear him, they would that maybe they would hear him, but they wouldn't publish anything about it, they wouldn't present this to their members, they wouldn't give him a response. And I it I think most of the book is about his quest to have somebody tell him what was wrong with this um his reasoning, or to admit uh that this very important theory, which is basically the foundation of modern physics, is simply incorrect and should be immediately discarded before it does any more harm. And for 20 years he went about this privately, trying to get some response without any success, except a few things that basically had no relevance and didn't address his question. And so finally, as he says, he was forced to write this book to put it in the public record that science is really at a crossroad and that it is uh essentially failing the public and that people don't know about this. And here's what he he has learned, and here's what happened, and here's why science is failing the public, and his plea that we need to do something about this before something really bad happens. And it's very much the story of virology, and it's the story of heart attacks, it's even the story of Strephanthus. And I thought then there's a whole lot of back and forth, and this is the absolute final paragraph, it's an afterword written by a physicist, Alberto Pellazzi, in April of 2018, who's going to talk about, uh, write about what what this whole controversy was about. And I thought it was very interesting, so I'm going to read this paragraph. So this is explaining what what this controversy was about from Pilazzi's point of view. And so here's the quote. From a psychological point of view, it can be assumed that this attitude of passing from one assertion to another without being aware of the inconsistency of the whole text corresponds to a singular cognitive disorder that probably afflicted Einstein's personality and lasted all his lifelong. But what is relevant to the life of the world is not the psychology of any author, but the meaning that is built into the reader's mind given the character of an author's text. Einstein contradicted himself in a direct and immediate manner, without modesty and without any scruple of justifying controversial assertions, probably because he did not realize the problem on account of some serious cognitive impairment, but the effect is that the text, written in good German, with long periods and intricate syntax, takes with it its own strength, a serious tone, and an aura of depth and authority. A text that dares to contradict itself brilliantly and without looking for arguments intimidates the readers and stimulates them to attribute to themselves the lack of understanding much better than a text that tries to corroborate contradictions with fragile arguments. So let me tell you what I think that paragraph means, which is A. Einstein contradicted himself many times in the presentation of this theory, that is without a doubt. And he did seemingly without any compunction or shame or ability to understand what he was doing, which he attributes to a cognitive defect. But the most important point of this paragraph to me, and why it's still so relevant to what exactly is happening in the world today, is that as he says, when this is done without any investigation about these contradictions, even though they're glaring, it somehow convinces the reader that, well, the problem must be that I don't understand it, rather than the obvious contradictions of the presentation of the theory. Whereas if you present arguments and try to clarify what are obvious contradictions, then people will usually learn to follow it and see that they're contradictions and not buy the whole story. And that's exactly the problem we get into with virology. They present contradictions which are glaring, and they never address them, uh, even with so-called fragile arguments, and people are left thinking it must be because I don't understand it, rather than this is nonsense. And so, with that introduction, let's talk about heart attacks and strophis. So I basically got into this because of contradictions. So I, you know, even when I was in medical school, I was skeptical of the whole thing. Uh, but I never occurred to me that the idea that heart attacks weren't caused by blocked arteries wasn't true. It's just not something that ever occurred. So let's go through the claim. So the claim of conventional cardiologist, cardiology is we have a heart, it's about 1.1 kilograms. It's a relatively thick walled muscle, although thick is a judgment, so it depends on what you mean by thick. And the muscle is essentially fed primarily, if not exclusively, by three main vessels, which are called coronary arteries. So essentially that means all the blood that goes to your heart goes through these uh three main coronary arteries. Now, they don't explicitly say there's no small or collateral blood vessels, but that would be, I think, in the category of it's an obvious contradiction, as I'll show you, but they don't ever mention it, they don't ever talk about it except when pushed to the extreme. So they essentially show you and tell you all the blood goes through these three coronary arteries, like a plumbing, and your pipe gets clogged up with uh either cholesterol or inflammation or LPA or LDL or that changes over the years. But something in the blood is settling in your blood vessels, in these coronary arteries, creating what we call plaque. And then someday the plaque gets too much or it can rupture, and then the plaque gets lodged in the blood vessel, and the blood can't get through, and the area downstream from that blockage then doesn't get enough oxygen and doesn't get supplied with blood, and so then it dies, which is called a cardiac uh ischemic event, otherwise known as a heart attack. And that theory uh or that claim is the basis for the entire cardiology with reference to heart attacks. So, for instance, you give different drugs like statin drugs or put people on different diets, the idea is to reduce the plaque formation or to reduce the inflammation or to reduce the LDL or to reduce the LP little a or whatever of the theory of the day is that's causing the plaque to build up. And then if that doesn't work and you still get plaque, anyways, because after all, this is clearly a genetic disease, they say that's part of the claim. Then you have a blocked artery, and before you go on to have a heart attack and die, they go in and unblock the artery, and that's usually done with a angiogram and a stent. An angiogram is where they put a thread in and then put dye in so they can see how much blockage you have in your coronary vessels, and then if it's blocked to a certain degree, usually 80-90%, then they essentially rotor it out and then put a stent in to keep it from closing up immediately. And that's a set, or they do a bypass where they put a vessel in to make a bypass around that part that's blocked. And that's cardiology with there's other cardiology having to do with arrhythmias and congestive heart failure, but we're talking about the realm of heart attacks now, and so that's what cardiology is in a nutshell. Again, the claim is this is all caused by blocked arteries. There's three major arteries, that's where all the blood goes through. And if you get one blocked or two blocked or three blocked, or if you have four blockages, then you need to get these blockages bypassed or rotorooted and stented, which means you put something in there to keep the vessel open. And by God, you should have stopped it in the first place. And that's what we do with uh statin drugs, which lower the cholesterol, which is the thing that's precipitating in your artery, or they may also reduce inflammation. And by the way, if you're a holistic doctor, it's the same thing, uh, except instead of doing a statin drug, you can do a paleo diet or a raw vegan diet or something that all reduces the inflammation or reduces the LDL or reduces the LP little A and stops you from building up plaque, which is the reason. And everybody accepts that. Everybody from the cardiologists and the cardiothoracic surgeons to the holistic alternative cardiac people, everybody accepts that basic claim. Well, not everybody, because I had heard there was a group in somewhere, Portugal, Argentina, Brazil, or somewhere, that had a different uh theory about this. And so I at some point looked into it. But before that, and this was around the time when I was working part-time as an ER doctor, mostly to make money as I was building up my real practice. And so I ended up seeing over the years literally thousands of people who came with heart pain, chest pain, or were having a heart attack, or thought they were having a heart attack. And then eventually I wrote a book about uh human heart, cosmic heart, which talks about what I'm talking about today. And so I saw hundreds of people over the years whose issue was I don't want to have a heart attack, I just had a heart attack, should I have a bypass or a stent? So I heard a lot of stories around heart attacks, angina, which is chest pain related to your heart, or unstable angina, which is bad chest pain that comes and goes related to your heart. So the first thing I ended up thinking was, uh, and again, this goes back to uh there's a there's a lot of assumptions in this, and I always wanted to investigate assumptions and see whether they were actually correct. And so I just used simple mental experiments to see what I what what I could make of this. So if the idea is there's something that's too much in your blood, like you have too much cholesterol, or you have too much LDO, or you have too much LP little a, that's a kind of fat, or you have too much inflammation, and it's in your blood. And I, of course, said to myself, okay, is the blood the same everywhere in the body? Answer, as far as everybody knew, yes. As far as I knew, yes. We don't have a special blood through the coronary arteries that's different from the splenic artery or the hepatic artery or the femoral artery or anywhere else. It's all the same blood. What about the blood vessels, the arteries? Yes, they're the same too. They're made of the same thing, they essentially have the same structure. So if the idea is there's something in the blood that's too much and it's precipitating in the artery, and the artery is the same and the blood is the same, why wouldn't it precipitate everywhere in there in the body where there's arteries and blood? And so you would get plaque buildup in the splenic artery, hepatic. Artery, femoral artery, toe artery, eye artery everywhere. And in fact, you do. You do get uh plaque, maybe not quite as much, but you definitely get plaque in all the different arteries of the body. So if that's the case, and that was the cause of heart attacks, then, and I've asked over the every time I gave a lecture on heart, I would ask everybody in the audience, usually these were live. How many people know somebody who had a heart attack? Everybody raised their hand. Bill Clinton, Dick Cheney, and Uncle Fred, and you know, everybody else. How many people know somebody who had a spleen attack? Uh, over the uh 20 years or so, I asked one person raise their hand and she misunderstood the question. The one ER doctor did, but he meant that somebody had a ruptured spleen, which is not what we mean here. So nobody has spleen attacks. How about liver attacks? No, kidney attacks. I've heard that happens, nobody has ever seen it. So, how come the only organ, actually it's not the only organ because we have brain attacks, which we call strokes, how come only the brain and the heart have attacks caused by this uh blockages, whereas the other parts of the body have blockages, but they don't ever have attacks. That suggested to me that there's something different about the heart and the brain than there is about the spleen and your foot and your liver and your eye and everywhere else. So that was my first question. The second question I had was uh over the years, and this started in the ER, and then over the years in my practice, I heard this story literally hundreds of times. I was hiking with my wife, and we were going up Mount Tam or some other place that was in the Bay Area, and I started not to feel so good, and I had a little chest pain, and my wife said, I don't want you to die, so you go into the cardiologist, and he does some tests, and then he does an angiogram, and he says, You got a 90% blockage, and we're gonna have to put a stent in. Uh, it is if it blocks any more than that, you're gonna have a heart attack. Some variation of that story I heard over and over again. You have a 90% blockage, you have a 95% blockage, uh, you have a 93% blockage, etc. And if it blocks anymore, your curtains. And I remember thinking to myself, wait a minute, if all the blood goes is has to go through these three arteries and you have a 95%, 93% blockage, meaning you have five or seven percent going to this major area of your heart, how did you walk up Mount Tam? How are you even alive? And you mean to tell me that if you block from 5% blood flow or seven down to four or six or three, that somehow that's going to make a difference and kill you? And that made zero sense to me. Uh so the next step was I started looking into uh, okay, somebody must have come up with this theory and somebody must have proven it. In other words, you take people who die of heart attack, you do an autopsy on them, and you see how many of them had a blockage in the artery leading to the part of the heart that had the attack. Now, I was aware even then, I think probably vaguely, that just because somebody has a blockage post-heart attack, post-death, in an artery leading to a certain part of their heart, that does not mean that it caused the heart attack. Because there are many reasons why the blockage could have happened after the heart attack, not before. And I've given the analogy of if you have a free-flowing stream and then a beaver comes and builds a dam in the stream, you will get debris upstream from the dam. And if the beaver builds a dam that completely blocks off the flow, you'll get even more debris upstream from the dam. The blockage upstream from the dam was not the cause of the restricted flow, it was the beaver. And so, similarly, if you have a necrotic dead area of your heart, which is what a heart attack by definition is, you might see the flow into that somehow uh constricted, or you might get debris backfilled, backflowed up the artery. And so you might end up seeing more debris or more inflammation or more plaque in arteries that uh are leading to the area of the heart attack, but you don't know that that happened before the heart attack as opposed to against, as opposed to afterwards. And I never saw that problem addressed even once in the medical literature, except with a guy named Giorgio Baroldi, who I will show you a paper in a minute. But, anyways, I the first step was to look through the medical literature and see, okay, they must have done autopsy studies, and they can tell me what percentage of people have a significant blocked artery leading to that area of the heart. And to my interest, I would say not surprise at that point, I found that the range was, and again, uh this goes in the category which uh people have pointed out, the claim is this is the reason, the only reason why people have heart attacks. And so this is the uh swan story. If you claim all swans are white and you find a black swan, you have falsified the claim. So if you claim that all heart attacks are caused by blocked arteries, which is the reason behind why you say if you do an angiogram and you find clean coronary arteries or not significant blockages, you say, oh, you're fine, you're not gonna have a heart attack. So you can only do that if that is the only reason. So what I found is the lowest percentage of significant blockages on autopsies. So this is people who died of heart attacks. So these are the worst of the worst, not people like most of the time have a heart attack and they live and then they go on and you have to do something. These are people who died of a heart attack. The lowest was 18% had a blockage, which means 82% didn't. Uh and the highest I found was 78%. And that's not insignificant, that's a fair, fairly high number. But it also means there's 22% of the swans were black. 22% of the people had no lesions in the coronary artery, no blockages leading to the area of the heart that had the attack. So the obvious question is so why if they have a heart attack? I mean, we're told that's the only reason. So how how is this possible? Uh, and then I found this uh website by uh Knut Sroca and this video, which I'm gonna show you, which I think really clinches the deal for me. And so let me try to share that with you, and we're gonna watch the whole video. So I make sure that I have this on the internet so anybody can look at it at any time uh from now on. So I have to share my sound, so share. Uh let's go to this here. Hopefully you can see it. And here's the heart attack new, and this is the Wayback Machine, whatever that is. And so here's the video. And I'm not gonna blow it up because I'm afraid that will ruin it. In this short film, may it you I'm gonna I'm gonna stop it at occasionally. First of all, this is the kind of drawing that people show you with these three major coronary arteries, one, two, three. And this is obviously not a real heart, right? This is a drawing. But every time the cardiologists show you and they show you where your blockages are, they show you not a real heart uh with its blood flow, which actually, when you do that, you see uh thousands of little blood vessels, but they show you this picture, uh, which is fake.

SPEAKER_00

During an NGO, the right coronary artery at left hand will be filled with contrast medium using a heart catheter. Before we start the film, I want to show you the most important result of this examination in advance. You can see a severe narrowing is the noses in the midsection of the artery. Now let us take a look at the angiole. So that you can study the procedure in detail. Here is the first photo. At the upper edge of the picture you see the heart catheter with its curved end still empty of contrast medium. Now the contrast medium starts to appear. You can see the roughly S-shaped form of the upper section of the artery, marked by contrast medium. This is the most intriguing photo. Why is this? The most important feature is the dark strip marked at the bottom left of the photo. This shows contrast medium in a section far beyond the stenosis. Nothing can yet be seen of the narrowing itself. Despite this, a section of the coronary artery far beyond the stenosis is already filling up. Here for the first time the stenosis circled appears. This is the same photo. The narrowing can be vaguely recognized due to the descending flow from above, but mainly as a result of the ascending flow from below. Things now become clearer. This stenosis hardly allows a single drop of blood to pass. The stenosis allows practically nothing to pass. It's not the case, as a lay person might assume, that the blood somehow manages to squeeze through the bottleneck and struggles to fill the lower part of the artery. Yet it is exactly this section beyond the narrowing that is well filled. The blood must come from somewhere. Even if the collaterals, the vessels that make a detour around the stenosis, are not clearly seen. These photos are proof of their existence and effectivity. This is a perfect illustration of a ninety percent stenosis. However, this method fails to provide decisive information. It's not possible to show the extensive network of collaterals using the heart catheter. This leads to considerable false interpretations regarding the importance of coronary artery stenosis. In the very small narrowing, a little blood forces its way from above and a little from below. The blood in the stenosis is stagnant. If the narrow passageway is closed completely by a blood clot, a thrombosis, what happened then? Does a heart attack occur as generally assumed? By no means. The blood is already standing still in the stenosis. A complete closure would have no effect. There is no alteration whatsoever. There can be no better illustration. The blood supply to the heart muscle beyond the stenosis is completely unaffected. The right coronary artery is clearly and powerfully displayed far to the regions of its finest branches. The stenosis does not damage the heart. To familiarize yourself with these invisible collaterals, do take another look at this short film.

SPEAKER_01

Okay, so in other words, um and I'm I'm not going to switch to full screen for a minute here. In other words, uh we're uh bypasses and stents fix a problem which doesn't need fixing, because as you can see from this, and I've seen scores, if not hundred, other cat uh heart catheter films, angiograms, this is the same thing, the same story with just about every one of them. And the body uses collateral circulation, which is probably 90 to 95 percent of the blood flow, goes through these small vessels, and even when there's a blockage, there the body knows how to make its own bypass, use these secondary vessels to bypass the stenosis, and as you can see from the film, it has no impact on the blood flow to the heart muscle downstream. And that exactly correlates, and this is again, you make these assumptions, and then some things are hard to understand, like why don't stents and bypasses have been shown, why haven't they been shown to increase lifespan? Why haven't they been shown to prevent further heart attacks? And even in the best study, which was in the Lancet, I think 2018, uh, where the first time they uh did a actually control group, and half the people they put a stent in, and the other half they didn't, and six weeks later they had the same amount of chest pain, showing that not only do they not uh prevent further heart attacks, that means stents and bypasses, they don't uh lengthen your life and they don't even actually reduce your chest pain compared to a placebo react uh dummy experiment where they put in a catheter, they tell you they put a stent in, but don't. Six weeks later, you have the same outcome as if they put a stent in. So all that stuff, which is just assumptions that it must be right because you have a blockage, but nobody ever actually goes through the logic and the details, turn out on examination to not be true. And this perfectly explains it all these findings about and why that um the blockage is not the cause of the heart attack. And I just want to show this uh study. This was a paper by Giorgio Baroldi and a few other people, and you can see let me just get it a little bigger. Um he's the second author, and he's the pathologist from Italy who essentially diagnosed or looked at thousands of people on autopsy uh who died of a heart attack and asked the question: did they die? Is the edio pathogenesis of heart attacks actually blocked arteries? And I'm not gonna spend a whole lot of time on this, but what you can see from this is the occurrence of thrombi, that's blockages, was associated. Hang on, let me back up a little. So the first anomaly of this, this is from 1980, um, and here you can see the reference, it's uh circulation, official journal of American Heart Association, volume 61, February 1980. In other words, your first problem is 55% of the people who died of a heart attack had no significant blockage in the artery leading to that part of the heart. Now, 45% did, and when he goes through this, he tries to ask himself the question uh or ask the question: do we know that these uh thrombi that were found in 45% did they actually come before and not after? And he goes through this, and you I won't go through this because it's pretty complicated. But the bottom line, uh, let me just read the the conclusion. Two other morphological feet forms of myocardial necrosis were found associated with infarcts. Their pathogenesis and role in acute infarction must be clarified. These data support the concept that an occlusive coronary thrombus has no primary role in the pathogenesis of myocardial infarct. In other words, the blockages did not cause the infarct. So there must be some other reason, and whether we know the reason or not, he and Sroca give evidence that the reason is a suppressed parasympathetic nervous system. In other words, you could almost say stress, and that becomes uh a decreased energy flow through the heart, and that would also be through the brain, which are the two organs that require the most energy. They have the most mitochondria, which are allegedly the energy uh creating organelles in our tissues, they're they're most prevalent in the heart and the brain, and those are the two organs that can't stop. So if your leg uh essentially runs out of energy and you start building up uh acid, uh as happens when you do a so-called glycolytic shift. And I don't want to get too much into this right now, but you you switch your metabolism, then you build up lactic acid, and that causes cramps and pain in your leg, just like it causes cramps and pain in your heart, and we call that angina in your heart and leg cramps in your leg, and then your leg stops and the lactic acid gets flushed out, whereas in your heart it can't stop, the lactic acid builds up and that acidifies the tissue and then causes a breakdown of the tissue or a necrosis, which is exactly what you see with a heart attack. So the two reasons that are primarily given for heart attacks uh as opposed to the coronary occlusion theory are having to do with an imbalance in the parasympathetic nervous system, meaning a suppressed stress uh parasympathetic nervous system, which means a excessive stress or excessive sympathetic tone, and the buildup of acid because of decreased energy supply and flow through the tissue. Now, whether or not those are actually proven to be the case, is uh I don't want to get Into trying to prove some other theory. I think at this point, all we can say for sure is the claim that all heart attacks are caused by thrombi occlusions, plaque buildup in the three coronary arteries has been shown to be false. So now we have the problem of what do we do with these people who have chest pain, and it's not to say people don't have chest pain, it's not to say people don't actually die from heart attacks. That is not what we're saying. We're just talking about so why does that happen? And is there anything else we can do about that? And so here we go to the frequently asked questions. And again, I want to get this on the internet so anybody at any point can see it. And it's under the uh heading of Wabain, the wasted opportunity. So let's go there, and hopefully anybody who wants can see this. Now let me make a few introductory comments. So, first of all, he calls it wabbeene, which is the so-called active ingredient or the chemical uniquely found in the seeds of the Strephanthus plant. But I would say that at uh I because I know what uh medicine containing wabbein uh Sroca used for his career, and it was basically uh originally Stratoval, and then he also used the extract from T Brazil. So at no point did he actually use or were any of these studies actually done on the pure chemical called Wabine. You can buy Wabine from many different chemical supply stores. It is supposedly the exact copy of the active ingredient found in Strephanthus seeds. But at no point were any of these studies which he's referring to done with pure wabeine. They were all done with strophanthus seed extract that contains wabbeine. That's very important. Stratoval, which was the main form of strephanthus seeds used in Germany for decades, uh, was a Strephanthus seed extract. And that essentially, when the Stratoval company went out of business, it morphed into the capsules that Soroka and De Busman and others had a hand in formulating, which was essentially just a reformulation and essentially an upgrade of the original Stratoval formulation, and they were uh Strephanthus seed extracts, as is T Brazil, which is basically soaked for a month or so in alcohol, uh, strophanthus seeds, and then we and others have checked them for wabine content, which positively identifies that the seeds were from strophanthus, because as far as we know, that's the only source of wabine in nature. We've also tested our supply of strophanthus capsules to make sure that they have wabeene in them, which positively identifies them as being from Strephanthus. The other thing I want to say is it's when you look at studies, and I've been over this many times, and I'm going to go over it probably many more times in the future. I am to the point in my evolution of my thinking where I pay no attention to any study that uses uh essentially cell cultures or purified chemicals on biochemical pathways as having any relevance to what happens in a patient or a member of our clinic or to somebody that I know or anybody. As far as I can see, any study on putting chemical wabine in a cell culture and seeing what happens, or a uh interacting it with an alleged BRCA2 gene, or there's I looked and found 1,200 different studies on wabine and cancer, and literally every single one of them was they took a cell culture or they took a growing cells that are allegedly from breast cancer and they put some wabine on them and it did this or it did that. And as far as I can see, that has no relevance to what anybody wants to know, which is if I take Strephantha seed extract and I have chest pain or I'm worried about having a heart attack, will that help me out? The only studies I want to see these days are a study that you have a hundred or a thousand or ten thousand or ten or some amount of people who have more or less similar, if not identical, symptoms. In other words, they can walk a hundred feet without having pain, but then a hundred feet or up a certain hill, they get pain in their chest. You divide them into two groups. The only thing different you do with the two groups is one you give them a strophanthocide extract, and the other you give them something that looks and smells and tastes exactly like a strophanthocede extract, and you say, go live your life and come back in a month or a week or six months or whatever it is. And maybe you do some tests that don't interfere with people's physiology, like you do an EKG, or you do a cardiac echo, or uh you put them on a treadmill and see how long they can walk, or something like that, uh, where you can see how they're doing, and the independent variable is the Strephanthus seed extract, and the dependent variable is predominantly how are you feeling? What is your function? Did you have more chest pain? Can you walk longer? Do you feel better, etc.? And then you can use some uh supplemental uh objective tests like EKGs, etc. And that is exactly the kind of studies you see with Strephanthus. So here's some examples. So in 1984, 150 heart patients suffering from attacks of angina were treated with wabine, and again, he means Strephanthus seed capsules, they're probably Stratoval, in a clinic in Berlin. They had some were told to do bypass, do the severity. The usual medicines were stopped. After one week, 122 patients were free from anginal complaints, and after two weeks, this was 146 of 148. Uh, they had minimal unpleasant side effects, headache, dizziness, lack of appetite, but all these disappeared. Only two patients decided not to keep going due to some probably diarrhea, which I have actually the only side effects symptom that I've ever seen. Uh, and then they had EKGs or ECGs to document that they had better uh electrical activity of their heart. And then there's some other ones, uh, the doctor, and these are mostly observational, but they're the kind of things I'm looking at. Uh, they were treating people with exertional angina. After two weeks, the patients who had taken wabine, again, meaning strophanta seed extract capsules, a clear decrease in the number of heart seizures or pain during activities, and their physical capacities had increased. Objective proof was improvement in the patient's EKG recordings, and their subjective well-being was greatly improved, and they did a full placebo group, and they showed no notable improvement. Uh, here's another study that he mentioned from a university clinic in Freiburg, Germany. It was found that uh patients who took with angina chest pain who had taken one dose of this concentrated Wabine drops on the tongue, and I'm not sure what they're referring to there, uh, but probably it was Strepanthocet extract concentrated, the stroke volume and performance of the heart significantly increased after half an hour. There was also an improvement in the EKG, indicating that the metabolic disorder, or what I'm calling the energy flow through the heart, had disappeared. This uh this was only after a heart uh one half hour. Uh, and then there was the study of 1800 miners working underground. This was in the 1970s. It was done by a guy named uh Professor Kern, and they had a lot of heart attacks and people dying of heart attacks in the mines, and then they gave everybody surfanthus, and then there was only two deaths instead of around 30 deaths, and so Wabain uh made it possible to drastically cut the rate of death by heart attack in the large coal mine and almost reduced it to zero. Uh and then there's some other things here that Wabaein Strephanthus extract, leading medication for treating heart weakness or what we call congestive heart failure for over half a century. Um and other things here about people's uh subjective response to being treated with strophanthus seed extracts. So here's a little bit of the history of it and the so-called alleged, I would say, chemical formula for Strephanthus. And then the he talks about the scandal and how they got rid of it. And mostly uh this was because they were introducing the plaque theory, and there's nobody was claiming that Strephanthus Wabine had anything to do with decreasing plaque or bypassing it, so it must not be working. This is again an example of even though the evidence was clear through the small studies that they did, and by the way, I'm not claiming that any of these studies are definitive. Uh, I would love to see more scientific studies doing just that, having the Strephanthus seed extract being the independent variable, and chest pain or EKG changes or and EKG changes, and uh incidence of heart attacks being the dependent variable, and have these all clearly defined because what I've seen for my 30 years of using it is so many different people who had results that I never would have thought possible with any other way of decreased chest pain, increased performance, increased stamina, uh seemingly needing to have bypasses, who went on to be asymptomatic and lived five, ten, or more years. I saw very few uh, if any, negative effects, except a little bit, as I said, of some intestinal distress. And so I just thought it was important to put the uh whole history of Wabine and what studies we do have in, and then there's some mechanism of action. Uh, as I said, it stimulates the uh parasympathetic nervous system and it inhibits the sympathetic nervous system, which is exactly what they say uh beta blockers are doing, which is blocking the sympathetic nervous system. So this is not an unknown mechanism of action, even for normal cardiology. Uh seems to do that in the brain. And there's uh a thought that it's actually wabene is a naturally produced hormone, if that even exists, that's found in the adrenal glands, and that somehow these uh Strephanthus seeds are just essentially making a kind of bioidentical copy of this naturally occurring substance, which is there to stimulate our rest, digest, life is good, relaxation, nervous system to help us combat the effects of stress and metabolic uh inefficiency in ways which we probably don't know and may never know, but you can see the effect on what happens with people, both from just observing the effect over and over again and the few studies that were done. So one of the uh pleas that I had from Dr. DeBuzman was we cannot, those of us who are understand the benefit of Wabaein, it is a wasted opportunity, uh, and we cannot let this amazing medicine, this amazing plant just die out and never heard from again. So hopefully, by putting uh this article, and I hope everybody goes to it, if you can find this uh on the Wayback Machine, goes to it, reads the whole website yourself. I'm not sure how long it's going to be here, and you can see the whole history of the theory uh or the issue around why we have heart attacks, what we actually know, what has been shown and not shown, and a medicine which may be uh the what the native people call it the gift from paradise. So thanks everybody for listening, and I hope this gets some wide distribution uh so we actually don't let uh Wabaein be a wasted opportunity, as could otherwise be the case. So thanks everybody and have a great week.