➡ The text discusses the concept of genetic diseases, focusing on a specific syndrome believed to be genetic. The author questions the validity of genetic theories, stating that many aspects of genetics are unproven or even disproven. Despite this, the author assumes these theories are correct for the purpose of examining a case study about a woman with a supposed genetic disease. The woman and her husband, after discovering she carries a gene mutation linked to a fatal insomnia condition, leave their careers to become scientists and potentially find a treatment.

➡ Fatal Familial Insomnia is a life-threatening condition that resembles Alzheimer’s or dementia, caused by a mutation in the PRNP gene. This gene mutation leads to misfolded proteins in the brain, specifically in the thalamus, which regulates sleep. However, the exact function of the normal PRP protein is unknown, and there’s no clear correlation between the amount of mutant protein and the severity of the disease. Despite the mutation being linked to the disease, many aspects of its effects and how it leads to the symptoms remain unclear.

➡ The text discusses a study about a disease, comparing it to a house built with defective nails. The severity of the disease doesn’t correlate with the number of defective genes a person has, just like a house’s stability doesn’t depend on the number of defective nails used. The text suggests that there’s no clear understanding of how these defective genes (or nails) cause the disease (or house to fall). The author concludes that the theory lacks evidence and correlations, making it hard to believe.

➡ The speaker criticizes researchers for developing ineffective drugs based on unproven theories, which he believes are misleading and harmful. He argues that there’s no clear link between the supposed cause and the disease, and suggests that this issue is common in genetic disease research. He expresses regret for not questioning these theories during his medical training and ends by apologizing for the poor sound quality and wishing everyone a good week.

Okay, welcome everybody. Today is another Wednesday webinar. Today is Wednesday, May 28, 2025. And as always, thanks for joining me. So today the main topic is going to be about genetic diseases, so called genetic diseases. And but before I get into that, I have a few other things to bring up. The first is I actually just tried the, just original, I guess you say, plain sauerkraut that we’re selling on our website, Dr. Cowan’s Garden. And I gotta say that I’ve probably made hundreds of jars of sauerkraut in my life going back at least 30 years, maybe more.

And this is one of the best sauerkrauts I’ve ever eaten. Enough so that I may end up, even though I have four crocks and a bunch of things, you know, with springs and all that I can make it in jars or crocs, etc, and I’m pretty used to making it, I may end up not making it, not growing cabbage and just getting our own sauerkraut because I recognize a better tasting product when I see it. So I hope everybody gives it a try. And if you’re a sauerkraut devotee like I am, I think you’ll really like it.

So that was the first thing. The second thing is I actually got an email this week from Mark Bailey, a good friend of the show and of us, telling me about how the mainstream media, and I’m not sure which part of the media in New Zealand has done at least one piece and maybe more on Sam, his wife, Sam Bailey, and, and specifically criticizing and maybe even mocking her so called no virus position. And I just want to say that when I heard that, I was profoundly. What’s the word? Offended. Yes, profoundly offended by when I heard that.

It was similar experience to. I remember a few years ago when they came out with the dis information dozen. And even though I had written books about the dangers and the horrors of vaccines and how nobody should ever get a vaccine and the COVID shot, etc. I somehow was not on that. Disinformation doesn’t. And I remember my son Asher saying at the time that I needed to up my game. And I’m sure he was correct. So that’s really when the weekly webinar started. And I’ve had more to say about it. And I don’t know if they came out with a updated disinformation dozen, I would, I would make the list.

I hope so. But analogously, to do a story on the mainstream press and not mentioned my work on the no viruses or Mark’s work on the no viruses position. I mean he’s written probably the definitive paper and they’ve written a maybe the definitive work on the science falsifying the viral hypothesis. Not mentioning the numerous, countless lectures and webinars and public talks that Andy has given. And same with Mike Stone and that, you know, I don’t know, scores or hundreds of of articles and information that he’s come out and to not mention any of us and only pick on Sam is just not right.

So I think Mark and I and probably the others will offer to have a conversation with any members of the New Zealand or literally anywhere in the world press or media to go over this issue of has a virus actually been proven to exist? So I await their response and hopefully it will be soon the next thing and hopefully this is going to be short. I just wanted to give a brief update on the bird flu situation because I was in made aware of a paper and let me show you this paper. So I’m going to share that the Department of Health and Human Services sent to I guess it was the director of the Canadian Food Inspection Agency.

So that’s probably sort of like the FDA or something in Canada talking about they value our partnership and collaboration and they had certain requests and I just want to point out the anti scientific nature of this, this letter to President McKinnon. So for instance, they highlight three things. The flock is a controlled environment which enables longitudinal studies of the natural history status post H5N1 infection which of course we know doesn’t exist. So that’s pseudoscience. The ostriches can live up to 50 years. That’s probably true. Providing the opportunity for future insights into immune longevity associated with the H5N1 virus.

That is complete pseudoscience. There is no immune longevity to a non existent virus. Then the potential to study both antibody levels and cellular immunity to help further our scientific understanding of the virus and the immune physiological response. There’s obviously nothing scientific in any understanding of a virus that doesn’t exist or a antibody or cellular immunity response to a virus that doesn’t exist. And the opportunity to study the important principle of antibody dependent enhancement and possible therapeutics in the setting of prior in the setting of prior infection. It’s obviously another example of pseudoscience as is this whole paper because there is no evidence as I went over last time that there is a virus or a antibody or otherwise so called immune response to something that doesn’t exist.

And while as I said last time, I support wholeheartedly the non slaughtering of these innocent ostriches because they didn’t do anything. I also need to see that or wish to see that in conjunction with stop torturing them by injecting them every two weeks with a poison which has no scientific value and stop using this as a pseudo scientific experiment. Just raise the oyster, the ostriches, let them live happy, healthy lives. If they need to breed them to further other ostrich farms, that’s fine. But I think that anybody involved in this really needs to demand that they stop these pseudo scientific experiments and just get on with raising healthy ostriches and maybe breeding them for other farmers to raise healthy ostriches and stop all this pseudo scientific experiment.

Now, it was interesting to me to see, well, who wrote this stuff, this paper, and here you see the second sheet on the paper here. I won’t enlarge this. And it’s obviously signed by three people. The first is Robert F. Kennedy Jr. Who’s the secretary for the United States Department of Health and Human Services. And I think it’s also interesting, as I just found out, somebody put in the comments, the word Kennedy is a Gaelic word that means head wound or ugly head. So I thought that was interesting. But anyways, so we know from his own mouth, from his own words that he doesn’t understand or doesn’t know how a virologist proves there’s a virus and shows that it exists.

He said that a few years ago. And my guess is he hasn’t updated his knowledge. So it would therefore be not possible for him to have written this, this, this, this letter because he doesn’t know whether there’s a virus or not. Which is an interesting thing to have a, the director or the secretary of the most important department in the United States government, the Department of Health and Human Services. The leader of that is somebody. And the Department of Health and Human Services is obviously very much connected with the whole virus story and probably spends billions of dollars a year researching viruses and managing viruses.

And to. It’s ironic to have a leader of the department who doesn’t know whether there’s a virus or not, doesn’t know how a virologist would know that, and doesn’t seem to be interested in the subject. So then I thought, what about the next guy, which is, I think his name is Dr. Bought a Chair. And I think that the reason he was brought in was because the NIH was doing sloppy research. This is by all accounts, and one of the reasons they thought this might be the case was they didn’t have enough chairs. And the researchers had to stand on their feet all day long.

And of course then all the blood rushes out of their head into their feet and so they can’t think properly. And then they end up doing poor research. And so they did the only sensible thing, which was to bring in somebody who could buy some chairs. So they brought in doctor bought a chair and he was able to buy some chairs. And hopefully that will result in better research. But I don’t think that he could have written this letter either because he’s mostly concerned with buying shares, not the subject of virology. And then it was very clear that the third person, the commissioner of the Food and the FDA, Food and Drug Administration, I think his name is Dr.

Malarkey. And since this paper is 100% Malarkey, it was pretty obvious that it must have been Dr. Malarkey who wrote this paper. And so I think we now know who wrote this paper couldn’t have been Kennedy or Dr. Bought a chair, so it must have been Dr. Malarkey. Okay, so let’s stop this for a minute. Let’s go on now to the main subject, and that’s about genetic diseases. And so I wasn’t planning on doing this, but you know, one of the purposes of these weekly webinars, as well as, you know, obviously having some interaction with the people who seem to care what I say and what I think, which is kind of fun for everybody.

So hopefully that’s going well. But it’s also to put a body of work out there examining the actual evidence for our current science, so called science, and our current system of biology and medicine. And as we probably all know, the whole concept of genetics and in particular genetic diseases is, I would say, rampant in our world. You know, it’s one of the main things you hear when you go to a doctor’s appointment that while your diabetes is genetic, your heart disease is genetic, the reason you have blood disorder is genetic, the reason your psychiatric case so called, is because of genetics.

Everything is because of genetics. So I ran across this article with which was a article about something that is a clear claim for a genetic disease. And I thought it would be interesting to look at the evidence that they present. It is presented in various papers on this particular syndrome. Now, I want to just be clear that when I’m doing this, I’m going to be assuming or working under the assumption that the basic concepts and what we call genetics are correct, which is actually, as we probably all know, is not actually the case. They’ve never isolated a DNA.

They’ve never isolated and proven that nucleotides exist. And as far as I know, there is no direct proof that so called genes or sequences of DNA directly code for specific proteins. So all that I would say is speculation. In other words, it’s a kind of story that’s being told. But I’m going to assume that all those things have been shown to be true. There is something called DNA. It does organize itself into sequences, segments that we call genes. And the genes code for proteins. And that when one of the nucleotides, the component of the gene, essentially the letters that make up the sequence of letters in the DNA sequence is changed, that’s called a mutation.

And that mutation results in the production of a different protein which has health consequences. Now again, I want to be clear that I consider all those things that I’m assuming now to be true to be at least not actually proven at this time, if not actually already falsified. So let me just be say that once more. As far as I can see, none of those things I just said the existence of the DNA, existence of nucleotides, the sequence of DNA coding for a specific protein, and a change in the sequence being a mutation and creating a different abnormal protein.

And there’s a final one which is that it becomes the engine for evolution. All those things are given are taken as fact, fact in the study of genetics. And I don’t think any of them are actually facts at all. Some of them have been falsified and some of them at least have not been proven to be true. But for the next half an hour or so, we’re going to assume those things are accurate and we’re going to look at the case for whether this syndrome is actually a genetic disease, assuming that they have the basics of genetics correctly.

So I just want to be very clear about that. So what led me to look at this particular syndrome was a paper that I found. I don’t know where I found this, but I typically never know where I find anything. Okay, so like a lot of stories in science so called and biology and medicine, there’s often an emotional hook to get which helps you or convinces you or facilitates people believing in the story because they’re already emotionally invested in the story being true. So this is the story is called One Woman’s Race to diffuse the Genetic Time bomb in her genes.

So already we have a sort of heroic story. So we’re going to have a heroine in the story and how DNA sequencing and new genetic drugs raise the chance we can cure any inherited disease. So this is exciting news. And this was in the MIT Technology Review. So the story is 2011, this woman was handed a genetic report that contained a death sentence. So again a very emotional story here. But it also held a map for her how to escape her body. She learned harbored a gene mutation, a wrong letter of DNA in her quote quote prion gene that would eventually lead to a rare brain condition called fatal familial insomnia, which I must admit I’ve never heard of and sounds like somebody who just goes can’t go to sleep ever.

And it runs in families. They say her mother died of it the year before and the test revealed that she had inherited the flaw as well. This led her to make a heroic decision which they call a prion love story called by the New Yorker. And they dropped out, the husband and wife out of their careers in law and engineering and they became scientists dedicated to diffusing this gene or this syndrome. They got PhDs in 2019 and then after seven years they thick they have found a treatment that they can do it. I also want you to I pointed out to notice the words they often use in these so called scientific or this isn’t a scientific paper but they use they may have found or they think they found or it’s possible that they have found a treatment which of course also means it’s possible they didn’t find it and they may not have find it.

But anyways they use those same words over and over again in scientific papers and it’s called an antisense drug, which is of course not to be confused with a nonsense drug like most of the drugs. So this is not a nonsense drug, it’s an antisense drug. It’s a mirror image of the molecule that reaches the brain could greatly reduce the amount of the prion protein. Of course that means it could not. This could potentially. So there’s the use of two words, could potentially, which means it could not and potentially doesn’t forestall the mysterious chain reaction of misfolding proteins that characterize prion disease.

Less of the protein shape, she reasoned, less chance she’ll get sick. I want you to remember that line they’re saying here, less protein, less sick. So they announced that they’re pioneer or working with a commercial firm, a California biotech company which specializes in nonsense compounds. I mean antisense. And for the first time she’s optimistic. It’s plausible, she says, that antisense could treat the disease in our lifetime. Which means it’s also plausible that it doesn’t so let’s stop there and go on to the next. So then from here I decided to look into this disease because I’ve never heard of it, never saw anybody with it, and also particularly wondering about, about what the difference is between fatal familial insomnia and other diseases.

So let’s look at the next paper. So this was a paper I found called fatal familial insomnia. And here’s the claim. Remember that we’re always looking for the claim to see whether the claim is true. If you make a claim then you have to be able to substantiate it. So I first I had just read the story about the couple that has decided because they found out because her mother died and she found out she has the mutation that causes fatal familial insomnia. And they set out to get PhDs in biology or genetics or something. And now they’re hot on the trail of anti sense drugs, not to be confused with nonsense drugs to treat the condition.

So then I went on to look at. So what is this fatal familial insomnia? So here is the claim and as always, the claim is what the medical establishment, the doctors are saying. We know about this. This is the, the. Yeah, the claim. So fatal familial insomnia is a rare genetic condition. So first thing, they have definitively said that this is a caused by a genetic defect that causes sleeping difficulties, insomnia, memory loss, dementia and involuntary muscle twitching. The condition gets worse over time and it’s life threatening. There’s no cure, but treatment temporarily slows down the progression of symptoms.

At this point, I think they’re talking about things like sedatives and Klonopin and stuff like that. Okay, and then we go down to the symptoms. So how do we know somebody has this? What are the symptoms of fatal familial insomnia? Include difficulty sleeping that gets worse over time. That’s progressive insomnia, nervous system overactivity, including high blood pressure, faster than normal heart rate and anxiety, memory loss, hallucinations or seeing or think thinking that something’s there that where it isn’t. Like viruses. So if you see or think there’s a virus there, that constitutes a hallucination, involuntary muscle twitching or jerking, otherwise known as myoclonus.

So interestingly, these are very similar to what we call Alzheimer’s disease or dementia. And now there’s something that I also want people to remember, which is the symptoms of fatal familial insomnia begin between the ages of 20 and 70, the average onset of symptoms is age 40. So it starts anywhere between 20 and 70, which pretty much covers most of adult life. And I want you to remember that because we’re going to get back to it. Early symptoms, they look very much like Alzheimer’s or dementia. And then if you have any of these symptoms, you should see a health care provider and it can be life threatening.

So then let’s go down here a little bit more. What causes fatal and familial insomnia? A mutation or change of the PRNP gene causes fatal familial insomnia. So again, there’s a mutation in a gene, and that is the gene responsible for making the prion protein. That’s a kind of protein. And the prion protein, prpc, exists in your brain, specifically in the thalamus, which helps regulate body functions like sleep. When there’s a mutation in this PRNP gene, the amino acids that build up the proteins don’t have the instructions to build the proteins correctly. This mutation is similar to folding your laundry.

If you’re unsure how to fold a T shirt, you might ball up the fabric and put it in the drawer. Over time, the drawer becomes progressively more difficult to close because you have several T shirts that aren’t folded correctly. So misfolded T shirts are PRPC proteins that collect in your brain, become toxic to your cells and your nervous system, which creates symptoms. So it sounds from that like they’ve got this all worked out. You got this mutation in the gene and that creates a different protein and it doesn’t fold right. And then your brain gets clogged up with T shirts or these misfolded proteins, and that specifically happens in your thalamus.

And then you can’t go to sleep and you jerk and you see viruses and stuff that isn’t actually there. So that is a very specific claim as to the cause of this. And we’re going to get back to this a little bit later. So now we go to the next study, which is called fatal familial insomnia, a prion disease with a mutation at codon 178 of the prion protein gene. So you got a bunch of authors, New England journal of Medicine, 1992, for fatal familial insomnia. New England Journal of Medicine, 1992. And so there’s just, just.

There’s only one thing I wanted to talk about, even getting more specific about the, how they found this. And they say in the method section, in the abstract, we used antibodies to Prion protein to perform dot and western blot analysis with and without proteinase K and et cetera. They go on from there. So the important point I wanted to mention is they use antibodies without in the paper demonstrating that these are actually specific antibodies to this PRP prion protein, which, and we know from many talks before that the antibodies are not specific. Okay, so that’s the next one.

And then this is the most important study which was next, and this is called Molecular Pathology of Fatal Familial Insomnia from the journal brain pathology from 1998. And I was going to read the whole abstract, but I don’t think I’m going to. But it’s the same thing. Fatal familia insomnia is linked to a mutation at codon 178 of the prion protein. It’s the same. And they talk about infectious proteins instead of infectious viruses, and they talk about what they did in here. And it’s all very complicated, specific, hard to understand for anybody, myself included, about what they actually did and how they demonstrated this.

But the reason I wanted to show this, and I do want to spend a little bit of time on this, is to go over what they call the unresolved issues in fatal familial insomnia. So the major issues remain to be solved in order to reach a clear understanding of the pathogenesis of ffi. And first of all, that’s interesting because it seems like they’ve got it all worked out here. But anyways, they say now we have some major issues. The first question concerns the potential effects of the mutant PRP on protein processing, cell function and structure. Our cell model indicates that the in FFI, the D178N mutation, probably through an effect on confirmation, destabilizes the mutant PRP.

Consequently, only 30% reaches the cell surface, allegedly the site of the normal function, while the remaining aggregates or is degraded, probably by the quality control system of the cell. So I want to just point out that they’re weaving a story here, which is clearly a story they don’t have evidence for any quality control system of the cell, a mechanism thought to promote the repair or breakdown of harmful proteins in the endoplasmic reticulum. In addition, the protein that reaches the cell membrane shows this significant alteration. And here’s the first important line in this. The effects of these changes, however, remain difficult to assess at a molecular level because the function of the normal PRP is not known.

So in other words, this whole paper is about the abnormal function of a mutated PRP protein, a mutated gene resulting in an abnormal protein. But then they admit that the function of this protein, even though they have this whole story about where it is and how it appears, is actually not known. And then they say tests such as PET and polysomnography have failed to demonstrate any abnormalities in the carriers of FFI before the clinical onset of disease, suggesting that the dysmetabolism of the mutant protein has no major dysfunctional effects. So in other words, they can’t find any evidence of this mechanism that they just spent the last six pages and they actually have doubts whether the mutant PRP has any major dysfunctional effect, which is the whole point.

In other words, the whole point of this story is that a mutant PRP has major dysfunctional effects, meaning you can’t sleep and you twitch and you get demented and then you die. Here they’re contradicting themselves saying there’s no major dysfunctional effects since in patients with clinical symptoms, even in case of very short duration prp, the abnormal one, is invariably detectable. It may be surmised that the clinical onset only occurs when sufficient amount of the abnormal one is formed. How this conversion of the mutant PRP to the abnormal one occurs and why it occurs only at a relatively advanced age remains to be determined.

In other words, they don’t know why this doesn’t this only the people are normal until relatively advanced age. And then all of a sudden they get a seemingly sufficient amount, although they, as we’ll see in a minute, there is no increased amount. And then suddenly they get all these symptoms. Okay, I’m going to skip down a little bit here. So in the last paragraph, I want to take a look at this. The mechanism regulating the topography of the mutant protein formation and its relationship with neurologic neuronal dysfunction, histopathology, and ultimately the clinical course of the disease and FFI remain enigmatic.

So let’s, let’s dissect that a little bit. They’re saying that the relationship of the abnormal mutant protein, which is the whole story they’re telling, so they’re saying you get this mutant DNA which makes a mutant protein, and the mutant protein, like socks in your drawer or misfolded laundry, builds up in your drawer and then it causes you to not be able to sleep and be demented and have muscle twitches and then die. And now they’re saying the relationship with the dysfunction of the nerves and how this actually works and the clinical course, like how it actually relates this, the buildup, so called, of this protein Remains enigmatic.

In other words, we don’t have a clue. As mentioned before in ffi, the distribution of the abnormal protein prp, this one, as well as that of the hypometabolic brain area detected by PET scanner are more widespread than the histopathological lesions. In other words. So they’re saying that the place in the brain that it affects because they’re saying the thalamus controls you whether you go to sleep or not. And so you should see it in the thalamus, but turns out you see it essentially equally in many other parts of the brain and that doesn’t make any sense.

So when you start looking for it, they don’t see it. A correlation with the place you find the protein, allegedly and the symptoms. In addition, there is incomplete correlation between the levels and the severity. And again, I want you to take a think about what they just said. In other words, there is not a correlation between how much allegedly of this mutant protein you have and how bad your disease is. Think about that for a minute. There’s not a correlation. In other words, if you have a lot of this protein, you may have no disease or little disease.

If you have a little bit of this protein, you may have horrible disease. Either one could be true. There is incomplete correlation. For example, the thalamus and the brainstem continues contain similar amounts, but the thalamic lesions are much more severe. In other words, you could have a lot there and a lot in the other place, but you only see symptoms in the one place. Similarly, apoptosis, a recent finding, does not correlate with the amount of PRP mutant one. So they say, even though they observations suggest that accumulation may be a cause dysfunction. That contradicts what they just said.

There’s a selective vulnerability that’s a escape route. Saying it could be that there’s increase causes more symptoms, but not actually. But there’s actually a vulnerability and we don’t know anything about that. And this needs to be investigated. The duration of the symptoms among subjects with homozygous or heterozygous is also puzzling. There is no overall correlation with the severity of the pathology or the degree of accumulation, since the subjects with the shortest course have the least amount pathology in most brain regions. In other words, here they’re saying whether you have two copies of the gene or one doesn’t correlate with how bad the disease is and the severity of the disease doesn’t has no overall correlation with the degree of accumulation.

So then they go on to make excuses for this. So there Must be other factors unidentified. That impair the neuronal function before the appearance of significant pathology, etc. Now one of the things that I keep talking about that has to do with science and medicine and virology and just about everything we’re talking about is if you try to. Let me just make sure I got all this. I think I do. When you try to read this. Let me stop the Share when you try to read this paper, if anybody decides they want to do such a thing, you, your head will spin as did mine because there was no way I could get through and understand and have any clue what they are talking about in that six page review article of this, of this study.

So the natural tendency is to say I don’t know what these guys are talking about. There must be something to it because they seem like smart guys and they couldn’t possibly be making this stuff up. It’s like the old story. If you tell a huge lie, people think it must be true because nobody would make that up. So they telling this huge story about how this happens. But then you go down and you find the contradictions. So I thought I would try to put this in a way that hopefully brings this all together and you can understand because probably most of us, including me, didn’t really understand what they were talking about.

But here’s the, here’s, here’s the way to try to understand this. Compare this to a house. So you decided you’re going to look at this house to buy and the house was recently built and then you were told by the builder that the people who built the house possibly, again that’s important word here, possibly used abnormal nails which are defective in abnormal and defective nails which might impact the integrity of the house and therefore in the integrity or the decision you might want to make on whether to buy the house or not. Let me say that again.

You come onto a house newly made, you talk to the builder, he or the agent, he says, the builder says that they used abnormal mutant nails or they may have and the nails may be defective and they may have used them in the house. So you asked the agent or the builder if they in fact used these mutant defective nails, how long would they expect the house to last with these mutant nails? And like in our story with the FFI, they say, well, the house should last 20 to 70 years. Okay, so what about if all the nails were the normal nails, how long would it last then? So now this is the question of when is the onset of normal Alzheimer’s or normal dementia in People? Well, it’s anywhere between 30 and 70.

There is an early onset Alzheimer’s. So the builder says, well, it’ll last between 30 and 70 years if all the nails are normal. In other words, let me say that again. If the nails were the defective ones that were used, it’ll last 20 to 70 years. And if the nails were the normal nails, it’ll last 30 to 70 years. Okay, now, if the nails were defective, were they only used at certain parts of the house, like the bathroom or the mudroom or the kitchen or so? Or were they? And in the place where they used these defective nails, are those areas of the house more likely to fall down and disintegrate? No.

In other words, whether they used defective nails or not in the bathroom, there is no correlation with whether the bathroom will likely fall down or not. Because that’s what they told us about. There is no correlation between the site of the disease, which they say is the thalamus, and whether you find accumulation of this mutant protein there or some other place in the brain, you see the same level of accumulation or no accumulation. And as they said, there is no correlation between whether the nails are found in the bathroom or in the mudroom or whatever, the likelihood that that place will fall apart.

So then the next question. If you find more defective nails rather than fewer defective nails that were used in the house, is that more likely to result in the house falling down sooner rather than later? Answer no. Doesn’t matter how many defective nails were used. It has no correlation, no impact on whether the house will fall down. Because that’s what they told us about this mutant protein. There is no correlation between the amount of mutant protein found in the brain or whether there’s two copies or one copy. It has no effect, no correlation with the clinical symptoms or in other words, what’s likely to happen.

So then you say, well, how do these defective nails actually weaken the house compared to normal nails? Answer, we have no idea. We know they’re defective. At least we think they’re defective. We have no idea how a defective nail correlates or causes the house to fall down. And that’s exactly what they told us. We have no idea what this normal protein does. We made up some story, but we don’t really know whether the story is right. And frankly, as we admitted, we have no idea what this normal protein does or what the abnormal protein would do differently.

So let me reiterate that. So we don’t know whether the defective nails were even used. We don’t have any correlation between the site of the defective nails being used and the core on the likelihood of that part of the house falling down or not. We don’t have any correlation between the amount of nails that defective nails and the likelihood that the house will fall down. And we don’t have any mechanism to under to explain to us how these defective nails would result in the house falling down. There’s no correlation with the amount, there’s no correlation with the, with the location.

There’s no actual proof that the defective nails are even there. We have no way to understand how these defective nails actually work. How many of you, I would love for this to be in person would raise their hand and say, yes, I believe it’s the defective nails that are causing the house to fall down. My guess is, since most of you are very intelligent people listening to this, nobody would raise their hand because it’s actually preposterous to think given those lack of correlations and that lack of understanding, there’s actually no evidence that this abnormal protein has any relationship to anybody not being able to fall asleep or getting dementia or having muscle twitches.

There’s no, no, there isn’t even a correlation, let alone what you would expect if you say it’s the cause, which is you’ve identified the mutant protein as the independent variable and shown that it and only it causes these symptoms. So we have a situation, and again, this is on their own terms, where we don’t have a defined condition, we have a non specific symptoms which are basically identical to early onset Alzheimer’s or early onset dementia. And then later onset. It can happen anytime in life with no understanding of why, given two people with the same genetic condition, so called, and the same amount of protein made, one person gets it at 30 and the other at 70, which already should tell you that this is not related to this protein.

And then they tell us there’s no correlation between the amount of protein that somebody has and the severity of their symptoms. There’s no correlation between the site where the symptoms are allegedly originating from, which is the thalamus, and the accumulation of protein, this protein in that area. And, and furthermore, we have no idea what this protein even does or what an abnormal copy of it. If you put it like that, with our House example, nobody would buy this because they would clearly understand that this is another example of malarkey. And maybe Dr. Malarkey can write something on genetic diseases, because this is an example of, of exactly that.

And I would submit that if you go through basically every so called genetic disease, you end up with the same sort of lack of correlations, lack of a defined clinical entity, lack of the basic correlations that would even make you think there’s something to investigate. I mean, if somebody says to you that there is no correlation between the amount of monkeys in my yard and whether the bananas are gone or not, no correlation at all, nobody in their right mind would conclude that it’s the monkeys eating the bananas because there’s no relationship between the amount of monkeys or even whether.

Or whether the monkeys are even in the location, whether the bananas are gone. We don’t even have a correlation relationship to think that we should develop a hypothesis to actually investigate the cause. So this isn’t even a case of no correlation, or correlation doesn’t equal causation. That’s obvious. We don’t even have correlation here. And this is using their own words. And so I think that these heroic people who have unfortunately spent their whole life investigating what they call anti sense and what I would call nonsense, will actually get nowhere and accept producing a drug which doesn’t work and just poisons people worse and gets further and further away from any honest and realistic understanding of what in the heck is happening to these people in the first place.

And again, I would submit that this is the same thing you could find with literally every genetic disease you investigate, because everyone that I’ve investigated, you find the same sort of obvious stuff. And my only last comment and question to myself is, you know, we heard this stuff in medical school and we didn’t somehow have the sense to say, hey, wait a minute, this just does not sound right. There’s not even a correlation here. How are you possibly saying this is the cause of this disease? Okay, so again, sorry about the sound. I think we’re going to have to fix this before the next webinar.

And I hope everybody has a great week. And thanks for joining me.
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