➡ The speaker in the text is hosting a webinar where they discuss a variety of topics, including an upcoming biology event at Polyface Farm, the visualization of an atom, and the use of mathematics in proving scientific models. They question the accuracy of a visual representation of an atom, arguing that the depicted distances between the nucleus and electrons are not accurate. They also critique the reliance on mathematics to prove the existence of scientific models, suggesting that mathematical proof does not necessarily confirm the physical existence of a model.
➡ This text discusses the limitations of math and DNA testing in proving certain facts. It argues that while math can accurately measure and calculate, it cannot prove the existence of something. Similarly, DNA testing, often seen as foolproof, has its limitations, as shown in a case where a woman who gave birth to a child was not genetically linked to the child. This challenges the belief that DNA is the ultimate indicator of our identity and heredity, suggesting that our understanding of these concepts may need to be reevaluated.
➡ Cystic fibrosis is a disease caused by changes in a gene that makes a protein that helps cells in the lungs and other body parts work properly. To have this disease, a person must inherit two copies of this changed gene, one from each parent. People who have one copy of the changed gene and one normal gene are called carriers; they don’t have the disease but can pass the changed gene to their children. The existence of this gene and its role in causing cystic fibrosis is questioned by some, who argue that there is no proof that genes make specific proteins, a key part of the theory behind cystic fibrosis.
➡ The text discusses the complexity of cystic fibrosis, a disease caused by a single gene mutation that results in a wide range of symptoms affecting lung function and digestion. The author questions the genetic approach to understanding and treating the disease, suggesting instead to focus on observable symptoms and imbalances in the body. The text also introduces a new virus, HMPV, found in California, and criticizes the methods used to isolate and identify it, arguing that the process is flawed and unreliable. The author concludes by questioning the validity of current scientific methods in understanding and treating diseases.
➡ The speaker discusses the controversy surrounding the HPV vaccine in India, where it’s planned to be given to 15 million girls. He questions the existence of the HPV virus and its link to cervical cancer, arguing that the vaccine may cause more harm than good. He criticizes those who misinterpret his stance as wanting young girls to die from cervical cancer, clarifying that his intention is to protect them, but he disagrees with the strategy being used. He compares this to the negative effects of rent control, where good intentions lead to poor outcomes due to flawed strategies.

Okay, welcome, everybody. Today’s another Wednesday webinar. Today looks like it’s March 11, 2026. Hope everybody had a good week. And as always, thanks for joining me. And just a reminder that we are having a new biology experience in June at Polyface Farm. And they’re still spots available and sounds like they’re going fast. And we’re going to have. We, as I announced last week, we have three wonderful musicians lined up, lots of good food and good friends to meet and reconnect with, and hopefully some good talks, a lot of learning and a lot of fun. And I hope to see everybody there.

I think that’s all the announcements. Let me just check. Don’t have anything written down, so let’s get into it. And I just have a number of fairly short things here, and I’m not sure I’m going to even go a whole hour, which is probably okay, but I have a few things I wanted to just put out there. So this means I’m going to share my screen, but I don’t think I need to share the sound. So we’re going to start with what I showed last week because I missed probably the main point. And I used to do this fair amount when I was seeing patients as a doctor, and I would call them my patient intelligence tests.

So this is an audience intelligence test, although I can’t see you raise your hand and I can’t call on people, so I won’t know whether you got it right. But. And by the way, like most of these intelligence tests, I also missed it last week, which is why I’m doing it again this week. So this is a reportedly important finding in the world of atomic physics because it was the first time they looked at an actual photograph, they claim, of an atom. And so you’re looking at a crystal at a magnification of over a million. And I showed this last week.

And so you. Here you see the outline of the nucleus in the middle and then an electron cloud that orbits the nucleus on the outside. And the reason the electron cloud is fuzzy, they say, is because the electrons are moving fast. And so like anything that’s moving fast, it blurs the image. And the nucleus we know is real because nuclei have two, two major components, I.e. protons and neutrons. So there you see the two major components of the nucleus. So again, this was reported as a sort of watershed milestone in actually being able to visualize, therefore, document, the validity of this nuclear atom model.

So I’m going to give you a minute or so just with what’s wrong with this picture. And again, I missed it last time. And then I’ll after a minute. So if anybody wants to venture something, they could put it in the chat, although I’m not going to look at the chat and other people can see it. So what’s wrong with this picture? Then you could say, so maybe I’ll talk while you’re writing or thinking about it. But you could say, well, this is a computer generated image, so it’s not a direct image. And that’s true, and that’s a problem.

But one of the reasons I wanted to show this and the point that I really want to make with this is one of the fascinating things about science, and we’ve run into this over and over again, is often the scientists will make directly contradictory statements and you’re supposedly not meant to notice that these two statements can’t possibly coexist and be accurate. So it’s not that this isn’t a computer generated image, which it is. It’s not that we’re reifying the nucleus, so we don’t really know this, that it’s got two components unless we prove that first, because they say there’s this picture of it.

And so I think I’ll stop there. And so what I did was say, okay, if this is a real image, I asked the search engine thing that like the AI, I, I guess I can make this bigger. If the nucleus were the size of a pinhead, how far away would the electrons be from the nucleus? So just to remind you, here’s the nucleus and it’s actually a little bit bigger on this image than a pinhead, I think. And the electrons are maybe an inch or an inch and a half or two inches or so away. So that’s what they’re showing you.

Now, getting back to this, the answer I got. So the question was if the nucleus was the size of a pinhead, and how far away would the electrons be? And the answer was nucleus were the size of a pinhead, the electrons would be approximately one mile away. This illustrates the vast difference in scale between the nucleus and the electron cloud in an atom. And then the scale when considering the size of an atom, the nucleus is extremely small compared to the overall size of an atom. If we scale the nucleus to the size of a pinhead, which is about 1 millimeter in diameter, we can estimate the distance to the electrons and it would be about a mile.

So this isn’t a mile, this is an inch. And so if they’re telling you that the electron should be a mile away, they would have to show you if it was an accurate actual picture, the electrons would have to be a mile away from the nucleus. But they’re not, in which case both of those can’t possibly be true. And so you have to wonder, you say which one is true, or more likely, neither is true because they’ve never seen a picture, they have no evidence really that it exists. So they made up a, a size and then they made up a picture that, that falsifies the size.

But that doesn’t seem to ring a bell with the people who are doing this, that, that means they falsified their model. So their model at this point stands falsified. That is not true, but that doesn’t seem to make any difference to most scientists. So there you go. So hopefully some of you got that. Again, it. I didn’t get it either. Okay, next subject. I, We’ve been looking a lot at DNA. Oh, before I get into that, let me stop the share for a minute. This isn’t exactly relevant to what we just looked at, but when, when we’re talking about proving a model or falsifying a model, which is really the realm of science, somebody makes a claim.

And if it can’t be falsified, first of all, if it can’t be falsified, it’s a belief. And if it can be falsified but is unable to be falsified, then at least tentatively, it stands as being true until somebody can come up with some sort of falsification. And the point I, the next point I want to make is there’s a habit now, and interesting, the guy who’s called Tesla mentioned this and a lot of other people have mentioned it, and Steve Young mentioned it with regard to his physics training, which was mostly mathematics. And what you get into when you’re, when you’re having a conversation with somebody about whether something is true or not, or in particular whether something exists or not, they often will use some form of mathematics to attempt to convince you that something is true.

And I had a hard time coming up with a good example of this because it’s hard to come up with examples in from the real world, but there are probably many. But the example that I did come up with was, let’s say somebody says, I have a bucket and it’s made of fairy dust. Okay? So then you say, well, what, what other characteristics of this bucket? So they say the bucket is 2 inches by 2 inches by 2 inches. Those are the dimensions the, in the, let’s say, the internal dimensions of the bucket. So the bucket is 8 cubic inches.

That, that’s the volume inside the bucket. I think I got that right. Okay. And then they’re attempting to essentially demonstrate that we can, we know there is this bucket and it’s made of fairy dust. And there at. One of the explanations, it’s a little bit of a stretch here, is that we have measured the internal dimensions. Then when you say as is obvious, and that’s why it’s not a great example, but just because you have a, you are able to measure a 2 by 2 by 2 inch, therefore 8 cubic inch entity, doesn’t mean you have a bucket and certainly doesn’t mean it’s made of fairy dust.

Now the amazing comeback that you’ll hear on that from many people, particularly physicists and other so called scientists, is are you saying that a 2 by 2 by 2 bucket isn’t 8 cubic inches in volume? Because that’s the math. Are you so ignorant about math that you don’t know that that’s true? And the answer to that of course is that’s true. 2 inches by 2 inches by 2 inches. That means the inside volume is 8 cubic inches. I’m not disputing that. But I’m disputing that if you have an entity of 8 cubic inches in volume, that that proves you have a bucket and B that it’s made of fairy dust.

And they will inevitably keep on you about the math. But what you realize hopefully from that example is the accuracy of that math, that is to say two by two by two does in fact equal eight cubic inches. That’s true. It can never be used to prove you have a bucket made of fairy dust. And you see this over and over again. You see it with the genome, but I have a genome and it’s 10,000 base pairs. Therefore it proves there was a virus. Because if I had a genome of 20,000, that’s a whole other virus.

So the math may be right in what you’re doing, what you did with the chemicals. And although you never saw a lining up of base pairs, that’s also a myth, which why it’s not a great analogy. But that has no bearing. The math can never prove the existence. Math is only there to once you approve that you have a bucket made of fairy dust, if such a thing is possible, then you can measure the internal dimensions and then you can find the volume and it can never be used going backwards to prove that you in fact 2x2x2 means you have a bucket made of fairy dust.

So when you’re talking to people and they start going down the math pathway. Just realize that the math will never prove the existence of something. It’s only to characterize the characteristics, to elucidate the characteristics of something that you have already independently verified. Okay, next topic. We talked a little about genetics and, and whether that’s accurate or not. And this will get into the bit on cystic fibrosis as well. And it also has a lot to do with a lot of things in medicine. And I ran across this article and I’m not sure where I got this from.

It doesn’t lie. So who are you? What happens when a DNA test show a woman is not the mother of the child she gave birth to? So somebody wrote a book about this and you can purchase it on the site. And DNA is often considered the ultimate indicator of our identity, a foolproof way to determine our origin and how we connect to our parents and previous generations and. But his excerpt, hidden Migrating Cells in the New Science of Microchimerism is redefining human identity. So there’s the reference for the book. Author and science journalist Lise Barneaude explores an unusual case that exposes the limitation of DNA testing.

When a maternity test suggested a woman was not the mother of the child she gave birth to. Lydia Fairchild was 26 when she applied for welfare benefits to help her raise her two children on her own. As part of the application, she had to undergo a maternity test. A few weeks later, she was called into a meeting with social services, where they accused her of not being the mother of her children. At first I kind of laughed, but they were serious. I could see the seriousness in their face. Fairchild said DNA is 100% foolproof that it doesn’t lie.

A social worker told her, so who are you? So there’s some cartoons. At first, Fairchild was suspected of attempting to defraud the welfare system by inventing children. The state prosecutor launched an investigation and quickly confirmed that the two children did indeed live with her. Could she have kidnapped them? And Fairchild showed them photographs of herself pregnant. Her mother, her children’s father, and her obstetrician all testified the fact that she had given birth. Could she be a surrogate mother who kept the children she carried? After three hearings in court, Fairchild feared the worst. Every day it felt like she was going to be the last day I’d see them.

I called every lawyer in the phone book. None of them believed me. It was my word against DNA. It was me against everyone else. Fairchild was pregnant with her third child at the time, and the judge asked that both mother and child be tested immediately after birth. And the impossible happened. Fairchild’s third child just emerged from her womb, was not her son either, genetically speaking. And that apparently was the end of that. And so this is another principle besides helping to demythologize the whole DNA thing. So maybe DNA isn’t what we think it is and certainly it’s not a hundred percent foolproof and we don’t really even know what they’re testing and maybe the whole thing is just a bunch of nonsense and maybe they do some sort of investigation of your name or something.

They can find out when you send in those reports and they find your ancestors. And by the way, as I pointed out last time, how do you say you’re a match to a distant relative or distant ancestor? Who them? Who them who? They never had undergone any DNA testing. So how do you match with something that has never been investigated? And I’m not sure what the answer is. But the other point this brings up, and this is something hope. So essentially I’m helping people and helping myself to understand how to have conversations with people who seemingly don’t, who seemingly believe in the so called scientism way of seeing the world.

And so they certainly believe that DNA is foolproof and DNA is the source of heredity, etc. And so what they’ve set up here is what they call an unfalsifiable hypothesis. In other words, we can type your DNA, you and the child, and therefore tell you with 100% certainty whether you’re the true mother or father or relative of this other child, this person. And so what this example shows you is that when that claim has been falsified, in other words, here we have a true gold standard, meaning we see a child come out of the mother’s uterus, there could be no more definitive proof that this child is the progeny of that mother.

So that is a proof for that. And yet, as they point out, you do a DNA testing and it says you’re not the offspring of this mother. In other words, you falsified the claim that the DNA testing is foolproof and determines who your parents are. And what’s so interesting about what’s happening with scientism now is that doesn’t seem to make people think, well, maybe there’s some flaw with the whole claim, with the whole theory of DNA being the foolproof way of understanding heredity. Rather they make up, which goes, they go into this in the book, in the rest of the article, there is such a thing as DNA chimerism.

In other words, it isn’t that DNA isn’t the hereditary material, it’s that in some people, and we have no idea how many, their DNA has somehow changed. And even though that it doesn’t match with their offspring, they are that it is still the hereditary material, it is still a match, except the test shows that it’s not a match. In other words, there’s no way to falsify this claim because if you, well, there is a way, you falsified the claim, but that doesn’t make the people change their theory. So there’s no way to get them to change the theory.

The theory has to be true. And so then you have to make a sort of post hoc reasoning to explain away an obvious contradiction and an obvious falsification of the theory. So you claim that somehow, and some people, and we don’t know how many, but obviously anybody who it doesn’t match your DNA has changed and dummy, that’s why it doesn’t match. And so there’s nothing you can say to somebody like that to get them to understand that the whole thing is, is a house of cards. Okay, so that was the second topic, the third, and this came from a interesting comment and maybe a challenge.

So somebody has some nephews or grandchildren or something. So there were two children who were born allegedly with a disease called cystic fibrosis. And isn’t that a genetic disease? And so that doesn’t that prove that there are genetic diseases or something like that? And this is a very interesting question. And another point of science here is we don’t need to come up with another theory as to why children or people have cystic fibrosis or even whether cystic fibrosis is actually a specific entity, which we’ll get into a little bit here. We’re just investigating the claim that cystic fibrosis is caused by mutation in a certain gene located on a certain chromosome.

And this has been definitively proved and shown that this mutation is the cause of this malady in many, many people. And it’s an important issue in the history of medicine because like sickle cell anemia, which I’ve talked about, it’s one of the most important so called diseases that medical students and doctors are told is a pure genetic disease. It’s been proven hands down, no argument, there’s no possible way to argue this case. It is a proven genetic disease. So I decided let’s take a look and see what we can find. Is there really the proof? And again, the claim is all of these symptoms, there is a specific entity which has specific symptoms which we can identify either through the symptoms or through various tests or both.

And this is caused by a genetic change, in other words, a mutation in a specific gene. So let’s take a look. So, first thing I tried to find, again, it doesn’t come out quite right, but you’ll see. So this is just a general article on the cystic fibrosis genetics. The basis every person has two copies of the cystic fibrosis transmembrane constuctance regulator gene. A person must inherit two copies of the CFTR gene that contain mutations, one copy from each parent to have cystic fibrosis. This is actually called an autosomal, meaning it’s not on the sex chromosome recessive, meaning you have to have two copies.

Now, the first thing, which I’m not going to get into much here that caught my attention is that there is a transmembrane conduction regulator. In other words, they claim there is the reason for the abnormality in the sodium potassium distribution is because of a protein transmembrane regulator that, that spans the from the inside to the outside of the cell membrane. And I’ve been over the possibility of cell membrane receptors and pumps and regulators, and there is no possibility that any of these things have been shown to exist. So already we have a problem with the theory.

And again, I’ve done many other talks on sodium potassium pump and other transmembrane entities. And all this you can get from Hillman, who basically proved that none of these things have ever been demonstrated. So the summary is cystic fibrosis is caused by mutations in the gene that produces this cystic fibrosis transmembrane conductance regulator, CFTR protein. People with CF mutations in the gene disrupt the normal production or functioning of the protein found in the cells of the lungs and other parts of the body. Cystic fibrosis is an example of a recessive gene, meaning you have to have two copies and it’s autosomal, meaning it’s not on the sex chromosomes.

That means a person must have a mutation of both copies of the CFTR gene To have cf. People inherit one copy of the gene that contains a mutation and one normal copy are considered to be cystic fibrosis carriers. CF carriers do not have the disease, but can pass their copy of the defective gene onto their children. And this was one of the main drivers of genetic testing and geneticists and genetic screening and screening at birth, et cetera, et cetera. So again, so we’re looking for the proof that there is this gene and that you get a mutation in this gene and that produces the symptoms we call cystic fibrosis.

And again, our first problem is we already know that there is no transmembrane conductance protein regulator. And so that becomes the first problem. So the second problem, And this I would say is an even bigger problem, is there is a theory. So all of this is based on the. The, well, let’s call it a hypothesis that we have these chromosomes and the chromosomes are long strands of DNA, which again, I’ve done many webinars attempting to disprove that we actually know that and that on these long strands of DNA there are segments that we call genes, even though nobody can actually define what a gene is anymore.

So that’s a problem. But I’m going to forget about those issues for now and say the fundamental claim here, although it’s not so much stated directly here, is that each gene codes for a specific protein. That is the theoretical foundation of the claim that cystic fibrosis is a mutation in a gene. Since the claim involves that we know that the gene codes for a protein, this is a important protein in the imaginary transmembrane receptor. And so if you get a mistake in the transmembrane receptor protein, you will obviously get a mistake in the function of it, which is to regulate sodium, potassium.

Hence you get abnormal sodium, for instance, in the sweat, which is why you can do a sweat test to find the abnormal sodium concentration in the sweat. And it all goes back to the claim that genes code for proteins. Now. So I decided to do what I always do, which is go to a bunch of papers, not just this one, and ask the question and ask it of these, you know, search engine things. Tell me the foundational paper that proved that these segments of DNA that we call genes code for a specific protein. That was the question.

And I asked many different search engines and I looked at many different paper, and the good thing is that almost all of them, it may be even all of them actually gave me the same reference. And I don’t have this on the computer, so I’m just going to have to tell it to you. And I know that annoys people, but this is from a paper, Nature 1961, December 30, 1961. It’s number 4809. The page number is 1227. And the title of the paper is the General Nature of the Genetic Code for Proteins. And the authors were Dr.

Francis H, Dr. F.H.C. crick, F.R.S. barnett, Dr. S. Brenner and Dr. R.J. watts Tobin. So this is the same Crick, or as I like to call him, Francis Crook, who came up with the bogus paper on the double helix model of DNA. And I don’t know what happened to Watson, but he’s not part of this paper. So this is the paper that allegedly proved that genes code for proteins. And so after that, everybody refers back to this paper. Since this has been proven, we don’t need to do that anymore. We can just accept that as fact, and then everything downstream follows from there.

So I’m not going to go through this too much, except this on the section called the Explanation in Outline. So he’s basically giving an overview of what this paper says. And there’s a whole lot of very technical stuff in this paper with the usual cartoons and all, but I’m going to read you the explanation and outline. So this is basically a summary of what the paper is going to explain. And again, this is the paper that pretty much everybody referred to as the paper that demonstrates that the genes, the segments of DNA strands, they code for specific proteins.

Okay, reading and quoting. Quote. Our explanation of all these facts is based on the theory set out at the beginning of this article, although we have no direct evidence that the beta cistron, that’s what they used to call the gene, produces a polypeptide chain, probably through an RNA intermediate. In what follows, we shall assume this to be so. In other words, they’re not going to have any direct evidence that genes produce a polypeptide that is a protein. They say that it’s probably through an RNA intermediary, which is where we got the whole thing about DNA makes MRNA makes protein, and it’s all very specific.

Then what follows, we shall assume this to be so. And like I said, this is the proof that it is. So. So there you go. That’s pretty convincing evidence. And the rest of it is essentially math. So they get the math and they talk about the sequences and nobody can tell you. And they don’t even investigate because they just assume that sequences came from the genes. And so there you go. Okay, so now we go back to the specific example of cystic fibrosis. And this stuff really gets you into the weeds. So here’s the paper. This was the American Journal of human genetics.

And four pages, 827 to 834. This is from 1989. And some people may criticize this. Why am I using such old papers? Because these were the foundational papers that attempted to prove this and all of them followed from there. So I’m going to read some from the intro just so you can see what the claim is. So, cystic fibrosis, the most common genetic disease in the Caucasian population. So obviously this is an important subject. Inheritance autosomal recessive trait with an estimated carrier frequency of 1 over 25. They give you a reference. So this is a very important.

Like I say, autosomal recessive incidence of CF in other populations is rare, which is interesting. Clinical expression of CF is heterogeneous. It usually comprises chronic obstructive lung disease and malfunction of the exocrine glands leading to pancreatic enzyme insufficiency. But all patients show elevated electrolyte concentration in the sweat. So the importance of this statement is the clinical expression is variable. So it isn’t just one disease or one set of symptoms. It’s a whole lot of things. Some people have lung disease, some people have problems with pancreatic enzymes, some people have problem with digestion, some people have problem digesting fat, other people get sick a lot, other people seem to have a normal life.

And all of that is supposedly because of a mutation in one of the genes. 15% have sufficient pancreatic exocrine function. That means the production of the enzymes that help with digestion for normal digestion and do not require pancreatic enzyme supplementation with meals. So, in other words, the same genetics, 15% of them have no problem with making the enzymes for digestion. Allegedly, enzymes are responsible for helping digestion. CFPS patients have far superior overall prognosis than do patients with pancreatic insufficiency with improved survival, pulmonary function and growth. Despite progress in perinatal diagnosis, medical care, the primary defect in cystic fibrosis is still unknown.

So basically, and so then it goes on to talking about other things and how they’re going to identify the gene. But the first thing we note is this is not a single disease. This is a whole wide spectrum of symptoms that involves lung function and involves digestion. Some people have poor lung function, some people have normal lung function, some people have poor digestion, some people have normal digestion. And all of this is because of a single mutation on a single gene. And then there’s a whole lot of other stuff here which really gets you deep into the weeds here.

And I’m not going to go through that. And I, I must admit I didn’t have the bandwidth for going through this with a fine tooth comb, but what I did get take a look at. So again, what is the claim? The claim is there is a single mutation on a single gene. I think it’s located on chromosome number seven, they call it. And here are the. What they claim are the different mutations. So different errors found in the same gene that all end up with a diagnosis of cystic fibrosis. So this is the haplotype analysis of individual CF patients with pancreatic insufficiency or not.

The taplotype designations are the same in Table 2. They correspond to the each dot is a certain person and they all have a different mutation allegedly in that gene. And when I looked in papers that are more recent than that, you come up with literally hundreds of different possible mutations of this same gene that allegedly all make for a similar abnormal function of a protein in an imaginary transmembrane receptor which somehow ends up with similar, although not the same symptoms, which have many different prognoses depending on God knows what. And they try, because they’re wedded to it must be the gene and the, the different protein they try to lump them into that certain genes make certain prognoses and they’ve been doing that for the last 40 or so years and basically getting almost nowhere.

So we have no proof that certain of these mutations carry a specific, certain prognosis or have a specific set of symptoms associated with them. All we have is a whole lot of different types of protein, a whole lot of different so called genetic material from this gene located on chromosome number seven. When you do chemical analysis, meaning you take stuff and you put chemicals in it and you end up with color changes which allegedly tell you the sequence. So even that is a problem, you end up with a whole mess of range of possibilities. And these all are supposedly meant to say you have the same diagnosis.

And all I can say is the way that I prove things is not like that. That would be. Everybody has. We’ve proven that the gene makes the protein, we’ve proven that the protein regulates the sodium balance in and out of the tissues. We’ve proven that there is a specific change in the protein caused by specific gene and that in everybody creates more or less the same symptoms. And it’s so far away from that that I don’t see how anybody can come away with this thinking that we have proven that cystic fibrosis has been proven to be caused by a specific genetic mutation creating a specific protein, creating a malfunction in a specific transmembrane receptor which then causes different symptoms.

And I would advise anybody with this diagnosis to forget about the whole genetic thing and treat what you see and only give you one hint which is anytime you’re seeing an abnormality in the sodium, potassium or sodium or salt balance you’re talking about the earth property is out of balance. And that’s caused by this formation of the water structure structure inside the tissues. And so that’s where you should start to ask the question what has disturbed the fundamental structuring of the tissue water in this person. And I think you’ll end up with a much better prognosis than if you go down the genetic route which leads you nowhere.

Okay, so that’s enough of that. And then moving on. I have a few more minutes here. I happen to see this paper, see if I can find it or this article a hide the women and children because there’s a virus without a vaccine or treatment that is hitting California. What you need to know. And it’s called the meta pneuma pneumovirus or hmpv. Somehow I thought it’s called the Mimi virus. And I had a cousin named Mimi, so I thought that was interesting. Maybe she had something to do with. Although I doubt it. Anyways, so that it was got my attention.

So there’s a new virus and. And you can see this guy on the bike. He’s at risk and he may pass it to this lady going into this store. And you should never go into stores in Northern California that have high concentrations of HMPV virus in the local sewage. That’s where they found the virus. So what is the evidence for this? And the reason I wanted to show you this because I guess today’s theme is unfalsifiable hypotheses. So here’s a paper called the human meta pneumovirus hmpv, the virus who came with the common cold. This is in a recent infection.

20, 26, 54, pages 1 through 13. And then they tell you about how it’s a significant cause of respiratory infections worldwide, particularly in children, elderly, immunocompromised. So it was discovered in 2001 and major contributor and all that stuff. So we’ve been down this story many times. But I. There was one thing that I couldn’t help but pointing out here, and this is. So here’s the virology section and they have a whole lot of diagnostic category methods and description advantages, disadvantages of doing it and different genomes, genome size compared to RSV and influenza, et cetera, et cetera.

But the most important thing here, and of course there’s the cartoons here because you can’t have a Scientific paper without cartoons. We get to the always the question that we like to ask, how is this virus isolated? And so reading across culture of HMPV in cell lines, e.g. lLC MK2, followed by serological or molecular detection of ant antibodies. So what does that mean? And again, we’ve heard about this hundreds of times. They took some stuff from somebody they claim has HMPV and they put it on this cell line which is called LLC MK2. And I’m not sure where that cell line comes from, but it’s some growing, it’s like the equivalent of the monkey kidney cells.

And so then this is the gold standard for pathogen characterization and supports vaccine development. So this is important because this is as we’ve talked about and once again we hear from the virologist, the isolation of the virus in a cell culture is the gold standard, is the way to, to prove the virus exists and then to characterize the virus and then you can get into vaccine development. So what are the problems with this? Well, one, it’s labor intensive, so you have to actually get somebody to do it. It’s a slow growing virus, cytopathic effects rarely observed.

Now let’s think about what that means. So what, the way you say there’s a virus is you take some stuff from somebody you claim has this virus, has this illness, you put it on a cell culture in a few days, like three days up to seven days, the tissue breaks down. That’s called the cytopathic cell killing effect. And that tells you that it could have only been the virus that killed the cells. Even though we know that’s not true and this has been proven many times, and that is the way we isolate the virus. There is no doubt of that.

So what they’re telling you here is this is the way to isolate this virus. Yes, this true, this is the gold standard, the most important way. But this virus doesn’t cause the cytopathic effect except, quote, rarely. So in other words, most of the time there’s no death of the cells. And apparently if that happens, it happens after such a long time that one has to wonder whether because they took away the nutrients and because they poisoned it, whether the cells just died. And so essentially what you have here is a situation where if the cells die, that is the proof that this is the isolation of the virus.

And if the cells don’t die, in other words, there is no cytopathic effect. That’s also proof that there was a virus present killing the cells. It’s just that the virus doesn’t do it very well, or it takes a really long time, or it’s slow growing, or it’s got another date with somebody else, or it has some other reason why it took so long and you almost never see it. But never mind, because whether it happens or not, it still proves that in fact that is the virus that was, that had done it. And so this is yet another example of, of a, essentially there, it is a falsifiable hypothesis.

You can demonstrate that the cytopathic effect does not come from the virus and partly because you can demonstrate that they never had a virus to test in the first place. But when they do things like this, they end up with an unfalsifiable claim. So whether it happens or not, it still means that it’s there and therefore the whole thing is totally, totally useless. Okay, so this virus has never been isolated, never been shown to exist. Therefore it’s yet another example of virological nonsense. And I just want to finish with a brief comment because I happen to go on a show by this Indian fellow.

Some of you may have seen this or seen clips and very nice guy, good, good intention, good hearted guy. I liked him. Kamal was his name, I’m not sure what his last name. Singh maybe. And I think you’ll be able to find some of the clips and maybe the interview. And it was all about the fact that India had rolled out the HPV Gardasil and I think maybe not Gardasil, but an HPV vaccine. And their intention was to vaccinate 15 million girls, young girls in India with this vaccine, which as we know will result in probably hundreds of thousands, if not more direct injuries and the same and 15 million with young girls who will be injured.

So the reason I’m saying this is because I, I saw some of the Instagram posts and I saw some of the comments of the people and apparently this guy is well known and a lot of the doctors, some of them were in Indian so I couldn’t really read it, but some of them were in English and it was, almost all of them had nothing to do with my claim of course, that there is no hpv. There is no evidence that therefore that any virus could cause cervical cancer. And therefore there is no possible benefit from this so called vaccine.

It’s all risk. And as far as I can see there was no argument about the science. And the reason I’m bringing this up, and this is another thing to watch out for when you’re having a conversation or maybe you would want to put an argument or trying to help People to understand this and that they, almost all of them would say things like, so in other words, you want young girls or young women to die from cervical cancer. That was the. That was their comment or their rebuttal of what I would say. And I was thinking about this and thought people should really think about this.

And you can think about whether you think I’m correct. And what this is is a confusion of intention versus strategy. It’s also a confusion from intention versus, you might say facts. So, and you see this from a lot of people when they argue with you. So. So I say there’s no evidence that there is such a thing as a measles, as a disease. There’s no evidence of measles virus. And so they say, so you want people to. Children to die of measles. So what they’re arguing about is my intentions. Now, let’s just say that most of us, probably not all of us, our intention is the same.

That is, we want children to be as healthy and active and vibrant as possible. I want that. You want that. The people who argue from the other side, that is not the issue. And to bring that up is a confusion with intention and strategy and facts. The issue is whether there’s a disease, whether there’s a virus, and whether this strategy helps prevent that. And so this is what pretty much everybody said. They questioned our intentions, me and the interviewer, not the facts, not the strategy, just the intentions. And I would submit that the intent. You’ll never get anywhere arguing with intentions.

You should, in fact, agree our intention is the same, to protect young children, girls, young women, as much as possible. I accept that you want that, and I want that. Now we’re talking about strategy and facts. And I thought of giving an example, and this may not be a great example, but people in a more political, economic sense, they talk about rent control. You say, well, there’s people who can’t afford to live in a certain place, New York City or San Francisco or Hudson or a whole lot of places. So the government comes in and institutes rent control, and that helps people afford to live in a certain place.

So isn’t that a good thing? And again, the intention of everybody is to help have as many people as possible, poor people, rich people, and everywhere in between have a safe, comfortable, healthy, adequate place to live. That is not the issue. The issue is whether that’s an effective strategy. Now, I would submit that if you do rent control, what’s going to happen is you’ll end up with the people who own the places, who Rent them out will not be able to make a living doing it. And so inevitably what happens is the quality and quantity of the places for rent will deteriorate.

There will be fewer, therefore the prices will inevitably go up, which is exactly what happens. And the quality of these places because the landlords can’t make any money off renting it. And so they can’t make the necessary, you know, fixing up things that we all have to do with our dwellings and our places we live. And so the inevitable outcome will be a deterioration in the quality and the quantity of the rental places. And the rental places will be more expensive. And that’s exactly what we’ve seen in case after case. And it even hurts the very person who you supposedly were trying to help by giving them a lower rent because then their landlord can’t afford to make improvements.

So they end up living in a horrible place where the pipes leak and things don’t work and nobody can afford to fix them and they can’t afford to move because there’s so few other places. And, and therefore the rental prices on the other places have gone so, so high up. And so in a funny sort of way, while the intention may be to help the person, the strategy was so flawed that you end up hurting them. And that’s what we see over and over again. So don’t fall into the trap of arguing about intentions. The intention of any program to help young girls is to help them be as healthy and happy and safe and vibrant as possible.

We all agree on that. What we’re talking about is strategy and facts. Is there an hpv? Does it cause cervical cancer? If there isn’t, it can’t possibly. Does this so called vaccine prevent it? All those I would say have been definitively proven in the negative, shown to be false. And so there is no argument and so that this is a good strategy and the only thing they have to go on is so you mean you want young girls to die. And once you hear that, you know you’re talking to somebody who literally cannot think and cannot be reasoned with.

So watch out for that. It happens in many different areas of life and I guess I went all the way to three. And so thanks everybody for listening and hope you have a great week.
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