Okay, everybody, welcome to today's meeting of Medical Doctors for COVID Ethics International
on this Tuesday night, the 5th of November, London time, which is Wednesday morning, Australian
New Zealand time, which is, which is midday, LA time on election day.
In the US presidential election, 2024.
Well, not only presidential, but all of the House of Representatives, Senate as well.
So special day.
And so this group was founded by Dr.
Stephen Frost over three years ago with a desire to pursue truth, ethics, justice, freedom
and health.
Stephen has stood up against government and power over the years and has been a whistleblower
and activist. His medical specialty is radiology.
We remember another freedom warrior at this moment.
And at all of our meetings is Rainer Formick, German and US lawyer who's unlawfully incarcerated
in a German jail undergoing a German show trial.
Please do what you can to highlight the outrageous behaviour of the German government in attacking
Rainer Formick.
It's clearly scared of Rainer's work as a freedom warrior.
I'm Charles Covets, the moderator of this group.
I'm Australasia's passion provocateur.
And we love passionate people in these meetings.
I practiced law for 20 years before changing career 31 years ago.
And over the last 14 years, I've helped parents and lawyers to strategise remedies for vaccine
damage and damage from bad medical advice.
I'm also the chief executive of an industrial hemp company.
We comprise lots of professions here and we're from all around the world.
Many of us thought that vaccines were OK.
Now, most of us know that vaccines have never been properly tested for safety and efficacy.
And yes, I am a passionate anti-vaxxer.
And please, I urge all of you to become passionate anti-vaxxers.
God does not need help in producing healthy babies.
If this is your first time here, welcome and feel free to introduce yourself in the chat.
If you publish anything, put that in the chat as well.
Most of us understand we're in the middle of World War 3 and that the medical science
battle is only one of 12 battle fronts in this latest world war.
And there's no time to be tired.
I assess we're four and a half years into a seven year war.
So look after your health.
So you're up for the fight.
Most of us understand the development of science and the science is never settled.
And our presenter today is an expert in this space.
Dr David Resnick, I'll introduce him in a moment.
Some of us believe that viruses exist.
Some of us believe that viruses are a hoax and some of us are on the fence.
And most of us consider that debating the existence of viruses is a distraction from
the real war that we are in.
This meeting runs for two and a half hours normally, after which for those with the time,
Tom Rodman runs a videotelegram meeting.
Although today, because of the election, Stephen and I have discussed and will keep the meeting
running for as long as people want to sit here to discuss what's happening in the election.
It'll be a special deal.
We will post this recording and we will keep the recording going.
We won't publish that until unless something brilliant comes out of it.
I point out that, yes, we'll talk about cloud up later.
We will listen to Dr David Resnick for as long as David wishes to speak.
And then we have Q&A.
Stephen Frost, by long established tradition, asks the first questions for 15 minutes.
This is a free speech environment with appropriate moderating.
Free speech is crucially important in our fight to preserve our human freedoms.
However, as occurred on Sunday night, we do not allow ad hominem attacks.
You attack ideas. You don't attack the people not interested in your views about other
people, whether they're, whether they are, whatever they are.
No attacks on people, number one.
And number two, appropriate moderating means we stick to the topic.
Some people seem to think that because David Resnick might be presenting something, you can
ask him what he thinks about stuff that's irrelevant to what he's been talking about.
That's what appropriate moderating means.
If you're offended by anything, be offended.
We are lovingly not interested.
We reject the offence industry that requires nobody to say anything that may offend another.
We similarly reject the triggering industry.
The triggering industry, both the offence industry and triggering industry are both
free speech censorship attempts.
We come with an attitude and perspective of love, not fear.
Fear is the opposite of love.
Fear squashes you, enslaves you.
Love, on the other hand, expands you, liberates you.
These twice weekly meetings are not just talk fest.
An extraordinary range of actions and initiatives have been generated from linkages made by
attendees in these meetings.
It's just extraordinary.
Like if it were, it would take us, it would take us an hour for Stephen and I to go through
what's happened as a consequence of these conversations.
If you have a solution or a product or links or resources that will help people put the
details into the chat, the meeting is recorded and is uploaded on the Rumble channel.
And now welcome to our guest presenter, Dr David Resnick.
And we thank you, David, for giving us your time and wisdom and insights.
David has presented to us previously.
Let me tell you a little bit about David for the purposes of the recording.
David received his PhD in chemistry from Georgia Tech in 1978.
He worked 20 years in pharmaceutical biotech industry and founded four biotech companies.
He developed inhibitors against the enzymes responsible for the tissue destruction caused
by cancer, emphysema and arthritis.
The same class of inhibitors are powerful anti-parasitic agents.
They've left the pharmaceutical biotech industry in 1996 and joined UC Berkeley.
And Professor Peter Juesberg's fight against the blatantly wrong dogma
that HIV causes AIDS.
And David's history on fighting against that fraud is similar to the fight that we're going
through now on the COVID scam.
David is former president of Rethinking AIDS, the group for the scientific reappraisal of
the HIV hypothesis and former president of the International Coalition for Medical Justice.
He was also a member of South African President Thabo Mwembeki's presidential AIDS advisory
panel that met in 2000.
Along the way, Peter Juesberg and Dave Rasnik proved the aneuploidy chromosomal imbalance
theory of cancer.
Since February 2020, similar time to many of us on this call, Dave has been working
with people around the world fighting the COVID-initiated global coup d'etat.
His full CV and four decades of information are available on his website, davidrasnik.com.
And David, you introduced to us in your first presentation here Leopold Kaur's book,
The Breakdown of Nations, written in 1957.
And I have shared that with many people.
I'm sure you'll tell us where you can find it on your website.
It's a wonderful, wonderful book.
And in the times that we're right now, we're in an election, the message of Leopold Kaur
that the number one cause of all failures is bigness really resonates with me.
I love that idea.
So David, thank you so much for speaking to us again.
And thank you, Stephen Frost, again, for creating this group and for organizing David to speak
to us today.
Well, I'm looking forward to presenting my cancer work today because it's something that
I'm the most proud of as a scientist, scientific work.
And it never would have come about had it not been for AIDS.
That's when I joined up with Peter Duisburg just to support him for a little while.
And I found wound up being with him for about 10 years.
And when we weren't fighting the AIDS scandal, we'd take a breather and we'd work on cancer.
And Peter ran out of, he couldn't get any grant support anymore.
So right before he left to go on a sabbatical in Germany, the first one in his life, because he
couldn't get any grant support anymore, financial support from the government because he
challenged HIV.
So he decided he's going to work on the chromosomal or chromosomal imbalance theory of cancer that
Theodore Boveri produced back in 1914.
And he went to Germany to do some experimental work on that.
And I stayed in California and I went to the library to learn about chromosome, I knew about
chromosomes, but about Boveri's work and about chromosomal imbalance.
And it turns out that had it not been for AIDS, Peter and I would have not done our most important
work that we did as scientists on cancer.
And we got together and in a few years we proved Theodore Boveri's original theory that
unbalanced chromosomes and only unbalanced chromosomes are what's behind cancer.
And that's what I'm going to talk about today.
Because I don't know how many opportunities you're going to get to hear this story, but I'm
going to start right now by showing you, I need to share my computer if I can do that.
Is there a share button on here someplace?
Yes, there is.
If you've got zoom, it's at the bottom of your screen.
There's the green button that says share.
Oh, I see it.
I see it.
Okay.
And I want to share my screen.
David, which state are you in?
I think you said earlier, but...
North Carolina.
That's right.
Okay.
This is the screen.
Let's say I want to, this is the one I want to share.
Is that a picture of North Carolina behind you, David?
No.
All right.
Okay.
Tell me what you see.
Yeah, we've got David Resnick PhD, your website, we can see.
That's right.
I wanted to start with this so people can see.
If I click on the home screen, that's where we're at right now.
We can see your desktop as well.
Is that okay, David?
Do you want that?
Don't worry about that.
All right.
I've had problems doing this sort of thing over the past few years,
and I think I haven't figured out well enough for today.
Okay.
So anyway, this is my website.
And the stuff that I'm going to be talking about today...
Let's see.
Why don't they see, stop sharing?
No, I want to share.
Yeah.
Why does that pop up?
You are sharing.
I don't want to stop sharing.
Why doesn't this come forward?
What do you want to see?
Oh, it just disappeared.
There was a little notification about that.
I was sharing my screen.
Move your mouse.
Just move your mouse.
Yeah.
We've still got it.
Okay, good.
All right.
Now, what I would like for people to do,
I'm going to show you right now where you can go.
Actually, I go too high and it brings this thing back down.
But you can go up here to cancer.
You see this where I'm going to go here?
I'm going to click on this cancer tab.
Yep.
We can see that.
Now you see the chromosomal imbalance theory of cancer.
Yep.
You can come down here.
This book right here, I published it, I forget when.
It was early 2000, I guess.
It's the explanation of our chromosomal imbalance theory
of cancer that Peter and I worked on.
And this book, you can click on this image here
and you can download my book.
It's 358 pages.
It's free.
And you can go to that and read it.
You can read it on the screen or you can download it
and get it any way you want.
The other thing is this is David Hansenman,
this guy right here on the right, the second photo to the right.
I'm going to be talking about him.
I'm just showing you these things where you can go to
and you can click on it and you can get his book.
It's a biography of him for people who are interested.
The same thing here with Theodore Boveri.
Click, he's an important guy.
You can click on it and you can download his book.
It's only, let's see, 59 pages, but it's concerning
the origins of malignant tumor.
He published that in 1914 and he was absolutely right
about unbalanced chromosomes.
He explains in there how unbalanced chromosomes
cause cancer and people can go to that if they want to.
It's especially good for historical information.
All these things, these are just examples,
but these are the ones I want to talk about today.
If you scroll down on the same thing here,
down here at the bottom you see this cancer book.
It's the biology of cancer by Weinberg.
It's the second edition, it's published 2014.
You can click on it and it's a very big book
and you can download it and you get the gene mutation explanation
of cancer, which is government dogma.
All right, for those people who would like to compare
the gene mutation stuff with the chromosomal thing
or anything else they want to, and I just wanted to let you know
that you can go to my website and you have access
to any of this stuff that's on there.
Okay, so if there's no questions about this,
I'm going to go ahead with my presentation.
Yep, go for it, David.
That's well explained, Leah.
Okay, let's get this done.
Let's get this out of the way, get that out of the way.
And here, let's see.
Yeah, we can see that.
Okay, everybody can see that.
The essence of cancer, all right?
What it really is, that's what I want to talk about today.
It's basically a comparison of the chromosomal imbalance theory
of cancer, which is government, I mean,
what Peter and I have proved, Theodore Boveri came up with it.
110 years ago this year, actually, versus the reigning gene
mutation theory of cancer, the idea that there are cancer genes,
that you have a normal gene, you get a mutation in it,
and it turns into cancer, all right?
That's untrue, and we're going to go through that today.
So I'll move on to the next slide here.
Okay, up here.
There you go.
Okay, this is that book I've mentioned that you can download if you want.
It's The Hallmarks of Cancer, published by Robert Weinberg,
originally in 2000.
Oh, this is our, up the top is a paper that he published in 2000,
where he says cancer biology and treatment will become a science
with a conceptual and logical coherence
that rivals that of chemistry and physics.
And the whole pharmaceutical field industry that I was in there for about
two decades is all about molecules, all about molecules.
And it's very simple to understand that because that's what pharmaceutical
companies do.
They make molecules to target other molecules.
And that's the only way they can conceive of any disease, including cancer.
You find a gene, you make a drug, a molecular drug for that gene
or whatever they think is the cause of a problem.
And they can just keep going on forever like they have.
Then totally, completely, abjectly a failure, an abject failure, this approach.
All right, there's the Cancer Genome Atlas, which is part of the reason they have this.
There was Nixon's war on cancer.
It was like it was 1975 when he launched the war on cancer.
And the gene mutation hypothesis became government dogma.
And it led to the looking for gene mutations and they've cataloged over 10,000 different tumors,
cancer tumors.
And 10 million, actually more than 10 million now cancer-related in quotes,
cancer-related mutations.
In other words, they find these mutations in cancer cells, but they don't say they're
actually cancer-causing.
And each one of these cells, these cancer cells, has an average of 1,000 mutations per tumor,
per tumor cell.
I'm sorry, per tumor that has all these different cells in it.
Now, for the folks who don't have a background in biology or biochemistry,
you hear these things about gene mutations, about sequencing, about what is an oncogene.
I'm going to help you a little bit for those who don't understand.
The DNA is like, we'll be talking about this later, it's a biological dictionary.
The genes are a biological dictionary.
And they code those genes, the DNA and RNA code for amino acids, basically, sequences of them.
And this normal here that you see lower down, that's a normal sequence of any protein,
or any product of a gene.
And the three-letter codes at the top, the code for these amino acids like lysine,
histidine, leucine, glycine, those are amino acids.
And the string of those make protein.
And the AAA, the CAC, the TTG, the GGT, those are adenine,
cytosine, thiamine, and guanine.
Those are the four nucleotides.
The different sequences of those nucleotides code for different amino acids.
Now, this little yellow box that I have here shows a mutation.
What they mean by a point mutation, you have your normal sequence up here,
lysine, histidine, leucine, and glycine.
And the histidine has the code of CAC.
But that A now is going to be replaced with a G.
That's a gene mutation, a point mutation right there.
And now you have the code CGC, but it no longer codes for histidine,
it codes for arginine, a completely different amino acid.
And they say down here that hypothetically, that the CGC,
and this arginine replacement, now is responsible for turning that cell into a cancer cell,
hence the red little cancer here.
I want to emphasize repeatedly throughout this thing,
that's never ever been demonstrated anywhere.
But that's the hypothesis, that's the theory.
But the vast majority of these mutations are totally irrelevant.
I'll keep going here.
Now, in spite of the National Cancer Institute dogma,
leading cancer gene researchers know that mutant genes don't cause cancer.
But they keep working on gene mutations because if anybody who
goes against the government dogma, they can't get funding for that.
But here, let's start back with this fellow back in 1994, Gerald Dermer,
his book, The Immortal Cell, Why Cancer Research Fails.
Perhaps the most damning evidence against the oncogene or cancer gene theory
is the fact that the supposed human oncogenes do not transform true normal cells,
which have a normal set of chromosomes.
He said that they don't exist as of 1994.
It continues, there is absolutely no evidence from observations of human tumors
to indicate that the mutation of any proto-oncogene,
that means a normal gene before it's mutated into an oncogene,
that these mutations of any kind is essential for cancer initiation.
In fact, in many tumors, all of the supposed proto-oncogenes are normal
and there are no oncogenes present.
Now we go back to Weinberg.
He, even though he published that book in 2014 that I already showed you folks about,
the Molecular Biology of Cancer, and it was also in 2014, but he published in the journal Cell
in the same year, these comments.
He said, the actual course of research on the molecular basis of cancer
has been largely disappointing.
Rather than revealing a small number of genetic and biochemical determinants
operating within cancer cells, molecular analyses of human cancers
have revealed a bewildering complex array of such factors.
Even within a given type of cancer, there were no uniform successions of genetic change.
Instead, each tumor seemed to represent a unique experiment of nature,
acquiring a unique set of mutant genes and in the unpredictable chronological order.
The coupling between observational data and biological insight is frayed, if not broken.
This is from one of the world's leading gene mutation supporters of that idea of cancer.
Bruce Alberts, he's another heavyweight.
This is from his book, a 2014 book, I guess 2014 was a big year.
His book was Molecular Biology of the Cell, chapter 20, page 1094.
You can see it's a very, very big book.
This book is used in universities to educate upcoming scientists, molecular biologists,
and that sort of thing.
Here's what he has to say, it's very, very interesting.
Human DNA has three billion nucleotides, that's those ATCs and Gs,
we have three billion of those, all right?
Every time a cell divides, there is about one uncorrected mutation per every one billion
nucleotides.
Thus, there are about three random mutations every time a cell divides.
But I can tell you right now from a chemist, a scientist, anybody,
that's an extraordinarily, extraordinarily stable and resilient system.
When you have three billion nucleotides and you only have three mutations,
and it could be anywhere on that genome, on the DNA.
No scientist, nobody could do that, just only nature can be that precise, that accurate.
But then he goes on, there are 10,000 trillion cell divisions during the course of a human life.
Based on this, every single gene is likely to have undergone mutation about 10 billion
separate occasions, 10 billion separate occasions, every gene in your body.
Just by using that one mutation per billion nucleotides, but we have so many cell divisions,
you get these mutations.
From this point of view, the problem of cancer seems to be not why it occurs,
but why it occurs so infrequently.
That's absolutely right.
If gene mutations cause cancer, and with this rate of mutation that happens in everybody,
this rate of mutations happens in everybody, why don't we all have…
Life would not even be possible.
Bert Vogelstein is another big gene mutation guy, and this was in 2016.
He said, the search for cancer-causing gene mutations is hindered by the lack of a gold standard.
That is, bona fide driver gene mutations.
In other words, there is not a single cancer gene or gene mutation anywhere in the world
that has been demonstrated to turn a normal cell into a cancer cell or combination of these.
There's no single gene or combination of gene mutations that anybody has ever been able to
demonstrate that turns a normal cell into a cancer cell.
Yet, that is the current dogma that virtually every researcher who's working on academics or
any grant for the National Cancer Institute, they're all working under the assumption
that gene mutations are the source of lots of problems, especially cancer.
This is what they're facing.
Any of the people who are here in the Zoom meeting today who are scientists or certainly
a biological scientist, you've probably seen one of these metabolic or biochemical pathway
charts on the hall in your lab somewhere.
They just keep getting bigger and bigger and more amazing as the years go by.
You see, these things take up a sizable fraction of the wall in a laboratory.
There's no way in this slide that I could make it…
I can't amplify it big enough right here, where you can even see a name of any one of these little
genes or proteins or enzymes that are part of this network.
This is a biological roadmap of life, basically.
It's got oxidation in there, replication.
It's got all kinds of stuff in this thing that people have mapped one gene at a time in a group
of them.
They've been doing this now for decades.
They come up with these maps.
They know a lot about the enzymes, the kinetics and everything, but they don't have a clue
other than to map these things up.
But they have no clue about how to change things other than just try it, have a hypothesis,
make a molecule for it, inhibit or change this enzyme for that enzyme or whatever,
which they can do.
Usually, it's an utter failure.
Nothing happens.
Occasionally, something does happen.
If they have a hypothesis like they do with cancer, even though they've never found a
cancer-causing gene, they come up with these hypotheses from that atlas of oncogenes and
tumor suppressor genes, a whole host of different names for them.
The drug companies then or the academics will design inhibitors or some way to interact,
a molecule or some way to interact with these hypothetical genes or molecules.
Low and behold, it either causes havoc in the patient.
It doesn't stop cancer.
If anything, it can increase cancer.
It's insane.
These people know this.
This is one of the points that I want to stress here.
I'm not more brilliant than these people are that make these maps and do this stuff
and write these grant proposals and everything.
The people who have been doing this for a couple of decades at least, maybe even a decade,
that's a shorter time, know that what they're doing doesn't make sense.
But they keep doing it because if they want to keep their grant support, if they want to
keep their little company going or the pharmaceutical industry, they have to just keep doing the
insanity and how they live with it, I don't know.
I know for a fact that they know this.
It was just like with the AIDS stuff.
The people at UCSF and also UC Berkeley during the 1980s with the AIDS stuff, and certainly
in the 90s, most of those people knew that AIDS was not contagious and HIV did not cause AIDS,
but they kept their mouths shut and they kept working on it.
So the way the system is set up, it looks like people are making a lot of progress.
Look at this map here, this map of all these biological interactions and everything.
Oh, we really know something to be able to do a map like that.
They don't have any idea of how to use it or what to make sense of it other than it's just
kind of impressive to hang on your wall.
Okay, I'll stop preaching.
I'll keep going here.
All right, this is a big point that I want to make.
Our genome is not an instruction manual.
A lot of people think it is.
It's a biological dictionary.
The best way to see this is that the genome of the mouse and humans, 99% of our genomes
are the same, same genomes in mice and humans, and over half of our genes we share with the worm.
You know, and there aren't really, really worm genes,
there aren't really mouse genes, there aren't really human genes.
It's like a dictionary.
Think of the Oxford English Dictionary.
You can, all of the, anything that's ever been written in English,
you can find those words in the Oxford English Dictionary.
But no matter how hard you look and you go through those 23 volumes of the Oxford English
Dictionary, you cannot derive a novel or a lecture or a published paper or anything.
No, those are just a little building blocks.
They're just the bricks that you put together to make a sentence, an idea, or a book.
The same thing is with the genes.
That's what the genes are.
They're just the little bricks that the whole intact organism or the cell puts together
in a particular way and makes these proteins and these enzymes.
And then you get something magical.
Like with the same genes, same genes you can make a human.
Not scientists can, but people can.
Or you can make a mouse.
A mouse can make a mouse, you see.
And even though they're the same genes, so trying to find, looking for an oncogene,
a cancer-causing gene, makes as much sense as looking for the human genes in humans
to distinguish us from a mouse.
It's not possible.
It's not possible to do that.
And yet that's the logic that is being used with cancer right now and all other
major complex biological phenotypes or characteristics.
Okay, part two.
Carcinogens cause aneuploid chromosomes.
Aneuploid means unbalanced chromosomes.
Last week, I guess, I brought up the word aneuploidy.
And most people hadn't heard about it before.
Aneuploidy is the state of unbalanced chromosomes.
All right, that's just a technical word for it.
So aneuploid chromosomes cause cancer and only aneuploid cells cause cancer.
And that's what Theodore Boveri understood 110 years ago.
And he put it in that book that you can download from my website.
One of the first guys, it was David Hanselman back in 1891.
And he was a German guy, just like David Theodore Boveri.
And he used microscopic analysis to examine cancer cells.
And he looked at hundreds of cancer cells.
And there's a book, like I said, you can go to my website and download this biography of him.
There's also other articles that he's written that you can get too.
And what he noticed was, is that all cancer cells have these abnormally called chromatin.
And you can see these pictures of these cells.
This number 10 down here looks like probably was a control cell lower right,
where you have the chromosomes, the dark things,
are chromosomes that are being pulled apart as the cells divide.
The cancer cells, every one of them is different.
The chromatin is unbalanced.
The two cells, when they divide, they don't have the same chromatin or chromosomes,
just the normal cells do.
And he never found a cancer cell that was not like that.
And the normal cells are very, very reproducible.
No two cancer cells are alike.
And the cell of a malignant tumor is a cell with a certain abnormal chromatin content.
He said that before Boveri did, and he was absolutely right.
Boveri and Hanselman actually knew each other.
Now we'll go to Boveri.
Here's the big guy.
He formulated the aneuploidy theory of cancer in 1914.
And that was that book that you can download.
I think it's 59 pages, something like that.
He said, the essence of cancer was a certain abnormal chromatin constitution,
the way in which it originates having no significance.
Each process which brings about this chromatin constitution
would result in the origin of a malignant cancer.
He was absolutely right about that.
And now let's talk about these chromosomes.
And he explained in his book, he explained how that would happen.
Karyotype is just a fancy word, the technical word
for a collection of species specific chromosomes.
Remember, mice and humans share the same genes.
99% of our genes are identical.
But we don't have the same complement of chromosomes.
In other words, it's like taking the Oxford English Dictionary.
Standard, it comes in 23 different volumes,
just like the human genome comes in 23 different volumes,
23 different chromosomes.
But the mouse has the same genes, but it only comes in 20 volumes, not 23.
And these volumes are called chromosomes.
And with sexually reproducing organisms like mammals,
with sexually reproducing organisms like mammals,
you get for your 46 chromosomes, 23 unique chromosomes come from the mother,
23 unique chromosomes come from the father, the mother and the father,
for a complement of 46 chromosomes in humans for a total of 20,000 genes.
And with the mice, the male and the female,
I do the same thing for a total of 20,000 genes.
So they have backup, think of it like backup chromosomes,
because the two copies are identical in terms of genes.
They're duplicated, but it's very, very important
that you have two copies to get into that.
Now here is a modern way of looking at the chromosomes.
On the left, we have human chromosomes,
and they're using modern stains, which makes it much easier to identify the chromosomes.
On the left, we have a human with 46 chromosomes, it's normal, it's euploid.
It's male because it has one lower right, it has one X chromosome,
and one Y chromosome is the male.
And over here on the right, females, by the way, have two X chromosomes and no Y chromosome.
On the right, you have cancer with its unbalanced chromosomes.
You can see there's chromosome one up here, chromosome two is missing up here.
You have three copies of chromosome three, you got two of four, you got one of five over here,
and then you see these numbers are changing all along down here.
And then down at the bottom, you see this whole array of different,
they're stitched together chromosomes, they're called marker chromosomes.
And no two cancer cells have the same complement of chromosomes.
That's extremely important.
All normal cells have the same complement of chromosomes, they're balanced.
You can call them diploid for meaning two, their ploidy is diploid,
or you can call them euploid for meaning it's normal.
And euploid means they're unbalanced, they're abnormal.
There's no two cancer cells that have the same complement of chromosomes.
They have the same genes, but not the same complement of chromosomes.
I emphasize that because it's so crucial, a lot of people don't know that.
And here's some of the terminology, I've already been using it.
Ploidy is just how many chromosomes do you have in your cell?
Euploid means a balanced set of normal chromosomes.
Humans, we have two copies of 23.
One, half of them come from the mother, half comes from the father.
For a total of 46, aneuploid means unbalanced chromosomes, for example, down syndrome.
The down syndrome kids are actually aneuploid.
They are born with the usual 46 chromosomes plus an extra chromosome 21
for a total of 47 chromosomes.
I don't have time to go into the consequences of that today,
but we can in the discussion area if you want to.
And then there's pseudodeploid, where you can have like this DLD1 cell line,
it's an artificial cell line, which to use it in cell culture and laboratory.
It's aneuploid.
It has the right number of chromosomes, 46, but they have, for example,
three copies of one of the chromosomes and only one copy of the other one,
which makes it aneuploid, but the total is still 46.
Now, this is what a pathologist looks at through a microscope.
This is from the Pap smear that most everybody is familiar with,
that George Papadikala developed back in the 50s.
And they still use it to this day because it's the best cancer,
as of right now, the best way to diagnose cancer is still with the Pap smear, the Pap test.
And this is normal cervical cancer, normal cervical cells up here.
They're stained with the cytoplasm green and the nucleus of these things are purple.
And then they have 46 balanced chromosomes.
And here is what the pathologist sees, for example.
These are cancer cells that he sees along adjacent to the normal cells that happen to be
in the Pap smear or on the cervix someplace.
And you can see they're very, very different.
They have between six, typically between 60 and 90 chromosomes.
That's why they're so much larger.
And the nuclei are much larger.
That's one of the rules that pathologists use.
They look for nuclei that are about three times larger than the normal cell has,
as an indication that's possibly a cancer cell.
And you can see that they're all different sizes and types of things,
just like Hanselman, SAAW, and Bavaria.
No two cancer cells look like each other.
A theory of cancer must explain these and other features pathologists use to diagnose cancer.
It must explain the time course of carcinogenesis, chromosomal instability,
and other characteristics of cancer, such as drug resistance and abnormal metabolism,
the Warburg effect.
We're going to be talking about some of those things.
Part three.
How does chromosomal imbalance cause cancer?
That's where Theodore Boveri came into, and he explained it.
And Peter Duesberg and I proved it.
For cancer to happen, the cells have to be able to divide.
Cancer requires cell division.
And let's just say we have a normal cell right here.
It starts out with the normal 46 chromosomes.
Before that cell has to divide, it has to double its chromosomes in order to,
when it divides, such that each new cell, the two new cells that are a product of cell division,
will both wind up having the balanced set of 46 chromosomes.
That's what normally happens when cell division happens.
The 46 chromosomes in one cell are duplicated to make 92.
The cell divides.
46 goes to the left.
46 goes to the right.
And you have two new cells.
And right here we show a cell getting ready to divide.
You can see the chromosomes here.
And then they line up in preparation for that cell to divide.
They line up with what's called the centromeres.
That's where the proteins that pull the chromosomes apart.
That's what they're called centromeres.
That's where it's attached.
They have to line up on what's called a metaphase plate and get lined up such that they can then
get the forces balanced so that the cell, the chromosomes can be pulled apart.
And here is the cell on the left.
You see the chromosomes are starting to be pulled apart.
The blue things are the chromosomes.
And the spindle apparatus, or the red protein, so they're attached to the chromosomes.
And they're pulling those chromosomes apart during cell division.
If you rotate this image on the left, just 90 degrees, you see that what you're looking,
it looks like a donut.
That's what it looks like when you rotate that metaphase plate and you look at it head on.
The thing on the left, the image on the left, is pulling the chromosomes left and right.
The image on the right, the chromosomes are being pulled towards you
and then away from you into your computer.
And you can see that these are balanced.
There's a symmetry here that's absolutely essential to balance the forces.
It's a little donut.
Right here, right in the middle where I'm moving my little cursor,
that's where the centromeres are.
And that's where the spindle apparatus are attached so they can pull those chromosomes apart.
All right, now here's where we're going to generate some aneuploidy.
Let's say there's some carcinogen or x-ray or cosmic rays or whatever happens.
The cancer results from unbalanced cell division.
So you had your 92 chromosomes all ready to go and something happens.
Asbestos or something in your cytoplasm interfering with chromosomal separation.
All carcinogens interrupt one way or another, normal cell division,
and they cause an imbalance of forces.
And then when they're, if they, most of these cells,
once they have an imbalance in chromosomes, they die.
They can't divide.
But on the rare occasions that they do, they adjust these things,
move them around or whatever to try to balance the forces.
And if they are able to divide, then unbalanced division happens.
Like moving to the left, there are 41 chromosomes.
Moving to the right, there are 51 chromosomes.
Now we have two aneuploid cells.
All right.
And then they're going to divide.
And we have two new aneuploid cells.
So when they divide, then they can either propagate or die.
They usually die.
Thank goodness.
But if you have lots of exposure to carcinogen,
you generate a population of these things.
And at some point, some of them will figure out how to survive, unfortunately.
But even those usually die.
We'll get into that here in a little bit.
OK, cancer phenotypes.
Phenotype just means a characteristic or a property
that you can look at under the microscope
or it's like a physical something that you can measure
and compare the good and the bad.
So for example, large size and variable morphology
that pathologists use, those are phenotypes.
The appearance of tumor-associated antigens,
that usually means like on the surface of a cell,
that these proteins are on the surface of a cell,
on cancer cells that are not present normal cells.
You have high levels of secreted proteins
that are responsible for invasiveness and loss of contact inhibition
that allows cancers to progress and metastasize.
And then, of course, there's the chromosomal instability
that's responsible for progression and drug resistance.
All of these things are due to aneuploidy and the overexpression of protein.
Important observations.
Aneuploid cancer cells have substantially greater amounts
of DNA, RNA, and protein.
The DNA, or the nucleotides, or those 3 billion nucleotides,
the 20,000 genes that code for RNA,
which leaves the nucleus, it goes out in the cytoplasm,
it takes that coded information,
goes into the cytoplasm of the cell,
and it turns that coded sequence of RNA
into a sequence of amino acids to make a protein.
And so, the cancer cells, the aneuploid cancer cells,
have substantially greater amounts of this DNA, RNA, and protein than normal cells.
And that has dramatic consequences.
This is most important of all for me personally,
when I was trying to understand chromosomal imbalance
and try to explain all the phenotypes.
Of cancer phenotypes.
And this is very crucial data that's important,
it's been known for half my life
that the relative proportions of DNA to RNA
and RNA to protein are constant.
In normal cells, the euploid cells, which are normal cells,
and aneuploid cells, those relative proportions,
in other words, if you increase the amount of DNA in a cancer cell,
you automatically proportionally increase the amount of RNA and protein.
And that has the profound biophysical consequences for these cells.
Biophysical and biochemical consequences of aneuploidy.
There's a 70% increase in the nuclear volume,
that's why we saw those big nuclei in aneuploid cells.
There's 70% increase in nuclear volume due to aneuploidy,
produces only a 40% increase in the surface area of the nuclear membrane.
Now those are out of balance.
The physical properties of the membrane,
which surrounds the chromosomes,
now they're out of balance, they're disproportionate.
And consequently, a change in the number of chromosomes
alters the interactions between the chromosomes and the nuclear membrane.
Cancer cells have a 10 to 100% more protein than euploid cells.
The excess protein has even a greater consequence than the RNA.
And the excess protein has profound consequences for the cancer cell
because they're really big molecules.
The consequences of extra protein.
Biochemical changes are proportional.
In other words, if you double an enzyme,
the amount of an enzyme present,
you double its activity, its ability to do work.
That's the biochemical approach, all right?
But the biophysical changes are exponential.
They go up, they have much, much greater consequences than the biochemical.
Here's some of the examples below.
Says the effects of increased cellular protein.
There's lots and lots of extra protein in cancer cells.
The membrane-bound proteins, for example,
we'll just talk about those right now.
If you have a 10% increase in cellular protein,
that's CP, you have a 100% increase in proteins
that are bound to membranes, whether it's the nuclear membrane
or the cellular membrane.
And that has profound consequences.
That explains a huge amount of things about invasiveness of cancer,
just how the metabolism is all screwed up.
And then the same thing with secreted proteins.
If you have a 10% increase in the secreted protein,
there is a 400% increase, or cellular proteins,
or 400% increase in secreted proteins.
And a 40%, you can see up here, a 40% increase in cellular proteins,
the 3,100% increase in membrane-bound proteins.
But there's typically a 70% increase in protein in cancer cells.
And I don't know what those numbers are,
but you can see how big these consequences are.
Now, the Warburg effect, that has to do,
the Warburg effect has to do with energy production.
Aerobic glycolysis takes place in the mitochondria of the cells,
the mitochondria of big organelles inside your cells
that produce ATP, adenosine triphosphate,
which is the energy molecule for most living things.
Aerobic glycolysis in the mitochondria is much more efficient
at producing the energy molecule, ATP.
You get 32 molecules of ATP per one molecule of glucose by the mitochondria.
Why then do cancer cells resort to the less efficient fermentation to produce ATP?
Because that's where the Warburg effect.
Instead of relying on mitochondria, now the fermentation comes in here.
Increased production of ATP in the mitochondria of cancer cells
is limited by crowding due to the extra chromosomes in protein.
Mitochondria require five to 50 times more space than fermentation does,
which happens in the cytoplasm, to produce the same amount of ATP.
Fermentation produces ATP up to 200 times faster than the mitochondria,
and it takes much less space to do it.
And it does it in the cytoplasm.
And as a consequence of this in cancer cells,
many of the mitochondria shrink and die away.
Mitochondria-like cells, I mean, they go away, they can reproduce, and they come back.
But a large fraction of the mitochondria in normal cells disappear in cancer cells
because they're just too big for the biophysics of all that aneuploidy.
They're still there, but they're very, very reduced.
And to make up for the lost ability to produce ATP,
that's when fermentation comes in there,
and it produces all the energy that cancer cells need.
Those cancer cells turn to fermentation of glucose
to provide the additional energy required for the synthesis of extra protein.
Now, chromosomal instability.
Chromosomal instability is absolute.
If you don't have chromosomal instability, you don't have cancer.
Without chromosomal instability, there is no.
Once you get the aneuploid cell from a carcinogen,
if there is no progression, you don't get cancer.
There is no cancer, there's no metastasis,
there's no drug resistance without chromosomal instability.
That's the only way a cancer cell can progress
is because unbalanced chromosomes are unstable and they're constantly changing.
And we'll talk about that here.
The evidence strongly suggests that the relationship
between aneuploidy and chromosomal instability
can be envisioned as a vicious cycle where one potentiates the other.
The vicious cycle can lead to a rapid broadening of the karyotype.
The karyotype is the collection of chromosomes.
And it broadens the karyotype diversity,
the variety of combinations of chromosomes,
in a population providing the substrate for natural selection.
I know that lady.
In other words, as soon as you get an imbalance,
you get progression, which leads to more imbalance, leads to more progression,
up to a point until the cells just can't handle it more and they almost always die.
Aneuploidy and chromosomal instability are inseparable.
That's basically what she was talking about.
Aneuploidy increases the complexity of managing all cellular activities.
Chromosomal imbalance disrupts the mitotic machinery
that separates the chromosomes during cell division,
leading to chromosomal instability.
Every time aneuploid cell divides,
it's struggling to try to get the chromosomes lined up so it can separate
and keep dividing.
Almost always they fail.
A single extra, an extra copy of a single chromosome
is sufficient to produce chromosomal instability.
Remember Down syndrome kids?
They have one extra copy of the smallest human chromosome, chromosome 21.
They have elevated risk of lots of different types of cancer
that have nothing to do with cigarette smoking.
They used to, they noticed that Down syndrome kids
have much lower levels of lung cancer,
head and neck, throat cancer and everything.
That's restricted to people that smoke a lot basically.
But they have elevated levels of all other kinds of cancer
and don't have enough time to really talk about all those details right now.
But they really do.
They have hugely elevated levels of cancer,
just because the extra copy of the smallest chromosome.
The greater the imbalance of chromosomes, the greater the instability.
The result is a heterogeneous population of aneuploid cells,
leading to, once you have mature cancer,
like in the solid cancer that takes decades to develop,
once you have a tumor with all those cancer cells,
no two cancer cells are identical.
Every one of them has a different collection of chromosomes.
Yet they have all the same genes, just a different collection of chromosomes.
Aneuploidy always damages the cell.
However, gaining chromosomes is more survivable than a loss.
The survival advantage of cells with gained chromosomes
plus chromosomal instability leads to the automatic progression of aneuploidy
with an increase in chromosomes.
That's why when you have aneuploid cells dividing,
the ones that survive are the ones that have more chromosomes,
than the ones that die off faster, the ones that have fewer chromosomes,
compared to those that have more chromosomes.
But they're generally dying off anyway.
Here is just a schematic of the progression of cancer.
Here you have a normal cell where its DNA index equals one,
which means you divide the 46 chromosomes by 23 chromosomes,
whichever way you want to look at it.
The normal number of chromosomes by itself, that's the DNA index of one.
In this case here, we have two copies of each chromosome,
so you divide each one of these copies, two copies by two,
DNA index of one, all along the border.
That's normal.
You come in and there's carcinogen, asbestos, radiation, whatever,
you get an unbalanced cell, a cell with unbalanced chromosomes,
and it starts trying to divide.
You get these low level of chromosomes with DNA indices between 0.5 and 1.2.
1.3, anywhere between 1.2 and 1.3 seems to be a barrier that cells
have a very, very difficult time of progressing.
That's why cancer is so rare.
These cancer cells are wimpy.
They die out in droves spontaneously.
But if you keep getting doses and doses of carcinogens,
and you keep feeding them, and keep doing this, and your health goes down,
then eventually you're going to have some cells that are going to be able to survive.
And then what they do is they have enough of them around,
they do what's called chromosome doubling, where the tetraploidization,
where the cells that have DNA index below 1.3, they can't divide.
A lot of them can't divide.
A lot of times they just die.
But some rare occasions, some then just double their chromosomes again,
and then they're able to get a balanced set of chromosomes, higher DNA index,
and they pull the cells apart.
They divide, pull the chromosomes apart.
Then they get these cells that are called tetraploidization.
They're much larger cells.
They have roughly twice the amount of chromosomes available.
But they're very, very unstable.
Since they have extra chromosomes, they can afford to lose some.
So as these progression goes along, there is a balance among these cells
to lose them.
They can afford to lose chromosomes.
And it's better that they lose these chromosomes.
It turns out nature has figured out a way to balance the survivability of aneuploid chromosomes.
The DNA index that seems to be the most stable for these aneuploid cells
is around a DNA index of 1.7, meaning they have 70% extra protein, 70% extra DNA.
But it's wide.
Varies from 1.5 to 1.9, but typically hovers around 1.7.
And they can just keep dividing.
So that's the progression part of this thing.
Now into the quantitative theory of chromosomal imbalance.
More details about this.
Every one of these little subjects that I'm talking about, believe me,
is an hour talking in its own right.
But I'm just trying to give you the highlights here.
And there's my book again.
You can go to that book, my book on my website, and get more details.
But this book was written for scientists.
It's got a lot of technical jargon.
But I tried to make it as much as possible in English.
I've written another book for the general public.
It's not published yet, but maybe it will this coming year.
It's in the hands of the publisher right now.
Thank goodness.
So the phenotypes of cancer cells are determined by the fraction of the genome.
This is another crucial feature about aneuploidy.
It's the fraction of the chromosomes that are out of balance that determines cancer.
The phenotypes of cancer cells are determined by the fraction of the genome phi.
That's a Greek letter phi there.
That is out of balance relative to the euploid cell.
And that fraction is typically again about 50% to 70%.
You see it's a large, large fraction right there.
And here is just a diagram of this.
It shows this is a plot of balanced, unbalanced phenotypes.
The horizontal axis, the ploidy factor, just says,
how many chromosomes do you have?
Ploidy factor one means you have a DNA index of one.
It means you have two copies of each chromosome.
And then that's a little green thing down here on the x-axis, the horizontal axis.
And then the cellular activity is arbitrarily designated one up here,
just as your normal background phenotypes of your cell.
Normal phenotypes of a cell are at this FD right here, flux.
The F stands for flux.
It's the activity or the output of a cell.
Number one is just arbitrarily designated number here.
And this just means that you have balanced chromosomes down here at one.
These other things that I have up here are like we have cancer.
That's why I have it in red right here.
It has, like I said, a DNA index of around 1.7, which would be right about in here someplace.
Or phi about 0.7.
Here's 0.5.
Then you have 0.2.
And then down here we have this.
This phi down here equal to 0.01.
That's for down syndrome.
That's like the kid that has the three copies of chromosome 21.
It affects 1% of the genome.
1% of the genome is affected.
Now the seven gene mutation theory of cancer, that's this one over here.
That little seven, that 0.00007, that's the phi of the seven gene theory of cancer.
People early on, they thought it took seven gene mutations to cause cancer.
Well, that's a very, very tiny fraction of the genome.
And this dotted line right here shows you the effect of those genes.
In other words, the phenotypic effect, that's what is measured here on this y-axis,
on the vertical axis right here.
It has no effect.
The normal effect right here at this one down at the bottom and this one over here on the left.
Right there is the normal cell number.
Right there, it's at one.
And look, this dotted line right here is the dotted line for the seven gene mutation.
It has no effect on the phenotype of a cell.
If you want to change the phenotype of a cell and all its properties like cancer cells,
you have to change, you have to increase the fraction of the cell that is aneuploid.
So here is 0.2 and then you get up here to 0.5.
In other words, 50% of the chromosomes are out of balance.
You're up here in the cancer zone.
And typically they hover between 0.5 and 0.7.
Somewhere in here is cancer.
Then you have this here, this vertical, this straight line up here, phi equal to one.
There's these three places up here where, I already talked about that one.
Here you are for tetraploid cells.
There are actually examples where the egg, a fertilized egg that divides,
has four copies of every chromosome.
Remember, your normal cell has two copies of every chromosome.
But rarely some eggs will have, the fertilized eggs will have four copies of every chromosome,
which means they're balanced.
They're not out of balance.
They're still in balance.
And that's what this line, the straight line shows you.
That's for balanced chromosomes.
You can see these are infants.
They're born dead.
I couldn't find any of these tetraploid babies.
But look at it.
You can recognize them as a human being.
Their phenotypes are normal because the chromosomes are balanced.
But the physiological effects of having so, so much protein
in their cells that can't survive and they're born dead.
But then you also have the rare occasions where the child is born with three copies
of every chromosome in the cell.
And many of these are born alive.
Most of them aren't, but many of them are born alive.
And they can survive weeks to months, but they always die.
And you can see this is a typical example of one of these poor things.
These poor things.
So this illustrates balance.
Normal, if you have two chromosomes, two copies of each chromosome,
you get a healthy human being.
You get three copies of every chromosome.
You get the poor little kid like here.
And then the one that we had before, these have four copies.
But if you have unbalanced chromosomes, you get cancer cells.
And no two are alike.
Okay.
Right.
And then I know I'm talking a long time.
I know y'all are getting tired of hearing me, but I'm getting close to the end now.
Also, the theory of chromosomal imbalance are able to actually calculate the stability.
But all this stuff we're able to predict, by the way.
We have all these publications.
We're able to predict and advance this stuff based on the chromosomal imbalance theory of cancer.
And we can compare our theoretical calculations with the real world data
that other people did.
So we didn't do it.
So we weren't biased in terms of experimental stuff.
But here was an equation that I came up with and published it, I guess, was 90.
I can't remember if this was 1999 or 2000.
Came up with this equation here.
Stability index based on chromosomal imbalance.
And then it shows that the least stable cells down here, very, very low stability index right here.
One is the most stable.
Zero, of course, would be the least stable.
So as you go down, it's less and less stable.
And the curve shows the least stable cells have a DNA index of about 1.5.
But cancer typically has a DNA index around 1.7.
Right in here, your cancer cells.
Like, they vary.
They vary right in here.
So they're a little bit more stable than the ones at 1.5.
So the ones that are 1 or 2, aneuploid cells are still pretty stable.
Now here is, this is a comparison of real world data that was published by, I forget who it was.
I think it was one of the Vogelstein.
This was Vogelstein's data on cell lines from cancer cells.
Colon cancer cell lines.
Looked at a lot of different ones.
And what I did was I plotted Vogelstein's fraction of cell,
the fraction of cells down here on the left.
That's how stable the cells are.
And on the horizontal axis is a DNA index.
And you can see that the cells that have, that are close to the DNA index of 1,
these are aneuploid cells, though.
They're actually more stable than the ones that have a DNA index of about 40.
With 40 chromosomes instead of the 46.
And then when you have twice the number of chromosomes,
just as the stability index function shows,
these aneuploid cell lines, they're a lot more stable.
The least stable cells are the ones down here with the DNA index exactly halfway in between.
Just as this theory up here predicted that the least stable would be right about here,
DNA index of about 1.5.
And then as you go either side of the most stable,
then the stability drops off rapidly.
These are all real cell lines right here, real cancer cell lines.
And they follow the predictions exactly.
Okay, time course of carcinogenesis.
This is John Karens.
He's a critic of the gene mutation theory.
Clearly, we cannot claim to know what turns a cell into a cancer cell
until we understand why the time course of carcinogenesis
is almost always so extraordinarily long, like decades for solid cancer, for example.
So true.
Oh, here's the rates.
This is the 2000 paper I published.
This is the Auto-Catalyzed Progression Maneuploidy.
Explains the time course of human cancer.
I generated this equation here that I'm showing you right now.
And I applied it to real world data.
And I have highlighted here phi in the red.
Phi is the fraction.
Remember, the fraction of the genome is the important thing.
The closer the fraction is to one or two, the more stable the cells are.
The more further away you get, like we said, if you're halfway in between,
it's the most unstable.
But cancer cells tend to be around about 70% of the genome.
All right, so you can, I apply this to the genome.
I applied this data, this equation to real world data from Amortazh and Dole,
goes back to the 1950s.
And I did it to every one of the head, I forget how many.
Laura, they must have 20 or 30 different cancers that they plotted.
And they plotted the data.
And I just here just applied it to all of them.
But these are just representative examples.
Okay, so these are deaths per million.
That's the y-axis or the horizontal axis here, the deaths per million.
And the horizontal axis are age, it's in years.
All right, basically, what is the prospects if you have lung cancer?
You know, when do you expect to see deaths?
So like lung cancer in men, these circles, these little circles here,
are the real data from Amortazh and Dole.
The 7G mutation theory of cancer, that's the dashed line right here.
That one goes up that way.
This equation that I had back here, this is the solid line.
And you can see it fits the observational data of Amortazh and Dole.
It fits it for lung cancer in men.
It fits it for lung cancer in women.
It fits it for breast cancer.
It fits it for cervical cancer in women.
It fits it for prostate cancer in men.
And it fits it in colon cancer in men.
But notice that both the 7G mutation curve and the aneuploidy curve,
both fit the data, the same data for the colon cancer in men.
The reason is that most colon cancer in men usually survive it.
You know, something else kills them later in life.
And if they survive it, that's why it doesn't show this curve up here.
But I just wanted to show it.
Okay.
Almost done, everybody.
Aneuploidy is diagnostic of all stages of cancer.
This was a study, this was Bolton and colleagues.
They understood that aneuploidy was a very, very good thing to use to diagnose cancer.
This is all the way back in 1998.
And they were looking for a way of using chromosomes.
You can see on the right here, the lesion.
This is the old nomenclature.
When a pathologist, let's say, looks at a cervical cancer, they look at the normal cells.
Then they categorize the abnormal ones by CIN1, and increasingly worse, CIN2, CIN3,
invasive cancer.
Stands for cervical interepithelial neoplasia.
So you can see here that the cancers, the severity increases as you go down this list right here.
And that also increases with, here in these little, I put these little,
they used eight chromosomes that these guys looked at.
And then they looked at these four categories, normal CIN1, CIN2, CIN3, and invasive cancer,
for each one of these chromosomes.
So you have left to right here, this list going top to bottom.
And you can see that they're all, at some point, every one of the chromosomes is aneuploid,
or abnormal in these things.
Their hope was that they would get a different distribution in these chromosomes
for some chromosomes relative to others.
So they could use that distribution to characterize the differences between CIN1, CIN2,
CIN3, and invasive cancer.
All they can say is, up here, if you look at these chromosomes,
we can't tell whether you've got any of these things or not.
So they were a little disappointed.
It turns out that their idea was right, if you looked at the spread of the chromosomes.
But I don't want to get into that right now.
So they're a little disappointed.
But the main thing to notice here is, here's all the normal chromosomes down at the bottom.
These are cells, normal cells.
Normal cells had very reliable chromosomal counts of chromosomes.
And these little bars that are separating it just shows how well they varied from cell to cell.
Of course, up here are all of those different things.
The wide range, the chromosomal instability, they're all up here.
But there's this quantum leap.
There's this quantum leap from normal cells to all of these abnormal cells.
And the primary reason for that is that normal cells with those low level of aneuploidy,
like I say, if you have just a few chromosomes,
they're not readily distinguishable by eyeball with the PEP smear.
So everything below CIN1, it can still be aneuploid precursors to cancer.
But the pathologists can't detect it by eye with those stains.
It's just that the cells are just too normal.
But you can see all of them.
That explains why these things are all up here.
They had to have massive, they had to have already undergone that chromosomal doubling step.
They had to have already gone past that in order to get the level of chromosomes
that pathologists can easily detect.
Okay, so where, I'm almost done here.
I think that's it.
Where are the diploid cancers?
It goes all the way back to the little theater of Boveri in 1914.
This is what he said in his book concerning the origin of malignant tumors.
If it should turn out that an exactly diploid chromosome number was regularly found,
then our hypothesis, chromosomal imbalance hypothesis, must be false.
He's absolutely right.
But to this day, nobody has come up with diploid cancer.
The end.
Okay, everybody.
I know you're probably sick of hearing me talk, but...
No, David, it was very good.
So stop your share now.
Okay, stop the share.
I stopped share.
Okay, I stopped here.
Oh, good.
I can see you guys now.
Yes.
Anybody left?
Well, we're so happy we got left.
It was very good.
And the depth of your work is extraordinary.
And Stephen will go for 15 minutes with the first series of questions.
And, Dave, the question that I have for you while Stephen's gathering his thoughts is
you knew that the HIV virus, if it exists, didn't cause AIDS.
Yes.
As did Peter Duesberg.
And here you are seeing the same COVID scam going on.
And then, you know, Bobby Kennedy writes about AZT and all of that information that's available.
And yet the mass that most people go, oh, yes, HIV causes AIDS.
So how do you maintain your passion for finding the truth?
Because, you know, it's clear that you and Peter were right, as were a minority of others,
but it didn't change much, did it?
People weren't held to account for the fraud.
No, no, no.
And as you saw in my little bio, I've been fighting this for 40 years, basically.
Yeah.
And I've never stopped.
The thing, one reason why I really wanted to talk today and talk about cancer
is because of what happened with AIDS and the HIV.
There are a lot of us, a lot of scientists knew, even the mainstreamers that kept working on it
with HIV and everything, they knew the truth.
They knew HIV did not cause AIDS.
The older people certainly knew it.
That's why they were so mean to Peter.
Those people, you know, if they thought we were just wrong,
they would have ignored us, you know?
But the people that knew that we were right, which were a lot of people,
knew that we were right.
They couldn't have it.
And I've talked about this in other talks about AIDS.
And so they had to control the dogma.
The HIV dogma is what we were fighting.
Now Peter and I have been fighting the gene mutation dogma.
There's so many dogmas out there, so many dogmas.
Every profession has their own dogma.
And the people that if you go against it, you get punished.
You get fired or whatever, or you can't get grant support or anything.
And so one of the really remarkable things about this crazy thing that's
passed almost five years now is that we are now getting together as a group of people,
because we're so curious, we want to know what's going on.
We want to hear other people's story, you know?
And everybody has stories that other people need to know, you see?
And I have a story about AIDS and I have a story about cancer.
And I want to share that where the sharing is good.
Well, people are hungry to find this stuff and there's avenues for them to do it.
That's why so many of us go to your Zoom meetings and other Zoom meetings or whatever.
It's because we're so hungry for other people's stories, you know?
That's the way we solve problems.
That's the way human beings solve problems.
They don't appreciate it, but we are beginning to understand that.
I think that it's not a case of the science or logical thought.
It's a case of human beings getting together, sharing their stories,
and making sense of what has happened in the last five years in this case.
That's how I see it.
But...
Well, Stephen, the next 15 minutes are yours.
I go for it, Stephen, but David, we honour your work.
It's an extraordinary volume of work and I love your passion.
Stephen, over to you.
So, David, you know you were talking about the dogma of the HIV virus was the cause of AIDS.
And as I understand it, AIDS is a collection of symptoms and diseases.
It's not a disease as I can understand it.
But anyway, do you think that the defence of the dogma over AIDS was absolutely crucial
to the successful defence of that?
Was it absolutely crucial to the rise of virology and the possibility of 2020 happening?
Was that...
Do you think that they knew in the time of AIDS and HIV virus?
Do you think that they knew what they planned in the future, i.e. pandemics, you know?
Endless deadly pandemics which they could terrorise populations with so that
human beings would capitulate to world government, for example, that kind of thinking?
It was intentional.
I've talked about this.
I've talked about it was intentional.
Well, April 23rd, 1984, it was a press conference.
Margaret Heckler, Secretary of Health and Human Services,
they brought out...
I had a press conference out there, brought out Robert Gallo.
And it became government dogma that day that AIDS is contagious caused by Robert Gallo's virus.
Ultimately, it was called HIV.
It started in Africa, sexually transmitted, and is invariably fatal.
That was government set dogma to that day, on that day, April 23rd, 1984,
which continues to this day.
That was intentional.
Anthony Fauci was made director of the National Institute of Infectious Disease.
Infectious disease, I can't even think of it now.
But viral diseases, okay?
For the purpose of defending that dogma and pushing it,
National Institutes of...
Damn, I can't think of it now.
Also, this is gone.
Yeah, and he was brought in November of 1984 to push that program, that dogma.
It was intentional.
Allergy, infection, everything.
Every one of his viral pandemics since then, the first SARS, the MERS, the Ebola,
all of those were all of the same thing.
Prepare the way to do this.
And also, benefit the pharmaceutical companies and things because they make drugs,
I mean, make chemicals, sell them to people, whatever.
But it was basically part of a ploy to control the whole system.
Mm-hmm.
Yeah.
You look back at the history of it, it's clear.
So David, it was intentional, yes, but was it...
Do you think in the 80s, they were already planning a world where virology kind of took over
from immunology, if you like, where the immunologists could appreciate that human beings
and for that matter, other animals had incredible immune systems.
And it was highly unlikely that mere men, i.e. man, you know, the capital M,
were clever enough to improve on God's immune system, if you understand.
So do you think that they planned to control people in the future with the threat of deadly viral
pandemics?
Do you think they planned it then or do you think that came about later?
And it was intentional over AIDS, the deception, but do you think they knew in the 80s that they
were going to push virology to achieve, as a Trojan horse, for totalitarianism?
Well, I knew it was intentional to push it.
Absolutely.
Now, I don't know if it was designed to be the weapon of 2020, 2021.
I don't know.
But it definitely was pushed because all you got to do is look at everything they did during the
almost four decades of Anthony Fauci at the Institute of Allergy and Infectious Disease.
That's what he was the director of.
He had more money, more power than even the Secretary of Health and Human Services.
He did.
That was intentional to control that place.
What the goal was, you're asking the goal.
I don't know what the goal was other than to have massive control over this health and human
services, which the pharmaceutical industry was very, very big at this time.
And 70% of the FDA's money comes from the pharmaceutical industry.
And I'm sure they made hundreds of billions of dollars during this period that we're talking
about.
Incurable disease is what money is made of, like cancer and things like that.
I'm sorry.
Go ahead.
Did Fauci take over from Gallo, Robert Gallo?
No, Gallo was just at the National Cancer Institute.
It's not at the Institute of Allergy and Infectious Disease.
So he wasn't in charge of anything really big.
But he was a cancer virologist, Gallo was.
He was not the director of it or anything like that.
And he was originally found guilty of scientific misconduct and fired.
Started another facility later, but you never heard of it.
He just sort of disappeared.
So when was that?
Oh, Lord.
That was in the 80s.
He was fired in the 80s.
Congress had some hearings on Gallo.
They found him guilty of lying scientific misconduct.
And of course, the government, it was the Reagan administration at the time,
they could not afford to have that embarrassment to come out.
The guy behind their policy of contagious AIDS and everything found guilty.
What they did was they dismantled that whole thing and they were going to require him to be
retried, so to speak.
And they realized the people that did it the first time, they found him guilty,
realized that the government, the powers that be, were not going to let him be guilty.
But they got rid of him.
They just had to get rid of him.
And that's what they did.
And subsequently, so Luke Montagnier won the Nobel Prize for Medicine in 2008
for the discovery of the AIDS virus.
Isn't that right?
That's right.
Not for the discovery that it caused for the virus.
Yes.
Sorry, for the HIV virus.
Sorry.
By the way, and Luke Montagnier later on acknowledged that that virus did not cause AIDS.
Exactly.
But that was pretty much, it was quite a lot later, wasn't it?
It was after 2020.
No, he actually, it was actually, it was 2000.
It was 2000.
I think it was 2000.
They had the AIDS conference, the big AIDS conference in San Francisco.
I was living there at the time.
And right downtown San Francisco.
Fauci, that was the first time he came out in opposition to HIV being the cause of AIDS.
And he introduced an alternative agent that was not a virus.
I forget what it was.
Just proposing it.
And then after, God, it was in the early 2000s when he and others and a bunch of Europeans
found HIV free AIDS cases.
And so it started to be a stampede away from HIV.
Anthony Fauci got on, I think it was Air Force Two, went all the way to wherever it was,
in England, I think it was, or France, or wherever it was.
And he shut that whole thing down about HIV free AIDS cases.
That's when they came up with HIV 2 or something like that, another retrovirus that caused these
other HIV 1 AIDS cases.
They had to keep the retrovirus thing going.
So they could not have a virus free AIDS cases.
And that's when, like I say, Anthony Fauci got on Air Force Two and flew out there very,
very quickly to shut that down.
And he did.
Yeah.
So who won the Nobel Prize in 2008 then?
Was that just Montagnier or was it Gallo Two?
Gallo No.
Gallo didn't get it.
No, exactly.
He wasn't happy about that, was he?
He thought he was going to get it instead of Montagnier.
Yeah.
So Montagnier, when he accepted...
He might have chained it with somebody, I don't know, but it wasn't with Gallo.
So Montagnier was awarded the Nobel Prize on his own for the...
I don't know.
I don't know if it was on his own or not, but it was not Gallo.
I think there was someone else, but I can't remember who it was.
But anyway, but the point was in 2008, Montagnier was probably aware
that the prize that he was being awarded was for something which he didn't believe was true
at that time.
He didn't get the prize for discovering the cause of AIDS.
He got the prize for discovery of the virus.
Absolutely.
That's exactly...
Yes, exactly.
Not given the Nobel Prize for discovering the cause of AIDS.
No.
Yeah.
I mean, that was weird.
It was very, very weird.
It was one of these politically engineered Nobel Prizes.
It's not the only one.
Maybe it was necessary to give Montagnier that to keep the false narrative going.
Yes.
Because Montagnier was the biggest threat at the time, maybe?
Nobel Prize is a very powerful tool for propaganda.
Sure.
And Keri Mullis won the Nobel Prize for chemistry, which is your subject, in 1993 for the invention,
if you like, of the PCR technique.
PCR.
Is that right?
PCR, yeah.
Ten years earlier, yeah.
So all these names are all linked.
And it seems to me that Keri Mullis turned up in Paris and asked Montagnier when he was
surrounded by his colleagues.
And he said...
So he'd come up with a statement.
The HIV virus is the probable cause of AIDS.
So he asked Montagnier, because he couldn't find any justification for this statement,
and he asked Montagnier whether he could provide some references for him.
And Montagnier suggested a couple.
So I think this came directly from Keri Mullis's mouth.
And Keri Mullis said, no, that's not good enough.
And two suggestions.
And then Montagnier gave up and walked away, apparently, and left his colleagues, too.
And they were a little bit surprised.
So Keri Mullis said.
But Keri Mullis ended up, because he had a Nobel Prize, he was able to defend Peter Duisburg.
And I wonder whether you could tell us something about that.
To some extent.
After Keri talked with Montagnier, he was furious.
He was really, really furious, because he realized, man, this is a scam.
Total scam.
He sort of knew...
You don't think he knew beforehand or suspected it?
He suspected it, absolutely.
Oh, right.
Oh, yeah.
But he didn't get furious until he talked to Montagnier himself and asked him,
if Montagnier didn't know, who the hell does?
Yes.
So that was a very important story from Keri Mullis's point of view and also from human beings point of view.
But I think we ought to get that story sorted out in our minds so that we can...
Or you, maybe David, so you can explain to the public what, you know, in simple terms,
the connections in that story.
Because Keri Mullis ended up dying, in inverted commas, in August 2019 of pneumonia, as I remember him.
But of course, if you think about it, there's no way...
Because he was saying things like...
He hated Fauci, Anthony Fauci.
So he was saying things like, Keri...
I've actually heard it with my own ears.
Him saying that there's a video on the internet,
he's talking about Fauci and he says, he, Fauci, doesn't know anything about anything.
That's right. It's true.
And then he goes on to say, and I would say that to his face,
so this guy, Keri Mullis, had to be dead at the beginning of 2020.
He couldn't be around, they couldn't have done what they did at the beginning of 2020
with Keri Mullis around, in my opinion.
Or Montagnier.
It's very, very suspicious.
It's circumstantial at this point, but it did not escape my notice.
Keri Mullis died, and also, Luke Montagnier and Peter Duesberg had a stroke.
Those are the three most powerful, outspoken, credentialed opponents and critics
of Anthony Fauci in the world.
Those three people.
All right?
Two of them died, one of them had a stroke.
I mean, how fortuitous could that be?
Well, one of them died before 2020, but Montagnier died in February 22, I think.
Look at it this way.
They knew it was coming as a planned thing anyway.
They had the injections already in the vials before 2020.
Sure.
So is it true?
Because it came before, just because of 2019, that's beside the point.
It's all in the same time, you know?
Just too close.
Too close.
So David, is it true that Montagnier, one week before he died, he was in Milan?
So he was 94, was he, or something like that?
93?
He was an older fellow.
I mean, Keri was the youngest.
You know, Keri was old.
Peter was old.
I'm getting there myself.
Yeah, so Montagnier, apparently in the speech in Rome, he said, and I'm pretty sure I've got a
transcript somewhere, but whether I can find it or not is another matter, but he said that
the unvaccinated would save humanity.
Is that true?
And a week later he was dead.
Dead, I don't know.
Right.
So there ends the interrogation, David.
I could go on, but I'll bore people to death.
So Charles, are you there?
Thank you for answering those questions.
So these are really important names.
Luke Montagnier, Peter Duisburg, Keri Mullis, and they are really, really important.
There's a great story there that needs to be told, and it hasn't been told properly,
I don't think, so we should do that.
Get Celia Farber.
Invite Celia Farber.
You may have had her on before.
I think you have.
We have had her on, yeah.
She knows all these people.
She's very, you know, very, very tight.
She can answer a lot of your questions on the internet.
She can answer a lot of your questions that I can't.
I see you're not as au fait as her, you mean, on the stories?
I know about it, but I didn't dig into it like she did, you know?
Ah, yeah.
A journalist has a broader spectrum of views and questions than I do.
Yes, sure.
They can get the nuances and dig into things and ask the...
They can ask the kind of questions that you're asking me.
So I don't ask the same questions that Celia does.
I'm not a journalist.
Oh, about cancer, just one quick question I thought of,
which was about your presentation.
I'm sorry the questions I've asked now weren't really about your presentation,
but you do know stuff that...
So the cancer, the site of toxic drugs, which do they work?
And if they work, by what mechanism do they work?
And is it a kind of blunt instrument that kills everything and thereby cancer?
Or is it...
How finely tuned do you think it is as a chemist?
You mean the chemotherapy?
The site of toxic drugs, which are said to be wonder drugs, you know?
Oh, no, they should all be illegal.
All of them?
Yeah, I can't think of any...
There's no such thing as a cancer drug.
There isn't one.
Not in the sense of a pharmaceutical drug.
Remember the Warburg effect and the importance of glucose to...
Every cancer, I don't care, even though none of them have the same combination of chromosomes,
they're all absolutely dependent on fermentation of the cell.
The so-called Warburg effect because they have a requirement for energy.
They have a huge demand of energy, more than normal cells and tissues.
And that has to go through if you keep glucose out of your diet
and change it with something else.
I think they call them keto diets or whatever.
There are approaches.
There are approaches that take advantage that you can take advantage of.
One of them is the Warburg effect.
And a lot of people are doing that around the world,
primarily in Mexico and Europe, but especially Germany.
They know to...
They know diet.
Fasting, very serious medical monitor dieting.
The cancer cells...
Every component in my presentation, those little numbered areas there,
I could talk an hour on each one of those.
Like about the...
No, the cytotoxic drugs.
So this is really important in my...
They're carcinogenic, by the way.
I cannot think of a cancer, anti-cancer drug that is not carcinogenic.
Okay.
So, but most people believe that they work, these things.
Maybe they want to believe they work, but...
So they don't work, in your opinion?
They absolutely don't work.
Okay, let me answer the question this way.
There's no target, there is no genetic target.
The only metabolic approach that you could go after, like I said,
is the production of fermentation,
which no drug company goes after that because they can't, they don't know how.
It's a dietary thing.
But they...
Lost my...
So how do they...
I'll answer that question one more time.
I derailed it.
David, how do they produce the illusion that they work then?
How do these criminals...
The illusion, yes.
Okay.
They're all toxic.
And people...
Cancer cells are very, very wimpy cells.
They die on their own all the time, all the time.
Okay.
And one reason why it takes decades is because they're so wimpy for solid cancers, all right?
For these things to come along.
And we probably all have cancer cells in us.
Maybe even little micro tumors or whatever.
But our innate immune system takes care of it because a normal, a healthy person,
you're much more healthy than any aneuploid cell.
The aneuploid cells are not healthy at all.
They go, they come and they go and they disappear.
And we're exposed to carcinogens all the time.
And if you're healthy and you don't have so many carcinogens,
you're not going to die of cancer.
It used to be a very, very rare thing, cancer was.
Now, you know, cancer is now the second leading cause of death in the United States.
Second, it used to be third.
Now since they use these injections, it's number two.
And they're all toxic drugs.
Our cells, our normal diploid healthy cells,
they're so much healthier than any cancer cell.
What the chemotherapy does, it kills all the cancer drugs.
They kill the cancer cells.
Cancer cells always die faster than normal cells.
That's why they're so hard to culture.
Before the HeLa cells from Henrietta Lacks in the 50s,
nobody could culture a human cancer cell.
In fact, nobody could really hardly culture human cells, period.
But until Henrietta Lacks, the HeLa cell,
they're still going in the lab right now.
They're extremely difficult to grow.
And when you take a biopsy of a tumor,
it's always a mix of normal healthy cells and cancer cells.
And if you try to culture them, in no time at all,
all the cancer cells have died off in cell culture.
And the normal cells are the ones that keep going.
That's why people used to think that there was such thing as diploid cancers.
Because when they analyzed those cultured cells,
they were all diploid because all the diploid cancer cells had died off.
Now everybody knows there's no such thing as a diploid cancer cell.
All right.
So what happens is instead of keeping your much higher health,
that health difference, cancer is low, you're high,
the chemo and radiation and everything lower,
it kills the cancer cells faster than you,
but it's also destroying your health.
So that distance between you and cancer is getting smaller and smaller,
your health and the cancer cell.
And after therapy is done, your health now is way down here.
They do it to the point where they can't detect the cancer cells anymore,
but they're still there.
There are probably millions of them left, you know, low cancer cells.
And they're the ones that could survive all that,
but they have to take you off the drugs and the treatment before they kill you.
Every technique, every medical technique other than surgery, just pure surgery,
but if you use any chemotherapy or radiation,
they're killing you because they're your cells, it's just the cancer cells.
There's no target that a chemotherapy goes after,
that a cancer cell has a target that your normal cells don't have.
Remember they're your cells, your genes, the same thing.
They're targeting your normal cells at the same time they're targeting the cancer cells.
The cancer cells just die faster.
That's it.
Yes, but the point is, even if you are doubtful about that,
I'm certain of it.
If the cancer cells are killed off almost at the expense of the patient dying,
but not quite dying, and then the patient recovers,
and then they achieve a so-called, yeah, they've been cured of cancer eventually,
you know, after five years, whatever it is, allegedly.
Then you could argue that they've achieved their goal, even though they put their,
they didn't really know what they were doing.
They used a blunt instrument to kill off the cancer cells, which almost killed them.
Do you understand me?
But at least the patients have survived.
But most don't.
Most don't make five years.
Absolutely not.
Right.
So you think the whole thing with cancer drugs...
The cancer comes back and there's nothing they can do about it.
There's no therapy and it winds up killing them.
David, you think that the whole cancer treatment, that's a fraud too, do you?
So all the cancer research...
Absolutely, totally and completely.
Right. That's interesting.
So last question, very quickly, Charles.
Very quickly answers as well, David.
Was there a pandemic in 2020 or not?
A pandemic, a fraud?
Yes, exactly.
Did you know in the United States, fewer people died in 2020 than they did the previous five years?
Yeah. So do you think as I think, you don't have to agree with me,
but I think that it's highly possible, probable in fact, that pandemics can't occur because
a deadly virus, if you believe in viruses, kills its host.
Therefore it can't spread all around the world.
And so the whole thing about pandemics is a construct for these criminals
to use the Trojan horse for totalitarianism.
And the second question I have is, was there a disease called COVID-19?
No.
Absolutely.
All you got to do is look at the CDC, go to the CDC's own website.
They actually have it and I do it in my presentations.
I take an image of the CDC's website and they have a comparison of the symptoms of the flu
and the symptoms of COVID-19.
They're identical.
Absolutely.
You know, so all they did was change the name.
There's two things and this came from the AIDS, HIV and AIDS started this.
The CDC knew as early as 1982 that the so-called AIDS defined, early AIDS defining diseases
were in gay men using chronic doses of nitrite inhalants and recreational drugs.
And the heterosexual IV drug users.
Those were the AIDS cases in the 70s and the early 80s.
And the CDC knew as early as 1982 that that was what was causing those symptoms that later
be called AIDS and they could be adding new symptoms for AIDS.
The definition is huge.
So to sum up David, AIDS was a false diagnosis and so was COVID-19.
It was a fraud.
It wasn't a false diagnosis.
I agree with you.
It was a scam.
They knew it.
They, I'm telling you right now that they decided in 1984, the federal government decided,
and that's when they hired Anthony Fauci to do this intentionally, was to lead the AIDS thing
as an uncurable viral disease that anybody could get.
And he killed any other.
Anthony Fauci would not allow anything else, any publications, any outspoken, anything.
That was by design.
They didn't care what it was, but they had this thing and they wanted to have this virus.
And they wanted to make a contagious disease because people are afraid of contagious diseases.
Absolutely.
They wanted to make a contagious disease lethal.
Yes, exactly.
Exactly.
Make it really an object of fear in the minds of human beings.
Lots of hands up.
One last point, Charles, just very quickly.
So in my opinion as a medical doctor, David, I think that it's highly probable that these
pandemics, the deadly viral pandemics, you know, which have caused, so we've got to do
something about the next pandemic and all this.
I don't think pandemics are possible.
No, we've agreed on that.
I think that's a con.
Come on.
I'm just trying to ram the point home.
You've rammed it beautifully.
I'm with you on that.
Good.
Very good, David.
Thank you so much.
All right.
Thank you, Stephen.
Lars.
Thank you, David.
That was fantastic.
I have two questions for you.
The first one is Thomas Seyfried in Boston.
He says that cancer is a metabolic disease.
Do you agree with him on everything he says?
Or do you have differences with him?
It is a metabolic disease.
That's the Warburg effect that I talked about and he talks about.
What they're doing, they're saying the thing where I absolutely disagree is that
they agree that aneuploidy is a big deal in cancer, but they say that the Warburg effect,
or this metabolic disease, leads to chromosomal imbalance.
It's the absolute opposite.
If that were true, there would be diploid cancers.
You'd have the fermentation leading to cancer without aneuploidy.
There's no example of that.
The question is, what causes this massive Warburg effect where you have these healthy cells
and all of a sudden they decided to go stop using mitochondria.
Much more efficient producing 32 ATP's per one glucose.
Why give that up and now start using fermentation to produce only two ATP's?
You see, the explanation is what I just said.
When you have this overabundance of protein, you have chromosomes, you have 70%, 50%, 60%,
80% extra protein in the cell.
It's called macromolecular crowding inside the cell.
It just changes the physics.
Like I said before, the phenotypic consequences,
the more biophysical consequences than biochemical.
The biophysical consequences go up exponentially.
Exponentially, like tenfold or more.
And that's what produces all of the phenotypes.
The membrane-bound proteins, the secreted proteins,
are a consequence of the overproduction of protein.
The only way you can get an overproduction of protein, you have to have a hell of a lot of ATP.
If you starve a cancer cell with ATP, you can't completely because you're generating the
fermentation in the cancer cell too.
But if you just really cut it down, the aerobic glycolysis,
not all of the mitochondria are destroyed in cancer cells.
Once you see it, it's obvious.
The metabolic thing, if you're talking about therapy, that's where you go to, I think.
Starve the cancer of glucose.
Starve it of ATP, but not the person.
Humans can live without glucose.
And David, Danny Dukoc, and others are saying precisely that in the chat.
Starve the cancer of glucose.
That's right.
Starve the cancer.
Yeah.
It's not toxic to people.
It's a non-toxic way to do it.
I have one more question, if I may.
A lot of cancer doctors talk about terrible cancer now.
In your view, what's the mechanism and is there anything people can do about it?
Don't get injected.
I don't know how you treat it.
I frankly, honestly, I don't know how you would do that.
Okay, I've answered this.
I've talked about it.
I put it in my new book, actually, too.
Knowing the chronology of the progression of cancer, it takes decades for solid tumors and
everything.
Because knowing the cancer cells, knowing the aneuploidy, how damaged these things are,
that your immune system is really just absolutely extraordinary.
Just get, if it sees them, it gets rid of them.
And if it can't get rid of them, it just like guards around it.
Now just sit there benign because they can't progress.
For example, you can have these partially progressed cancer cells, but if you go in
there and take a biopsy, on occasion, you'll free them up and then start dividing and progressing
and then turn into cancer.
It's rare, but a few percent, that happens even with just biopsy.
The turbo cancer, from my perspective, has to be, like I said, we all probably have these
little cancers and tumors in us to varying degrees.
I think it's the innate immune system that is just totally being destroyed.
I have no doubt that some of those things that they're injecting into people are carcinogens.
But if you had a functioning immune system, it would still take years to get a blood cancer
from scratch and decades to get a solid tumor from scratch by doing that.
You see?
So I'm convinced that these turbo cancers are those tumors that we have in our body.
They're in us already that are dormant, that you probably never ever know.
You probably survived it or whatever, or if it did show up, okay, or whatever.
But now once you've destroyed the innate immune system and you prevent that, you basically
with no immune system, you're turning people into petri dishes in the cell culture.
It's the tumor that is already there.
These aneuploid cells, like I said, they're very weak compared to normal healthy cells.
They don't have a prayer usually.
But as soon as you destroy the immune system, there's always a population.
Because no two of them have the same karyotypes.
There's always these different viruses, like bacteria.
Cancer is like a single cell organism, like bacteria.
The individual cells are on their own, really.
They can do what they want to.
You will always find an antibody-resistant bacterium in a population of bacteria.
Because you kill off all the ones that are susceptible to it, and you leave the ones
that just happen to be resistant to it, and then they repopulate the bacteria population.
Well, that's what I think is going on with the turbo cancer.
Every one of these cancer cells, remember, is unique.
Just like people are unique.
No two have the identical phenotype or karyotype or anything, like bacteria.
There's always going to be some that will take advantage of the environment.
You give them an environment with a weakened immune system.
Those that can proliferate will proliferate, like cell culture, like mad.
I think that is the explanation for the speed with which these things.
David Martin suggested that the pseudo-uridine downregulated interferon 1,
so that the immune system just couldn't handle it.
Does that make sense in your world?
I think it's more dramatic than that.
That's the molecular thing.
The interferon, or the cytokine, or that thing.
The immune system is at least as complex as our central nervous system, I think.
Everywhere you look, it's just so huge.
I think it's just in mass.
It's just being reduced.
One of the things that they've noticed with these,
have you heard of IgG4, immunoglobulin 4?
Yes.
That one, and I think too, but IgG4,
that's the one that's the least available antibody in our body.
When it proliferates, its function generally allows us to overcome allergies.
Like my brother had a lot of allergies, and they exposed him a lot of allergies when he was a kid.
Finally, his IgG4 came up there, and now he doesn't have these allergies anymore.
It basically shuts the immune system down to this, aspects of it.
But the IgG4 levels now have gone up 200, 500 fold, something like that, in these people.
And they have been exposed to these injections, and they're also getting used to these cancers.
If they have anything to do with cancers, they're going to stop the immune system from attacking
cancer cells.
I'm not an immunologist.
I don't know all the nuances because it's complex, complicated stuff.
But I know the general principles, and the general principles make perfect sense to me.
Thank you very much.
Thank you.
Thank you, Lars.
Zoe, good to see you again.
Sorry, I was on mute.
Can you hear me?
Yep.
Yes.
We could momentarily, but not now.
We've lost you now, Zoe.
And we can hear you now.
There we go.
Can you hear me now?
Yes.
I touched it.
Hello.
Thanks for having me.
Zoe, are you the medical coder?
Are you the medical coder?
That's me.
All right.
Can you put your email address in the chat?
Because I meant to invite you, but somehow you've slipped off the radar.
I sent an email to both you and Charles.
I think it was when Holland was on.
That's good.
Okay.
I'll look for it then.
So I hope it went through.
I have a proton mail address.
It's zoeSmith at protonmail.
So hopefully, I can send you another one.
Oh, that would be good.
Yeah. If you could do that.
Yeah.
So my question for Dr. Rasnik, it actually has to do with HIV, but it connects to COVID.
So my question, and this is in my book, because I used to work in a lab,
and there's an exposure protocol for anybody that works in a lab.
If you're exposed to a body fluid, you're supposed to go down to the ER,
and they will run a PCR test on you and see if you have HIV, and then they start you on
HIV prophylaxis if you've been exposed.
And I did not know what that drug was.
So for researching my book, I looked into it, and I can't remember the name off the top of my head,
the brand name.
But when I looked into the actual brand name and who makes it and what is the dose and
how are they prescribing this PrEP or prophylaxis treatment that they're giving to hospital
employees that are exposed to body fluids, it appeared to me it was AZT but in a reduced dose.
And what we know from HIV is that AZT was causing the AIDS symptoms and making it appear as though
there was an epidemic of HIV at the time.
And another thing that I talk about in the book is that there was this drug Remdesivir
in connection with the ventilators that were used to make everyone think that COVID-19 was
this massive respiratory failure disease, and that's how they got everyone to believe that there was
a pandemic happening.
It was actually the treatment in the hospital that was causing that.
So I'm finding this other parallel, and I'm just curious if you've discovered that,
if you knew that that was the treatment that hospital employees were given,
because I had always known, and I didn't know what the actual drug was that they were prescribing,
but everybody that worked in the lab that had ever, and I had a friend who actually did have
to do this treatment for two months because she was exposed to body fluids.
We all knew that it had these massive side effects, and I looked up what the side effects
were, and it was like two pages.
It includes death and organ failure.
I was definitely afraid of being exposed and having to be put on this protocol
in order to stay employed and come to find out there's this connection with AZT.
So I was interested in your perspective on that.
Yes.
If you could.
Happy to talk to you about that.
Yeah.
It's PREP and PEP, pre-exposure prophylaxis and post-exposure prophylaxis.
This came out in the end of the 90s, early 2000s, something like that.
It was the idea, it was a way to, you're right, they use these tests.
It's the same key here all the way through, antibody tests for HIV or PCR or something like that,
to label you with something.
Then they come up with the toxic thing to give you as a consequence of that.
The test, the PCR test, for example, is totally bogus.
Antibody test, PCR, it tells you in all of those tests, the PCR test for HIV,
the antialysate test and all that, it says in the package inserts that there's no reference
standards that these tests are not to be used to diagnose the presence of HIV
or the virus.
You cannot use it to diagnose AIDS or the presence of HIV.
Believe it or not, it says it in the package inserts that come with all those HIV tests.
But yet they're doing it anyway, and they're giving you these drugs.
Since they started using these things, the post-exposure prophylaxis and pre-exposure
prophylaxis, so many people were coming down with AIDS-defining diseases after that,
were killing a lot of people and keep adding these new diseases or consequences,
that they came up with another disease.
It was called immune reconstitution inflammatory syndrome.
Originally, it was immune reconstitution syndrome, IRS.
You come down with the same diseases as an AIDS person plus additional ones.
But if they show up only after you take the drugs, it's not called AIDS.
It's called IRS or immune, or IRIS.
That's what it is.
I've got posters.
I've talked about this.
They are causing more harm.
AIDS diseases plus a whole host, more than double the number of diseases that were associated
with AIDS are part of IRS and immune inflammatory reconstitution syndrome.
They're causing these diseases that they're trying to...
This has been going on since the late 90s.
Well, they're doing that with long COVID also.
They have a diagnosis for COVID.
After you've been given this test, they label you as COVID-19, and there's a diagnosis code for that.
But if you come in and you've been vaccinated and you have these long COVID symptoms,
they're calling them long COVID symptoms, they have specific diseases for that.
They're not categorized as vaccine injuries.
That's one reason that I titled my book what I did, because the COVID code, it actually
the code that I'm talking about when I refer to that, is the vaccine injury code that they
did not publish in the United States or in many other countries.
It was published on the WHO website, but they did not make it available
to report internationally as a code.
It was a way of burying a needle in the haystack, and they've recategorized...
Well, not only did they use the initial COVID diagnosis code to recategorize all the respiratory
symptoms that used to be flu, asthma, and all those things into COVID,
but they've also used this long COVID thing to categorize vaccine injuries as that.
Right.
So it seems to me in multiple levels, they use the HIV
fraud to parallel the COVID fraud.
They basically pulled the rules from the HIV scam and applied them to COVID.
Yeah. In fact, the AIDS thing was the blueprint.
When they kept that, that was the blueprint for everything since then.
I'm literally meaning everything since then.
I agree. So I was correct in the current treatment that they are still giving to
hospital employees and also marketing currently to gay people for as PrEP is AZT,
just a reduced dose. So it is continuing.
Absolutely. They're giving the anti-HIV drugs as prophylaxis.
Perfectly healthy. But if you had sex with somebody and you're afraid
that you might get HIV from them, then it's pre-exposure prophylaxis.
It's perfectly healthy. They give you the exact same AIDS drugs.
And if you come down with AIDS diseases or any of the other diseases, they don't call it AIDS,
even though you have the AIDS symptoms. They call it post-exposure prophylaxis.
I mean, immune reconstitution inflammatory syndrome. They just rename it.
Wow. Wow.
I think a lot of people are not aware of that.
They're not. That's why we have to share this stuff.
You know, and since you're a coder person, you could look that up.
Certainly with AIDS, you look at that.
So David, couldn't you and Zoe go to the equivalent of the police in the UK in America
or go to the sheriffs and tell them about this?
But you know, I don't go to people like that. They have to come to me
because I'm not a preacher. I can't convert anybody.
They have to look like moms and everything.
You know, they had to go through some horrible thing with their child,
to become a warrior and fight the horrible things that are going on.
That's what's going to happen with COVID.
They have to have enough people injured, whatever that is economically,
so they get so pissed off, they either give up or they die or they fight back.
I mean, look how long it took to talk about AIDS after all these decades.
But also, people like you, David and Zoe, working together,
could actually create a counter narrative which could destroy the false narrative of them.
So as you say, I'm happy to be sorry, all these people knew that.
Sorry. I'm eager to do it.
I would be happy to as well, whatever I can do.
I know in the United States, all the institutions down to the individuals that used any COVID
measure from the vaccine to the PCR tests are covered under the PREP Act.
So I don't think going to a sheriff would do any good in the United States because of that.
But anything that I can do, I'm happy to do, to fight back.
That's why I wrote my book.
And Dr. Rasnik, if I may, I'd like to send you an email later and maybe we could discuss this on
my sub stack and help get it out there more. By the way, everybody, I prefer Dave.
Zoe, I do think that- I don't like people that I don't like.
I come from the healthcare industry, so I'm programmed to show that kind of respect.
So thank you for being down to Earth, Dave.
Yeah, we'll do that.
So Zoe, I think there is a point in going to the sheriffs, even if they don't do anything,
because if you formally put a complaint in, a criminal complaint or whatever you call it in
America, then you know that you have told people, certain people, named people,
that what's going on and that you know that they knew then, at least so there's a marker
in the future. But if everybody says, oh, there's no point in going to the sheriff
and there's nothing recorded, then it's just all in the air, isn't it, in the future.
And that's not very- so I do think that notices of liability or whatever you want to call them,
you know, are very important because then in the future you can say this person,
this named person knew this then, two years ago, five years ago, whatever. But at the moment,
you know, HIV and AIDS has never been solved, I think because nobody's formally made these
complaints to anyone. Formally. Oh no, we tried. Listen, what happens, you get fired, you lose your
grants. I mean, if you know you're on the right track when somebody comes after you.
Absolutely, yeah. Your insolence is a testament to that.
It's far more important that Zoe and I and other people share the information so that we can
distribute it broadly. That's what I- Yes, very good.
All right. Thank you, Zoe. Glyn.
Hi, David. It's interesting, as a deep researcher, you've sort of done things in your own space and
all of these crazy ass hoaxes are all around you, which is, I think you've done a marvelous job of
describing it. And there's three primary ones here. The HIV hoax, the COVID hoax, and the
hoax and the pharma health correction industry hoax. Am I accurate in saying that?
I got it. But like I said, I got 40 years of that sort of stuff on my website. I mean, a lot of
stuff. And a lot of it- Okay, so what I would like to suggest is I think a lot of these are connected
and especially around who was the primary sponsor. So I want to name a number of other hoaxes and
see if you have an answer. So very quick answer, please. Just either say, yes, you think so and
you haven't, or I'm not sure. Just give me one or the other. The climate change hoax.
As who is the sponsor of the climate change hoax?
I don't know, but it's- Okay. Let me- the transsexual transformation improvement hoax.
I don't know, but I think they're all the same. The President Trump is a threat to democracy
hoax. I don't know the answer to these things. Okay. I'm just trying to- yeah. The women's lib
hoax. I'm glad for women's lib because I'm old enough to know when they didn't have a whole lot
of rights. Well, that's a- well, I won't go deep. That's a little deeper. Now, another one from you
having lived in California for a long time, the OJ Simpson murder trial hoax that he was the culprit.
He was definitely guilty. Oh, no, no, no, no. Oh, no, no, no, no. He was definitely not guilty.
In fact, she was killed. Both of them were killed by a mob who had held a very large loan out to
them and they weren't able to pay it back. So they were murdered for that mob action. I'd like to see
that evidence. And sure, if you want to get a hold of me. The reason I said he was guilty is because
I knew Celie Farber. You know, I know Celie Farber and she and I went down to LA. I drove her around
because I knew the area. She was going to interview him, OJ Simpson, about this thing.
And she's convinced he did it too. Well, he didn't and it was the mob and the people.
Let me just connect them all. Okay. So that happened to have been perpetrated by Bill Clinton,
who happens to be by bloodline a member of the Rockefeller family. The Rockefeller family is
behind the COVID hoax. They're behind the HIV hoax. They're behind the
pharma health industry all the way back to the early 1900s.
Well, the big ones, I think, are probably right. The big thing. It's OJ's thing, I doubt it.
Well, it's a quirky item, but that's why I brought it up because that's one I've been handed the
reality information. The hundreds of hoaxes of who killed JFK. That was LBJ and it was John D.
Rockefeller III. So my point in all of this is, you sort of wonder how did all these things happen?
All these, well, it's all a common cause. It's all connect the dots. It's all back to the Rockefeller
family. All right. So why was OJ Simpson involved in that?
So what happened was Bill Clinton needed something to take over the news chain.
And that trial lasted for nine months. And it was right while he was being impeached and
everything was going on with Monica Lewinsky. So that was all a frame up. I mean, where have you
ever seen trials that last that long? They intentionally made that trial last forever
as a diversion to what was going wrong with his presidency.
All right. Thank you. Let's get to it.
Why did OJ Simpson go along with it? Or you mean that he didn't go along with it?
What do you mean he went out? He defended himself as innocent.
Oh, I see. Why did they pick on him then?
He's a convenient, you know, it just, you know, that happened and they could use that as a diversion.
As soon as they spotted him, he became a huge patsy. He was a huge patsy.
Yeah. Okay. All right. Let's keep going. We're tight for time. We've got seven minutes to go
because the numbers here, Steven, are dropping. We've got 32 on the call. So Tom.
Tom. Okay. Thanks for the presentation. Yeah. I am Kui. JJ Kui does a lot of this biological
one-on-one kind of training and I pick up a little bit of, you know, my curiosity is,
you know, I'm trying to learn from you and kind of a neophyte in a lot of these areas, but
just the basic thing about the chromosomes and the X shape and then the X and the Y chromosome,
and then there's numbered chromosomes. You know, I find that interesting. And then there's the issue
of the DNA getting integrated, you know, the work by Kevin McKernan. So I'm hitting you just with a
bunch of different topics and you can comment on one or all or whatever. In your presentation,
there was a measurement that you used as a metric to determine, I think it was a DNA index or
something, the amount of, yeah, that seemed to be really fundamental. So I'm curious about how you
measured that. And as the cells divide, like one cell might have less chromatin, right? So,
and then the other has more. So that confuses me. It seems like the total, yeah, so let me see if
there's anything else. Oh yeah, your exponential functions and the math you did, that was kind of
interesting. And then maybe finishing up here, you said we all have this meme about the PCR being
faulty, but more people trust these grocery store lateral flow tests. And everyone knows,
I keep asking that question. Cui said, Cui has an answer, which is that had those tests existed back
in 2014, they would have had the same results. The background, you know, he has that whole argument
about the background noise and that those, so can you dismiss those tests as well? So yeah, those
are a few points. And that, well, maybe the last one is why do we have to have these chromosomes?
Is it just that the pack, if you concatenate all these base pairs at a certain point, you just need
to package them up in a chromosome. You know, what's, why did life do that? Oh man, we don't
have another two hours. Oh man, I don't know how to even respond to that. What's your number one
on top of the list? Well, yeah, to your presentation, then the DNA index and how you,
the DNA index. Yeah. It's easy. Okay. I got 10 fingers, you know, I got two hands,
a total of 10 fingers. And I define, I define my finger index, my normal finger index as 10
divided by 10. How many fingers do I have divided by the normal number? 10 divided by 10 is one.
Now I've been amputated, lost a finger. All right. Now I've got nine divided by 10. So the DNA index
is 0.9. You see, cause it got nine divided by 10 is 0.9. Okay. Now let's say some people are actually
born with more fingers than five. So now let's say I've got two little fingers or two thumbs
or whatever. Not let's say I've got three extra fingers. But okay, these are chromat,
are these chromosomes? Divided by 10, I have a finger index of 1.3. Now think of my fingers as
chromosomes. Right. So the big bundles of DNA. It's just a ratio. It's just a ratio of the number
of chromosomes present to the normal number of chromosomes. That's all it is.
Okay. And so going to the cancer cells are on average around 1.7. In other words,
they have roughly 70% more chromosomes, but it's very, very broad. You know, it's broad because
no two are alike, but they all over around 1.7. When one of those cancer cells that has an excess
number of chromosomes divides, it's another asymmetrical division, right? But because you
start from a, okay, you start from a big one, both pieces are still maybe greater than one.
Yeah. They never, yeah. They never, the thing is, is that the ones that have the fewer chromosomes,
you know, like, you know, always unbalanced. One will have more than the other. The one that
has more chromosomes has a survival advantage of the ones that have fewer. So there's a, there's
an advantage as an advantage. That's why the progression goes up. And that's why the 3.0 lived
maybe, right? That strange being. What was that again? There was a baby that was alive that
survived and wasn't that index like three or something? Oh yeah. Yeah. Yeah. Those are balanced.
Those are all balanced chromosomes. That's why it was a baby at all. So it had three copies
instead of two. And since it was balanced, that's why the cells were able to divide. And they kept
being balanced and they kept always being three copies instead of two. So that's not, that's not
aneuploid, but- No, aneuploid is unbalanced. Okay. That's called polyploid. Polyploid is if you have
more chromosomes than normal and that polyploid can either be aneuploid. In other words, they're
not balanced or they can be polyploid and balanced like the baby. If you have unbalanced chromosomes,
you get, you, except for like Down syndrome, you know, you, you can, you can be born and have
Down syndrome, but you know, they typically die in their fifties and they have lots of chance.
Try to be the last question. So the integration process wherein the plasmid, that's the other
issue, plasmid DNA and how the circular DNA compares to the chromosomal chromatin stuff.
But the integration process wherein the plasmids from the jab get integrated into the chromosome.
Can you discuss that a bit? And in terms of aneuploidy, it's irrelevant. In terms of it's
in the sense of the amount, the amounts are so small. The amounts of that are so small,
they're irrelevant. But if they may have a function where they, where they disturb normal operation
and they cause some sort of havoc, but it has nothing to do with their size. Like with the
aneuploidy thing, it has to do with the size of the genome. But you can go, go in and you can
disrupt, you can disrupt normal, normal genome by putting things in or changing their nucleotides,
like they do with those, those injections. You know, they forget, they take it, replace the
uracil or something else, or forget what it is. You know, and if you, a healthy cell would not,
could not survive with that substitution. But that's in the injections.
So you think they get cleaned up that Kevin McKernan stuff gets cleaned up pretty quickly?
I have no idea. I know what he did, but I don't know the details. That's not my field.
You know, they get down to the weeds and the minutia. I look at the big stuff.
All right. Thank you, Tom. Last question, Stephen.
Exactly, David. Well, actually, David, so, oh, you've disappeared now. You there?
He's there. He's there. He's doing something. Don't worry. He can hear you.
Oh, I did that by accident, I guess.
Oh, there you are.
So we lost you.
I'm back. I hadn't disappeared.
So David, you just said you like the big stuff and I'm exactly the same, but it's strange, you know.
So I've realised that not many people are like us who like the big picture, you know. So they have
all the information and they don't do anything with the information, it seems to me. And, and,
but you kind of assume that everybody thinks like you do, you're like we do, you know, and, but they
don't. And it seems to be quite rare that people want to join the dots of the information that they
have and then to seek other information. And I think that is your strength.
I'll tell you how I approach things. It has to do, a lot of it has to do with what we're confronted
with on a daily basis, all the way from school to jobs and everything. Scientists are like artists,
where you have this conception, you know, artists and scientists really start with the big thing,
the question. What is the question that you care about? It's usually trivial. I mean,
not trivial. If it's trivial, it's more engineering or technology. You know, it's how do I change this
to increase that twofold or whatever? You know, that's not science. Science is when you have a
question that nobody has an answer to and you're just driven by that question. The questions are
big. Then in the process of understanding it, you drill down and you know, you start with big and
then you go down into the details like I did with cancer. You know, I had this question about soon
as Peter Duesberg, he and I, we were at a coffee shop right before he went on the sabbatical in
1996 to Germany. We were talking about this aneuploid stuff and I had always been working
with single gene products, single enzymes, you know, for this disease or that disease or what are
making inhibitors for it. And then he was talking about all these chromosomes and everything. I was
saying, oh, jeez. And then I said, with cancer, I said, Peter, you mean it's just numbers? And he
said, yes. So then I started looking big, you know, about cancer, cancer big, aneuploid, then,
you know, then I get a big picture, big thing. Then I drill down on the details as my questions,
my focus was big, but my curiosity led me to sort of look at this detail, that detail, this detail,
for all of those little points and things that I were talking to you about, you know,
but most people in life think of it in school, your jobs or whatever, you're not allowed a big
picture. You're not even encouraged to have a big picture. Nobody respects the big picture, you know,
the details, you know, memorize this, do that, be able to calculate this, you know, and, you know,
you're not encouraged to look at the big stuff.
Exactly. So in the last five years, I've been really shocked as to what's happened on multiple
levels in many areas. And I wonder, what's the most shocked at whether you have been similarly
affected? And if so, was this last five years worse than the HIV AIDS era? And what's the most
shocking thing of all that's happened in the last 50 years? Say?
Most shocking thing? Well, what we're going through.
To you, to you. Not to you, not to what's happened to you, but to you, what is the most shocking
thing that's happened in the world in the last, in the scientific world or whatever in the last,
the fraud, if you like. Oh, oh, okay. Oh, I see what you're saying.
Oh, that's what you mean by shocking. I mean that, yeah.
Unacceptable. Correct.
Yeah, yeah, yeah. Okay. Oh, Lord. Anti-human, whatever.
God, I hadn't thought that way before. I can't answer your question.
For example, I don't think you were very impressed with the lockdowns,
you know, but also people talking about the science as if it never changes.
And there's no such thing as the science. Correct.
Yeah. So I just wonder, you know, sorry.
I know it's important to you, but I'm not getting it.
Oh, I understand. Yeah. So to me, I think the worst thing of all is the psychological torture,
deliberate psychological torture of human beings by their own governments.
It's outrageous. And the treason, the necessary treason. So yeah, I think it's just.
There's nothing new there, though. There's nothing new there. That's bad. I absolutely,
totally agree with you, but it's nothing new there. The scope, like World Wars and all that.
Oh, sure.
Racism.
But it completely blew my world apart. And I think it's blown many people's worlds
apart and they haven't recovered. No, you're right. I mean, look at my situation. You see,
I had my light bulb moment in 1985. You see, you never know when that light bulb moment's
going to happen. You're not looking for it. You know, other people are having it now.
They're a lot older, you know, and it's a thing that you can't forecast. It just happens,
you know, and you just have to be open to it.
Yeah. And once you've seen it, you can't unsee it.
That's right. And how do you respond? You see, so many people, professionals,
like other scientists and academics during the 80s, were confronted with what I was confronted with.
I knew there was a serious problem with the contagious HIV hypothesis in 1985. It didn't
make sense. But I didn't think it was a fraud or anything at that moment. You know, I just thought
well, they just got it wrong. Until I tried to discuss my reservations of problems with that
hypothesis with my colleagues at UCSF and UC Berkeley and places like that. They wouldn't talk
to me. You see, and that never happened before. You know, look how I love to talk.
Scientists used to love to talk, you know, and then when they stopped talking about something so big
and important, boy, that was a wake up call to me. There's something weird going on here. It's sick.
You know, and then that's what led me to delve into it. And I've been on that road ever since 1985.
Haven't gotten off of it. Good for you, David. It happens to most everybody at some point in
their life. It might be the last hour of their life. I don't know. So when you speak, David,
you have this great authenticity, which I think most human beings would recognize. And I don't
think many would disagree that, you know, I think it's very difficult for you. It would be very
difficult for you to lie, even if you were trying to lie. You know, you're just incapable of lying,
it seems to me. And so what you've said tonight, it just strikes me as so authentic and.
Yeah, there's so much more fun telling the truth. Absolutely. I mean, you know, it's just,
I don't know how you address that. I mean, people, it's funny if how open people are,
you know, when you're around people who are open, it's just sort of attracting, you know,
sort of attracted. And then you got the people that are closed up and tight. That's off putting.
Well, yeah, it's gas. Yeah, it feels like gaslighting when you're with them.
Anyway, thank you so much for David for coming on. And Charles, I don't know whether you want
to say anything. Thank you, David. Wonderful. We honor your great work. 40 years. May you keep
doing it for many years to come. And there are so we'll get this chat sent to you, but save the
chat as well, David, because it's a great conversation in there. And thank you, Stephen,
for organizing. Thank you, David. Thank you. I just I'd say one thing, David. I think that
Peter Duisburg, from the fact that he was so viciously attacked rather like an Andrew Wakefield,
you know, I think he was brilliant. I've never met the man, David, but I've just gathered that
he must have been brilliant. And obviously, you must be very, very talented. Otherwise,
you would not have been working with him. Yeah, well done to you. I'm just I consider myself
extremely lucky. All right. Yes, exactly. Thanks. Thank you, David. Thanks, everybody. Thank you so
much. Thank you. Bye bye. Don't forget to get it. Oh, it's gone now. Yeah. Oh, Charles,
Lee, can you leave it open for the election if people want to stay on?
No, there's only 25. Everyone's going, Stephen. Let them go to the Tom Rodman group,
and you should join the Tom Rodman group as well. You know how to do that?
No, I won't bother doing that. But anyway, I would have liked to keep it open so that people could
come back tomorrow as well. Charles, but you don't have to publish it, obviously.
Well, I'm going to stop this recording now. So, Pinter keeps