Yeah.
Now, Dr. Gallo and Dr. Fauci talked a lot about isolation and purification.
Can you tell me what the difference is between the two?
Isolation, what was it?
Isolation and purification.
Of the virus?
Yes.
Well, you isolate a virus by
finding the virus which causes a disease.
You purify a virus by making a lot of, I mean, just by purifying it so you get a pure virus.
I don't understand what the issue.
I see.
No, it depends on how they used it.
Well, didn't Dr. Gallo do that?
I mean, he actually isolated it, so... I mean, why should I do all of this?
This is all textbook stuff you're asking me.
Come out to the coast, we'll get together, have a few laughs.
do do
Good morning, ladies and gentlemen.
This is GigaOM Biological coming to you live from my garage in Pittsburgh, Pennsylvania.
It's 1116 on the 12th of December.
I'm happy to be here to bring you another Biology 101 session.
Today is another one of these Bad Biology 101 study halls.
Good to see everybody in the chat.
That was indeed the Chips theme.
I've got a number of pictures of me when I was a small child before first grade where I was riding around my neighborhood in Indiana with a black square radio strapped to the front of my bicycle and a Cubs batting, you know, plastic
faux batting helmet on and sunglasses pretending to be Poncharello and riding around my neighborhood with a blonde friend of mine named Shane, who was, of course, Andy.
And it was, I don't know how many years we did that, but for a very long time, Poncharello was me on TV.
And all these years later, believe it or not, I have a,
a BMW California Highway Patrol motorcycle in my garage that I very rarely ride and had originally purchased to do JC on a bike on the bike and then very quickly realized that
That was a level of danger combined with large machine operation that didn't really combine very well with my filmmaking desires.
And so I've since abandoned that idea.
I only ride that bike when I want to have fun and completely forget about everything else is what you do on a motorcycle.
Today we're going to try and combat this bad biology evolution because DNA thing again by trying to take a look at and practice watching and listening to other people swim within it.
And if you listen to them swim within it, you can hear some of these big ideas, these big assumptions bubble up.
And as they bubble up, you can see how often they have to come back to that well of assumption in order to keep talking about the things that they want to talk about, or in order to frame the particular paper that they're talking about within what appears to be a relevant discussion framework.
They always have to go back to this bad biology 101 and evolution because DNA.
And so I think one of the ways that I can help myself to develop the big points of a curriculum that would try to combat this would be to try and work daily at trying to find ways to quickly and succinctly show
how people are trapped in these ideas.
And so I have proposed many times that there are a number of quick and short combinations of words that can be used to try and shake the enchantment.
And I said yesterday, I think pretty well, how actually words that have elaborate meanings and elaborate concepts attached to them can often function as enchantments because if those
in-depth meaning and in-depth concepts that are tied to the meaning of that particular word are provoked or evoked in people's minds because of the nature of the way they understand those things.
Very similar to how someone who has grown up his whole life thinking that, you know, saying for Christ's sake would be a very, very bad way to swear.
Much worse than say, I don't know, son of a bitch or something like that.
And I apologize for the sensitive ears out there, but there are different
ways of swearing, and some of those swear words are very corrosive to our ears.
Swear words in other languages might not be.
For example, if I said kankerhoor, do you really, does that, maybe that one is a bad example because you can kind of hear what it says already.
Sorry.
So that's a Dutch swear word, of course, which means cancer
Oh, it would be conquer wife is what you say, I think most of the time.
But anyway, it doesn't matter.
Now I'm being I'm going down a bad place here.
What I'm trying to do is to give you this concept that words and the more colorful their meanings are, the more
elaborated on the meanings of these words have been, and more importantly, the more we are unconsciously aware of how uniform these meanings are, the more likely it is that they are to function as an enchantment.
One of the, you know, things you might look at in this context is history, and what we understand as history, for example, around
the assassination of John F. Kennedy.
There is a mythology around that, and that mythology has been built up over time, and it is the shared understanding of what that mythology is that gets evoked in our mind when someone says, hey, you know about the JFK assassination?
Do you know about that?
Do you know about the 9-11 conspiracy thing?
Those are pretty complex combinations of words relative to, say, some of the words that are used in biology that provoke magnificently detailed concepts by their simple mention.
And this, I think, is where
We have to find the language that will help high school teachers, high school students, freshmen and sophomores in biology, first year medical students break out of this.
this cognitive trap that they're in.
And it is a cognitive trap.
And you don't have to see it as malevolent.
You can see it as something that lemmings would have happen.
This is where the mass psychosis is.
And it's not a completely innocent one.
It is one that has been influenced by those people in our past
who consider themselves some of the wisest people around, those people are the influencers and the people that have codified these ideas in such a way that have allowed them to propagate across generations.
And their students that they have mentored are the people that are helping to propagate it to the next generation, and we need to break that.
And I think the way to break it might be to explore the truth and mythology of the Human Genome Project.
I think one way to break it might be to challenge doctors and nurses to really consider the biology of intramuscular injection and challenge themselves to really assess how much they understand of human biology and whether or not they can really explain why intramuscular injection is something that they use in their professional
in their professional existence.
And finally, RNA cannot pandemic, I believe, is still the best three combinations of words to throw at an academic biologist who is probably most likely not in the field of RNA virology, not in the field of pandemics, and challenge them to say, hey,
You remember when you did your PhD and you had this oral examination and somebody asked you the question about the central dogma of molecular biology and cellular biology, and you answered that it was DNA to RNA to protein.
How does the idea that RNA can pandemic fit into that?
Because in the dogma of modern bad biology, DNA is the stable, the magic,
encodes everything part, the protected in the nucleus part, the telomeric senescence part, the Hayflick limit part, the evolution acts on genes part.
And the RNA is the local temporary signal that is regulating the protein expression that changes all the time as part of the pattern integrity.
So how does that work that outside of the context of what you would call life,
RNA itself can sustain itself in the background in the terms of endemicity, which basically means in perpetuity.
How does that figure into that?
Because even species can't maintain themselves in perpetuity and change and go extinct.
And so how is it that outside of this, without all of the elaborate machinery of DNA, how can RNA accomplish this?
in the context of a coronavirus and who told you that?
That's maybe the biggest thing.
Do I have to crank it up a little bit?
I can crank it up a little bit.
That's some of the biggest thing that we have to deal with here is the idea that maybe the microphone is just not quite pointed right.
that we have to deal with is the idea that these people have accepted these preposterous notions as proven and therefore just move on again with these assumptions on the wall.
And one of the worst ones is that RNA can pandemic, that RNA is something we need to fear, that free range RNA is something that if you make it right, oh my gosh, it could be worse than a nuclear bomb.
And this is absolutely absurd.
And we cannot let our children grow up in a world where they believe this.
We are in 2024.
One way to challenge your doctor might also just be say, you know, intramuscular injection is the single worst way to be exposed to a toxin.
Can you tell me a worse way?
And maybe they'll say, well, IV injection.
And you might say, well, IV injections actually not as bad because it will never fool you.
You're never going to not know that it was what you injected.
You're never going to think, oh, wow, maybe it was something else.
Maybe it was something that I ate.
Maybe it was my genetics.
But if you inject it intramuscularly and the onset of the symptoms is over the course of days or weeks or months, then you're never going to attribute it to the acute exposure to whatever was in that injection.
IV, it's very, very much harder to divorce the effects from the cause.
And so it's a lot less dangerous because you're a lot less likely to misattribute your suffering to something else.
And it is a very great way to be exposed to toxins or be exposed to dangers that you don't want to be associated to the exposure.
It is a great way to be exposed to a toxin if you don't want the dangers of the toxin exposure to be revealed.
If you don't want to see the effects temporarily related to the exposure of the toxin, the intramuscular injection's great.
If you want the exposure to a toxin to be longer lasting and to ramp up and crescendo and decrescendo on a different time course than IV injection, well, yeah, sure, this is great.
And so New Biology 101 is based on the idea that life is a pattern integrity with a trajectory across time.
This is an idea that I am stealing from Buckminster Fuller, among, I think, probably other biologists before him.
But Buckminster Fuller has stood out to me in my reading recently as one of the greatest thinkers of the late modern era, and a curious omission from all of these people's pantheon of brightness.
Almost nobody talks about Buckminster Fuller, even though Buckminster Fuller was an enthusiastic biologist.
So it's very curious to me.
And so that's why I'm very confident to try to establish this new biology idea that way.
And it's not new, it's just new for me.
Let me slide down here to the bottom.
Still keep doing that a little slow.
Remind you that I am doing JC on the hardwood.
Um, I did not manage to shoot a video yesterday.
Um, I will not manage to shoot a video today.
However, I should be able to get around to it on the weekend or else next week.
Um, it's actually during the week that I have the most opportunity to do it around two in the afternoon, because that's when the gym is completely empty and I can hog the whole half court.
And today I don't think I'm gonna make it there at two o'clock because we do have a freshman game this afternoon.
But it is a project that's not gonna stop.
And it's also because of, I'm focusing first this week on five days a week, and then next week we'll get five days a week plus JC on the hardwood and probably also the probability course once a week, which we might actually do on Thursdays now, we'll see.
So Bad Biology 101, watching a slow motion train wreck is basically what it's going to feel like when you hang out with me nowadays, because this is where we are.
We're surrounded by thousands and thousands of academic biologists who have spent their lives specializing and pigeonholing their brains so that they can excuse themselves from having to think usefully about many other topics.
They don't have to think very much about what food they buy or what school their kid goes to.
They only have to really focus on their career because everybody else around them also only gets by by only focusing on their career and only hyper-focusing on that little question, that little receptor subtype, that little experimental model, that little knockout mouse, and trying to get as many slices out of it as possible.
And so these are the people that I am trying to wake up with these small, succinct, semantic word bombs, like RNA cannot pandemic, or intramuscular injection is dumb, or transfection was criminal, or these kind of, you know, that's what I'm trying to do with those things.
But ultimately, I can only coach people.
I can't make them do the exercise, and a lot of those people require a lot of exercise.
just like I required a lot of exercise.
I did not get here in 2020.
It was with a great amount of effort and pain and self-doubt and rechecking and double-checking and making mistakes that I got to the stage where now I think I understand exactly or close to how they're doing this.
And we have to get our thinking on different time horizons.
We've got to get our thinking on different time scales.
We have to understand that these people have raised us to misunderstand ourselves.
They actually raised our parents to misunderstand themselves.
And our parents raised us with their guidance to misunderstand ourselves.
That's where we are.
And so it is a long and arduous trek that we are gonna have to help these people.
We're gonna need to be Sherpas in a way.
And so we're gonna have to climb the mountain lots of times.
We're gonna have to get accustomed to being at high altitude and to carrying the heavier loads for people that have just gotten there and can barely even put the left in front of the right.
And we're gonna have to do it for a while.
Until people understand that there is a way up this mountain.
There is a peak up there.
And there's a safe way down.
But it's going to be a slow motion train wreck.
I can guarantee you that.
And so what I want to approach it with and how I want to coach you to approach it is to ask what questions are they asking and really try hard if you ever do this on your own, which I hope you do, try really hard to write them down, write down the question, what are they asking?
And then what model are they using to ask it?
Because almost invariably in modern academic science, they're not gonna be using a model of
of what they're testing.
They're not gonna be testing autistic kids.
They're not gonna be testing, you know, they don't, they always have to have a model system.
How far away from the actual question is the model system?
These are the kinds of directions I want you to take your curiosity rather than the direction that they want you to take it and using the tools that they want you to assume are useful.
And so that's the other thing that we want to listen to as we listen to these guys talk.
What biological ideas do they assume are proven?
Assume are certain concepts, certain concepts in the sense of sound concepts, proven concepts.
If you talk about extraterrestrials as if they exist, that's one thing.
If you talk about Vulcans as if they exist, that's another thing.
And so how many times are they talking about extraterrestrials as a general proposition?
How many times are they talking about Vulcans?
Because again, that's where this here, I'll even put my little thing on right now.
I'll play science officer.
And we will try to answer the question, okay, so how many times are they talking about extraterrestrials?
Which in theory would be fine, right?
It would be fine to talk about extraterrestrials as a possibility.
And how many times are they talking about Vulcans?
Because that's very different.
And so if you hypothetically talk about a mechanism or you hypothetically talk about a
Biological phenomenon, that's one thing.
If you certainly talk about an existing phenomenon that doesn't exist, that's another.
If you talk about a possibly existing phenomenon with some indirect evidence as if it's already a proven fact, that is very similar to talking about Vulcans.
talking about extraterrestrials as a possibility and admitting that they could also be based on silicon or something like that, that's all hypothetical.
Talking about what planet they live on, what they look like, and their language is another thing entirely, right?
And I would suggest to you that there are concepts in biology right now, in bad biology, that have been built up into a false mountain of knowledge.
And every time these words are said, that false mountain of knowledge is in the background, subconsciously.
edified by the collective acceptance of the people in the conversation.
So for example, we have four people on the screen, that's what we're going to see soon.
Four people on the screen, three people from the United States, one person from Scotland.
And if they say something like, Big Macs are really tasty because the secret sauce is Thousand Island dressing, and they all go, yeah, that's true.
That's an illusion of consensus.
And then they go on to say, yeah, but fast food's bad for you.
That's an illusion of consensus.
But if they just said Big Macs, and then all of them said, mm, mm, that's also an illusion of consensus that leaves a lot more to your imagination, a lot more to what do you know.
And so if you don't know very much about fast food, and you don't know very much about Burger King or McDonald's, and somebody says Big Macs, and they all say, oh, wow, those are tasty,
What happens?
Well, you're pretty curious about Big Macs.
What if they say prions and they all go, oh wow, yeah, those things are really interesting, wow.
Because that's how this works.
That's what happens to academic biologists, too.
As I said yesterday, when they go to a seminar and they hear a story that has a big word definition with several sub definitions or subcategories, and they are looking at one subcategory, and you pay attention and learn all these terms and how this person proposes they're working together, then the next time you hear this little term, all of these ideas will be provoked.
And if that person did their job right, they will be provoked as ideas that make sense.
And more importantly, you might want to assume are right because that guy's working on them.
That woman was working on them.
She's dedicated her whole life to studying that stuff.
She was really nice and very charming over coffee.
She can't be, she's obviously not an idiot.
That's an interesting idea.
I'm going to come, I'm going to, I'm going to run with that in my own understanding of her own system for the rest of my life.
That's what happens.
And we start sharing each other's models as all being as certain as we write it in our grant application.
And because our salaries and our wonderful job with its wonderful perks and its wonderful schedule and its wonderful feeling of authority and prestige and whatever else it feels like to be on the faculty of a medical school, all prevents these people from snapping out of it and saying, wait, what are we doing here?
And so like I said, we're gonna be Sherpas.
It's gonna be a lot of hard work, a lot of carrying heavy stuff for people who don't really think that we're doing very much, who are super proud of themselves for just being on the trail.
Until they realize what we're doing and what we've done and how they're really not doing what they thought they were doing.
Maybe we can end the,
the academic Mount Everest climbing forever.
But first we're gonna have to walk with them and show them what they're doing is so ridiculous.
So of course, he's going to raise a little money.
I might have to fast forward through this part.
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From microbe.tv, this is Twip.
This Week in Parasitism, episode 248, recorded on November 22nd, 2024.
Oh, nice choice of music, you monkeys.
Wow.
I try very hard not to watch these beforehand because my reaction is a lot better.
And you're listening to the podcast all about parasites.
Joining me today from New York, Daniel Griffin.
I think that's a hairstyle commitment that at one point in time, I think George Clooney made the commitment to, and that's where he's living right now.
Maybe in the late ER stages of George Clooney's thingy, Bob.
Hello, everyone.
What you got on your tie?
It's Friday, so it's got to be an STD, right?
Gonorrhea.
I know, exactly.
The gonococcus.
Is that like cocktail hour or something?
Also joining us from Fort Lee, New Jersey, Dixon DesPommiers.
And ditto.
Hello, everybody.
Today was an auspicious day in the fact that it was cloudy and it was not warm.
And yesterday was even more auspicious.
It actually rained.
So that was an event that hadn't occurred since late September.
Still raining now, supposedly.
It's 40 degrees.
Yeah.
Well, it's not raining here right now, but it might pick up again.
It's cold, it's wet, it's raining where I am.
That sounds like your sailing season has come to an end.
Sounds like Glasgow weather.
No, this is winter sailing season.
I'll let you introduce our last co-host.
Also joining us from Glasgow, Scotland, Christina Nowla.
Hello, everybody.
I think I'm beating you all with the weather because it's been quite nice, freezing cold, but no rain.
I thought it's always cold and wet and rainy in Glasgow.
It's usually wet and windy.
Cold, I don't know, I suppose that's relative.
It's below freezing.
Is that cold?
Yeah, it's cold.
It doesn't usually get that cold, so that's quite unusual.
Anything below 10 C is cold to me.
Okay.
I've had to scrape the car today, so it's definitely cold.
Oh, that's cold.
I was going to tell Dixon that in the winter, I race sailboats every Sunday.
I usually do that with my cousin.
There is this one guy, John Browning, who basically is a professional sailor.
He was a trimmer for the America's Cup, more Newport Bermuda races.
You can look at how many books he's got behind him that are entitled for this thing.
So infectious diseases, parasites, parasites, parasites.
This is not always what he has behind him.
He's got several backgrounds because he's on several shows, I guess.
So he moves his laptop around a little bit and he's always got a new bow tie.
And he looks a lot older after five years.
It's a lot of these people have aged very, very poorly.
I've also aged very, very poorly.
If I look back at my 2020 videos, I was a lot younger.
My kids were a lot younger.
There you can see behind him some cups.
That's, I guess, periticism and that's virology.
So they're making cups.
They got lots of money because all these people are getting stipends.
And he's going to say it again.
He's got this studio in Manhattan, right?
Exactly right.
Yeah.
Could be quite productive.
And also, you know, the fish seem less.
I apologize for the blower in the background.
It's the heater.
It's cold in here.
The river and everything.
And it's beautiful.
Beautiful.
Daniel, did you say nymphing?
Yeah.
So, you know, as Dixon well knows, 80, 90% of a trout's diet is subsurface.
It's not on the surface.
And so if you're surface fly fishing, it's actually not as productive as if it's called nymphing.
And so you actually put a little weight or use a sinking line and you're actually going to get the earlier forms of the arthropods down there to where the trout, you'll often see it looks like they're rising, but they're not rising.
It's the tail.
breaking the surface as they're going down.
That's right, that's right, that's right.
I've never heard that term.
I've only been fishing once, so... There's even a term called euronymphing.
It's a specialty, a way of handling... This all sounds too obscene to me.
Well, it depends on how you do it, but you're right.
Also these beautiful maiden spirits of the water.
That's right, that's right, that's right.
That would be nigh-adding.
Enjoy these conversations.
We'd love to have your support.
Okay.
I just wanted you to see what they're trying to do They're trying to put together a little hokey, you know kind of nice You know for old people and young people alike to love these, you know these very interesting people that talk about biology and so now these four are gonna discuss a paper that's gonna blow your mind because We need I've looked at the paper.
We're gonna have to do some stuff but you know science is under siege and
We have the nomination of RFK Jr.
as head of Health and Human Services.
Someone who has zero qualifications and has contrary views to the health of Americans.
And so, in fact, you should write your senators and oppose his nomination.
I have a website to send you to, safecommunitiescoalition.org.
And of course, this is a very large possibility for Jay Bhattacharya, for Robert F. Kennedy Jr., for any of these people.
They could just be taking up time and space in our head, living rent-free until their nomination is spiked and they make a big story about that.
And then in four days, they confirm somebody else that used to work for Big Pharma.
Why isn't that more than likely?
And now you have none other than Vincent Racaniello saying that this is the thing, we have to really get, we have to figure this out, this guy's terrible.
He's already done some streams with Paul Offit about that, the same guy who's been in front of that mic for the last 10 years.
So it's, it's, it's, this is just theater.
You don't have to get really excited about it, unless you're getting excited about it from the pretense that Robert F. Kennedy Jr.
could be freed from the people that are currently influencing him and refocused on the most urgent,
of dangers in the United States to our freedom and to our sovereignty.
But I don't think that's going to happen.
And it's not because I think Bobby's a bad guy.
I think it's because the Truman Show-like operation that's being used on all of these people, where groups of people lie to them about the dangers, groups of people lie to them about the biology and about what bioweapons mean and what national security means, and lie to them about who to trust.
And it is the coordinated effort of these people to lie to these puppets, these victims, that gets people into places where they have a book, and they have a single message, and they push ivermectin for five years.
Or they have a substack, and they have a single message, and they push VAERS and the spike protein for several years.
This is all part of the same nonsense.
It's just the opposite side of the coin.
So it looks very foreign.
It looks very mainstream because we're not watching mainstream media.
But this is the alternate side of media on that alternate side of the narrative.
And so it's of utmost importance that we listen to this because these people are the most committed to the bad biology.
FK, you can put your little letter in there, and they have a draft already made for you.
You put where you live, and we'll send it to your senators.
I have a solution for this, by the way, Vincent.
What's the solution, dilution?
No, the solution is that only the Republican kids don't get vaccinated.
Well, you know red states had higher incidence of COVID, right, Daniel?
Red states?
I think Danny Rancor said that it had to do with economic status, but okay, red states, that's good.
Unfortunately, there was what they referred to as red COVID, because early on you saw a lot of the deaths, hospitalization, morbidity in urban centers.
But then, unfortunately, once vaccines were available, once we had a lot of therapeutics available, there was sort of this reverse phenomenon.
where a lot of the other areas were really hard hit.
It really was tough.
I don't understand the messaging.
There was a lot of uptake of the monoclonal antibodies, which, you know, thumbs up, that was fantastic, you know, 80-90% reduction in
and progression in hospitalization.
Unfortunately, no reduction in long COVID.
Where in other areas where you had the vaccines, not only did you get that 90% reduction in hospitalizations and deaths, we're also now seeing really significant impact.
Probably about the same, probably about a 75% reduction in the risk of long COVID, post-acute sequelae.
Yeah.
So, you know, and I think that, you know, the solution is that.
OK, so now Griffin is going to tell us about the the status of the 30,000 foot, the 30,000 foot view of what happened during covid.
And so let's just take notes and see what kind of.
Let's just see what kind of thing, let me see if I can get this over here.
How does that work?
I think it's this one.
Yeah, let's just take some notes and see what he says about this.
And see if we can, we can succinctly, you know, sort of critique what it is, sorry, what it is that he says here.
I'm very curious about it myself, because it's, it sounded very short through the corner, as they would say in Dutch, it sounds like he took, he left a lot out.
Let's say it like that.
Here we go.
COVID, because, you know, early on, you saw a lot of the deaths, hospitalization, morbidity in urban centers.
But then, unfortunately, once vaccines were available, once we had a lot of therapeutics available, there was sort of this reverse phenomenon where a lot of the other areas were really hard hit.
It really was tough.
I don't understand the messaging.
There was a lot of uptake of the monoclonal antibodies, which, you know, thumbs up.
That was fantastic.
You know, 80, 90 percent reduction in
in progression, hospitalization, unfortunately, no reduction in long COVID.
Where in other areas where you had the vaccines, not only did you get that 90% reduction in hospitalizations and deaths, but we're also now seeing really significant impact, probably about the same, probably about a 75% reduction in the risk of long COVID post-acute sequelae.
Yeah.
So, you know, and I think that, you know, you know, what is it, the solution to pollution is dilution.
So maybe if we can dilute out the misinformation with accurate information from those of us who are not trying to sell you a snake oil, then yeah, maybe, maybe we can make a difference.
So, but we, yeah, we need your money so we can get our, our, absolutely.
We need your money.
Wow.
So early on, early on, it was in urban areas, that would be the blue effect.
And then after we got vaccines and therapeutics, it kind of reversed to all the red states, which, okay.
90% of reduction in hospitalizations and death in the vaccinated population is of course wrong.
And a reduction in long COVID is comical.
I mean, I don't even know.
But again, remember what we're doing here.
This is what happens at a seminar in any university when they give their introduction and they say that there are several genes for autism and one of the genes for autism is this one, according to that paper.
And so we made a knockout mouse of that gene and now here's the data from it.
And what happened there?
Everybody in the room accepted that there are genes for autism and that it has a list and that list is there.
And so when they go on to their next talk, that's already what they think is real.
No different than everybody listening to this talk, listening to this thing says, oh yeah, that's right.
I heard that once, that there was a 90% reduction in hospitalizations and death.
That's great.
I'm glad that Nate took it.
I'm sure Nate's daughters are really glad he took it.
Because that 90% reduction in hospitalization and death due to COVID is also balanced out by a few people every year having an aneurysm they shouldn't have had, having a stroke they shouldn't have had, having a heart attack or three that they shouldn't have had.
And so the Bad Biology 101 starts right away, right off with a COVID bad biology, a pandemic enchantment.
All through this discussion that you just heard right there, everybody that's listening to this, that listens to it often, is confirming in their head that these four people agree there was a pandemic, there's long COVID, there is COVID, it's still spreading, vaccines helped, the vaccines were great, there were therapeutics, some of them are called, I don't know, Paxlovid and Remdesivir.
Dilution is the solution to pollution and dilution is in fact what they've done to me.
By taking little bits and pieces of what I was saying in 2020 and twisting them around in my head and forcing me, coercing me, encouraging me to become the expert on lab leaks.
And less of a skeptic of the basic biology of a pandemic.
Less of a skeptic of the basic biology of a pandemic.
please be less of a skeptic of the pandemic.
You can be skeptic of the shot, just don't be skeptic of the pandemic.
And that is what they do here.
Every time, no matter what they're going to talk about, they first got to reinforce the overarching narrative of evolution because DNA and RNA can pandemic.
This is a lie.
but they just reinforced it with a long, long, long diatribe about all the details that supposedly confirm that RNA can and is in the process of an ongoing pandemic and transition into endemicity.
Wait, speaking of snake oil, you know, Dr. Oz was nominated as head of Medicare, Medicaid services, right?
What do you think about that, Daniel?
Unfortunately, as well, I think many of us, three of the four of us, Columbia faculty, there was actually a letter, which I think was signed by maybe 10 or 12 Columbia faculty, basically calling out for the fact that he was knowingly misinforming people so that he could sell his products, he could sell his
So I think that's probably what brings it up.
So that's not OK to take someone, put him in the head of Medicare, Medicaid, CMS, who has a history of ethical laxity, of actually basically misinforming, lying for their own financial self-interest.
That's not OK in my book.
I apparently also owns a lot of Medicare companies as well.
So that would benefit him.
Oh, interesting.
So yeah.
Well, I hearken back to that quote that I am often.
So while they're talking about Medicare, I'll take the time to remind you that the cost of old people and that whole program is about half of the US budget.
And because of the population pyramid problem, that budget was about to balloon.
And so I am making the argument along with a few other people that they murdered people and lied about it in order to manage that problem.
And so it's very funny that these people are talking around that, you know, talking about it, but not talking about it.
The one big elephant in the room is that this increase in all cause mortality, this increase in Medicare, Medicaid burden, this increase in retirees relative to the productive taxpaying working class, this has been foreseen for a couple decades now.
And these people may not be sophisticated enough to know it.
It's very possible that they're not, because again, these are academic biologists who spend their whole day trying to focus on the most important problem in the world.
And that's the one that their lab does experiments about.
Almost their entire life has been spent focused on that.
To the chagrin of their kids, their marriage, their hobbies, their physical health,
prone to say when this topic comes up, but it rings true virtually every time I say it.
Mark Twain was quoted as saying that there's only one criminal class in America, and that's Congress.
The other thing that Mark Twain has quoted, another one that I like a lot better than that, is that he always told the truth because then you don't have to remember anything.
And that's kind of my shtick.
That's kind of how I get through this and make sure that I don't lose my mind.
I just keep telling the truth all the time and show all my cards as often as I can so that nobody ever doubts.
Nobody can ever doubt.
Nobody can point to me and say that I just tried my best and made a mistake for more than a year and a half.
And so people I love died because they took this shot as a working vaccine.
They took this pandemic as a potential lab leak disaster.
And everyone laughed, and then they stopped laughing when they realized it was true.
It's true.
Yeah.
I mean, I don't want to make all our programs a, well, maybe it is okay.
All our programs really are about combating anti-science and misinformation.
Without funding, there is no science.
Yeah.
And the funding all comes from government.
One of the things that RFK Jr.
has said before is that he would like an eight-year pause on infectious disease research in the U.S.
Many of our programs are about infectious diseases, right?
Today we're going to talk about a paper that involves infectious disease research.
So to think that you could stop it for eight years is the silliest of silly notions, to put it mildly.
Okay, so they're going to talk about some infectious disease research today, and we're going to critique that research as whether or not it's valuable or not.
It's not even possible.
It reflects an ignorance of what infectious disease research is.
Where is the Scottish lady?
Why is she just a voice in the background?
Maybe that leads us right into our paper, which is where infectious disease research may actually be tapping into Alzheimer's disease, which, you know,
So remember that Alzheimer's disease could not be the exposure, the intramuscular exposure to toxins, could not be that.
It can't be the ingestion of toxins, the inhalation of toxins, the cutaneous exposure to toxins.
It can't be any of that.
Alzheimer's disease is a specific phenomenon that these parasitologists are going to define based on what they've heard from other biologists, not because they've done the experiments or read enough to know.
I assure you, no, none, no, none of these four have spent any significant time reading into the neurobiology of Alzheimer's disease, none of them.
They only know what they've read in maybe a review article.
But more likely, they know what they have heard from a seminar that came to their department sometime where somebody told them about Alzheimer's and a mouse model of it.
And you're going to see it very clearly when they expound on and you know,
dissect this paper, and nowhere on their radar is the idea that what they're doing is absurd.
What they did in the paper is absurd.
The data is absurd.
The model is absurd.
The whole question in the context of that model is absurd.
Nowhere are they going to get to it except for one guy, and that's Dixon, and they hate him.
And they have to talk over him all the time.
That's this old dude here down in the bottom.
I guess he can barely see my cursor there.
Um, so I'll, I'll make them big for a little bit and then, uh, I'll keep taking notes and we will, um, we'll see what we get here.
We shall we jump into it.
Okay.
So this is why you're here.
So we're going to discuss what's real FSA.
It's a, it's a great paper.
A great paper.
And so this is a paper entitled Toxoplasma gondii infection of Alzheimer's disease mice reduces brain amyloid density globally and regionally.
And you know, I'm old school.
I printed it out.
So the authors are Catherine Yanes, Nathaniel Guanzon, Ricardo Azevedo, Damian Wheeler, Sunil Gandhi, and Melissa B. Loden.
And a lot of these authors are from California.
So Department of Molecular Biology, Biochemistry, University of California, Irvine, Irvine, California, Institute for Immunology, University of California, Irvine, Irvine, California, and also Translucence Biosystems, Irvine, California.
So it helps to clarify the title a little bit.
And that is that we're not talking about globally and regionally, geographically, we're talking about it in the regions of the brain.
It's a little, you know, for anyone not really up on this literature, perhaps they would be a little bit confused about the
How did you get mice out of a regional... No, we're not going there.
Which part of the world does it help the mice?
It just confounds the issues.
No, but they do talk about the brain as... So he's there, kind of, but because he's so entrenched, so deeply lost in the bad biology of evolution because DNA, bad biology that there's no...
There's no firm line between things that are pattern integrities and things that aren't.
There's no even mental energy expended on trying to discern where pattern integrities borders are or anything like that because they're not thinking that way.
And this guy starts to see it already, but wait until you see the details of what he's really talking about.
None of these guys are neuroscientists.
None of these guys are neurobiologists.
And it's an interesting combination paper where they're using neurobiology to do a parasitology paper.
They're using neurobiology to do Alzheimer's research.
And you can see exactly how shitty academic biology has become.
And now think that some of those authors that we watched there a second ago, some of those authors are in training.
Right?
Some of those authors are post-docs in training.
Global Institute for Immunology.
So the.
Ah.
No.
What happened there?
Oh, I went back, I went, I went over to slide, what did I do?
Yeah, ships.
Alzheimer's is a form of dementia.
This is Alzheimer's what's going on.
It just confounds the issue geographically.
biology, biochemistry, University of California, Irvine, Irvine, California Institute.
And so this is a paper entitled Toxoplasma.
Yeah, so these people right here, this one, you know, this is the, this is the person who's teaching everybody, this might be a postdoc, this might be a technician, this might be a technician, this might be a PhD student, this might be a PhD student, or they could all be
PhD students and grad students that are all learning about biology, and all think that they're learning about how Alzheimer's disease works by working on this mouse.
And so you can read here, oops, darn it, I did it again.
Where is it?
I'm sorry.
And so now what we need to think about to answer the questions that I want to ask, what questions, what models, what we need to think about is, okay, first,
Background.
Toxoplasma gondii infection of Alzheimer's disease model mice decreases amyloid beta plaques.
We aim to determine if there is a brain regional difference in amyloid beta reduction in the brains of gonadi infected compared to control mice.
So apparently they already had a paper
where they showed that amyloid beta in the brain of these mice was decreased when they were exposed to or infected by Toxoplasma gondii.
Whatever the hell that is.
I think that's the stuff that comes out of cat litter boxes.
I know that there was a person who contacted me a couple years ago who wanted me to think about the possibility that COVID was actually this.
So I find it curious that this is a paper that TWIP or whatever this one is called, has decided to cover.
So that's the reason, one of the reasons why I'm here.
Another reason why I'm here, of course, is because amyloidosis was something that a lot of people were saying the spike protein could do, that it was an amyloid generating protein or it could cause amyloidosis.
And that's very different.
Please understand that saying the spike protein can cause amyloidosis is very different than saying that transfection can cause amyloidosis.
It's very different than saying transfection with a pseudo-uridine M1 modified mRNA, it could cause amyloidosis.
It's different than saying, you see,
And so these people, of course, first need to tell you what they know about this stuff, even though they don't actually know it.
They were just told it.
They were handed these tools and they are going to tell you how these tools work, even though they're just all air tools.
You know, this is how an air hammer works.
This is how an air screwdriver works.
And so now we're going to build an imaginary tree house.
And because so much of this is cerebral, this discussion, that's essentially what you're doing.
Globally and regionally, and I'm old school, I printed it out.
So the authors are Catherine Yanes, Nathaniel Guanzon, Ricardo Azevedo, Damian Wheeler, Sunil Gandhi.
I just wanted to make that point.
I apologize.
We'll just let this play because otherwise I'll screw up where it is.
And a lot of these authors are from California.
So Department of Molecular Biology, Biochemistry, University of California,
Irvine, Irvine, California, Institute for Immunology, University of California, Irvine, Irvine, California, and also Translucence Biosystems, Irvine, California.
So it helps to clarify the title a little bit.
And that is that we're not talking about globally and regionally, geographically.
We're talking about it in the regions of the brain.
It's a little, you know, for anyone not really up on this literature, perhaps they would be a little bit confused about the
How did you?
So one of the things that they didn't they're not going to say and not explain is that they're they're using an anatomical measurement and a stain for for amyloid.
So what they do is they use this very special thing called I disco, which is a acronym for some way of clearing the brain.
What they mean by clearing the brain is that a couple of three, four years ago, five years ago, somebody
I don't remember who it was first figured this out.
You could do it with urea and you can do it with other ways.
There are lots of different methods for doing it.
You can essentially make a
the lipids and the fats of a mouse brain translucent.
And you do it by like dissolving things and, you know, maybe you replace some things.
I don't know all the details of it, but in this paper, they use something called iDisco, which is a methodology to clear the whole brain so that you can image through it from top to bottom.
And so on the back of that, the proteins are still supposedly all there.
They can use an antibody that's fluorescent to stain
where the amyloid is, and then they can image through the whole brain and see in the control mice versus the mice that were infected with Toxoplasmoda gandhi, have different distributions of amyloid in their brain.
And that's what he means, they're going to look at anatomical regions in the brain where the amyloid is present in the control group, and then look to what extent is the amyloid present in the group that is infected.
So that's already
It's already a very bad representation for what's going on because on that background, what is the mouse?
And maybe as a non-academic biologist, this is one of those crucial questions that you need to ask very early on.
What is the mouse model they're using?
Is it an inbred line with a name like Sprague Dolly rats or Long Evans rats or C57 Black 6 mice?
Or is it a knockout mouse?
Is it a knock-in mouse?
Is it a regional knock-in mouse?
And so it matters very greatly because if they are using a genetically modified inbred strain, then they're using a pattern integrity that probably is orders of magnitude and distance away from any relation to how our pattern integrity works.
A mouse is already quite a distance away from how our pattern integrity works.
They're lacking the complications that we have.
And so it's not gonna be possible to understand how we work by looking at them.
The analogy that I used the other day was if you want to study the finest Swiss watch, you better not start by, or you're not going to get very far if your only experiments are done on cuckoo clocks.
You'll learn a lot about how clocks work.
You might learn a lot about how the basic gear mechanisms, you might be able to identify the timekeeping parts of a Swiss watch, but if it's got all the calendar functions or a date wheel or all these other things, you're gonna have to, you're not just gonna learn very much from a cuckoo clock.
And this is a horribly short analogy for the difference between the pattern integrity and, and the requirements and, and, and, and operation of it at a mouse level and the pattern integrity and the operational requirements of it at the human level.
because we live longer, because our development is longer, because our intelligence is higher, because our conceptual ability is higher, and all of those things require necessarily an infrastructure of biological mechanisms that don't exist at the level of a mouse.
And yet here these people already are accepting
this mouse model, without inadequate description even, a mouse model as equivalent to and useful to studying a phenomenon in our own pattern integrity.
And why?
Because this mouse has a homologue of a protein that some very poor scientists in academia have convinced us is crucially related to the mechanism of Alzheimer's disease.
when in reality it's turned out that most of those papers were fraudulent.
It's not that amyloid beta isn't there or is there or whatever, but it doesn't appear to be the central cog of the mechanism.
It doesn't appear to be the spike protein of amyloidosis.
It doesn't appear to be the spike protein of Alzheimer's disease.
It's there and it does stuff, but what they can show or pretend that it does in vitro is not confirmable in vivo.
There's lots of other things that happen like neuronal death and the retraction of long myelin tracks and all kinds of other changes that occur that yeah, amyloid might be there, but amyloid is not causing all this to happen.
But now we are going to have a mouse model that qualifies as a model of Alzheimer's because there is overexpression of amyloid in the brain.
I mean, this is extraordinary.
Get mice out of a regional, no, we're not going there.
Which part of the world does it help the mice, but no.
It just confounds the issues.
No, but they do talk about the brain as a globe.
a global issue because it's got so many parts.
Yeah, no, and I think that that's going to be an area that we'll touch on.
I mean, I think they could have just gone away with, you know, Toxoplasma gondii infection reduces brain amyloid density.
But there is some parts where it becomes interesting for those sort of deeper in the weeds about the different areas of the brain that they're going to look at.
So,
Right.
What an interesting choice of words deeper in the weeds.
They're not in the weeds.
They're lost, not even in, they're lost in the weeds of ideas that don't make sense.
For sure.
But the funny thing is, is that these people think they're not lost in those same weeds.
So maybe we should start off just by talking about Alzheimer's and the current theories about what causes Alzheimer's, what's going on.
So I'll start off with just the clinical perspective.
What is Alzheimer's?
So Alzheimer's disease is a form of dementia.
And one of the things clinically we make a distinction from is it's memory loss.
sort of this memory loss that we expect, unfortunately, as people get older, just forgetting things, compared to dementia.
There are lots of mouse models where the entorhinal cortex and the cells of the entorhinal cortex that present, project to the hippocampus are the first cells to deteriorate during Alzheimer's.
And so this actually could be the key because that is a central part of the memory circuit of the hippocampus and as part of the
memory circuit that I spent my time studying.
And so from the perspective of the hippocampus, I think the state of the art would be to say that certain cells of layer two of the medial entorhinal cortex may be the first cells to be lost, and that may explain why specifically Alzheimer's disease people have a short-term memory problem and a problem with navigation.
So amyloid is on a lot of places that cells don't die.
And so it's, again, I'm just saying that I'm not one of, I played in this sandbox before, so I know what they're talking about.
Dementia is really a cognitive dysfunction.
It's confusion, disorientation, trouble, activities of daily living.
So Alzheimer's is a form of dementia.
And it's one of the neurodegenerative forms of dementia.
So breaking them in, we have vascular dementia.
So someone might have major or minor infarcts, ischemia, damage to the brain, not getting enough blood supply to different parts of the brain.
So we have our vascular dementias.
And then we have a whole group of these neurodegenerative, where it seems that the brain itself is degenerating over time.
When we get to Alzheimer's And so it's not related to toxins.
It's not related to intramuscular toxin exposure.
It is related to the brain deteriorating I guess There's been I'm gonna say three major theories on Types pathogenesis what's driving and the number one that people have probably heard most about is the the amyloid
theory.
And it's interesting because they talk about camps.
They talk about people who are in the amyloid camp.
They talk about people who are in the tau camp.
So the other is there are these tau that form.
And then there's this inflammatory, the idea that, oh, those are all just sort of markers of an ongoing inflammatory process.
and if people had any comments sort of there before we go moving forward.
It's interesting the way there's- Anybody have any comments there?
Because I don't really know what I'm talking about.
I'm just kind of regurgitating what I heard in a couple seminars or what I read in a very cursory book a long time ago or in the introduction to the last paper.
There's an amyloid camp, a tau camp, and an inflammatory camp, and they all do bullshit experiments and bullshit mouse models, and they all justify themselves as being right, and that's why you have to fund them.
And none of them ever attack each other.
These guys are not gonna, the tau camp is not gonna do experiments to show that amyloid camp is full of shit.
And the amyloid camp is not gonna get funded to do tau experiments to show that tau experiment people are full of shit.
And for sure, the inflammatory camp is not going to get any funding to do experiments to prove that amyloid and tau are just byproducts of some other thing.
They can get experiments to show that inflammation is important.
They can get funding to show that tau might be important.
They can get funding to show that amyloid might be important.
But none of them will ever get funding to show why the other ideas are wrong.
And they are discouraged from doing that.
And so what you get is three different sources of bullshit.
And it's bullshit guaranteed because by definition, they aren't trying to disprove other people's model to make their model sharper.
They're barely trying to test their own because they're using p-values and null hypotheses.
And the null hypothesis is based on the idea that amyloid has something to do with Alzheimer's disease.
And so a good model of Alzheimer's disease would be a mouse that expresses a crap ton of amyloid in its brain.
There's camps here.
It isn't a bipartisan.
You've got the partisan here.
You've got one side, the aisle, the amyloid people, they want all the funding.
You've got the tau people, they want all the funding.
Is this the Green Party, the inflammatory people?
Only if there's pus coming out of us.
You also might want to add that Alzheimer's disease is on the rise.
And I believe that's a global problem.
It's not just a regional problem.
It's wherever you go, it's increasing.
So- I suppose that's got something to do with the aging population.
It might, very well.
The aging population has nothing to do with anything.
The aging population is not the pandemic.
It's not the rise in all cause mortality.
It's not the rise of death in hospitals.
It's not the rise of death as a result of not using antibiotics or supplemental oxygen.
Come on.
We're not expecting old people diseases because of old people.
We're not expecting old people diseases that come from a long life of exposure to toxins to start manifesting more if we have more old people, are we?
That would be crazy.
That's a good point actually.
Is it not, I presume you're meaning Alzheimer's in general and not early onset Alzheimer's that's on the rise?
Is that another camp?
I don't know.
So these purported experts, aka jackasses, are on here trying to lecture us about the biology of Alzheimer's, and they're not even aware that there's early-onset Alzheimer's.
Now this Scottish lady's gonna point out, what else, I mean, what else could she possibly point out here?
Parasitologist!
It is clear, I mean, Alzheimer's is- I don't know, I'm a parasitologist!
Wow.
It's just pathetic.
But I say it's pathetic with the self-deprecating knowledge that I was as gung-ho as these guys and then more so.
And if you'd have met me in Norway when I was a neuroscientist or a neurobiologist and talked to me about evolution, I would have eaten you for lunch.
Just make sure you realize that I'm very humbly submitting that all the time, that I was as bamboozled as these people.
And that's why I think I have a unique job to do because I can, you know, I was there and in it and all in.
I had the sweatshirts and the t-shirts and the hats and I wanted to have pit, pit, uh, chairs in my house.
And I wanted to wear the pit blue and yellow because I was proud to be working for that place.
The guy who invented the polio vaccine came from there.
Are you kidding me?
something in general associated with advanced age, like as people get older.
So as you have an advancing population, people stay alive long enough, then you can start to see dementia and some of it.
And there's a couple of things that go through here.
So the idea of the amyloid hypothesis, which we're going to talk quite a bit about today, is this notion that the amyloid plaque accumulation itself, like the amyloid itself is toxic.
And so the amyloid accumulates, it causes neural damage, it triggers the inflammation, it then leads to the cognitive deficits, right?
So that's going to be a lot of this paper is talking about.
And of course, tau is the same thing.
Tau just says that that protein is more important than the other protein, but it's an accumulation of, or it's a toxic accumulation of the same protein, depending on how you want to say it.
But they're both very different concepts.
It's important to be accurate about it or precise about it, or it's important to realize whether he realizes it or not, that those are two different things.
The accumulation of a toxic protein or the toxic accumulation of a protein are two different things, but that's okay, whatever.
Then, you know, you would think like, well, if there's some way to decrease the amyloid, then we can decrease the neurotoxicity, we can decrease the inflammation, we can make folks better.
And as mentioned, this is a... And so I guess the basic simple thing is, is that inflammation is caused by amyloid and so it's a chicken or egg question and they can go on forever like that.
And their only evidence will be that if we overexpress amyloid in the brain of a mouse, there's a lot of inflammatory signals there.
We're not even close to the worst part of this yet.
You're not going to believe it.
This is a huge problem affecting a lot of folks as they get older.
And they start off with this background.
And there isn't a lot of data in this paper, to be honest.
There's two figures that we'll go through.
That's right.
But there's a lot of background context.
So one of the things- There's a lot of background context, which you could also call mythology.
There's a lot of mythology, there's a lot of summaries of other labs' hypotheses that have yet to be proven, and that summary is presented as almost fact.
And if you read that crap all day long, it doesn't sink in in the right way.
I know because I did it for 20 years.
It sinks in in a way where again, you know, here's a imaginary hammer.
Here's an imaginary screwdriver.
Here's an imaginary drill.
Now let's build an imaginary tree house together.
And an hour later, you're climbing around in it.
As they point out, and I'm just gonna read this straight from the intro here, recent studies have shown a link between infection with the obligate intracellular protozoan parasite Toxoplasma gondii and protection from Alzheimer's dementia-associated pathology in mouse models.
So in mouse models, they have seen something, so they are justifying their further work in the mouse model because in the mouse model, they've seen something.
And it's not just a mouse model.
It's a inbred genetically altered mouse model.
And then they mentioned that T. gondii is estimated to infect 13.3% of the US population and up to one third of the world's human.
So why in the hell wouldn't we just do a survey and find out how many people with Toxoplasma gondii get AD and then be done with it?
And if there's a signal, you'll see it across all the old folks homes and all the old folks that live at home and all the people that come into the hospital because when they check the box, yeah, I like cats, they don't get Alzheimer's disease.
But instead we're working on a genetic mouse model.
I mean, and teaching kids that that's biology at the cutting edge population.
So it would seem a very straightforward study to say, do the people who have toxo get AD?
Correct.
There you go.
And there's certain areas like in France and Brazil where, what is it, 80, 90% of the population has an infection.
Do they have AD?
Wait, so in Brazil and in France, like 80% of the people have Toxoplasma gondii?
I didn't know that.
So then there should be a huge difference between the Alzheimer's in those populations and the populations that don't have it.
You see how stupid this is?
That it passed a grant review committee, that it got funded, that it was a grant call that this was answered with and it got funded.
And now these people are discussing it as a relevant set of questions and a relevant set of data to discuss so that we can better understand our own biology as humans.
In France?
Of course.
Yeah, they do.
They do.
They have over a million cases.
I did some background reading on this just to see if there was a relationship.
And it turns out
Well, France's population is about 63 million, and they have 1.6 million cases of Alzheimer's.
In the United States, it's 360 million, and we have 6 million cases of Alzheimer's.
And it's on the rise in both places.
In France, it could be that those million cases are the people that don't have toxo.
It could be.
I don't know if they ever checked or not.
Well, that's a pretty straightforward study, right?
And Vincent's first instinct was to assume that the paper was right, and so then explain France and America's difference, but America's difference is not explained then, see?
Well, then we can just use the French data.
We don't have to use the American data.
Stop lying!
And I shouldn't even play that.
They're not lying.
These people are lost in a maze of mirrors and they're bumping into things, but that's just normal because they do that all day long, bumping into mirrors and, oh yeah, that's right.
Sorry, I'm wrong about that.
You know that better than me.
Let's go this way.
Okay, here we go.
And they started in the hall of mirrors of Alzheimer's disease.
Now they're getting into the hall of mirrors of the causes of Alzheimer's.
I think they've looked at, I don't think there's a correlation.
I don't think there is.
Yeah, I think in the discussion, they talk about that.
Yeah.
I mean, the other, and we'll get into is, does it matter when you get infected?
Yeah, exactly.
Right.
There are other agents they mentioned as well that also cause a reduction in amyloid.
So Daniel, what is amyloid?
Yeah, so what is amyloid?
I got sidetracked here because amyloid builds up elsewhere too, doesn't it?
It builds up in other parts of the body as well and causes different diseases.
I got a little bit sidetracked.
I mean, is it a protein?
Is it a fat?
Is it a polysaccharide?
What the heck is it?
So it's a protein.
It's a protein that actually builds up.
And yeah, it can collect, as Christina points out, not just in the brain.
It can actually collect in a lot of other places as well.
Why is it called amyloid?
Oh, that's good.
So what is the etymology of amylase?
Oh, starch and cellulose-like.
I think that's where that's from, isn't it?
Look at that.
And so there's an enzyme called amylase, which digests starch and glycogen.
And if
People don't know what the chemical signature of this is.
They're wondering, how does that build up?
Why does this Rick Griffin guy look so sad right now?
Did she just say something she wasn't supposed to say?
I've never heard that amyloid was related to starch or to, yeah, that's interesting.
Interesting.
Up in your brain and how does it interfere with transmission of neurons and that sort of thing.
So I'm glad I asked the question rather than I was asked
So they're all happy not to be experts in this but they're also happy to take money and talk shit about this stuff, right?
And laugh about how they don't know enough to know really talk about it, but they're talking about it anyway.
They're taking they're asking for money to talk about it.
actually mean starch-like, but it's protein, right?
So we're starch-like, right?
Carbohydrates, so it's a starch-like protein.
Yeah, yeah.
Is this a repeated protein, like a polyprotein?
So it is interesting.
Is there a connection here between amyloid and misfolded proteins of a Crutzfield-Jakob, which almost has this PCR replication?
We don't think so.
What are those, the replicator things from?
Prions.
Prions, so.
Interesting, because I think Kevin McCarron and a lot of people like Stephanie Seneff often make a parallel comparison between amyloid, amyloidosis and prions and prion disease.
And I think that's intentional.
Because again, they're trying to blur the line so that our biology and the sacredness of it is lost in these details of molecular biology instead of a firm line being drawn where pattern integrities end and where molecular biology begins, where chemistry and physics begins and takes over.
Because life is emergent properties beyond physics and chemistry that can't be accounted for by physics and chemistry alone.
And yet we are still stuck in this idea that physics and chemistry alone do account for everything, the genes account for everything, that we can basically think of ourselves on a determinist track while evolution works in the background.
And if we would pull our big boy pants on, we would take control of it.
prions, depending on where you're from.
I mean, Stanley Prusiner thinks these are all, in the end, misfolding diseases.
Why not plug Stephen Prusiner, right?
The guy that went to the Vatican with Hilary Kaprowski.
Why not plug him with these giant books about prions?
And most of the stuff that they think about prions is based on experiments in yeast and anecdotal observations of people that eat other people.
And they want you to believe that prion diseases only take one molecule.
Right, Rixie?
Right, Kevin McCarron?
Just one.
It only takes just one.
It's really turning out to be a worst-case scenario, isn't it?
right?
Because the amyloid is misfolding and the tau is misfolding to make these plaques and tangles.
So they have a similar underlying mechanism.
A similar underlying mechanism?
Do you mean that amyloid misfolds other amyloid?
Because that's what prions mean.
And if you don't at least know that mythology well enough to make that parallel, you are really a pathetic biologist on faculty of a really pathetic university.
You should be ashamed of yourself.
That is sad.
I was also, yeah, I was also a protein as well.
And so the same sort of theory there that if you can get rid of these abnormal, toxic, misfolded proteins, you can have some benefit here.
So how are the proteins toxic?
Are they folded in such a way that they induce
inflammation, they just throw around these ideas because they are enchantments that they think are provoking very limited ideas in your brain that will add up into a cognitive picture that makes you accept what they're saying.
they're relying on the idea that most of the people that actually listen to them don't know what they're talking about.
So the interesting thing, we sort of get back to some of the things that we've talked about is, so does infection with T. gondii actually impact learning, memory, behavior?
And so they point out that
There's been some prior work where they've done T. gondii infection of this AD, so this Alzheimer dementia mouse model, so Alzheimer's disease mouse.
And they've actually shown improvement in learning and memory deficits, and that this actually persists after infection.
Follow the mice out for almost a year, right?
Which for a mouse, that's like an eternity.
Exactly.
I kinda miss that, I wanna listen again.
you can have some benefit here.
And so the interesting thing, we sort of get back to some of the things that we've talked about is, so does infection with T. gondii actually impact learning, memory, behavior?
And so they point out that they actually, there's been some prior work where they've done T. gondii infection of this ED, so this Alzheimer
dementia mouse models, Elmer's disease mouse, and they've actually shown improvement in learning and memory deficits, and that this actually persists after infection.
Follow the mice out for.
Wow, I would have to read that paper.
That seems like extraordinary.
So it's a mouse model.
But keep in mind, right, this is what he's essentially arguing.
I'm just going to switch over here really quick.
What he's essentially arguing is that they have this AD mouse, and it has amyloid in its brain.
And if they expose it to Toxoplasma gondii, then they have an increase in memory or behavior.
behavior score.
Doesn't matter what they do and they have some increase in behavior score.
So you have a mouse model that has a genetically predisposed bad brain with overexpression of what these guys assume is a toxic protein.
And so it's already got bad stuff happening.
And then when they give it this, they see a better behavior.
And so now they want to look and see if this infection reduced the amount of amyloid in that mouse brain.
And so they're not testing whether amyloid makes that mouse
silly, so dumb.
So my guess is, is that there's a lower behavioral score in this mouse relative to its wild-type counterpart.
But that's not also very surprising.
What you might ask yourself, the question is, if you took another mouse and you expressed another protein in it, let's call it XY, and you expressed it in the same places under the same promoter as amyloid, would you get the same results in this mouse behavior?
Would you have the same problems?
Because my guess is, is that that question has not been asked.
They have not transfected or permanently genetically engineered another mouse to express exactly in the same way that they are doing it in this mouse, but a different protein.
A slightly less, a slightly less toxic protein with very similar structural motifs, perhaps.
Maybe a protein with all the same amino acids in a different order.
They haven't done that control.
The control is this mouse versus a wild type control.
A wild type control doesn't have the alteration in it, right?
And so just like a lot of other experiments, the control isn't the right one.
The control isn't the right one.
Why?
The control isn't the right one because these people work in the amyloid camp and the amyloid camp gets the free pass.
to assume that the amyloid is accumulation of a toxin and so you can use any mouse model you want that produces that accumulation of that said toxin.
You get to have this assumption for free because you work in the amyloid camp and you wrote a grant to the amyloid grant call.
That's why they don't have to do this experiment.
That's why this experiment is dumb, because they've already working under the assumption that the amyloid is responsible.
And so rather than them teaching you this as they do this little thing, they're not teaching you at all.
They're just teaching you to accept
They're teaching you to accept the presuppositions of this whole model of Alzheimer's and that there are a limited list of possible causes and that it's sufficient for us to just think about these three causes and how they're related to each other.
They are no more sophisticated than the experts that they learned this from.
And the experts that they learned it from are in the amyloid camp, the tau camp, or the inflammatory camp and work under one of those three assumptions as a basis for their work.
Just a year, right?
Which for a mouse, that's like an eternity.
Exactly.
Right, what is it my cousin says, like if two people date in college, it's like you multiply it by seven, it's like dark.
I'm sorry, but the NIH takes these people very seriously.
Columbia University takes these people seriously.
The university somewhere in Scotland takes these people seriously.
A university in Texas takes this guy seriously.
A hospital in New York City takes this guy seriously.
We have to take these people seriously.
and we have to confront them as non-serious.
We have to rescue people from these people.
We have to rescue the people that take these people seriously.
And that goes all the way to the top of the NIH, the NIAID, all of these people in these bureaucracies take these people seriously, just like they take seriously anyone that has a tenure track position.
Anyone that has a faculty position is taken seriously by other people with faculty positions.
And they are very careful and very gentlemanly and very parliamentary procedure about how they interact with each other so that they don't step on the toes of somebody who's not in the camp that they're in.
Even if they're in the same field of Alzheimer's disease or neurodegenerative disorders.
And this creates an illusion of a whole sea of knowledge that has to be taken seriously.
And this little exercise is watching four people practice taking it seriously.
Yes.
This is exactly what we have to do.
Mouse, they need to have, what are mouse years, right?
It's going to be like two years on your toes, right?
I mean, mice live, what, three years?
Max, that's max, right?
So that's like each mouse year is like 30 of our years.
But interestingly enough, if the mice are kept on a minimal caloric diet, they live longer than their litter mates that are allowed to eat anytime they want.
That's a general thing for all animals.
Ooh, big deal.
Why bring that up now?
What in the world?
Dixon is funny.
Dixon is one funny old man.
But I like him because he's still one of the only guys who will say this is stupid.
So being normal weight, not just overweight, but just normal weight, appears to be a pathological condition, which eventually ends up shortening your lifespan.
That's a bizarre finding because there are a lot of people out there that believe that so much that they look like they're walking skeletons.
I mean, that's another one of those that might be true in mice, but we haven't necessarily seen that in people.
So yeah, so another question.
Oh, they're happy to bring that up whenever it's convenient for them, but not as a general rule.
I don't even know how you'd try it, how you'd test it in people.
You can't infect people with Toxo, right?
Yes, you can.
Oh, yes, you can.
Well, yes, so this is different.
There's a group in Japan, right, which, you know, sort of almost like a cultish type group that believe this is how they're going to live forever.
And they incredibly limited caloric intake.
Yeah, yeah.
And we'll see.
So, Dixon, you can infect people with Toxo?
Under extraordinary conditions, you can.
If they're in a state of ill health where no matter what you do, in the known medicine world, they're going to die, then they often approve protocols for extraordinary experiments like this one.
So, Dixon, if you get toxo as an adult, what are the consequences?
Well, you don't get the learning deficit.
As far as I know, there are no permanent effects unless it
activates as an adult, and that came out during the initial AIDS outbreaks, and that diminished your immune response against everything, including Toxoplasma.
A lot of AIDS patients died of encephalitis to Toxo.
But if you have a healthy person who does not have Toxo, and then they get infected at age 50, will it become a chronic infection?
Oh yeah, well, you know, it depends on how you define infection, because it gets into this Bradyzoite stage.
And the Brady's whites are not dividing.
So should we go back and do this, like, let's do basic toxoplasmosis?
We should probably do.
We did that once already, but we can do that again.
Yeah, so let's start off.
How do you get toxoplasmosis?
Do you have to own a cat?
Well, there are two ways.
One is that you eat the cat, and the other one is you take very good care of the cat.
No, I think the primary way, the reason why the French
have such a high rate of infection, their prevalence and incidence rates are very, very high, is that they have a set of cultural dishes and cuisines that if you don't eat them by the time you're two years old, you're not considered French.
And one of them is steak tartare.
And steak tartare is free of toxoplasma, by the way.
Steak, as long as it's steak, it's OK.
But they don't use steak.
They use lamb.
And they use mutton.
And those animals are not free of toxo.
And so a lot of toxo is transmitted by the ingestion of raw meat.
In nature, this is, by the way, the most widely distributed protozoan infection in the world.
The next most prominent is the one we had last time for a case history for Trichomonas vaginalis.
And then I guess malaria is third.
But this is probably the world's greatest
successful protozoan parasite.
Because Vincent, if you acquire this as an adult, and you have an intact immune system, you'll probably have six weeks of mild symptoms, a few swollen lymph nodes maybe, some fever, as the organism distributes itself throughout the body.
Thank you, macrophages, for picking me up and dropping me somewhere else.
It's like the taxi cab for Toxoplasma.
But we should say ingestion, right?
It tends to be an oral ingestion.
Oral ingestion is the only way you're going to catch this.
It's not a sexually transmitted disease at all.
So you get the infection by ingesting the bradyzoite stage, which is a dormant stage in muscle tissue, usually.
But of course, if you eat brain or if you eat other organs as well, you have an option for getting it that way as well.
But it's mostly through the ingestion of muscle tissue.
So then the organisms are activated by passage through the stomach.
And as they enter the small intestine, they receive environmental cues to sort of wake up, because now you're in the right place to start the next phase of your infection.
The bradyzoites change into tachyzoites.
Tachyzoites are the stage that we're used to looking at, these sort of banana-shaped, crescent-shaped organisms.
And they can penetrate cells.
and they penetrate the cells in the small intestine, and they set up an infection in the lamina propria, and it's loaded with all kinds of phagocytic cells, and some of them, like neutrophils, I believe, can actually destroy toxoplasma tachyzoites, but macrophages don't.
And in fact, John Boothroyd, a friend of mine who worked at Stanford on this, has investigated why that happens.
And it's because of the way it enters the cell and the kind of membrane it induces around itself to prevent the fusion of lysosomes.
And as a result, the organisms are not destroyed.
And that's one of its key survival tactics, is to avoid death by phagocytosis so that you can be distributed throughout the body.
The other remarkable feature about Toxoplasma is that there are no limits
to the kind of cell it can infect.
Now, this week in virology, of course, we talk about all of the receptors for various tissues or for various cell types and how specific some viruses are, at least for those cell types.
Toxoplasma has no bounds with regards to entering and leaving the cells as well.
In cell culture, you can watch this happen all over the place.
The cells are still alive.
So it can punch a hole in the cell membrane and then going through the hole that it just creates, seals up, allows the tachyzoite to go inside.
And if you leave it in culture long enough, of course it will replicate.
And you can use any kind of cell that you want.
You're free to study this in any cell culture.
And fibroblasts are good to start with.
Fibroblasts come from foreskin.
Okay, so in your body this is happening all over the place and you can imagine what effects this might have because as the organism... It's interesting that he had a very detailed mechanism for the distribution of one part of the life cycle in the body, but not a very good explanation for how they replicate.
Just if you wait long enough, they start to replicate.
I'm not saying it's not real.
It's not a virus.
So I'm open to the idea that it's definitely real and that they understand a lot about it.
But it's funny how certain they are about viruses and how viruses work and how specific they are.
And we talk about that on another program.
But this is actually supported by an awful lot of tractable evidence, which is very different than virology, even though, again, here he is making it seem as though they're equivalent levels of fidelity and understanding.
replicate inside of a cell, just like with malaria, and they're related to each other.
They're both epicomplexa.
Out come the tachyzoites to look for another cell.
And in doing that, it destroys the cells that they were in.
And that could go on for some time.
That could maybe, if your immune system is active, and your IL-12 is active, and you've got lots of ILs there that are not ill, but rather helping the cells around them survive,
Then eventually, eventually, with the help of interferon and several other immune-inducible responses, including immunoglobulins, the tachyzoites are brought under control.
And when that happens, in most cells, they die.
But in the brain.
In most cells, they die?
Why do they die?
Such a weird story.
And in selected other tissues.
in the eye, for instance, also, the choroid plexus, the organisms can live for a long time.
They inhibit immune responses against them by a very simple technology.
They just stop dividing.
They said, I'm not going to let you see me because my metabolism will go to almost zero.
And those organisms transformed from tachyzoids into bradyzoids.
which is a rounded-up form of the banana-shaped tachyzoites.
But the moment you eat the bradyzoites in the form of a cyst, they reactivate and become tachyzoites again.
So the other thing about this organism is that it's very specific for its hosts with regards to reproduction.
It's
It's got a male and female equivalent.
But he just said that it doesn't really matter what cell they replicate in.
You can do it in any cell culture, but now they're very specific, what?
And the only group of animals that it can reproduce in are the felidae, so cats of all kinds.
In fact, all- Do they cell culture it in cat cells then or what?
What is going on here?
Clearly he's not an expert, he just knows what he's been told.
Cats are susceptible to both the tachyzoite stage that it eats from an animal that it just killed, to the sexual reproduction stages, which never leave the animal and go in and disperse throughout the tissues.
What that stage does is it fuses
going from a haploid to a diploid stage protozoan, and then they produce two internal spores, and the Oocyst, which it's called the Oocyst, and that name was also used for the sexual stages of Plasmodium as well.
That stage is then excreted into the environment.
So another way to catch this infection
is by accidentally eating some cat feces contaminated with the oocysts.
And they almost instantly upon hitting air, mature into the infectious form that's... So I don't understand.
They can replicate in your body, but you don't poop them out.
I guess that's the point, right?
I mean, this is so bad.
This is so bad.
It doesn't even make any sense, even though he thinks he's telling a coherent story.
And viable for some time.
Of course, if it dries out, it dies, and that's the end.
But carnivorism and scavenging is the way this organism finds its way around the world.
And I think that's enough for the biology.
The biology is very complicated.
Once it gets inside of a cell, it's very virus-like in terms of its ability to interfere with normal host processes and even interacts with host genomics in a way that is reminiscent of the way trichinella
interfaces with its host genomics to cause the host to produce proteins that it never would have produced otherwise, at least under those circumstances, and enables the parasite to live a long and non-reproductive life until the next host comes along.
And all you have to do is die in order to transmit this to another animal.
And that's the real crux of the whole situation.
Most infections don't depend on death of host in order to transmit itself from one place to the other, but toxoplasma is famous for its ability to survive as these bradyzoites in tissue.
It's amazing how many human beings are infected.
We're really kind of a bystander to this sort of... Yeah, that's right.
We're a dead end.
That's right.
Except we're not a dead end necessarily.
I guess we're eaten by a lion, right?
Well, no, no.
There are cultures on the Himalayan mountains, mostly Buddhist cultures, which actually dismember a person who has died and put them on these platforms.
for the vultures to come and feed on the carcass, to recycle the body back into nature.
And other animals will scavenge on those parts as well.
And when they do, of course, they have the option of acquiring toxoplasma as well.
You can also catch it from the mother.
So there's a congenital toxoplasmosis as well.
And so that's a third way of catching this.
It's the one that causes the most damage in people.
An adult can usually fight off this thing.
If you're suffering from AIDS, then the answer is you can't.
But if you're an immunocompetent person.
So I'm going to see if I can speed this up.
What I'm going to do is I'm going to try and go here.
which is the original video on YouTube.
And I'm going to go down here and try to see if I can find the show notes.
That's this one.
And then I'm going to look at the paper that they looked at.
Because that's, of course, what we're talking about here.
Let me move my big head.
And reduces amyloid in the brain is this one.
And can I get that one?
Um, there they are.
5xFAD is the name of the mouse that they used, and so I'm gonna go back to PubMed, where is it?
And, uh, 5xFAD.
Mice.
So, mast cells, blah blah blah blah blah.
seizures, exacerbate, excitatory, inhibitory, imbalance, and Alzheimer's disease, and patch clamp recordings.
That's kind of a cool paper.
And this is a cool paper.
Okay, these are the two that I found before.
Background, alterations in gastrointestinal function and gut brain axis are associated with progression and pathology of Alzheimer's disease.
Studies in Alzheimer's disease animal models show that changes in the gut microbiome and inflammatory markers can contribute to, I hate saying it, Alzheimer's disease development in the central nervous system.
Again, animal models.
And so what are the animal models?
Six month old,
5xFAID, their transgenic Alzheimer's disease, and wild type, male and female mice.
GI function was assessed and expression of amyloid in the brain and in the colonic myenteric plexus, so I guess that would be
a little patch of nerves in the gut or else a little patch of nerves somewhere in the deep brain.
I don't know.
I haven't looked it up yet.
But the point is, is that in this one, they say they're not a robust model of Alzheimer's to study amyloidosis in the gut because these guys don't mimic that.
Thank you very much.
They don't mimic that effect.
And so this transgenic model of Alzheimer's disease only has the transgenic alteration in the brain.
It only has amyloid in the brain.
So it's not really a model of amyloid generating Alzheimer's disease.
It's a model of
of transgenic alteration of amyloid expression, altering the behavior of an animal, and them equating that to a model of Alzheimer's disease.
And depending on how bad that assumption, that jump is, that leap is, we could really be studying nothing, and maybe even two orders of magnitude removed from something.
Inbred mouse.
Transgenic expression of a protein that shouldn't be there.
And then the assumption that that protein is central to a human disease.
There's like three bad assumptions here all in one whole list of literature.
Remember what I just did here.
I did a whole search on these mice and got a whole list of papers that goes to 1,541 papers where they talk about this mouse model.
1,500 papers that taught at least 1,000 grad students, at least 1,000 postdocs, and spent at least a million euros each.
Because not any of these labs are doing one paper using these models.
That's not how you get grant funding.
I wonder if we can find something that would help us understand exactly what happens in these mice.
I don't know, but I'm going to go back to this.
than you can.
But a fetus, especially in its first and second trimesters, has got no immune system, basically.
So the parasite can take advantage of it.
And eventually, the parasite ends up in brain tissue, as well as other tissues.
And the one most affected, of course, is the development of the brain and the fetus.
And some horrible cases of congenital toxoplasma
Okay, we're going to forget that again.
I'm sorry.
I forgot what I was doing here.
Now I know.
I remember now that the coffee's in me.
We were getting this paper out, right?
Oops, wrong screen.
We were getting this paper out.
Where did the paper go?
Where's the paper?
Here's the paper.
They looked at a brain region specific manner.
They have some, oh, here's the data.
So if they infect, yeah, we can just blow this up because this is the whole point, right?
They are going to look anatomically at two different places.
These are sagittal slices of the brain, so they're slicing sideways like this.
This one might be a little more lateral than this one that's in the middle.
This is probably a lateral slice.
This is more of a midline slice.
And you see down here, I believe, amyloid density is expressed in this yellow color here.
So purple is low, yellow is high.
Hopefully you can see my arrow.
And so this is high amyloid expression here at the base of the brain.
Maybe this is the, I don't know, is that the nucleus accumbens there, something like that.
And then in the frontal cortex, you can see a lot of it there.
You can also see some of it back here.
This might be cerebellum, and this might be entorhinal cortex back here.
This could also be entorhinal cortex right here along the edge of these lateral slices, sorry, sagittal slices.
Are these sagittal slices?
Yeah, I think they are.
I've been so long since I've talked with Menno, I don't remember all the planes of the anatomy anymore.
I apologize.
But I think this is a sagittal slice.
It would be coronal.
No, coronal is like this.
And sagittal should be like this.
And horizontal should be like that.
I think that's right.
And if I'm wrong, I apologize.
But I'm definitely not wrong about the fact that they're looking at injection of phosphate buffered saline versus injection of the toxin.
And so the question is, how do they do it?
Let's look at the methods.
were bred, all mice were infected at three months of age with 200 green fluorescent protein expressing tachyzoids, injected intraperitoneally.
So if we believe the biology that the old man was telling us, the tachyzoids are the
Those are the live ones, right?
Those are the infectious ones.
And they do 200 microliters of phosphate-buffered saline containing 200 green fluorescent protein-expressing PA7 tachyzoids.
Intraperitoneally.
And intraperitoneally, just to make sure.
I think I know what it means.
But if I say it out loud and then I look like a fool, I don't want that.
So I think I know what it means.
I can't even spell it.
Interperitoneal.
Cavity of the abdominal organs.
That's correct.
So that's interesting, right?
Because they're not going to inject it in the brain.
They're injecting it intraperitoneally.
Hmm.
Also where they don't put vaccines.
They don't put vaccines intraperitoneally.
That's interesting, huh?
Females were used in all experiments, as females have been reported to have a more aggressive timeline for the development of AD pathology.
One citation.
Parasites were serially passaged in human foreskin fibroblasts, as previously described.
Isn't that such a great use?
Isn't that such a great use for medical remnants that are taken from infant boys under the pretense of keeping their penis clean during infanthood, making it easier for them to maintain the hygiene of their genitals?
What an awesome use.
And so this is the optical clearing, and then they use DISCO, and then they show you that basically they can see that there's some plaques and whatever the infection took.
See, they look at infection, and they see, and they don't see.
I don't know what they're showing here.
A, what is A showing?
Amyloid burden is reduced.
Three-month-olds were injected.
Representative Z-planes showing amyloid signal from PBS injected.
So this is apparently showing the amyloid and it's lower.
It's not that impressive.
This is more impressive.
B is amyloid density was quantified at each mouse and density maps were computed or analyzed or aligned across that atlas and then mean density of amyloid in the lateral medial sagittal.
Yeah, it was sagittal.
amyloid density, the number of plaques per voxel, and then they have some p-value here.
So p-value.
Pervuvian.
P-value says that there's a difference between this group and that group.
And so we have an effect.
You see how it works?
That's it.
It's done.
There's a difference between this group and that group, even if you just, maybe you should throw that one away.
Well, let's not.
Let's not throw that one away because then there might not be a significant difference.
There might not be a significant difference if you just threw that one away.
But it doesn't matter, because that's not how p-values work, ladies and gentlemen.
That's not how knowledge is created on the academic bench.
Shall we give them a chance to actually finish their discussion of this paper?
Because they haven't really started even discussing it yet.
I don't know.
Maybe we should.
Are available online for you to
become absolutely repulsed by the damage that a very small organism can cause to a very innocent bystander, basically, that had nothing to do with this at all.
The mother ate a piece of raw meat or had a pet cat that, you know, she was not taking
as good a care of as she should have probably.
So Daniel, tell us, tell us what they did in this paper.
Let's go into reality here.
No, no, this, I mean, this is reality.
Well, that's true.
That's true.
Yeah.
Clinically and people it's world.
This is reality.
you know, unless it's from mom, um, usually presents a model like illness, but yeah, then you end up with these, uh, intracellular creatures in the brain and in most cases.
And, and so that's, that's where we're going to go.
So let's get back to our paper.
Uh, we've gotten much of the, uh,
I think the other thing we should probably mention in the paper, we're still in the intro here, is that the impact of the T. gondii infection in mice is different, whether you're dealing with your lab BALB-C, right?
You're familiar with the little white BALB-C mice versus the wild type, or even the black 57 mice.
So actually, it depends which mice you're
Oh, so Toxoplasma gondii infects different inbred mouse strains differently, but we can learn a lot of human biology from infecting mice with it.
Holy shit.
Stop lying!
That is spectacularly dumb.
Infecting, as far as the impacts that you're potentially going to have.
So let me see.
Let me read the paper again.
The mouse model is weird, right?
It is because there's actually this, yeah, this special Alzheimer's disease mouse, right, which again changes things because you're doing the infection in a... It doesn't change things.
It nullifies what you find and makes it inapplicable to any other pattern integrity because the pattern integrities that they are studying in this study
are not relevant to natural pattern integrities.
It's not a natural pattern integrity.
It's a genetically inbred, transgenically modified mouse line.
It changes things.
Boy, that's, yeah.
It changes things.
In particular, inbred, genetically modified mutant mouse, which you can buy from the National Institute of Health Mutant Mouse Resource and Research Centers.
I'm sure they're going to get shut down.
In fact, they're transgenic mice.
And you can buy them and use them and get grant money to use them and learn nothing about how your beautiful child works.
that overexpress a human altered amyloid protein.
They express a human altered amyloid protein.
Even Vincent can see that this is bullshit, but not really.
Because again, that's what happens when you're trapped.
When I was trapped, I called everybody's bullshit out all the time, but not all the way down to the hardwood.
just down to them not wearing the right uniform, or your hat's on crooked, or you didn't say that quite right, or don't forget that that's not proven yet.
But I gave them all their assumptions.
I gave them their assumptions about amyloid, or I gave them their assumptions about genes, and about behavior related to genes, because that's what you gotta do to work in neurobiology.
So I was just as broken.
And I accepted vaccines and all that public health stuff, because I'm not a doctor.
And because I raised my children, luckily, in Norway, where the same level of public health mythology is not pushed on parents.
Not even close, because you know what they do in Norway?
They encourage you with three days in the hospital hotel room with a string that you can pull
where you can sleep with your wife and your newborn kid for three days and pull on a string for 24 hours every day for three days to have a midwife come in and help you as the father learn how to help mom to get the baby to latch and breastfeed.
Because mom can't see it.
Mom can't see if there's enough of the breast in the mouth so that the mouth is encompassing the nipple.
and Papa can help with that.
And they spend three days encouraging women to not underestimate how wonderful it is, how beautiful it is, how much it is worth the time and effort to learn how to do it and how important it is for the husband to be present during it and be an expert enough to help so that in the middle of the night when wife is crying, you can remain calm
And I can get chills thinking about those three days because I never imagined how wonderful it would be to bond with my wife in that way.
And I never imagined how important it was to understand that because that's the reason why moms feel the way they feel.
And I also believe that's the reason why these malevolent monsters want you to stop breastfeeding babies.
Because they don't want strong, independent moms.
They don't want strong, independent women who understand their worth and understand the irreducible complexity that is their little baby on their breast.
They don't want them to even experience it.
So these are mutations in the amyloid gene that are known to predispose to misfolding.
So they put five copies of the mutant genes into the mice to try and, you know, because mice don't normally develop Alzheimer's.
How would you know?
Well, I think they do know, right?
Because they would have loved to have found, this goes back to the history, they would have loved to find naturally occurring, you know, Alzheimer's malars, you know.
But yes, they had to make these.
They had to make these.
You can buy them up in Jackson.
It was actually up at Jackson.
And why did they make them?
And then we're going to stop.
They made them because there was an amyloid camp.
They made them because the Human Genome Project tells us that everything is genetic.
They made them because the Human Genome Project provided the techniques and the technology to make knockout mice that would allow the amyloid camp, the tau camp, the inflammatory camp, the genetic causes of autism camp to exist.
And in so doing, they have created an entire illusion of knowledge based on the genetic causes of autism
the genetic causes of amyloid, the genetic causes of Parkinson's disease, and some of those are genetic explanations.
And because some of those low-hanging fruit have a genetic explanation, then they think that they can say evolution because DNA.
Because Mendel did some experiments on inbred pea plants that made it seem like they were dominant and recessive genes, we now think that evolution happened because of DNA.
And this level of obfuscation of the truth, this level of irreverence for the irreducible sacred complexity of our children is facilitated and edified by that biological assumption that evolution because DNA and the way that it is used to create all of these little islands of investigation that execute steps of logic on false assumptions.
Ladies and gentlemen, this has been Gigaohm Biological, a high resistance, low noise information brief brought to you by a biologist.
I don't actually think I have a goodbye slide here.
And so I'm just going to use this one again.
Thank you very much for coming.
I'm going to go to the freshman basketball game in an hour or so.
And then I'm going to go work out with my son doing some, I don't think the gym is going to be empty enough for me to film an episode.
If it is, I will.
And otherwise we'll get a JC on the hardwood episode done on Monday and probably up on the internet by Monday night or Tuesday.
And as usual, or as I'm planning to do now, I'm going to try and take the weekend off.
Although,
Things may happen and I may end up doing a surprise stream on Saturday or Sunday.
Maybe we'll even do an interview with Oma who's here.
Maybe we'll just do a chat and discussion with Big Mike.
I don't know.
Most likely my plan is to take the weekend off and show up again next week for five days in a row, including another
Bad Biology, including another Monday Meddler Medley, and including a, tomorrow we're gonna do a Friday week update as well, which I already have ready to go.
We're gonna keep ringing the bell of that Scooby-Doo until people understand how bad it is.
Ladies and gentlemen, thanks very much for being here.
Thanks for supporting the stream.
Thanks for sharing.
I had a little glitch on the peer tube yesterday, so it took me a while to re-upload my stream from yesterday, but it is there now, so go check it out if you missed it.
It was also a really good one.
And again, I will see you again tomorrow.
Thanks for coming.