https://www.youtube.com/watch?v=p7vmIWYlFHQ
Dr. Garrett Smith
NutritionDetective.com
Tuesday, March 25th, 2025
NOTE: Automatic Translation includes errors. Ivermectin, Abermectin, Avermectin are often confused and probably other words we haven’t identified yet. I’m doing this work to see if we can make AI digestable transcripts that correctly grock the material.
-Joe Baker
https://docs.google.com/document/d/1LvomhjzMhRjkFEH4BlooeuCCzezF3YlHXctrSC3rT9E/edit?usp=drivesdk
Okay, hello, hello, hello everyone.
This is Dr. Garrett Smith, also known as the Nutrition Detective around these here YouTube
parts and today we have another exciting part of the Infertility PsyOps series.
Today we’re going to be covering some of the pharma aspects of it that have become quite
popular recently.
For all sorts of purposes, they think they’re going, they think that, people think that
the pharma cartel has come out with generic medications that are cures for things.
Now first I want to say, okay, the reason why medicine loves chemotherapy so much is
mainly because they make tons and tons of money on it.
But then I also want you to think about how the people up top really would like fewer
people around.
They would like that.
So you have to understand when people argue that these generic medications are not profitable,
well I’m going to tell you that profit is not always their motive.
And if they were losing too much money from generic drugs being sold as cures, they would
stop selling them.
They’re a cartel, okay?
They protect their own.
So do you understand that if they were doing things that were damaging themselves, they
would simply tell their teammates, the generic makers, you’re going to stop making this right now.
They just make it unavailable.
They’re not on your side.
They’re not tdoerying to help you.
If they were helping you too much, they would stop selling it.
You can’t say on one hand that they don’t make any money on these things and that they’re
trying to fix things and that it just doesn’t make any sense.
Like the arguments for all this don’t make any sense.
Why would they shoot themselves in the foot to not make any money?
And do you actually think they sell anything that they don’t make money on?
Like really think about it.
So we’re going to go into it today, ivermectin, the azoles, and methylene blue, which is a
pharma cartel drug.
If you don’t know, it is used in hospitals as a drug.
It has a black box warning and just because it’s only a little bit in the dropper bottle
doesn’t mean it’s not a drug, okay?
So we’re going to hit on all of these and they’re going to play together.
When you understand how all of these things play together, let me first give you an idea
here.
Studies are done with each one of these things by itself typically, right?
That’s how science works.
Well, in the real world, toxicity is often synergistic.
So you add one plus one and you get three.
The thing is with toxins, sometimes you get, you add one plus one and you get five in terms
of toxicity.
So remember, they haven’t done any studies combining these things until you get to the
idea that we get to ivermectin and P-glycoprotein inhibitors and then you’re going to go, oh
wow, this is really, really bad.
Oh yeah, I wanted to say thank you to Thief on the Cross in the chat.
He said, this diet changed my life.
And then Steph right after him said, same here.
So yes, hello everyone in the chat who’s here.
We’ll get started on all this right now and this is what we’re trying to help.
So we’re trying to understand what I want you guys to understand and what I think we
do better than just about anybody else out there is we actually understand detox.
And your priority is always to not take in toxins.
The other thing that we learn as we go is that toxins slow detox.
The more toxic you are, the slower your detox.
This is just the way it goes.
The dirtier a car engine is, the less efficiently it runs.
You know, you’ve got to use more energy to get it to go the same distance.
This is what happens.
So all of these things we’re going to talk about today basically slow detox.
They’re toxins themselves and they slow detox.
And this is what they do.
And when you do all this, especially we’re focusing on men today because sperm is the
easiest thing to see this stuff in.
But ladies, it’s just as bad for you.
And for those of you out there who might say, well, I don’t care about fertility.
I’m too old for that or I’ve already had my kids or whatever.
Fertility is health, folks.
Health is fertility.
Fertility is health.
If something’s ruining fertility in younger people, it’s ruining health as well in younger
people and older people.
So we’re using fertility as a surrogate marker of health.
Just because you don’t want to have kids doesn’t mean it doesn’t affect you.
And if you don’t want to have kids and you go and poison yourself, you’re going to get
sick.
So it all fits together.
So let’s head into it.
So Joe, I think posted the links doc in the chat.
Links for today’s show: https://docs.google.com/document/d/1LvomhjzMhRjkFEH4BlooeuCCzezF3YlHXctrSC3rT9E/edit?usp=drivesdk
And Joe, you can show the Twitter thread.
(80) Nutrition Detective 🔍 – Dr. Garrett Smith on X: “IVERMECTIN – THE NEXT PHASE OF “THEIR” INFERTILITY PLANS As I keep repeating, they want us sick, infertile, & dead early The pokeys did their damage & continue to do so How will they trick people–especially men–who DIDN’T get it into infertility? ENTER IVERMECTIN (IVM) https://t.co/Lyd657PrpU ” / X: https://x.com/NutriDetect/status/1711787826688233672
So let me just check.
There we go.
So this is my ivermectin thread on fertility.
I’m going to go over the links from this thread.
I’ve already been over some of this before, but this thread, it’s going pretty good.
You know, 200,000 views, it’s going all right.
Share this around to people who think that ivermectin is, the biggest lie you hear out
there about ivermectin is that it’s safe as water.
It’s not safe as water.
That’s a joke.
It kills parasites and it kills bugs.
As Kelsey said on Twitter once, she goes, if it’s killing all these things quickly,
it just, it accumulates in you and it just takes longer to kill you.
Okay.
So I kind of liked that idea that she said.
So now let’s go on.
What was I going to do here?
Oh, wait.
I didn’t want to do that.
Not that.
How did I get that to go away?
Joe?
I remembered how I got it to go away last time and now I’m not, uh, remembering, anyway,
we’ll just do this.
We’ll just refresh it.
And the glasp didn’t show up again.
Trial of ivermectin for treatment and prophylaxis of COVID-19 | The BMJ: https://www.bmj.com/content/369/bmj.m1432/rr-26
I wanted to go over this one from the British medical journal.
Now I know this says HCQ, but I wanted people to pay attention to, cause they think that,
you know, if, if, uh, Mr. Bill Gates is against something that therefore it must be good.
Well, let’s just make sure on ivermectin, um, research is proceeding on optimal doses
of efficacy and likely safety.
<sarcasm>The WHO who we love, right </sarcasm>, is directing additional focus to ivermectin and the Bill and Melinda
Gates foundation is supporting redirection, redirection of us $19 million of its grant
funds to repurposing ivermectin for COVID management.
Does that sound like they’re really against it?
Not to me, you may, you probably didn’t know that you probably thought they were all trying
to suppress it.
Oh my gosh.
Give me a break about the suppressing thing.
There’s people trying to make it nationally over the counter.
Okay.
That’s not suppressed.
That’s the opposite of suppression.
That’s promotion.
Okay.
(21) Nutrition Detective 🔍 – Dr. Garrett Smith on X: “Bill Gates, Population Control, & “vitamin” A: What We Can Learn By Following His MONEY$$$ Many are familiar w this “man” 😉 & his goals for humanity Did you know “vit” A is a CRUCIAL part of his approaches? What does HE know about it that YOU don’t? SHARE THIS / thread /” / X: https://x.com/NutriDetect/status/1599523128518098944
Now here’s my other thread as I’ve posted before, and I think we went over last week.
Bill Gates loves vitamin a Bill Gates loves, you know, they’re supporting ivermectin.
So please don’t think that it’s some like underground thing.
The WHO and Gates are supporting it.
Okay.
Assessment of Avermectins-Induced Toxicity in Animals – PMC: https://pmc.ncbi.nlm.nih.gov/articles/PMC8950826/
This is the ivermectin one.
Um, actually, let me, hold on, let me go check.
What did I do on this one?
Ah, forget it.
So that’s the ivermectin.
So now we’re heading into ivermectin is the family that ivermectin is in.
Okay.
So ivermectin is the big family.
There’s ivermectin and then there’s ABA mectin ABA ABA ABA mectin has, what was it?
Oh yeah.
Ivermectin Kelsey tells me the chemistry of this stuff.
Ivermectin has two more hydrogens on it than ABA mectin.
That’s it.
That’s the only difference between the two of them, two hydrogens.
Okay.
So hello, Beth.
Nice to have you here.
So let’s go over this assessment of Avermectin.
So that’s the whole family induced toxicity in animals.
Did I hear somebody say this was as safe as water?
Oh, let me check.
Many studies, many studies have reported the negative effects of Avermectin’s like ivermectin
ABA mectin, Dora mectin and aprinomectin on the host animals.
That’s you.
These harmful effects arise from Avermectin’s targeting GABA and glutamate gated chloride
channels present in both the parasites and the host animals.
Okay.
Stuff is going to get quite interesting in the future.
In this review, various model modes of Avermectin’s actions, along with the negative effects on
the host, like nephrotoxicity, that’s kidney toxicity, hepatotoxicity, that’s liver toxicity,
neurotoxicity, that’s toxicity to your brain and nervous system, reproductive toxicity,
that’s ruining your fertility and endocrine disruption.
That’s your hormones were discussed in detail.
Furthermore, other important issues like ecotoxicity to the ruining the environment, drug resistance,
where it’s not, it’s not working as well as it’s supposed to.
And drug residues in milk, drug residues in milk.
That means if cows are being given Ivermectin or they are eating it in the soil, in the
grass, it is coming out in their milk and it’s also in their tissues.
Okay.
And so if you’re nursing and you’re taking Ivermectin, you are feeding your baby Ivermectin
in the milk.
So associated with Avermectin’s uses were also discussed, which need special attention.
Wow.
That doesn’t sound good.
Okay.
Look at all this toxicity.
Safe as water, right?
Safe, safe as water.
Is that what safe as water looks like?
I just wanted to check.
Um, wait, wait, wait, wait, wait.
There we are.
Okay.
So let’s keep going.
Effects of abamectin.
Remember, this is just two hydrogens different than Ivermectin, but we’ll get to Ivermectin
for sure.
Effects of abamectin exposure on male fertility in rats: potential role of oxidative stress-mediated poly(ADP-ribose) polymerase (PARP) activation – PubMed: https://pubmed.ncbi.nlm.nih.gov/21945325/
Effects of Abamectin exposure.
What actually, let me just say this.
What I’m going to do today is I’m going to go over the families of the drugs to show
you that people will be like, well, that’s not the, with the azoles, they’ll say that’s
not the exact same drug.
Those, that’s not an antifungal azole.
That’s omeprazole.
That’s for stomach acid or what?
No, it’s all azoles.
And if you go and you look at the research on omeprazole and cancer, omeprazole is causing
all sorts of diseases.
They name them after the chemical structure of it.
And the same birds of a feather flock together.
The same chemical structures tend to do the same things.
Okay.
So that’s why we’re going to show this across the class of drugs.
Okay.
Effects of, this is actually roach poison.
Just so you know.
Avermectin is roach poison.
Two hydrogens different from that Ivermectin that you’re taking for your cough or your
cold.
Now is that, that’s what people are taking it for.
Effects of Avermectin exposure on male fertility in rats.
Potential role of oxidative stress mediated poly ADP ripose polymerase activation.
Let’s go down here.
Avermectin level was determined at high concentrations in the plasma and testicular tissues of male
rats exposed to this pesticide.
People will try to tell you that Ivermectin doesn’t accumulate.
They are absolutely wrong.
They’re either ignorant or they’re lying to you.
It accumulates.
What happens with toxic things that accumulate?
It means that the acute toxicity studies don’t matter so much because you can reach that
level of toxicity over time by accumulating it.
Avermectin administration was associated with decreased sperm count and motility.
Wow, that would be bad.
And increased seminiferous tubule damage.
In addition, significant elevations in the four hydroxy two nonanal, four HNE modified
proteins.
You guys may not know what this means, but we talk a lot about ALDH, aldehyde dehydrogenase,
and how it detoxes aldehydes.
Aldehydes are toxic to the testes and all of your system.
So if they’re seeing, this is four hydroxy two nonanaldehyde.
They don’t say aldehyde there.
They decide to shorten it.
I don’t know.
Maybe not to tell you that there’s aldehyde there.
But four HNE is often measured when they usually do malon dialdehyde as well.
So these are the two things that come about from PUFAs in your body.
When PUFAs oxidize, they turn into malon dialdehyde, four hydroxy two nonanal.
We process them through ALDHs.
So if we slowed down ALDH, you build up aldehydes.
Aldehydes are especially toxic to sperm.
I went over last week about how the goal of the male contraceptive pill approach is to
make an ALDH inhibitor that doesn’t ruin men’s health too fast or too quickly.
So do you understand that ivermectin is showing, or abimectin is showing that it is an ALDH
inhibitor because four HNE is going up.
They’re accumulating aldehydes.
It’s really hard to find research on ivermectin specifically being an aldehyde dehydrogenase
inhibitor, but we have the evidence here.
So this was observed in the testes of rats exposed to abimectin.
These results show that abimectin exposure induces testicular damage and affects sperm
dynamics.
Okay, that’s not good.
Let’s keep going because there’s plenty here.
Assessment of anti-fertility activities of abimectin pesticide in male rats.
Significant increases in the total number of resorptions.
I wanted to, shoot, I forgot.
I wanted to make sure that’s, that is, I believe that is, that’s an abortion where the embryo
is just absorbed back into the animal.
Hold on.
Yeah, fetal resorption, also known as fetus resorption, is the process where one or more
fetuses in the uterus disintegrate and are assimilated after organogenesis.
So, yeah, there’s not, they’re, they’re saying this is different than a miscarriage because
a miscarriage would actually come, you’d have stuff come out and on this one, nothing comes
out.
Okay, so, where were we?
Here we are.
So significant increases in the total number of resorptions and the number of females with
total number of resorptions and the number of females with resorptions were observed
in females mated with exposed males at all three concentrations.
Do you understand what they just said there?
The males were exposed to the abimectin and they just went over on that last paper, abimectin
accumulated in the testicles.
I’m assuming that they’re saying, yeah, let’s add this one.
The number of viable fetuses was significantly reduced in females mated with males that ingested
abimectin at 1.87 or 2.13 milligrams per animal per day.
The females aren’t on ivermectin.
The males are.
The pregnancies are not making it.
Do you understand?
So, the infertility PSYOP guys, it’s aimed at you.
It’s aimed at you conservative guys because they know you won’t take the pokey.
So, they have to get you thinking you’re real smart and oh, I don’t get the idea where people
think they’re somehow screwing over the pharma cartel by taking pharma cartel drugs.
Just stop saying that.
That is the most ignorant thing I’ve ever heard.
They’re like, yeah, screw pharma.
I’m taking pharma, but I’m buying it at a veterinary store.
Like, what?
Serious.
So, they’re seeing.
So, the males are exposed to abimectin and the females are basically aborting the pregnancy.
Oh, Thief on the Cross was saying aspirin shilling.
I’m going to go over aspirin in one of the infertility PSYOPs too.
So, epididymal and testicular sperm counts and daily sperm production were significantly
decreased in the exposed males.
The serum level of testosterone was significantly reduced.
Guys, what do they want to do to you?
They want to lower your testosterone.
They want to make you infertile so you don’t resist and so you don’t have kids that will resist.
This is their plan.
Whereas the serum level of follicle stimulating hormone, that’s what helps you make sperm,
was significantly increased in males that ingested abimectin at a concentration of 2.13
milligrams.
Histological evaluation of testes revealed several abnormalities, including infiltration,
things are going into places they’re not supposed to, with congested blood vessels,
with a marked hemorrhage and a significant accumulation of connective tissue,
that’s basically fibrosis or scarring, surrounding the seminiferous tubules.
These results strongly suggest the adverse effects of abimectin pesticide.
Pesticide.
Ivermectin is a pesticide.
Why do people argue that it’s not?
On male rat fertility.
I really want you to pay attention.
Because here, the effect of abimectin pesticide on fertility of adult male
sprague dolly rats was investigated.
So the female rats didn’t get it.
And the number of females impregnated by them was significantly reduced.
So the guys are not functioning.
The women are normal.
The females are normal here.
The guys are not functioning.
That’s who they’re going after.
I mean, it’ll affect women negatively, too.
But the guys, they’re going after you.
OK.
So now we have effective abimectin exposure on semen parameters indicative of reduced
sperm maturity.
A study on farm workers in Antalya, Turkey.
This is on humans now.
20 male farm workers who were using abimectin and 20 men not exposed to pesticides were
recruited as experimental and control groups, respectively.
Semen analysis, molecular markers of sperm maturity and semen reproductive hormone levels
were evaluated.
In experimental group, high plasma abimectin levels were detected.
These men have decreased sperm motility.
Moreover, diminished molecular markers of sperm maturity, such as decreased hyaluronic
acid binding of sperm.
That’s a marker of how well the sperm are functioning.
That’s a marker of how well the sperm are functioning because they have to bind to to
hyaluronic acid around the egg to penetrate it.
So they got to they got to break down the hyaluronic hyaluronic acid around the egg.
Increased numbers of aniline blue handling blue.
Gosh, that’s pretty close to methylene blue.
Positive sperm and increased percentage of creatine kinase positive sperm were observed
in abimectin exposed men.
Their serum testosterone, LH and FSH levels did not change significantly.
We conclude that exposure to abimectin may impair male fertility by affecting semen quality.
So we have roach poison, two hydrogens different from ivermectin causing problems in human
men, and they keep calling it a pesticide.
So now we’re going on to.
Effects of ivermectin and its combination with alpha lipoic acid on expression of these
genes and male rat fertility.
Furthermore, injection of ivermectin showed a significant decrease in serum testosterone
level, sperm count, motility percent, live sperm percent, and index weight of reproductive
organs.
And a significant increase in sperm abnormalities.
Moreover, ivermectin induced oxidative stress and pathological alterations in the testes.
Remember, it accumulated in the testes.
So a little bit over a long time will build up.
We concluded that ivermectin has undesirable effects on male fertility and altered expression
of IGFBP3 and HSPA1 genes in the testes.
So you see the same pattern as the abimectin.
We don’t need to do well, I don’t know how much we’re going to hit on this, but the titles
kind of says it all.
Ivermectin reduces motor coordination.
Boy, that would.
Gosh, if they didn’t want guys who fought back well, that’d be, that’d be a good thing
to induce, right?
Think about like a silent war on people.
Reduces motor coordination, serum testosterone, and central neurotransmitter levels, but does
not affect sexual motivation in male rats.
So these guys can still be horny, but everything else is breaking down.
You understand?
That’s what they’re doing.
But everything else is breaking down.
You understand?
That’s what they’re, you know, so they’re like, well, my libido is fine, so everything’s
fine.
No, your libido is not the only indicator of your testosterone.
It’s not even that great of one.
Data showed significant decrease in striatal dopaminergic system activity.
Gosh, does anybody seem like they have dopamine problems these days?
And lower testosterone levels, but no effects on sexual motivation or penile erection.
So things can seem to work okay, but in the background, the nervous system and the hormones
are not doing well.
Wait, was this the same one?
This is the same one.
Yeah.
Oh, no, I closed it.
Sorry, Joe.
Let me go share again.
And get on the right window again.
There we go.
There we go.
There we go.
This, this is the one we want.
The mutagenic effects of ivermectin in germinal cells.
These are sperm cells, basically, and serum protein of the mouse.
Ivermectin is a broad spectrum anti-parasite agent.
It’s also a pesticide.
It is extremely toxic to fish and aquatic life.
Some animals showed a reduction in the fertility, the number of variable fetuses.
I don’t know if they mean variable or viable.
Sperm count following treatment with IVM.
So they’re saying there’s all sorts of mutations.
Oh, did I miss that one, Joe?
I thought that one looked like another one.
That’s the one I clicked off of.
These findings support the mutagenicity of IVM.
Accordingly, cautious use of IVM is advisable.
Is this safe as water?
Just to be clear.
Just want to make sure if it’s safe as water.
Oh, yeah, Joe, we did that one.
That was when we just went over.
Yeah.
Okay.
Now, here’s the fun one.
Does ivermectin cause sperm problems in humans?
Now, this one’s a little small.
Try to make it bigger.
Nope, that’s too big.
Okay.
This paper is actually quite hard to find.
Effects of ivermectin therapy on the sperm functions of Nigerian onchocerciasis patients.
I don’t know if you guys have seen, but on Twitter, people are calling BS on
river blindness that’s caused by a parasite.
People are calling BS on all these diseases.
But let’s just see what ivermectin did to these guys.
The above parameters were measured before and after the patients were treated with 150
micrograms per kilogram body weight of ivermectin for 11 months.
And the results were compared and also with normal control reference range.
We observed significant reduction in the sperm counts and sperm motility of the patients tested
on the morphology.
That’s the shape of them.
There was significant increase in the number of abnormal sperm cells.
This took the forms of two heads, double tails, white sperms as an albino.
And that’s obviously abnormal and extraordinarily large heads.
It is suspected that the above alterations in the already determined parameters of the
patient’s sperm cells could only have occurred as a result of their treatment with ivermectin.
However, we could not record any significant change or alteration in the sperm viscosity,
sperm volume and sperm liquefaction time of the patients.
Oh, no, we found these things were normal.
We therefore suggest that caution be seriously exercised in the treatment of male oncocerciasis
patients with ivermectin.
Sorry, male oncocerciasis patients with ivermectin to avoid the adverse effects it has
on the patient’s sperm functions.
Are you seeing the pattern?
Abomectin, ivermectin, like same patterns.
Now, let’s go on to this one, because this is really, really, really important with all
the other things we’re going to go over.
OK.
P-glycoprotein is the mechanism of cellular detox.
It’s how your cells get rid of toxins.
Pretty important, right?
Your cells get rid of toxins via P-glycoprotein.
OK, so you want to know what would be really bad to inhibit?
P-glycoprotein.
Kelsey figured out that over time, and this made sense to me when she said it, that things
that inhibit P-glycoprotein almost always inhibit ALDH as well.
And the more lipolysis, the more lipolysis, the more lipolysis, the more lipolysis, the
more lipophilic or fat-soluble those things are, the stronger they are.
OK, so what are we not a big fan of?
Fat-soluble toxins.
How do we get more fat-soluble toxins?
Well, if it’s looking like if something is more fat-soluble, it tends to inhibit ALDH,
so it’s inhibiting your detox more, and it also tends to inhibit PGP.
So then the toxins that you want out of the cells don’t come out as well.
So in the research, when they want to cause bigger problems with ivermectin, when they
want to cause problems with ivermectin, they give it with a P-glycoprotein inhibitor so
you cannot get it out of the cells as well.
So it builds up more, and you get more toxicity.
So this P-glycoprotein inhibition is going to be very, very, very important as we go
on.
Funny thing, they’ve got people taking ivermectin with PGP inhibitors on purpose.
Wait until you see the azoles.
Combining ivermectin with febendazole, fenbendazole, or mebendazole, which are P-glycoprotein
inhibitors, what do you think that’s going to do?
Well, we’ll see.
Well, they don’t have studies on that, but you’ll understand.
Here’s the paper, effect of ivermectin on male fertility and its interaction with P-glycoprotein
inhibitor verapamil in rats.
Verapamil is the classic P-glycoprotein inhibitor they use in these studies.
They consider it like the baseline P-glycoprotein inhibitor.
It’s like the standard.
Administration of permeability glycoprotein, PGP inhibitors, can modify the pharmacological
properties or induce toxic effects of PGP substrates.
What does PGP substrate mean?
It means something that is detoxed by PGP, okay?
Just like an aldehyde is a substrate of aldehyde dehydrogenase.
It’s what the aldehyde dehydrogenase processes.
So PGP substrates are things that PGP helps get out of the cell.
So it doesn’t make sense that if they inhibit it, you’ll get more toxicity effects of those
things because it’s not working, okay?
The effects of administration of ivermectin anti-halmythic drug, PGP substrate, so it’s
anti-parasite and it’s detoxed by PGP.
Either alone or simultaneously with verapamil, a PGP inhibitor on male fertility were studied
by determining mounting behavior, epididymal spermatozoal analysis, so that’s the sperm
in the epididymis, weight and histopathological examination of male reproductive organs and
cytogenetic evaluation of meiotic chromosomes.
The results revealed that administration of ivermectin once weekly for eight weeks induced
slight fertility disturbances.
While pre-treatment with verapamil disturbed male fertility through altering different
sperm parameters and histological structure, that’s the structure of the reproductive organs.
Cytogenetic study, the cell genetic study revealed partial effect of ivermectin on meiosis.
Meanwhile, the combined treatment of ivermectin and verapamil induced stronger effects on germ
cells, increased frequency of meiotic structural chromosomal aberrations that they’re screwed
up and increased XY chromosomal dissociation, raising the attention to the genetic quality
of mature sperm.
We concluded that ivermectin has slight effects on male fertility, but when taken with verapamil
induced adverse effects on meiosis and fertility.
Key thing to get here, ivermectin gets worse when you combine it with PGP inhibitors.
Azoles are PGP inhibitors.
Methylene blue is a PGP inhibitor.
MK7K2 is a PGP inhibitor.
Quercetin is a PGP inhibitor.
Actually, I don’t remember.
Did I find, I think I found that beta carotene is a PGP inhibitor.
So vitamin A is a PGP inhibitor.
I don’t know if copper is too.
I’ll have to look that up.
So all these things that alternative health and pharmaceutical are trying to get you to
take are PGP inhibitors.
And then they try to tell you to take ivermectin.
Now, what does PGP have to do with sperm?
Well, let’s do that.
Is there a possibility that P-glycoprotein reduces reproductive toxicity in males, but
breast cancer resistant protein does not.
P-glycoprotein reducing reproductive toxicity.
Gosh, what could be building up?
In traditional understanding, P-glycoprotein and breast cancer resistance protein are regarded
as efflux transporters.
That means things are leaving.
Influx would be coming in, efflux is leaving.
That can decrease the concentration of their substrates, the toxins in the testes, thereby
reducing reproductive toxicity in males.
RTM means reducing or reproductive toxicity in males.
So reproductive toxicity in males and protecting spermatogenesis, the creation of sperm.
Furthermore, this study provides the first direct verification of the role of P-glycoprotein
in reducing reproductive toxicity in males and protecting spermatogenesis.
So does that last study make sense now?
They’ve got ivermectin combined with a PGP inhibitor and they get more reproductive toxicity.
Are you following?
I don’t need this one anymore.
So now let’s go.
So that is ivermectin.
It is not safe as water.
It is a pesticide.
It’s an antiparasitic.
It’s a toxin and it’s going to eventually accumulate and ruin your sperm.
If you’re taking it because you have a little cold, just sack up.
Like it’s a cold.
You’re not going to die.
So now let’s get to…
So remember the PGP stuff and ivermectin, they always tell people that everybody’s like
ivermectin and fenbandazole, ivermectin and mebandazole.
Do all three of them together.
Oh, and then take your methylene blue because a guy who’s supposed to be all about health
took some on a plane supposedly where we never see him drink it.
Okay.
So let’s do this now.
Drug interactions of azole antifungals.
Here’s a tip.
The more things a drug interacts with, the more toxic it is and the more it’s slowing
detox.
So you put these things together that are either a toxin and they slow detox or they’re
both, both.
They’re both toxins and they both slow detox.
You put them together, you get bad things.
Okay.
Azole antifungal agents show a wide range of interactions with other drugs.
This article reviews the clinical relevant drug interactions of commonly used antifungals
fluconazole and itraconazole.
So the part I want you to pay attention to in all these is that azole at the end.
People will try to tell you they’re all different.
They’re, they’re similar enough as you’ll see.
Azole antifungals act as substrates as well as inhibitors of cytochrome P4P, cytochrome
P450 enzymes.
These are detox enzymes.
So they inhibit, so they’re, they go through and they inhibit detox enzymes.
Do you remember what I told you earlier?
The more toxic you get, the more toxic you get.
Detox enzymes.
Do you remember what I told you earlier?
The more toxic you get, the more your detox gets slowed.
They are also inhibitors of membrane transporters such as P glycoprotein.
So we now know that azoles not only slow cytochrome P450, but they also slow P glycoprotein.
That’s not good.
Later, I’ll show you that they inhibit aldehyde dehydrogenase too.
And that’s going to be bad.
I want you to understand the reason some of these drugs help people is because they slow
and shut down detox, which then slows your bile production.
So it’s all getting stuck in your liver.
It’s not coming out.
Stuff is getting stuck in your fat.
It’s getting stuck in your liver.
It’s not coming out.
The toxicity didn’t leave.
Nobody has a deficiency of azole meds or ivermectin or methylene blue.
So if you’re taking them, you’re getting a drug-like effect.
Drugs often.
And then people be like, but I took this and it helped this symptom.
Wait, let me, let me check on that.
You took a drug and it helped relieve your symptoms.
Hmm.
Is that the entire basis of the pharmaceutical industry?
Yes.
I don’t know why people like ditched their brains and all of a sudden they’re like,
well, I took a pharmaceutical and my symptom went away.
And I’m like, all right.
Okay.
So you’re taking a poison to slow detox.
And the symptom of that detox of the toxicity went away.
Okay.
So I just want you to see all these things that it inhibits.
Oh yes.
So fluconazole has a variable dose dependent ability to inhibit cytochrome 3A4,
cytochrome P450 3A4, especially with high daily doses,
cytochrome 2C9 and cytochrome 2C19.
This cytochrome 3A4 is the most important one of all.
It processes the most things of all your cytochrome P450 system.
Okay.
Oh, fluconazole distributes readily into various body fluids and tissues.
Hmm.
Azoles are fairly lipophilic.
They like fat.
Gosh, what’s your liver?
Liver fat.
Kidneys got fat on them.
Central nervous system is all coated in fat.
Itriconazole.
Itriconazole is a highly lipophilic drug.
How do, where do fat soluble toxins get stored in your fat?
Gosh, where do you think cows store their fat soluble toxins?
In their fat.
What are people like going bonkers about right now?
Beef tallow.
What is beef tallow?
Cow fat.
Where are the fat talks, fat soluble toxins stored again?
In the cow fat.
So drug interactions.
Well, they interact with statins.
They interact with benzos.
Those are anti-anxiety drugs.
Warfarin, calcineurin inhibitors, corticosteroids, phenytoin.
Like the most, the more interactions they have, the more it’s slowing down detox.
Table one shows the less commonly encountered drug interactions of azole.
So what do we have?
So we have all, oh, another is all, that’s a different one.
3A4, 3A4, PGP, 3A4, like all these things.
So you see, C3A4 is showing up all over.
3A4 processes caffeine, does other things like important things.
So there’s that.
So we’re building a case against all the azoles right now.
Oh, wait, what’s this?
Interaction of common azole antifungals with P-glycoprotein.
We kind of already went over those.
Both eukaryotic and prokaryotic cells are resistant to a large number of antibiotics
because of the activities of export transporters.
I want you to understand what they’re saying here.
Cells are fighting against drugs because they have detox systems.
Animal cells fight against or detox drugs by having detox systems.
The most studied transporter in the mammalian ATP binding cassette transporter super family,
that’s a lot of words, right?
P-glycoprotein ejects, detoxes many structurally unrelated amphiphilic.
That means amphiphilic means it’s both water-soluble and fat-soluble.
And lipophilic, which is fat-soluble or fat-loving as they say,
xenobiotics, things that are foreign to the body.
P-glycoprotein detoxes water-soluble and fat-soluble foreign compounds.
Observed clinical interactions in some in vitro studies suggest that
azole antifungals may interact with PGP.
We already went over that.
In a cell line presenting an overexpressed amount of the human PGP transporter,
itraconazole and ketoconazole inhibited PGP function with 50% inhibitory concentrations
of approximately two micromole and six micromole respectively.
Therefore, exposure of tissue to the azole antifungals may be modulated
by human PGP and the clinical interactions of azole antifungals
with other drugs may be due in part to inhibition of PGP transport.
Gosh, PGP inhibitor azole taken with ivermectin.
That’s how you create a disaster.
And first, before anybody says, but what about all these people with cancer?
Just stop believing them.
Why are these people who are having this happen to them?
Why are they not?
Why are the people themselves?
Why is it always, oh, a friend of a friend or a family member or whatever?
Why are these people who got cured not going on video, on the record,
showing their labs, showing their imaging, bragging the heck out of it?
Why are they not coming to help other people?
Why is it always talking heads on the internet,
showing emails that are redacted of the names and the emails
of supposed people who got fixed by this?
Why are the actual people not doing interviews, not showing their imaging?
Call BS on all of this stuff these days, folks.
Like, call BS on it.
Proof or GTFO.
That’s what you tell these people.
Show labs, imaging, and the person, because now they’re cancer-free, right?
Wouldn’t they want to be bragging?
And then if they don’t give it, just say you don’t believe it.
Like, call BS on it.
It took me a while to realize that.
Like, I didn’t, this psyop is very, very deep.
And if you look into the background of the main doctor saying he has all these
patients supposedly getting better,
you need to look into his background, because it’s not good.
He does not have a good background.
He probably got offered something to do all of this BSing on the internet.
So,
P-glycoprotein plus ivermectin is bad.
Adverse effects associated with long-term administration of azole antifungal agents.
Well, wait, with this new chemo of ivermectin and azoles,
just call it N-E-U, you know, like new chemo.
That’s what it is.
Chemotherapy is using drugs to treat cancer.
They’re talking about putting people on it and, like, leaving them on it.
So long, that would be the definition of long term.
Oh, and also, find me a person who says that these meds worked on them
and they show proof and they’ve had it gone for a year.
These people should exist and they should be happy
as a clam to tell all of us and show all of us.
Where are they?
We are starting to get reports of it not working from actual doctors.
Long-term use of azoles is associated with liver toxicity,
hepatotoxicity and hormone related effects.
Shocking, including gynecomastia, that’s male breast development,
or as they call it, bitch tits, gyno.
Alopecia, hair loss, decreased libido, oligospermia,
azospermia, impotence, hypokalemia, low potassium.
Gosh, we never talked about that.
Hyponatremia, low sodium and rarely in adrenal insufficiency.
Voriconazole, another one, and posaconazole, another one,
have been associated with peripheral neuropathies.
That’s like diabetic neuropathy, you know, out in the hands and feet.
Or B6 neuropathy out in the hands and feet.
And itriconazole and voriconazole with pancreatitis,
which is the precursor to getting pancreatic cancer later.
In addition, voriconazole has been associated with periostitis.
That’s an inflammation of the bone.
Phototoxic reactions.
Gosh, we never talk about phototoxic reactions
where people become more sensitive to light
because they accumulate certain toxins in their skin.
That store, they’re like, oh, I don’t know, vitamin A,
because it slows down ALDH.
And squamous cell carcinoma.
Gosh, azoles are totally safe.
They’re totally safe, definitely.
You could just go on it forever.
Okay, the connection of azole fungicides.
So you’re taking a fungicide and a pesticide and an antiparasitic.
That’s going to end well.
With xenosensing, as in foreign sensing,
nuclear receptors, drug metabolism, and liver toxicity.
Okay, let me find the next thing that we’re going to look at.
How did I make it go away last time?
Oh, there we go.
Okay, azole fungicides, especially triazole compounds,
are widely used in agriculture and as pharmaceuticals.
So they’re in the animals.
Oh, they’d be in the tallow.
For a considerable number of agricultural azole fungicides,
the liver has been identified as the main target organ of toxicity.
Shocking.
Wait, what’s this?
Molecular aspects of azoles-induced teratogenesis birth defects.
Azoles are teratogenic birth defect causing in animal models
and are under investigation for potential human developmental toxic effects.
Infertility PSYOP, anyone?
Increasing evidence is linking disruption of embryonic retinoic acid homeostasis
as a crucial determinant of azole-mediated teratogenesis.
Wait, what did they just say?
Azoles are creating vitamin A-related birth defects.
Inhibiting ALDH, the main detox enzyme of vitamin A,
inhibiting that is what they want to do to make men sterile, the male contraceptive.
What am I telling you azoles do?
They slow ALDH.
They build up aldehydes.
Aldehydes cause birth defects.
Aldehydes ruin sperm.
Many of the birth defect things that you think are out there are caused
by things that slow ALDH, so you build up aldehydes.
It’s not about a lack of retinoic acid.
See, remember, when they say homeostasis, they’re hiding toxicity from you.
Disruption of embryonic retinoic acid homeostasis.
How about if we just said increasing evidence is linking vitamin A toxicity
as a crucial determinant of azole-mediated teratogenesis?
Actually, Stephanie Seneff wrote a paper about how the pesticides they were using
in South America were slowing down vitamin A detox in multiple ways,
and the same birth defects that they were seeing in South America
are the exact same as vitamin A birth defects, vitamin A toxicity birth defects.
Do you see the pattern?
Pesticides slow ALDH.
I have that research too.
Ivermectin slows ALDH.
Ivermectin slows ALDH.
Azoles slow ALDH.
Okay.
Oh, I think I already did this one.
Yeah, this is the same one.
Yeah, sorry.
Let me let me close that one.
We’ll go here.
Okay.
I won’t close it and kick us out, Joe.
Oh, so do azoles mess up hormones too, especially testosterone?
Things of this nature.
Azole fungicides affect mammalian steroidogenesis,
the creation of steroids, steroid hormones by inhibiting sterol,
14-alpha-D-methylase, and aromatase.
Some of you are going to think aromatase inhibition is a wonderful thing,
but when you do, when you see all these other things,
you’re going to go, well, no, that’s not going to be a good thing in combination.
At high doses, azole fungicides and other azole compounds.
Know how they say they group them all together.
They don’t separate them.
Azole fungicides and other azole compounds.
So they’re saying basically all of them.
They affect reproductive organs, fertility, and development in several species.
These effects may be explained by inhibition of sterol,
14-alpha-D-methylase, and or aromatase.
In fact, several azole compounds were shown to inhibit these enzymes in vitro.
So that’s in a Petri dish ish.
And there is also strong evidence for inhibiting activity in vivo,
in whole animals and humans.
Furthermore, the specificity of the enzyme inhibition of several of these compounds is poor.
So they’re not very specific.
They’re like shotguns.
They hit big areas, which is not good.
Both with respect to fungal versus non-fungal sterol,
sterol, 14-alpha-D-methylases and versus other P450 enzymes, including aromatase.
So it’s inhibiting other things.
I think that’s it on this one.
Yeah.
Let me make this one a little bigger.
So remember, we just saw that it inhibited hormone production.
Is that too big?
No.
So let’s keep going.
Azole fungicides inhibit human and rat gonadal.
Guys.
3-beta-hydroxysteroid dehydrogenases.
Structure activity relationship and in silico docking analysis.
This is the important part.
Azole fungicides inhibit gonadal human 3-beta-hydroxysteroid dehydrogenase 2
and rat 3-beta-hydroxysteroid dehydrogenase 1.
Diphenoconazole, another one,
is the most potent among 16 azole fungicides to inhibit this.
Azole fungicides inhibit progesterone production by human KGN cells.
If they’re saying it’s a cell study, though,
this very well may do the opposite in the whole system,
in the whole animal, the whole human.
So it may increase it in a not good way.
Guys, you don’t want to have high progesterone.
So again, like I said, they inhibit that enzyme.
What does that mean?
The inhibitory strength of azole fungicides was determined by their lipophilicity.
So the more fat-soluble they were, they are,
the more they inhibit these enzymes.
Wasn’t what that was what Kelsey was saying.
She’s a smart girl.
Overall, these findings suggest the use of azole fungicides have unintended consequences
on reproductive health due to their inhibition of gonadal 3-beta-hydroxysteroid dehydrogenases.
Yes, I’m not going to go into the details of that.
3-beta-hydroxysteroid dehydrogenases.
Yeah, you guys, no more super chats at this point.
I don’t know how long I have left on methylene blue.
I have a whole nother browser full of tabs.
So when we’re talking about 3-beta-hydroxysteroid dehydrogenases,
so again, I just wanted this paper to show both the lipophilicity,
the more fat-soluble they are, that means the more they store.
Wow, that would be weird that they would get stronger the more they store, huh?
I wanted you to pay attention to this enzyme.
Now we’re going to go into what that means.
Now, some of you are going to freak out because,
oh my gosh, I went to Wikipedia.
I was trying to get you a simple summary, okay?
This is not like politics or anything.
This is just a simple summary.
So if you freak out about, oh my gosh, you went to Wikipedia,
just go somewhere else then.
Like, grow up, really.
So this, oops, why did I do that?
This, 3-beta-hydroxysteroid dehydrogenase is therefore essential,
essential for the biosynthesis, the creation of all classes of hormonal steroids,
namely progesterone, glucocorticoids, mineralocorticoids,
androgens, that’s your male hormones,
and estrogens, that’s your more female hormones.
The 3-beta-hydroxysteroid dehydrogenase complex is responsible for the conversion of
pregnenolone to progesterone,
17-alpha-hydroxypregnenolone to 17-alpha-hydroxyprogesterone,
DHEA to androstenedione,
androstenediol to testosterone,
androstenediol to androstedienone.
Wow, that’s pretty important, right?
Gosh, azoles inhibit all that.
Hmm, that’s not good.
Gosh, what would they do to men, especially, by having them take these?
So let’s see the real-world evidence.
Azole fungicides and their endocrine hormone-disrupting properties,
perspectives on sex-hormone-dependent reproductive development.
Well, all reproductive development is sex-hormone dependent,
but anyway.
Azoles typically target the cytochrome 5-1 enzyme in fungi,
and by so doing, disrupt cell membrane integrity.
You think it only happens to funguses when they disrupt cell membrane integrity?
Do you think it…
Wait, weren’t they just saying this wasn’t specific?
It’s a non-specific effect?
However, azoles can also target various cytochrome enzymes in mammals’ detox pathways,
including humans, which can disrupt hormone synthesis and signaling.
Signaling is another word for toxicity.
They hide it with the word signaling and homeostasis.
So you’re seeing that again.
For instance, several azoles can inhibit enzymes of the steroidogenic pathway,
we just went over that,
and disrupt steroid hormone biosynthesis.
This is of particular concern during pregnancy.
Didn’t we already go over birth defects?
Sex hormones are integral to reproductive development.
In other words, exposure to azole fungicides during fetal life
can potentially lead to reproductive disease in the offspring.
Okay, you hand down your toxicities to your children, folks.
Exposure to azole fungicides during fetal life.
So if you have this stuff stored in your fat while you’re pregnant,
and remember that what the ivermectin thing or the abimectin thing was handed down,
and it even affected the women’s pregnancy.
So the dads being poisoned by abimectin caused failed pregnancies.
Do you remember that?
Exposure to azole fungicides during fetal life,
so when the pregnancy is happening,
can potentially lead to reproductive disease in the offspring later.
The children inherit the toxicity of their parents.
The more toxic they are, the slower they detox.
The slower you detox, the more health problems you have.
In addition, some azoles can act as androgen receptor antagonists,
so they’re blocking male hormones,
which can further aid to the disrupting potential following exposure.
Gosh, would be kind of weird if they were attacking men like this.
Like this.
When used as pharmaceutical,
systemic concentrations of the azole compounds can become significant
as combating fungal infections can be very challenging
and require prolonged exposure to high doses.
What do you think they’re doing in cancer treatment?
You think they’re doing low doses for a short time?
Probably not.
It worked before, and now it’s not working.
Anyway, whatever.
Okay.
Does it cause damage to the testes?
The azole drugs.
Transcriptome analysis of fetal rat testes following intrauterine exposure,
so during pregnancy.
So they’re going to look at the baby’s testes
following the mother being exposed during pregnancy to the azole fungicides
triticonazole and flucilazole.
Two more.
Reveal subtle changes despite adverse endocrine effects.
So they did have big hormonal effects,
and they’re saying, oh, we only saw little changes.
Triticonazole displayed strong androgen receptor antagonism in vitro,
whereas in utero exposure, it resulted in anti-androgenic effects in vivo,
so in the whole animal.
So they saw it in petri dish and in the whole animal,
evidenced by shorter anogenital distance in fetal male rats.
So this is less androgen, less male hormone activity when it’s shorter.
Flucilazole displayed strong androgen receptor antagonism,
but less potent than triticonazole and disrupted steroidogenesis in vitro,
that’s in the petri dish,
whereas in utero exposure disrupted fetal male plasma hormone levels.
So that’s in the whole animal, in utero.
This suggests that the observed influence of flucilazole on hormone production
may be by directly targeting steroidogenic enzyme activity in the testes at the protein level,
whereas observations of shorter anogenital distance,
so less masculinizing effects by triticonazole,
may primarily be due to disturbed androgen signaling,
disturbed androgen signaling in androgen sensitive tissues.
You see how I just keep finding, there’s all these people will be like,
but you’re not looking right at fenbendazole and mebendazole.
Do you see the patterns?
Like, do you see the patterns?
How many different ones do I have to go over?
Human relevant concentrations.
Human relevant concentrations of the antifungal drug clotrimazole
disrupt maternal, motherly, and fetal baby steroid hormone profiles in rats.
Human relevant concentrations.
Recent studies have raised potential concern
about the unsupervised use of clotrimazole during pregnancy,
especially since it is a potent,
potent inhibitor of cytochrome enzymes of the steroidogenesis pathway.
Uh, let’s be clear here.
Clotrimazole is a non-prescription and broad-spectrum antifungal drug
sold under brand names such as canistin and lotrimine.
Sure, many of you here in America are familiar with lotrimine
for athlete’s foot mainly.
Okay.
It’s over the counter.
What are, what are they trying to do with ivermectin right now?
Trying to make it,
Gosh, do you think maybe they should have thought twice about clotrimazole
being over the counter before finding out now?
Or is it all part of the plan?
However, steroid hormone profiles were sick.
And this is, this is an over the counter one.
Imagine how strong the prescription one is.
Imagine how strong the prescription ones are.
However, steroid hormone profiles were significantly affected in both the mother
and the fetus plasma in particular pronounced suppression of estrogens was seen.
Gosh, does anybody complain about hormonal problems these days in fetal testes?
So in the testicles of the babies marked up concentration of hydroxyprogesterone was observed,
which indicate a specific action on steroidogenesis.
So for all you Peters and your progesterone obsessed people, this is not good.
This is really not good.
We’ll do progesterone as part of the infertility psyop too.
Don’t want that.
They’re saying it’s a bad thing because of toxicity.
It’s capacity to significantly alter steroid hormone concentrations.
However, suggests that clotrimazole should be used with caution during pregnancy.
Now let’s do the one that I took as a teenager.
Ketoconazole.
Pretty, you know, doctors will give this out like candy.
Ketoconazole blocks testosterone synthesis.
Wait, another azole messing up hormones.
So they’re saying it inhibits testosterone synthesis,
but then what happened here, the development of gynecomastia,
so male development of breasts in two patients
prompted us to investigate the effect of the drug on testosterone production.
After a 200, 400, or 600 milligram dose,
volunteer male testosterone serum concentrations fell markedly,
but returned toward baseline eight to 24 hours later
as ketoconazole serum concentrations wanes, they went down.
A marked but transient, a marked, that’s significant,
but transient drop in testosterone levels occurred in patients receiving long-term therapy.
And continuous testosterone depression was noted in one.
A block of synthesis was demonstrated in vitro.
So they’re saying it was blocking the making of testosterone.
Ketoconazole at concentrations achievable in serum with currently used doses
blocked basal and gonadotropin stimulated testosterone production.
So that’s LH stimulated.
It blocked it by rat Leydig cells.
The diminution or the decreasing of testosterone synthesis
could be significant as further therapeutic trials
may use larger doses or more than once daily administration.
Wait until we get to the next one.
You know how I say that these azoles are part of the infertility psyop?
So here’s the paper.
Ketoconazole in initial management and treatment of metastatic prostate cancer to the spine.
The first line is all we care about.
Ketoconazole in high doses causes castrate levels of testosterone
within 24 to 48 hours.
It’s a chemical castration agent.
Infertility psyop anybody?
Now they’re going to have people take two azoles together.
Phenbendazole and mebendazole with ivermectin.
Not going to make it.
Let’s just hit another azole while we’re here.
People will say, oh, well, that’s just the fungicide ones.
FDA medications that impair human spermatogenesis.
Many labels had information relevant to sperm ejection,
such as ejaculation disorders, delayed ejaculation, retrograde ejaculation.
That’s where your semen is going backwards.
Erectile dysfunction, prospermia, et cetera, which were not included in this study.
They’re looking at drugs that affect sperm,
but they’re saying if it’s just the sperm going,
if it’s not coming out right, we’re not going to count it.
We excluded these findings because they’re not directly
related to sperm production or maturation.
What is this?
Omeprazole.
Another azole.
But people will say, well, that’s for your stomach.
Do you see the pattern here?
Here are in this category of causing sperm ejection problems.
Oh, wait, fenbendazole.
We do have one study on it.
Effect of fenbendazole on turkey semen quality.
However, when we use fenbendazole to treat nematodes in mature breeder toms,
so the male turkeys,
we observed a decrease in semen quality in a subsequent precipitous.
Significant, like very strong decline in fertility to less than 20%
within six weeks of administration.
Precipitous decline in fertility.
That’s like falling off a cliff is what they’re saying.
This drug significantly reduced sperm mobility.
That’s like the one of the most important things that sperm have
is the ability to move.
They kind of have to, right?
That’s really, really important.
OK, so we do have research on fenbendazole.
Oh, wait, do we have research on mebendazole?
Mebendazole induced blood testes barrier,
injury in mice testes by disrupting microtubules,
in addition to triggering programmed cell death.
We’re not talking about cancer cells here.
We’re talking about normal cells.
Triggering normal cells to die.
You have a blood testes barrier
to protect your testes from bad things getting in it.
Mebendazole induced an injury to it.
In this study, male mice were injected
with 40 milligrams per kilogram per day of mebendazole.
The treatment was for three and seven days.
Our results show that the injected mice
exhibited an abnormal spermatogenic phase
with a significant decrease in sperm.
Here we present our data indicating
that mebendazole impairs blood testes barrier
by reducing the expression of the microtubules
and blood testes barrier junction associated proteins.
So it’s causing leaky nuts.
We went over this last week.
This last problem, the leakiness,
leads to activating the caspase-3 pathway,
which triggers extensive sperm cell, basically.
Or these, yeah, it might be the,
when they say germ cell,
there may be meaning the cells that make the sperm.
I’m not sure, I can double check.
But extensive germ cell apoptosis.
So they’re dying.
This is, they’re not talking about cancer cells.
They’re talking about regular cells.
Basically self-destructing.
And then what do they start with here?
It’s a well-tolerated and commonly used.
Commonly used doesn’t mean anything
for the pharmaceutical industry, folks.
That’s not well-tolerated.
They’ll tell you it’s well-tolerated.
It’s just gonna destroy your balls, guys.
And let’s do this one,
just because it was a fun one
that I found that Kelsey had shared with me.
Vitamin B combination reduces fluconazole toxicity
in Wistar rats.
We don’t use too many B vitamins,
but you’ll notice a very important one here.
The major adverse effect
associated with systemic administration
of fluconazole is hepatic toxicity.
Hmm, liver toxicity from an azole.
Fluconazole is the most commonly used antifungal drug
in treatment of invasive fungal infections.
So what did they find?
Combination of B1, B2, and B3.
What does B1 do?
I’ve told you guys this before.
It binds to aldehyde.
Why would there be an excessive amount of aldehydes around?
Oh, because azoles slow ALDH.
So they would make, they would block,
they would bottleneck,
and you’d make more aldehydes
because ALDH is bottlenecked.
So B1 binds to aldehydes
and makes them less toxic while they’re in the system.
Doesn’t mean you get rid of them any faster.
That’s why people have to take these,
the people who do well with B1
have to take megadoses every day
is because the B1 is just binding
and making it less toxic.
And when those all fall apart,
you got to take more.
B2 and B3.
So they’re talking about,
they’re talking about nicotinic acid,
I believe here.
In fluconazole-induced toxicity,
we’re able to restore the level of alkaline phosphatase.
So that’s one of your liver enzymes,
near to normal,
but with a high level of alkaline phosphatase
in the B1 control group.
So B1, I’m guessing by itself,
didn’t quite work.
Aspartate aminotransferase,
this is AST,
one of the main liver enzymes,
was restored to normal in fluconazole plus B1,
fluconazole plus B2,
and fluconazole plus B1 plus B2 plus B3 groups,
and vice versa in fluconazole plus B3 group animals.
I’m not quite sure how to interpret
what they mean by vice versa.
Further, the level of alanine phosphatase
Further, the level of alanine aminotransferase, ALT,
was restored to normal in fluconazole plus niacin animals.
Pay attention to these words.
It proves the combination of these vitamins
proves the chemo preventative potential
of these micronutrients.
When they say chemo,
they’re talking chemicals, okay?
In fluconazole toxicity,
vitamin B combination reduces fluconazole toxicity.
What do we use nicotinic acid for?
Flesh niacin, what do we use it for?
It is the gasoline for making NAD,
which is necessary for what enzyme?
Aldehyde dehydrogenase.
You need nicotinic acid,
flesh niacin to run,
to make NAD,
which is necessary to run ALDH.
And then B1 binds to aldehydes.
Are you catching the pattern here?
If these vitamins help to fix the problem,
it’s an aldehyde related problem.
Okay.
So that’s the azoles.
I actually, I truly believe
that a lot of my health problems
started as a teenager when I took ketoconazole.
I do believe it damaged my testosterone.
Absolutely.
Apparently I fixed it,
but that’s what we do, right?
We fix the things that nobody else fixes.
So let’s go to methylene blue.
All right.
So I’m going to try to go through this one pretty quick.
You know me and quick, right?
Methylene blue interactions.
So remember how we talked about
the more a drug slows detox,
the more toxic something is,
and the more it slows detox,
the more drug interactions you’ll see.
Well, here, methylene blue interactions from drugs.com.
197 drugs known to interact with methylene blue.
129 of them are major.
66 are moderate and only two are minor.
This is a toxic drug that slows detox.
When we get through it,
I think I’ve been over this before,
but methylene blue slows detox
more than anything else I’ve ever seen.
We already saw the pattern with the azoles.
We saw, we saw a cytochrome P450 inhibition.
We saw aldehyde dehydrogenase inhibition,
and we saw P-glycoprotein inhibition.
Gosh, methylene blue does all that too.
Weird that they’re pushing all these together.
I actually saw somebody,
somebody was saying the other day,
it was a rumble video.
I swear they said,
take your ivermectin with your methylene blue,
like take them together.
They know not what they do
or they know what they’re doing
and they’re trying to hurt people.
Okay, next paper,
methylene blue loaded solid lipid nanoparticles.
Wait, why would they load fat with methylene blue?
Oh, it’s a fat soluble toxin.
I get it.
Okay.
Preparation optimization
and in vivo burn healing assessment.
Where was, what was the thing I wanted on this one?
Oh, with the positive charge
on methylene blue molecules
and lipophilicity loving fat
caused them to accumulate in the mitochondria.
Accumulation.
That’s all I wanted to show you here.
Methylene blue accumulates in you.
You take it every day.
It’s going to slowly accumulate.
You’re going to get problems later.
It doesn’t matter the dose so much per day.
If you’re taking in more than you get rid of,
it’s accumulating in yourselves.
Oh, I didn’t show my,
anyway, this, this post is from my methylene blue,
my epic methylene blue thread,
which I think is almost at 700,000 views now,
but I wanted to go over first
how methylene blue affects men’s erectile function, right?
That’s kind of important to sex.
So you can procreate.
Okay.
So let’s go into how does it affect erections in men?
Well, how does, how does,
I’m sorry, let me go over this one.
I think it’s, I wanted,
yeah, this one, this is what I meant to go over.
Methylene blue is an MAOI,
which is a type of antidepressant,
which means it slows down the breakdown
of your neurotransmitters.
That’s what it does.
So this is just this post.
Now let’s go into what the actual links are.
Antidepressants, which cause the fewest sexual side effects?
So you mean they all cause side of sexual side effects,
but they, some of them are fewer.
Okay.
Sexual side effects are common with antidepressants.
So your concern is understandable.
Effects on sexual function can include
a change in your desire.
So low libido,
trouble with lubrication or erection,
problems with sexual comfort and satisfaction,
not being able to reach an orgasm.
Antidepressants most likely to cause sexual side effects,
and oh, include, sorry, I didn’t share.
Oh, MAOI drugs.
Methylene blue is an MAOI.
It’s a drug.
It’s an MAOI.
It’s also an antipsychotic.
And it’s also a stimulant.
So people are like, I feel so good on it.
I’m like, yeah, you’re taking an antidepressant,
antipsychotic stimulant.
Neato. Cool.
You took a drug and you felt good.
Like crackheads love crack.
That doesn’t mean it’s good for them.
Okay.
Now let’s do this one.
So the title of this one,
selective serotonin reuptake inhibitor
induced sexual dysfunction,
clinical and research considerations.
Well, let’s go down here.
Antidepressants, including the tricyclic antidepressants,
monoamine oxidase inhibitors,
methylene blue,
and selective serotonin reuptake inhibitors
cause sexual dysfunctions such as
decreased sexual desire,
erectile difficulties,
and delayed ejaculation.
Such sexual side effects affect quality of life
and may result in noncompliance with medication,
the associated risk of recurrence of depression.
Depression may also be associated
with sexual disturbances,
especially reduced libido.
Oh, let’s see.
So let me zoom in on this one.
This is where was this from?
Let me see.
MAO inhibitors.
I forget where I got this paper.
Sexual side effects induced by MAOs
include anorgasmia,
inability to achieve orgasm.
So we’re not even like difficulty in orgasm.
We’re like, you can’t even do it,
and erectile dysfunction.
This is MAOIs.
Methylene blue is an MAOI.
Now let’s go into this one.
Methylene blue, what does it do?
It’s a good indicator of sexual dysfunction.
It’s a good indicator of sexual dysfunction.
It’s a good indicator of sexual dysfunction.
Methylene blue,
what does it do to your erections, guys?
So it’s an MAOI.
So we saw those sexual side effects.
Let’s go into the papers here.
I’m just going to hit the titles of these.
Methylene blue,
an effective therapeutic alternative for priapism.
So that’s when guys like take drugs
and they get an erection that doesn’t go away.
They inject methylene blue into it
to make it go away.
That’s how anti-erection methylene blue is.
You really want to go accumulating this
in your penile tissue over time.
So we’re going to hit this
because there’s multiple papers.
I don’t have anything to read on this one.
So they inject it into the penis directly.
Methylene blue,
an effective therapeutic alternative for priapism
induced by intracavernous injection of vasoactivators.
So they took,
they injected meds into their penis
to get an erection
because everything was pretty broken by then.
And then it gave them a permaboner
and then they injected methylene blue.
Methylene blue is a means of treatment for priapism
caused by intracavernous injection
to combat erectile dysfunction.
So they’re combating a medication side effect
with another medication.
And finally, another one,
use of methylene blue
and selective embolization of the pudendal artery
for high flow priapism refractory
or not responding to medical and surgical treatment.
So methylene blue is the Hail Mary at the end.
If it’s so safe,
why wouldn’t they use it first?
Okay, so now let’s go to this.
What does methylene blue in term,
do in terms of actually affecting
the mechanisms of the erection pathway?
We already went over
how it accumulates in your cell cells, okay?
So first I’m going to go over,
oh, sorry, I didn’t switch.
There it is, Joe.
First, I’m going to go over.
So MAOIs, remember MAOIs
stop the breakdown of catecholamines,
which includes adrenaline
and noradrenaline.
Those are stimulating, right?
Those are fight or flight kind of things, right?
So let me just hit on this paper real quick.
So we’re going into the erection mechanisms
that methylene blue affects.
So from the paper,
physiology of penile erection
and pathophysiology of erectile dysfunction.
Let’s go find these.
Basically, this is a long way of exp…
Oh, come on now.
I just want that to go away.
Sometimes it goes away and sometimes it doesn’t.
Okay, let me refresh this
so I can move it out of the way.
Man, GLASP has so many bugs.
Basically, okay, for a man to get an erection
is the parasympathetic nervous system.
That’s the rest and digest.
So you have to be relaxed.
This is why a lot of guys have ED
because they’re so tense and anxious inside.
They may not realize it, but that’s what happens.
So they can’t, they have ED, okay?
So parasympathetic, you have to relax
to get an erection.
And then sympathetic is the actual ejaculation, okay?
So what they’re saying here,
stimulation of the pelvic plexus
and the cavernous nerves induces erection,
whereas stimulation of the sympathetic trunk
causes detumescence.
So stimulating the sympathetic part of the nervous system
causes you to lose the erection.
This clearly implies that the sacral parasympathetic input
is responsible for tumescence,
that would be getting an erection,
and the thoracolumbar sympathetic pathway
is responsible for detumescence.
So too much adrenaline
is gonna be sympathetic nervous system
and it’s going to affect your erectile function.
Do you understand why they can inject this
into penises and make them go down?
Okay.
That’s that one.
Let’s go into this one.
So those of you who are familiar
with erection science,
nitric oxide is very important.
It is very important in it.
What does methylene blue do to nitric oxide?
Inhibition of nitric oxide synthesis by methylene blue.
Fairly straightforward.
Methylene blue appears to inhibit
nitric oxide-stimulated soluble guanylyl cyclase,
pay attention to this,
and has been widely used for inhibition
of CGMP-mediated processes.
Pay attention to this.
It inhibits this.
It inhibits this.
Our data suggests that methylene blue
acts as a direct inhibitor of nitric oxide synthase.
And it’s a much less specific and potent inhibitor.
So it still works.
It’s still an inhibitor of guanylyl cyclase.
Okay.
So we have two mechanisms.
One, inhibiting the breakdown of adrenaline
and noradrenaline would be the opposite
of what you need to get an erection.
Then we have that nitric oxide synthase inhibition.
Here we have modulation of soluble guanylyl cyclase
for the treatment of erectile dysfunction.
Now, what are they doing with this?
They were working on a new class
of erectile dysfunction drugs.
Sorry.
Here’s the title.
Sorry, Joe.
I’m trying to go fast
and that means I forget to change the screen.
So pharma was trying to create new drugs.
They’re trying to, let me see,
there was activators and let me see.
Come on, I can type.
Well, they were trying to stimulate.
There was stimulators and activators, I think.
I didn’t highlight this part.
Sorry.
What they’re trying to do
is they’re trying to make a whole new class of drugs
based on guanylyl cyclase.
So they were either going to stimulate it or activate it.
What does methylene blue do?
We already went over that.
It inhibits guanylyl cyclase.
So that’s another place it inhibits it.
And finally, we have androgenic male hormones
maintenance of the rat erectile response
via a non-nitric oxide dependent pathway.
So something outside of the nitric oxide synthase.
They talk about here methylene blue
and inhibitor of guanylyl cyclase.
Methylene blue inhibited the erectile response
in all treatment groups,
showing that cyclic GMP is critical
to the NO independent pathway,
as well as the NO dependent pathway.
So it inhibits both pathways.
Why would this be coming around
as part of the infertility psyop?
Oh, I don’t know.
Then we get into.
Does well, let’s get into this.
This is part of that thread.
So let’s go to these studies.
So long lasting effect on testes
following methylene blue injection
in laparoscopic lymphatic
sparing varicocelectomy.
So they’re injecting.
Methylene blue into the testes
to do their imaging
because methylene blue is an imaging dye.
Imaging dyes are all toxic.
Methylene blue is an imaging dye.
Imaging dyes are all toxic.
Injection of methylene blue to the testes
has been shown to have an adverse effect
in animal studies,
but is still being used frequently
as lymphatic mapping agent
during lymphatic sparing varicocelectomy
in adolescent varicocele.
So they’re still using it in teenagers.
Who do you not want to damage
sperm and testes in?
Oh, I don’t know.
Teenagers.
Why would they be using it frequently
if they know that it causes problems?
So they had 27 patients
who had methylene blue injected.
In group B, six patients
developed testicular changes
detectable by ultrasound.
The changes in their testes
were big enough
they could see it on ultrasound.
However, it has been shown
in other animal studies
that intraparenchymal injection
of methylene blue to rat testes
results in degenerative changes.
Our study is the first one
to describe postoperative
changes of human testes
on imaging after lymphatic
sparing varicocelectomy
with subdartoic
injection of methylene blue.
Six patients demonstrated
new onset testicular changes
on postoperative ultrasound,
although no statistically
significant testicular volume
reduction was seen in the group
with change on imaging.
These observations may serve
as a stand in surrogate marker
for testicular injury
or reduced testicular function.
They’re saying the changes that we saw
mean something most likely.
Not looking good for the testes.
Oh, let’s go.
So, well, gosh, if it affects
erections and testes,
it’s probably gonna affect sperm, right?
Adverse effects of methylene blue
on human sperm motility,
components of human reproductive
tract fluids and mouse embryo cleavage.
This is pertinent to you, ladies.
Because methylene blue exhibits germicidal,
it’s a biocide.
You can look up methylene blue biocide.
That means it kills life.
That’s why they use it as port-a-potty dye.
Oxidation and reduction properties.
The authors ask, so they’re saying,
they’re saying because methylene blue
does this and these,
the authors asked whether this agent
causes adverse effects on gametes.
And the answer is no.
Adverse effects on gametes.
They’re talking about sperm here.
Embryos and or secretions
of the reproductive tract.
Time and dose-dependent inhibition
of human sperm motility,
how well they move,
by methylene blue was observed,
as was growth inhibition
of two-cell mouse embryos.
That means the pregnancy
is not working right.
Furthermore, the presence of
methylene blue in uterine,
fallopian tube and peritoneal fluids
altered protein mobility
in polyacrylamide gels
and yielded apparent values
of follicle-stimulating hormone
and estradiol up to 260% of actual value.
So it messed up their hormone tests.
I think that’s it.
Yeah, OK.
Oh, no, no, wait, wait, wait, wait.
There’s the one part
down here at the bottom.
Hold on.
Is this the one?
Ah, yes.
Since we’re talking about
the infertility psyop,
how good is methylene blue at its job?
It does inhibit ALDH.
We’ll go over that.
But let me zoom in on this one.
I hope y’all can see this.
This is from that same paper.
This is from the full PDF.
Finally, these data suggest
that the utility of methylene blue
and compounds of this genera
be explored further
with respect to their spermicidal
and possibly viricidal potential
and use as a contraceptive agent.
Methylene blue is so good at his job
that these researchers said
we should look into this
as a male contraceptive agent.
Well, actually, they don’t say male or female.
Maybe for both.
This is the infertility psyop, folks.
They’re telling you.
They’re telling you what they’re doing.
I mean, maybe you need me to tell you.
But I’m here to do that.
So remember, what was the mechanism
of male contraceptive pills?
It was inhibition of aldehyde dehydrogenase, right?
I don’t think we need to look
at much of this paper, do we?
Inhibition of aldehyde dehydrogenase
is by methylene blue.
Hmm, pretty simple.
Gosh, I wonder how they could use it
as a male contraceptive then.
Methylene blue inhibited
the human erythrocyte red blood cell
and white red blood cells
and white blood cells, ALDHs,
and the rat liver mitochondrial
locam ALDH
inhibited in red blood cells,
white blood cells, and the liver
in a concentration dependent manner.
The inactivation was reversible by dilution.
So they had to dilute it
to get the effect to go down.
And kinetic analysis indicated
that methylene blue inhibits
the rat liver mitochondrial locam
and human erythrocyte ALDHs
competitively with respect
to dopal, dopaldehyde.
Always remember when you see al
at the end, it’s an aldehyde.
So, this is just another one
showing that it inhibits ALDH,
ethanol metabolism
and isolated liver cells.
Effects of methylene blue, cyanamide,
and penicillamine on the redox
state of the bound coenzyme
and on the substrate exchange
and alcohol dehydrogenase.
The results indicate
that methylene blue inhibits
aldehyde dehydrogenase.
Pretty straightforward.
Now, could methylene blue
that these ladies are taking
affect their children afterwards?
We kind of already showed
that all these things
affect children afterwards.
Ladies and gentlemen,
your toxicity is affecting
your reproduction ability
and it is affecting the quality
of the children that you make.
This is not a game.
You are seeing now
what they are doing to us.
They are propagandizing
toxic things that negatively
affect fertility,
trying to get people
to take them for health.
Let’s go into this.
Perinatal, so during
the pregnancy time,
perinatal MAO inhibition,
what does methylene blue do again?
Produces long lasting impairment
of serotonin function
in the offspring.
The things you have
that are toxic in you
during pregnancy,
both guys before
you get the lady pregnant,
it affects you too.
Remember that paper I went over
in previous work,
we showed that pharmacologically
inhibiting monoamine oxidase
activity during murine,
that’s mouse pregnancy,
increases the prevalence
of behaviors thought
to reflect impulsivity
and aggression.
We don’t see any of that today, do we?
Impulsivity.
Nah.
Let me find the next part.
Where is it?
There it is.
So prenatal.
This is prenatal before pregnancy.
Inhibition of MAO A and B.
So like all the Peters, right?
Because they’re not
going to get pregnant.
So it’s before they get pregnant.
Prenatal inhibition of MAO A and B.
Significantly,
it affected these things
persisting into adulthood.
It didn’t go away.
Remember how I tell you,
like if you’re toxic
and you don’t fix it,
it doesn’t go away.
It actually tends to get worse.
The data suggests
that inhibition of MAO activity
by 25 to 40%
effectively alters
serotonin innervation.
So you’re screwing up the system
in the child for good.
The current study
not only warns about
the long term long term
effects of the use of
certain antidepressants
during pregnancy,
but also of other drugs
such as cocaine,
nicotine,
and ethanol,
which inhibit MAO
or increase
extracellular levels of serotonin.
What’s the new psyop?
Oh, there it is.
Did you know this
also inhibits ALDH?
That would be a weird coincidence.
I guess I’ll have to
I’ll have to look into
p-glycoprotein as well
when I do
when I do that part
of the infertility psyop,
because that’s another part of it.
OK, now these next papers
are just showing
how toxic methylene blue
is to a fetus.
I’m just going to read these
toxic effects of methylene blue
on the fetus.
Fetal death
after exposure to methylene blue
died during mid trimester
amniocentesis
in twin pregnancy.
Hemolytic jaundice.
Oh, sorry.
Did I not show that, Joe?
I’m sorry.
Sorry about that.
Here we go.
Here’s the fetal death
after exposure to methylene blue
died during mid trimester
amniocentesis
in twin pregnancy.
Then we have
the next one I already read.
Hemolytic jaundice.
Gosh, that’s liver damage
in a newborn
after intra amniotic
injection of methylene blue.
Intra amniotic
injection of methylene blue
leading to methemoglobinemia
globinemia
meth hemoglobinemia
in one of twins.
You know how they say,
oh, methylene blue is given
for methemoglobinemia.
Well, it causes it too.
Do you understand that
that means it’s just a poison
and that whatever it fixed
with methemoglobinemia
was because it slowed
detox somehow.
Now, continuing.
Methylene blue induced
hyperbilirubinemia.
That’s bile leakage,
hyper bile,
too much bile in the blood.
In neonatal,
newborn glucose
6-phosphate dehydrogenase
deficiency.
Now, people who want to advocate
for methylene blue will say,
oh, it’s only a problem
if you have a G6P deficiency,
G6PD deficiency.
Well, wait, let’s let’s check that.
We report three premature newborns
exposed to methylene blue
that experienced severe hemolytic
that’s blood cells
getting basically cut apart,
falling apart reactions
requiring exchange transfusions.
Two newborns were subsequently
diagnosed with G6PD deficiency.
Where was the third one?
Wait, maybe it’s not
only G6PD people.
Only two of the three
had the problem.
Do they do they tell you
if your kid has G6PD
before they ever give you this?
No, they just do it.
Untoward talk about gaslighting.
They’re like, oh,
something bad happened.
We’ll call it untoward
newborn effect of intra
amniotic administration
of methylene blue.
How toxic is this to unborn kids?
Toxins affect.
The the most rapidly
dividing cells first.
Gosh, what’s happening
in pregnancy?
Why do things?
Why do toxins affect babies more?
Because they’re rapidly
dividing cells, they’re growing.
So does this?
So this means that these things
are toxic to the unborn.
It also means they’re toxic to you.
You’ve just already divided.
So it takes longer for them
to poison you.
OK, unfavorable neonatal outcome,
unfavorable
after intra amniotic
injection of methylene blue.
OK, now these are the warnings
about pregnancy.
So I’ll show you these links,
but I’m going to read them off here.
Methylene blue pregnancy warnings.
Australia and the UK,
you should be avoided.
U.S. contraindicated.
Just don’t even do it.
Australia TGA pregnancy category D.
U.S. FDA pregnancy category X.
That’s bad.
Risk summary.
This drug can cause fetal harm
when administered to a pregnant woman.
Intra amniotic injection
during the second trimester
has been associated
with neonatal intestinal atresia.
I believe that means
the intestines are
either not forming right
or they’re actually disintegrating
and fetal death.
This drug caused adverse
developmental outcomes in animals
when administered orally
during organogenesis,
the formation of their organ stages
at doses of at least 32
and 16 times, respectively,
the clinical dose
of one milligram per kilogram.
But it accumulates
when you have people
taking it every day.
It catches up.
More from that page.
This drug caused
reproductive toxicity
at all doses in animal studies.
Somebody remind me what all means.
All doses.
What does all doses mean?
All doses is what it means.
Intra amniotic injection
hours to days prior to birth
can result in hyperbilirubinemia,
leaking bile, hemolytic anemia,
skin staining, methemoglobinemia.
What is supposed to fix, right?
Respiratory distress
and photosensitivity.
That would be blocking your detox
and you’re accumulating
things like vitamin A
because it’s an ALDH inhibitor.
So the category D drug
drugs which have caused
are suspected to have caused
or may be expected to cause
an increased incidence
of human fetal malformations
that’s birth defects
or irreversible damage.
So that’s what methylene
blue is in Australia.
US FDA pregnancy category X
studies in animals and humans
have demonstrated fetal abnormalities
and or there is a positive evidence
of human fetal risk
based on adverse reaction data
from investigational
or marketing experience
and the risks involved
in use of the drug
in pregnant women
clearly outweigh potential benefits,
but they’re still using it, I think.
Anyway, so this let me show you
the link that this is from.
This is from drugs.com
methylene blue pregnancy
and breastfeeding warnings.
And then the next part
is breastfeeding.
Where do toxins go?
Fat soluble toxins in women,
where do they go during nursing?
They go into your milk.
Anybody who thinks that like
breast milk is like clean slate
and perfectly clean and pure?
No, I’m sorry, you’re wrong.
People say, well,
why is vitamin A and breast milk
if it’s not supposed to be in there?
And I go because the body puts toxins,
fat soluble toxins
into the breast milk
and vitamin A is a fat soluble toxin.
There’s your answer.
And then I show them
how many other fat soluble toxins
are in breast milk.
Then they usually just stop talking.
What about during breastfeeding?
You should be avoided
excreted into human milk.
Unknown.
They don’t even know
excreted into animal milk
data not available.
Comments, there is no information
regarding the presence
of this drug in human milk,
the effects on the breastfed infant
or the effects on milk production
because of the potential
for serious adverse reactions,
including Gino toxicity,
discontinued breastfeeding
during and for up to
eight days after therapy.
What does eight days after therapy mean?
It means it was stuck in your fat
and it’s still coming out
at a high rate up to eight days after.
We have in this thread,
I have the pictures from H Milo,
Milowitz, I think Milowitz.
I don’t know how to pronounce
how he put it on Twitter,
but anyway, he’s three years
or two or three years
past taking methylene blue.
He stopped taking it
and he got screwed up by peeting
and the methylene blue
is still coming out of his toe webs.
It’s coming out of his skin years later.
You are storing this stuff.
I like my little joke here.
I said no matter
how big a Star Wars fan you are,
don’t feed your babies blue milk.
I just I thought that was.
And this is from the same
drugs.com page,
which is in the links.
Oh, and finally.
As I’ve said before,
methylene blue inhibits
more things in the body
than anything I have ever come across.
What does it inhibit?
Monoamine oxidase,
nitric oxide synthase,
guanylate cyclase, CGMP,
aldehyde dehydrogenase.
What else does it inhibit?
Multiple amine oxidase
inhibiting activities,
glutathione reductase.
That’s inhibiting your production
of glutathione.
Methylene blue is inhibiting
your production of glutathione
inhibits xanthine oxidase.
This is part of how
you don’t get gout.
This is also how you
detox your caffeine.
Inhibits butylcholinesterase.
And as I mentioned here,
lowered butylcholinesterase
is associated with acute
and chronic liver damage,
inflammation and infections.
It inhibits at least
six cytochrome P450 enzymes.
1A2, 2C8, 2C9, 2C19, 2D6 and 3A4.
The most important one.
Oh, wait.
Oh, gosh.
It inhibited P-glycoprotein.
So remember what
I said that Kelsey said,
if things that inhibit
aldehyde dehydrogenase
also inhibit P-glycoprotein
and the more fat loving they are,
the more fat soluble are,
the more lipophilic they are,
the more damage they cause.
Okay.
So.
That is.
That is.
That is today’s presentation.
I know sometimes it might seem.
People go, well,
what should I take for cancer?
Well, don’t take pharma cartel garbage.
We’re working on getting actual
proof and real people with cancer.
Our approach takes longer
than others.
But, oh, Joe, we can,
I’m going to stop sharing.
Yeah, there we go.
So our approach might take longer,
but we are getting very good
initial reports from people
who have cancer.
And it’s very exciting
because I know when that comes around,
that’s going to be a big breakthrough.
So, yeah, there’s other options
that people go, well,
what am I going to do
if I’m not going to take these drugs?
Well, oh, my gosh,
there’s other stuff
than pharma cartel stuff.
I mean, there really is.
So.
Yeah, don’t don’t take these.
These are not good for you.
Do not run to pharma cartel medicines,
medicines.
For little things or to improve
your mitochondrial respiration
or whatever the crap
they’re selling you these days.
They are selling you a
methylene blue is a pharma drug.
No, there’s no debating it.
It’s a pharma drug.
It always has been.
It always will be.
It’s a toxic dye.
And just because people
get small little benefits
at the start doesn’t mean
it’s not accumulating,
it’s not going to cause problems later.
This is the whole duration paradox.
These things, lipophilic,
fat soluble things accumulate
and they cause problems later.
They may suppress a symptom at the start,
but they accumulate
and they cause problems later.
So.
Let’s see, Joe.
I didn’t.
I’m getting back to the.
OK, one.
One super chat from Will.
Good, that’s good,
because I got to get to
I got to get to the inner circle.
So we have one super chat from Will.
It was thank you, Will.
He said it’s dangerous to go alone.
Take this.
Yeah, that’s the good old
like like Legend of Zelda line.
I’m pretty sure that’s
where it was from, right?
Originally.
So, yeah, don’t.
If you are seeing something
that is pharma being promoted
by health people.
As a magical cure.
Pharma has never cured anything,
not even the common cold.
Think about how sad that is.
They can’t even cure the common cold.
So do you really think
that all this time
they’ve been hiding
ivermectin from you
and they’ve been hiding
fenbendazole and mebendazole
and methylene blue
and nicotine and weed
and all these things
are magical mushrooms.
And do you think they’ve been hiding
all these things from you?
Or.
Or.
This is the scary part.
Or do you think
they’re releasing it all on you
so you can’t figure it out all at once
and you’re going to screw you?
You’re likely going to screw yourself up
on one or more or all of them.
Because all of a sudden you go,
it’s this it’s like the
it’s reverse psychology.
People like, oh, oh,
they kept him suppressed for so long
and now they’re available
and they’re legal
and they’re easy to get.
Oh, this.
They must have been suppressing it.
And so now I must take it
because they suppressed it
and now it’s good.
That means that it’s good.
They know what they’re doing.
They’re doing reverse psychology.
They’re doing look up
the forbidden fruit effect.
Well, let’s just go over these.
I mean, reverse psychology, right?
You try to get somebody
to do what you want
by telling them not to do it, right?
Sometimes works on contrarians like me.
You know that that’s who
they would try to do it with.
I’d be like, well, you tell me
I can’t do that.
Well, I’m definitely going to do it.
That’s reverse psychology.
That’s easy, right?
So the forbidden fruit effect.
I don’t know if I’ve been
over this before.
Let me go.
Maybe we’ll share this, Joe.
Let me get my let me share my
let me find the screen share again.
The forbidden fruit effect.
This is an important one to know.
OK.
Let me see if I can find an easy one.
Let’s just go here.
Oh, stop.
It is a curious phenomenon
that humans are often drawn
to something that they cannot
or should not have.
So, gosh, during the couf,
the couf.
When they sort of kind of told you
that you can’t get ivermectin.
What did that create in people?
The forbidden fruit effect.
Oh, they want us to take the pokies.
Well, I’m not going to take that.
Oh, they’re trying to suppress this drug.
Hmm.
I should take that
because they’re saying no.
You see, it’s just it’s just
it’s another form of reverse psychology.
OK.
Who benefits from both sides of that?
Oh, the the pharma cartel.
What a weird coincidence.
So the last thing that we’ll go over
is, of course.
The Streisand effect.
The Streisand effect
is an unintended consequence
of attempts to hide,
remove or censor information
where the effort increases
instead increases public
awareness of the information.
So what did everybody go and do?
They spread all the ivermectin stuff.
It’s being hidden.
We better tell everybody about it.
And now if you mention
these things on Twitter,
let’s say all sorts of bots come up
selling it to you,
telling you you barely
even need a prescription.
And now they’re trying to make it
over the counter everywhere.
So they they hold it back
a little bit from you.
And then they open the floodgates
and then everybody who thought
they were being suppressed,
it was being suppressed.
They now want it.
Remember, if the pharma cartel
didn’t want you to have it
because it was a magical cure,
they would stop making them
all these things.
They would stop making it.
They are not your friends.
So.
I think that’s that’s basically that.
That’s what they’re doing,
basically, that that’s what
they’re doing to people.
And they’re going,
they’re getting people,
especially conservative men.
To pay to poison themselves.
Imagine they gave out
the pokies for free.
And you know what kind of people
tend to get those.
And now you have the other side,
the conservative side,
the capitalist side,
the side that says,
I’m going to figure it out myself
and I’m going to buy it myself
and I’m going to do it myself.
I think of how much they’re laughing.
At getting people to pay
to poison themselves
into into sterility and infertility.
They are laughing.
They are enjoying this.
I’m here trying to help people
to see all of this,
and I want to thank Kelsey
for all of her research
on ivermectin in the past,
and I want to thank
Tim Truth was actually very helpful.
He has several articles
which had some stuff on it.
And yeah, otherwise.
Don’t eat ALDH inhibitors.
Don’t consume P-glycoprotein inhibitors.
And yeah, you can look those up.
Like if you were going to go,
I don’t know,
maybe go search nicotine
and go look up nicotine
aldehyde dehydrogenase
and then go look up
nicotine P-glycoprotein.
And you can look up these things
and you can find them yourselves.
And then you go, oh, wow.
Now I know why there’s this new.
Psyop inorganic,
it’s not organic push,
and you guys just saw the thing
about where the influencers got caught
trying to say that, like,
people should be able to buy soda
with their welfare,
with their food stamps,
basically with their snap.
They got caught getting
like $1000 each to do that.
Well, first of all,
you need to know it’s a Psyop
that they got caught
and that everybody started
talking about it.
They do these things on purpose.
If it’s big news,
especially on social media these days,
they wanted it to be there.
You got to learn the game.
They know what they’re doing.
So that’s all I got for today.
So we’ll have another one,
I think, next week
where I’ll go over other
fun little ingredients.
There’s a company,
a company of wellness
likes to, you know,
promote ivermectin and HCQ.
And I don’t know if they’re
promoting these other things,
but they use lots of other supplements
that we will go over as part of it.
Those are going to be
kind of smaller topics.
We’re not going to do giant
ivermectin and azole
and methylene blue type
things on each one of those.
But yeah, we’re going
to go over new things.
So if you want to find me on the web,
nutritiondetective.com,
that’s where you can
find the supplements.
That’s where you can find
the consultations
with my health facilitators.
That’s where you can find
a link to the love
your liver program,
which again,
the love your liver program,
that’s at
members.nutritiondetective.com.
That is my do it yourself
program that also
has the community there
where you can talk
to other people and,
you know, get ideas
or tell people what worked
or didn’t work for you.
So then you can, you know,
we can all figure out our own,
our own, what we do best
within the framework.
So I give you the framework.
And then you have to
figure it out on your own.
So don’t don’t come thinking
that it’s just a magic pill.
Somebody actually
was wondering the other day,
like, do I actually have to read
and watch the stuff in the program?
Yes.
Yes.
I’m sorry that there
are actually things
you have to do.
There’s actually things
you need to do to get better.
We’re not doing that.
We’re not in the magic pill business.
I just went over
why the magic pill business
is horseshite.
The magic pill business
is not going to fix you.
Avoiding toxins.
Number one, facilitating
the removal of stored toxins
from your system is number two.
Number three is correcting
nutrient deficiencies,
truly essential
nutrient deficiencies.
That’s that’s how
you fix these things.
That’s how we’re fixing
these things.
And this is why we have people
like at the start of this saying
this is the greatest thing,
you know, the greatest diet
they ever found.
So that is everything for today.
We’ll be back next week
with another
another infertility
psyop part of the series
that might be the last one.
I don’t know.
I may come up with more down the line.
But anyway,
hope you all had a great day
or have a great day
and hope you all enjoyed this.
And I will see you all
next time.
Bye now.