Undoctrinate Yourself - #43 - Kevin McKernan

Episode Date: March 23, 2025

Kevin McKernan is a molecular biologist, founder of Medicinal Genomics, and covid mRNA vaccine whistleblower doing incredible work not only characterizing the contents of the mRNA jabs and their ill effects but also doing cutting edge work in sequencing the genomes of cannabis and psilocybe mushrooms, as well as spearheading decentralization efforts in academic publishing.Follow Kevin on X: x.com/Kevin_McKernanFollow Kevin on Substack: https://anandamide.substack.com/CannaMed Conference: https://cannmedevents.com/Medicinal Genomics: https://medicinalgenomics.com/team/kevin-mckernan/Click ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to support the podcast by becoming a patron: www.patreon.com.undoctrinateyourselfpodcastFollow the podcast on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠@undoctrinateyourselfpod⁠⁠⁠⁠⁠⁠⁠⁠⁠: www.instagram.com/undoctrinateyourselfpodFollow Dr. Alexis on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠@dralexisjazmyn⁠⁠: www.instagram.com/dralexisjazmynFollow Dr. Alexis on X @dralexisjazmyn: www.x.com/dralexisjazmynJoin ⁠The Incubator⁠ book club and think tank: https://dralexisjazmyn.thinkific.com/courses/theincubator

Hello everyone. Welcome back to Undoctrinate yourself. Today I'm sitting down with the incredible Kevin McKiernan. If you don't know his work, you need to follow him on X. And of course, in the show notes, I'll give you all the information, places you can find him, things he's working on. But Kevin is a molecular biologist by training as a very interesting background. It actually ended up defecting from academia, which was a sentiment that I probably kind of stuffed down multiple times throughout my PhD. And he has a great success story. So I'm really excited to talk about his training and the opportunities that arose. and with the recent issues with the Department of Education and the bills being passed there, I think it's an important conversation to have. We were chatting about that before we came on because there's this idea that, you know, people are outraged at, you know, this department getting cut. Meanwhile, you know, we were talking like the market isn't driving PhDs. And so what you end up having is a bunch of PhDs that can't find jobs, essentially, and the degree isn't really worth that much.

But anyway, we'll talk about that in a little bit. First of all, just welcome on to the show. show. I'm so happy to have you. Thank you for having you, Lexus. I've enjoyed your work as well. I've been following your stuff with Jack Cruz and a few others. So I usually go on podcast where I can learn something. So I'm high expectations here. Great. Yeah. And I definitely want to make sure we talk about the blockchain stuff as well. And I have my Bitcoin sign behind me. So we'll definitely touch on that at some point along the line. But let's talk about your training a bit and how you got interested in genetics, molecular biology, what your kind of winding path was to where you are now,

and then we'll get into some of the recent developments. Yeah, so I had an early start. I got really lucky. I got a job on the Human Genome Project back in, what was that, 96. And it was one of those scenarios where it was at MIT. And so a lot of this, a lot of people there that were running it were from MIT, but a few of them were running the research and development program there. I think they felt like they had to leave MIT. It was one of those things like they graduated and there was still at MIT. And so they took off and handed me the reins completely unqualified. And I had a kind of scramble to figure out, okay, how do I fit in here? I'm not a, I'm not a PhD in biology, let alone am I qualified to be running an R&D program on the Human Geno Project. But

thankfully, there were a lot of people there that just put faith in the fact that it was a hard worker and eager to learn. And I filled a void. And then over time, that program grew, tremendously. A lot of funding from Francis Collins, ironically. And I ended up learning on the job. And throughout that program, I kept getting tempted to go into a PhD program. Everyone kept telling me, while you're doing this exciting work, you should go get a PhD in this exciting work. And I started down that road, applied to a program out at Seattle from Lee Hood. If you don't know, Lee Hood, he was, he's one of these like Elon Musk-like characters in the biotech space, the genomic space. He invented some of the first DNA sequencers and synthesizers and just he's got a

great repertoire of bringing out really incredible technology in the field. I then deferred from that program when there was a family health issue here thinking if I moved across country from Boston to Seattle during a PhD, I mean, I get back for six years and that was a long time. And so I tried to get Eric Lander helped me get a position at MIT as a special student where I could start taking classes toward a PhD program. And as I started taking those classes, I realized they were like years behind what we were actually doing

on the Human Geno project. So I'm like, my day job's paying me. I've got to leave my day job to start paying them to get maybe a stipend where I can live as a student. So eventually I ended up finding an opportunity to start a company and just said, you know what, to hell with a PhD,

I'm going to go and start a company and I'll be a really insecure, 23-year-old CSO. What was that then? I don't know it was 23, but it was 19. It was 2000, so I was probably 27 at the time. And once that company got going, it quickly became profitable. We started selling off portions of it to different larger companies. And we started building some DNA sequencers. So that's kind of the compressed version of my history there, where I, you know, I toyed with doing the PhD, but it was one of those scenarios, which I think you'll often find if you're in a cutting edge field, the PhD programs, I would imagine, like maybe the PhD programs in AI today are probably, or blockchain are probably years behind what you could learn if you're just working in the actual industry itself. Totally.

Yeah. I feel like academia tends to be on the lagging end of things. And I mean, I can just speak personally as, you know, I finished my PhD at Princeton. And I saw a lot of my colleagues and peers, you know, vying for postdoc positions. and then from the postdoc, you're like, basically it's like a cutthroat situation to try to get a faculty position, or if you can't do that, then you go into pharma or biotech or something like that. And there's a very small amount of faculty positions relative to the amount of students that actually want to become faculty. Like there's a ton of people who like aspire to, you know, have their own lab and be a PI,

and there's just not enough positions for them. And that kind of ties into the conversation we had briefly before we started recording that the, the PhD programs are not actually market-driven. Do you want to talk about that a little bit? I think it's relevant given the whole DOE situation. Yeah, so it's a pricing signal thing, right? So how do the universities know what PhDs you're producing to satisfy what the market's building?

And that always is a bit of a chicken and egg issue. So they can overproduce the wrong types of specialties. If they happen to be academically in vogue, we might have an excess of gender study PhDs right now, which have no real market position. And maybe they did a year or two ago when they wanted to have a lot of this DEI positions in schools, but those are getting quickly eliminated because it was more of a zeitgeist and a market need. And so that can happen in science too, where we can funnel people into Alzheimer's research, all thinking about tau protein in APOE.

And we find out 20 years later that that was maybe a symptom, not an actual cause of the disease. I remember working at Emory. When I first did DNA sequencing was actually at Emory University, radioactively, and we were sequencing serotonin receptors because they were trying to fit serotonin selective re-uptake inhibitors. Now, the whole SSRI craze was going on in 91 to 95. And now we're looking back at that, realizing that's probably an antiquated model of depression. And maybe those drugs have suicidal ideation, and there's other things you could take for mushrooms that would probably do a better job. So sometimes that type of Fiat funding,

makes us go down rabbit holes that don't have a price signal on them. And I think this derives from printing money. And when we print money and we handed out to universities through a grant system, Anthony Fauci can decide that HIV is a significant threat to the world and we have to pile all this money into AZT, right? When AZT is in fact, you know, a toxic cancer drug and that wasn't really the right thing. It was kind of declared from on high that he is the science and that's what's going to get funded. And so huge, rabbit. holes get drilled by academic research that are dictated by $42 billion coming from on top. And that's not necessarily the market deciding that that's a right financial investment.

That's a few people at NIH that have a disproportionate amount of control over the expansion of the money supply. So I think it's a good thing of what they're doing is they're trying to tear some of that down and everyone's screaming because they think it's going to be the end of the world. The Department of Education, if you get rid of that, we're going to go back to being cave people. But reality is when I speak to teachers, they're like the Department of Education does. does nothing for them. It just makes more administrative cost. And then the admin budget is so large

over what the teachers get that they find themselves doing all these administrative assessments and behavioral plans, what have you, that don't benefit the students. So if you look at the administrative bloat on universities in the last like two decades, you'll see why college has gotten so damn expensive. That means if you're going to go into a PhD program, you know, or to med school, you're going to be building up almost a half a million dollars worth of debt that you've got to figure out how to pay off. And the price of your salaries coming out of those programs isn't necessarily escalating with the price of the cost of the education. So there's a lot, a lot of it comes back to monetary policy. And it's hard for people to see that.

But when they're flooding money into systems like this, it distorts everything. Everyone feels like they have to go get a college degree now. otherwise they can't get a job when they get out. But I don't think it's going to be true in five years. In five years, I think a lot of these intellectual jobs pushing spreadsheets and doing market reports are all going to be done by AI. And the only jobs that may be available are people who actually use their hands, you know, that are involved in, you know, maybe electricians and plumbers and actual trade school

types of professions, which are arguably cheaper educations to actually acquire today. So it is a, it's a complicated thing to unwind if you don't know about the money system. Yeah, the blow is a really big issue. And I mean, as like a personal anecdote, even if you get paid a stipend from a university, so like I was making $3,000 a month in my PhD, to live around Princeton for that rate is not really doable without going into some form of debt. And then you're there for five and a half, six years or whatever. You're accumulating debt over that time. And then, you know, you have to go get a job. And maybe, you know, if you're getting a postdoc, it's like not much better. You maybe get $4,000.

a month. So then the debt is still building. And then, oh, you get a wonderful faculty position and you start at like $120,000, which is an undergrad, sounds like a whole lot of money. And then by the time you have all this debt, it's like, this is nothing. Yeah, yeah, right. Yeah. Yeah. It's, um, so I mean, I don't know that it'll be interesting to see when they do. And when they, when they peel some of the stuff back, um, then the universities can have to decide, okay, how much of our endowment are we, like, how much do we really love teaching students? Because right now they're doing it because they can get, they can fund them off of some grants. They subsidize some of this type of activity through grant work.

And when the grant work dries up, they're going to have to ask, do we use our endowment for this? Do we or do we only focus on building PhDs? We know we can place in the marketplace and can hopefully contribute to the school through donations when they're successful. Right. I mean, that should be the model is that you build your endowments with successful alumni who contribute back to the school thinking it was a, you're going to pass it on to the next generation. but I suspect they're going to have to slim down the number of PhD students if the grant system needs to get overhauled. I mean, the most recent overhaul I think they were screaming about was that the overhead in the grants, they want to put back to 15%. All right.

That's not unreasonable. We've been involved in some of those grants, and yes, some of the schools at Harvard and MIT have really high overheads. They rake probably 65% of the money off the grant and put it into their institution for supporting the, what they call, you know, keeping the lights on. Yeah. But they're, they've now gone in and said,

no, we're only going to put forward like 15% for overhead. The rest you guys have to figure out. And now that's making them cut the PhDs. But what they really should be looking at is, why is our overhead so high? Yeah. The PhDs might actually make inventions and maybe you'll get patent royalties

or maybe they'll start companies. But the reality is the universities just have a really massive overhead they don't need. And their, their first reaction is to cut the PhDs, but they should probably be cutting their administrative staff that has bloated over the last 20 years and see if they can get by with a more streamlined operation. Yeah, I mean, it seems like most of the bloated

really comes back to middlemen of some sort that are like kind of superfluous, but they're kind of these fake jobs that are just adding to this overhead like you're saying, but they're not really serving a real meaningful function. I mean, that's like all insurance companies are basically like this. A lot of the administrative people,

and it's just like, it's the illusion of a job, but you're not actually an essential worker in any meaningful way. Yeah. Yeah. It'll be interesting to see what happens. I don't think it's going to be doom and gloom like everyone's predicting. It's the end of education. So I think having them put some pressure on there is going to be, we'll have some

interesting outcomes. I think that the very resourceful universities will figure this out and be like, okay, we have to, we have to get a trim our overhead if we want, if we really want the rewards of research, which they claim are it creates jobs, it creates companies, it creates IP, then they're not going to get that out of the people pushing paper around, making sure that they all have, you know, diversity, equity, inclusion and every step of the corridor, you know, that stuff's going to have to go away in order for them to get back to the basics. But there will be no shortage of screaming on the way there, I think. Yeah, I think it's mostly because we have this

warp sense of reality that's been going on for the past few decades where it's like we think certain things are normal and fine and they're actually not normal. It's just that we've become kind of desensitized to them thinking they're, you know, this is what happens. For example, like the journal model, the academic journal model and, you know, the gatekeeping that happens there and the publisher parish paradigm. And it's like, well, actually, before the 40s, like, most research was blue sky funded and it was like you were funded as a researcher because you know, let's say the government or whatever funding body believed in your brain to do cool things. And so, like, here's this money.

You don't have to have a project-driven funding model. It's not necessary, but yet it's become the status quo in the same way that, like, junk food and processed food has become a status quo for food, but maybe food isn't meant to be cheap and accessible. Maybe it's supposed to be a little more scarce than nutrient dense. You don't need to eat as much. And maybe it's supposed to be a little harder to work for. Like, I think we've just been so accustomed to thinking food. supposed to be cheap, that, you know, we're supposed to get our water in plastic bottles, that we're supposed to, you know, have this academic funding model that is gatekeeping

scientists from publishing. Like I like to always tell people in my research, if I wanted to publish something as an independent scientist, it would cost me $12,000 to put it in the journal nature because I don't have this grant funding to prop me up. Yeah, yeah. And of course, nowadays is the cost of publication is zero. That's all prestige and censorship that's going on there. It's funny, some of the reactions I've seen online about this is the academic seem to have the least understanding of economics on this. So they tend to act as if when this happens, there'll be no primary research. And so the economy will come to a crawl. So they have this belief that only the academic sector does this primary research, that like the private sector

doesn't do it. They just come along and sweep up the goods and go and go monetize it. And it's very bizarre perception that they must not understand like the size of private investment into research is like 10 times larger than the NIH, right? It's like 47 billion or something at NIH. And you go look at what the private health care and biotech space does, and it's 10 times that. And yet they sort of insist that the only way that will ever get these things that have no economic worth studied, which you should stop and say, why are you studying them? You know, they're like, we need people to do this primary research that has, you know, we don't know where it's going to go. It has no, it has no, you know, profit signal. So someone has to do it. I'm like, well, why? Why are they doing it?

If there's, if you don't think there's any, you know, market reason to do it, you should be doing it. And then they'll turn around and be like, you know, these private companies, they wouldn't survive if there weren't NIH grants. And I've been through NIH grants. And I can tell you that you can't get one without putting money down first. Like, you, you have to submit a grant application that could probably take you several FTEs to write the grant, several FTEs to create the preliminary research, and almost every grant people submit 80% of it's done it on submission. And you're just asking the government to take it over the into the end zone, if you will. So private sector is funding the application of a lot of those grants. And if it's not the private sector, maybe it's another

PI who's working money from another grant that happens to overlap with a field and he gets preliminary data, he can submit for another grant. So there's always somebody funding the submission of the grants. The grants aren't like, they're not throwing money from helicopters at cool ideas. You have to actually commit a significant amount of pre-investment in order for you to apply for one. So this concept of like market failure that, oh, the market is failing. Therefore, NIH needs to fund, you know, Tony Fauci ripping out the larynxes of dogs and putting fleas on their heads. Or, you know, NASA has to be funded so we can get tang. You know, like, no. that's not how research should work. You don't build a space shuttle so you can get tang. You build

tang because, you know, maybe athletes want it or something. And they're, but they're lost in this, this trap that if you don't have this primary research being funded by government, then greedy capitalist will distort science into a way that, you know, it'll become, it'll become corrupt. And they can, they can say this, they say this with a straight face after we just witnessed what happened with the Whiff, the one institute of biology, you know, a Tony, like, you know, out there like funding the gain of function research and then hiding the fact that they did it and then coming out with a vaccine that they profit from. And it's, it's mind boggling that they can't see that no, there isn't any accountability in government funding. And that's the problem.

In the market, yeah, you can do, companies can do nasty things, but people usually get fired or their stock goes down or the market has many more mechanisms to hold them accountable when they go off the rails. It doesn't always work, but putting unaccountable people in there doesn't make it better. And that's, that's what the, I think the spastic emotions we're seeing coming out of the academic institutions right now is that it's the end of science because we might actually penny pinch at the NIH. Yeah. Meanwhile, the most corruption and distortion has happened due to this government funding model, this grant funding model that's been basically propping up labs that are doing research that fit within their projects, you know, guidelines.

And then that's preventing labs from maybe doing things that they're interested in actually just intuitively or they think are important that maybe they can't get funding on. And it's pigeonholing science, especially translational medicine and that kind of science into a certain direction that is wholly unhelpful in a lot of ways. And I mean, if we look at also the reproducibility issues, there was, I think a paper that came out of, I don't remember what lab it was. I think it was somebody in California and they did like an analysis. Johnny D. He does a lot of work on that front. Yes. I believe it was him.

And I think he found something like, it was like almost 80% of papers can't be reproduced or something like this. It was a crazy amount. And it just points to, I mean, there's a lot of issues there. It could be like, you know, unknown unknowns, poor controls, things like this.

But it could also be like, you know, maybe the projects we're working on don't matter in the way that we think they matter, especially within the context of the NIH CDC that are developing these project guidelines for like developing cancer treatments that, kill the cancer just fast enough to not kill the patient. And it's like we're focused on these symptom management project, let's say,

or specific drug target projects at the expense of actual human health and creating health. And so I think that's where the decentralized model really comes in and can kind of shine. I learned this the hard way when we, so we had several government grants. But one of the largest one was a $27 million grant from NIH to be a genome center of theirs. And we got the grant because we had low over. That wasn't any like, you know, brilliance on our part. What we did is we moved the sequencing facilities out of Cambridge where the square footage was extraordinarily expensive. And we put it in the back of the shopping mall in Beverly, Massachusetts. So we cut every corner we could on cost

so that our overhead was like 20%. And the other people were getting 60% taken from the universities. So the NIH loved that cost saving strategy. Francis funded us, Craig Venter, Eric Lander, Bob Watersden at Washio and Baylor. So there was five of these genome centers, and we got really good at sequencing one type of plasma DNA, phosmids and plasmids in general, so that we had probably half the cost of everybody. And that's what kept us in that game. We then ended up building this DNA sequencer that we were billing the side with private

money. We had to apply for the $7 million grant. We got the grant when it was about 80, you know, it was 80% done probably on completion. but then that grant had spelled out a three-year research program of all these other tools we're going to build out of the sequencer. And by having that large grant, we were somewhat obligated to two masters. We had to keep going after those research goals. And even as the market was telling us, we don't want those tools.

We were still putting money into them because, hey, it was dilution-free capital. Our shareholders are getting a free ride on that. That's great. It has good prestige. But it ended up putting our company in a direction of, of putting too much investment into something known as mate pair sequencing when the market was going to paired end sequencing, which is, you know, uses less DNA and it was getting more traction. Illumina was our main competitor, and Illumina had less government funding. They're more privately funded,

and as a result, they were more responsive to what the market was demanding. And they doubled down in paired end reads, and they beat us in that domain. While we were still kind of capitulating being like, well, you know, the market's telling us to go this way, but we have this grant. that's funding all these people to go this direction, and maybe in going this direction that the government's telling us, it will discover something that will get us to this other end goal. So I think the lesson there was that the frequency of study review on your grants isn't as fast as the market review.

We did apply at one point to change direction for, we were building a sequencing chemistry using polymerases. We applied to NHDRI saying, look, we want to switch using ligases. We're getting more luck over there. that took us about six months to a year to get them to bless that. In the private sector, that would have taken like a week. We would have been like, look, the data's here. We know we have to go left.

Switch now and make the call because we don't want to have to wait for approval from an outside body to tell us that we're drilling in the wrong place. So the feedback mechanism from the market and from customers is you can't sever that. Otherwise, you're investing money in places that people don't find value. And if you don't find value in the marketplace, you're not, you don't have a perpetual margin machine that's going to help continue your R&D. So it always has to be directed by people willing to give you continual cash for what you're doing. And the grant cycle is just too slow. And the other thing about the grant cycle is the grant cycle attempts to be the market by bringing

in the subselection of the market in the study section. So they might bring in 12 experts. Like these are 12 gurus who would come from the market. They're going to review. your grant and say yes or no. But that's always a sub-sampling of the intelligence in the marketplace. And they often have conflicts. They have their own companies. They're usually involved in. They're not just people that are in, and they're not like academic monks and white cloth. They actually all are brilliant and tied to many industries. So there's some conflicts that you have to try and navigate. But the better thing is to actually get feedback from everybody in the marketplace than from 12 select people that are in the study section. So everything the NIH is doing

is creating a statistical sampling problem. They're going in and selecting a subset of intellects that say, this is where we think the research should go. When if you're in the market, you're listening to maybe 30 customers a month telling you that, no, we want you to build X, Y, or Z. And that's what's most valuable to us. So it's set up in a system that's meant to just distribute money

from the money machine with arguably with some sort of blessing from sages, some oracles come in and say, this is the right way to spend the money. but it's never going to be an Oracle that is like a polymarket type of Oracle. It's never going to be a, what are those betting markets they have now in crypto, right? You just don't have enough voices of customer, if you will, when you're going through that model. So I think that's where we learned that the market, the free market mechanism is, as flawed as people may think it is, we don't have a better system than that. and building up all these centralized means of distributing Fiat money are always going to underperform that.

I think it would be interesting while we're on the topic. You mentioned Fiat. You mentioned Bitcoin briefly. Maybe we can talk about the stark differences between those two forms of money as it relates to how science is conducted. And you've kind of alluded to it. But then also maybe mentioned a little bit about how you got interested in Bitcoin, the blockchain, and also finance in general because it's clear that you're very well-versed in these areas that a lot of scientists are not. So was that just by default as you're trying to navigate the space?

Yeah. So when you end up stepping out of academia, you have to start companies. You get a real rude awakening as to how to raise money and expectations on return of investment. And it sharpens your focus onto projects that are going to deliver as quickly as possible on return on investment. And you know, you learn about economics and time value of money. Where Bitcoin came into my life, because it was obviously, I started these companies in 2000. It wasn't around then. But one of the companies I started after we built a sequencer that went to market and was used in a lot of cancer programs, I started getting asked about cannabinoids for people because these are non-toxic drugs that are being used by patients in cancer therapy quite effectively. And, you know, there's no support for them.

like the NIH model just didn't entertain that because I think the reason it doesn't entertain that is because there is limited pharmaceutical interest in nutraceuticals because they can't get patents. They need patents to get through the FDA because the FDA process is so damn grueling. They will never approach it with something that's a generic. And we can talk about why the whole patent system is probably retrograde as well, but the FDA is even more of a retrograde in the patent system and that it creates such a massive hurdle that the only way you get through it is, with bribery and, you know, wrapped up as pedufa fees. So it, it, you, the pharmaceutical industry is not interested in anything that is cheap and anything that they can get that isn't exclusive.

So the whole cannabinoid space wasn't being addressed. So I started a company to go and sequence that genome, put it public and hopefully bring that market a little bit more mainstream, if you will, that if usually what happens if you sequence genomes and put them public, that the, the, the science in that field accelerates because people can now do knockouts. They can now do genetic manipulation of the plants. They can learn about the biochemistry of the plants so that they can figure out what to feed it to make it grow faster, right? There's just a revolution occurs once you know what the genetics are behind a particular organism. And if it's public, it lets like a thousand flowers bloom, no pun intended. But so, you know, we did that. But in doing that, I realized that this is a

horrible idea from a banking standpoint because that entire industry is unbanked. You want to try and get funding on kooky ideas in the research space. You know, don't go to the cannabis space because it's nearly impossible to get funding unless it's private funding. But then that private funding probably has to be from outside the United States or you got to move to Canada. When we started as in 2011, Canada wasn't even legal. And when Canada legalized, many of the people I knew in my field in the Canada space just moved. They picked up and went to Canada because they're like, it's never going to be banking free here in the United States. and it still has all types of banking restrictions on it.

So that opened my eye up to Bitcoin. And when I saw how that system operated, I realized this is a ledger. If you can track money, you could do peer review on chain, right? You don't need these journals anymore. The journals, you know, as you mentioned, this $12,000 fee to publish is ridiculous, right?

That's considering how easy it is to publish on Nostr or online anywhere, they don't really bring anything to the table. They bring a network of people who could potentially review your paper, and that's it. And that network you can now reassemble online through Twitter, through LinkedIn, wherever. There are all these networks for scientists

that you can use to sort of collect people to review your work. The only issue is there's no pricing signal in the peer review system. Right now they have it set up. So the journal takes 12K. They give nothing to the reviewers. The reviewers are expected to do the work for free in a weekend.

They usually hand it to their grad students because they're too busy. And oftentimes it's the only people that will pick up the job, the free work of peer reviewer, your competitors. And they'll act like, oh, I don't have a conflict. I'm not really their competitor. They'll review your paper. They'll trash it so that they can learn from it and then get ahead of you and push you back. And the editors try to police all this very poorly because they don't want to ruffle

too many feathers because their job is to keep all these people network. so that they can find reviewers. And then once the papers get out, they start charging the universities to buy them back again. You assign your copyright of your work to the journal, which is crazy. They then have it, and they can sell to universities or to individuals for 50 bucks of download. And then they have a page basis on their,

either in their journal or on their website where they sell the pharmaceutical advertisers and about a third or more of their revenues coming from pharmaceutical advertisement, just like the mainstream media. So it's no wonder they've become a gatekeeper. because they're not going to publish something that tarnishes their number one paycheck from Pfizer. And that alone makes them no more honest of a purveyor of information than CNN. They like to pretend they are, but look at the pandemic and see that the Lancet went through there,

the Lancet killed people with a hydroxychloric study. There's no doubt about that. They're complicit in murder, and they should be brought into a RICO case. I hope RFK does that. Nature has arguably killed people because they published and still stand behind the proximate origins paper, which is complete fraud, claiming that this virus didn't come from a laboratory. And as a result, there's no gain of function change in regulation in four years, while H5N1 is coming out of another lab, probably in Georgia.

So they're involved in a racket of distorting public information about what's actually happening with these pandemics and all this culling of birds and stuff. It's grotesque. So that whole system needs to be wiped out and annihilated and rebuilt with I mean, I don't expect people to regulate them into success. What's going to have to have to happen is like the Bitcoin community is going to have to just build a better system and make them completely obsolete. And they can do that by just intermeeting the journal entirely. You can just do peer to peer review.

Just put bounties up online that are paid in crypto and 500 bucks to review up front, five and later, whatever. Pick your own economic model for this. As long as it's transparent and people know that there's money moving, the reviewers are getting paid. Yes, that has to happen. And you can call that bribing reviewers. but right now you're paying the journal and expecting the reviewers to donate their time for free and for it to work out. It's never going to work out.

You're always going to get people, the only people who jump into that system are people who want to, who want to throw sand in the gears to the publication. And they have no motivation due to this quickly. The moment you put pricing signals into peer review, you can create a market so that papers that need to get through quickly can get funded with twice the amount, 10 times the amount of money. Small papers that don't have a tremendous amount of content in them. can go maybe through a fast one week review with one or two reviewers, and you can put bounties

on making them go faster, go slow like you can on the way you ship products from Amazon. That needs to happen in order for there to be any veracity in the quality of the work. The moment you rip pricing signals out of a marketplace, you get the U.S. healthcare system or the Canadian healthcare system. There's a good book from John Goodman called Priceless, which discusses this. When you pull price signals out of markets, how they decay, the directions they decay, and what things fall apart. But we don't have any price signals in what we consider to be the most foundational

aspect of science, which is peer review. It is communistic. It's a complete disaster right at the base layer of science. So I'm hopeful that the Bitcoin, this resonates to the Bitcoin community because they believe in consensus. They believe in building truth sets. And many of them were abused by the pandemic. because we have this Fiat system over here creating false science that's now affecting their civil liberties and their health.

And no amount of Bitcoin can buy back time. So I'm hoping some of them get incentivized to venture into this space and help us rebuild it. Yeah. And I think also if you're adding in, in addition to the financial incentives for reviewers and also adding in like a non-anonymous merit-based system where it's like as you do reviews and those papers are successful and the results hold up, you get like a little gold star next to your name as a reviewer so that like you know you could then be chosen for other reviews and then there's like competition happening right it's a good analogy is like the taxi cab medallions versus uber you know the uber drivers and the and the users of uber get rated you throw open an uber car you're not going to get you're not going to be easily loud in another one right likewise the drivers if they're if they're poor drivers and don't treat you treat you well they'll get it they'll get in a rating i think reviewers reviews can happen the same way and this might solve some of the phdd problems, right? Like we've got a lot of these students who are starving, well, they could be

making money on weekends reviewing papers while they're improving their domain expertise in the process. What's wrong with that? Why would academics get in the way of that? At the same time, the universities are turning around and allowing their athletes to get monetized with these new athlete words, which I'm all supportive of, but they won't apply, they won't allow the same thing to occur with their PhDs. The PhDs there have every right to earn an alternative living to supplement their income if they need to. And if it's working weekends, reviewing papers, why are they forcing them to do that for free?

Totally. And I think another, maybe an example of like the centralized versus decentralized way of doing this is like community notes versus fact checking. It's kind of a similar situation. I could even foresee like in the future decentralized journal model. Like it could be a community notes type situation in addition to the peer review where it's like you're getting feedback from multiple voices with different perspectives. I think it's valuable.

some of it might evolve on substack i mean i know substack isn't only science there's a lot of other content on there but a few of us are publishing stuff on substack and we're not publishing it with any intent of it being a perfect replacement for peer review i usually put things up there that are less mature than that they might be like at a poster level right where it's it's some experiments you did in the last few months you want to share it and get feedback it's probably not ready for what you consider full peer review. Although the only reason people pile up science before they submitted is that the review process costs 12 grand. So when that happens, you're not going to submit like a month's worth of experiment into a six-month peer review process

that costs 12 grand. The fact that it is that expensive and that long means that the cycle time of science gets slowed down. People basically bin their science into bigger buckets before they publish now because of that hurdle. If you, if you, remove that hurdle or put a market signal in that hurdle, people might publish every month. And they might do it on something like substack. And I've already had several of the substacks that I've written be cited in other peer review papers now. Awesome. From the DNA contamination front, I had one last week. I was just playing around looking at this hop-lating the thyroid that's devastating the cannabis field. And it was sort of publishing my stuff as a

real-time journal. And one of the premier plant pathologists in the space picked up on it and published a paper replicating some of that work in a peer review journal in Frontiers. And I was like, all right. Excellent. He didn't have to do that. Like in most cases, academics, they won't cite it if it's not like, at least in a preprint, right? And they'll just skip over it. But this happened to be a very honorable person who said, oh, yeah, that's a really good idea.

I'm going to replicate that and include that in my work and see if it pans out. And so you have a, you know, and there's a substact citation inside of a Frontiers article. So we have some of the tools to do this now. The real question is whether Substack is resistant. Like, they could get acquired and then turn into Facebook. You know, you just don't know if they're going to be, they're not decentralized enough to maybe resist a state level attack like that. But Noster comes to mind, right?

There's a couple of these other platforms that have publishing capabilities that could decentralize the sort of CEO founder risk that we have at Substack. But at the bare minimum, we have easy tools for researchers to build their sort of you know, online journals, if they will, or notebooks. But those are being shared at a faster rate. Yeah, there's going to be a slightly higher error rate because you're seeing people's early results. But you also get the journal of negative results with it.

Yes. Which doesn't happen right now. Exactly. Yeah, and so many people are spending money and time, repeating experiments that were already done and shown with negative results, but this just wasn't published. And so I think that's absolutely super important as well.

And you were talking about the blockchain briefly. So what does it actually look like when you're logging your results on a blockchain and time stamping it for IP reasons or what have you. How does that actually look in like a practical sense? So we did one project where we sequenced the cannabis genome in 2018 with PAC Bio. And specific bioscience has this really cool single molecule sequencer. And the cannabis genome up until then was only sequenced with aluminum sequencing, which meant it was really fragmented in like 100,000 pieces. So we couldn't really organize chromosomes from it. And PACBio has this thing that does.

was like 20,000 base pair reads, and we were able to build it into like a chromosomal map and a really, you know, beautiful picture. A dash, so that was a project where the dash blockchain funded it. Dash has a fork of Bitcoin, and they put in sort of a federated model where the miners of that network get to choose how to spend 10% of the block rewards. So, you know, in Bitcoin, the blocked rewards all go to the miners. In this case, the, they call them nodes where they, if they host a, a, um, a copy of the blockchain and provide some services for the network that they get to then vote

on how to spend 10% of the rewards. And it's a bit of a sort of a pooled model, if you will. And so they vote on these projects that they think may help the success of the network. And in one case, they like what we were doing is they like, lay, let's fund the sequencing of this genome and this model of people using blockchains to record. Now, at that time, they didn't have a dash drive, where you can put large data sets. And blockchains aren't good for putting large scientific stores of data. They're only good for really recording digital timestamps of when data occurred.

You can do that with a really quick hash function. But the data itself, you need to point to somewhere else, like IPFS or maybe Mega or, you know, some BitTorrent or something. We used IPFS for that project. So we took the big sequencing data, threw it in IPFS, and then every time we have, had an experiment we thought was meaningful, we would hash that data and spend it into a transaction on the dash blockchain. That would record it on a chain that was immutable so that you can always prove when certain data was generated. And then when the project was complete,

so it was funded in July of 2018 and we finished it in August and put it public in August. So from funding until publication was like three months, we then put out a bounty for reviewers. Three reviewers, you know, $500 in dash up front, $500 on completion of the review. Review's got to be done seven days. They all got paid out, but they all put their resume public and the review public and the fact that they received half and half of the funding. So everyone's transparent on, you know, what the incentives were. And we got a great review back. You know, there were critiques. It wasn't, I wouldn't say you deem it, it was a perfect story. You know, one person brought up that we could have analyzed a genome a couple of different ways. And they're right.

we ended up redoing it. And the other two people more or less signed off on it saying, yeah, this is a significant achievement compared to where the current references were. So a matter of like five months, we did what would have taken two years. And it was all, the whole genome cost about 50K. And so we got it sequenced, published, and reviewed faster than an entire review cycle could happen in a traditional project. So it was very, very, quick funding, very effective process to this. So the blockchains are really just being used as a timestamping mechanism and as a mechanism to coordinate peer review. Our peer review was coordinated internationally. So it was easy for us to get people crypto 24-7. We didn't have to wait for a bank

to open on a Monday morning to try and wire money to another country. And we didn't have to worry about PayPal interceding if we decided to use a reviewer who was canceled or controversial. So this all could, Now, maybe Dash isn't the right chain to do it now because they're not as the chain isn't as as heavily used as Bitcoin. But it is there as an option with has a faster block cycle and it has, you know, cheaper transactions. Now Bitcoin has lightning and a couple other functions on it that maybe some of this can get done there. But the architecture of the chain isn't terribly important.

As long as you believe it's immutable and it's going to have longevity to it. Like I think Bitcoin is obviously going to have the most longevity, the most proven history. It's got the most hash rates. That's probably the most secure places, but really important studies. But all studies don't necessarily need to be on the base layer of Bitcoin, taking up space. For those not familiar with Bitcoin, there is this function in Bitcoin where you can print into the opereturn. It's like a field, if you will, a notes field. And that's where people are using to stuff hashes.

It's called a hash and staff mechanism. You hash your file. It creates a unique fingerprint of your file. You spend it into a transaction in there. And that gets distributed to all the nodes and put into a transaction. And it's globally forever in the blockchain, you know, ever forward. And the actual large data sets, you got to, you know, you have a link somewhere else. And the websites that contain that link are a weakness.

Like we had it on our website, and our website has been hacked and attacked by people since we did some of this vaccine stuff. But you could put those links on Noster, which are more decentralized in our website. So the connection between the timestamp and where the data sets should be on something else that's probably more secure than your own web server like Noster. Got it. And so for that fingerprint, the file fingerprint, if you were to make any edits on that file, would the fingerprint change so that there's a way to prevent? Okay. Got it. That's an important aspect. So the way these shot 236 hashs work is if you change one letter in that file, the whole thing changes. The whole fingerprint comes out changes. So you can tell if it's been tampered with. You can't go the other direction, though, you're unidirectional. So you can't take a fingerprint and figure out what the original file was.

So anyone's seeing the fingerprint in the blockchain can't know that that came from this cannabis genome. So you have to have some other site that says, here's our sequence data, here's proof of timestamp. And if you run shot 256 in this file, it's much like an MD5 hash sum you get when you're downloading data to ensure that the data you download it off the website matches the hash to the manufacturer. that tells you a virus hasn't inserted itself into the software and you have the exact thing that was that was presented. If there's a change, all you can know is it's been tampered with, but you don't know how. So the unirectional nature of that's actually kind of important for Bitcoin, but we're leveraging that just to say that this file creates this unique hash, nothing else in the world can create this hash because the hashes are long enough in length that there's great videos on how unique

these numbers are, but they're enormous numbers. They're like two to the 256 power in terms of their size, which is like, you know, imagine all the sand grains in the universe, right? That's sort of a number. No one can guess that file, no other, that hash, no one else is going to create a file that collides with that hash because it's too big of a number space. So those unique fingerprints are really important. You change one letter in your file and the whole thing changes. Great. That's very good to know. So let's pivot a little bit into science. I asked people if they had questions for you. And I definitely had quite a few people asking about both the jabs and cannabis and cannabinoids

and their use in medicine. So maybe we can, I mean, we can start either direction. Which one makes the most sense for you? Well, I think the jabs are important to hit on just because I don't know that they're going to, I just read this morning from Mary, Mary Talley about in that like another nine million kids have gotten jabs since the election. Oh, my God. You know, so it's like, yes, they are, less people are taking them, but the people that are taking them are the kids because they're getting forced to. Yeah. And whether school systems, you know, vaccine schedules would have you. So I agree with Jack on this front that we can keep pounding our table on people to pull these, but we have to start focusing on how to fix the people who are going to hit by him because too many of it hit by them. And we can't reverse that. So it's great to stop them going forward, but no, therapies need to start to start, start, start.

hitting the forefront of the discussion. So, you know, he and you have been, I think, doing great work highlighting red light therapy and all of these other, you know, frowned upon fields of medicine that are cheap and effective and, you know, considered, you know, voodoo, if you will, by the mainstream funded Fiat machine. I've been focusing on these cannabinoids because I feel very similar about them is that they have been, they've been demonized because they are a massive threat to the pharmaceutical industry. When you start looking at the areas that they touch on, they touch on the pain market, which is like an 80 billion a year market. They touch on epilepsy.

They touch on autism. They touch on potentially vaccine injury. They touch on, you go down the list. And this is a much bigger market than the entire vaccine market that they can have an impact on. A lot of states that legalize them show there's like a 10% decrease in alcohol consumption. So that's another whole, you know, multi-billion dollar industry that is petrified at these things being legalized. So they, as a result, there's an entire institution at the NIH called the National Institute of Drug Abuse that doesn't look for drug benefits. They only look for abuse.

So they litter the scientific record of all the problems with cannabinoids. And if Ivermectin could only have such an institution, right? I won't be surprised if one gets built. The horse-based institution will probably be built shortly. But as you can imagine, that skews a lot of the scientific record in the direction of like cannabino. it's causing schizophrenia. And I saw a paper there day that was trying to blame some guy who chopped his ears off and cut his dick off after smoking weed and taking cratium. Oh my God. Yeah, the papers that come out are just like, oh, gee, you didn't bother to

highlight the fact the guy was taking meth. I mean, it was. It's so refer madness, right? It's like literally for madness. Not to say that they're obviously every drug can have negative effects and these aren't panaceas. But it's very difficult to start. sort your way through the literature. If you're starting from ground zero when someone says, hey, these cannabinoids might help with her kids epilepsy, a mother is going to be absolutely like petrified, trying to dig through, you know, nine out of the ten papers out there are going to talk about it causing you paranoia and cutting your ears off. And the real heart of the matter is a much different story there. So they're very non-toxic. If you look at the LD50 on drugs,

that's the important thing to look at is a lethal dose versus a therapeutic dose. And there's a huge margin of error with these things that you can't find with Tylenol. You can't find with a lot of the over-the-counter drugs that are out there. Tylonol is its own rabbit holds, actually a cannabinoid mymetic that no one will tell you about, but it makes a toxic liver byproduct called NAPQ1. Trying to, it's a pro drug. It turns into AM404, which is a not a web browser error. It's actually a drug from Andreas, which is named, Muck Grownis at out of Boston. but that's a cannabinoid my medic that they're trying to give you with Tylenol. But it comes with a toxic liver byproducts.

If you take too much of it, you kill yourself. The cannabinoids have the feature that you want without the liver byproduct tissue, but no one will tell you that CBD is probably a better drug than Tylenol for most of these situations. So there's all of this stuff going on in the farm industry that demonizes that thing. And as a result, people have had to vote this thing over the counter, or like Mary's trying to get done with ivermectin, state by state, and the red states are fighting back, and there's a big mess in how it's getting legalized.

They've legalized it in two different flavors, like in a hemp flavor versus a cannabis flavor, and the hemp flavor is banked, and the cannabis flavor is not banked. And in the hemp market, I advise people to stay the hell away from the hemp market right now. It is just contaminated with spice, K2. All types of drugs are getting sprayed on hemp

and sold at gas stations. including cratom, including opiates. Like, it's gone totally off the rails, which is upsetting because, like, five years or ten years ago, the people who are delivering CBD oils, the kids with epilepsy, that was the real, like, you know, Dallas Byers Club many years ago, and it saved a lot of kids' lives. But now these hemsters have come in there and used that loophole to sell all types of drugs sprayed onto hemp into gas stations and smoke shops and what have you. But anyway, so I got involved in this whole cannabinoid field because it looked like a way to decentralized medicine. Can we get drugs that you can grow in your backyard and get a better industry of information around them so that we can breed them more effectively?

We can test them more effectively than the FDA is ever going to test them. And we can give people confidence that you can grow safe drugs in your backyard. How that intersected with your initial question, I've lost track of. I think it was how it intersected with Bitcoin, I suppose. Oh, well, yeah. I mean, I was just, I'm really interested in talking about the cannabis and the cannabinoid story and the jab story. But, I mean, just to chime in briefly. So I think there's so many different types of cannabinoids, right?

I feel like new ones are being discovered all the time and different plants outside of cannabis as well. And of course, the body makes its own endocannobinoids as well. And actually, the lab I did my postdoc in at Penn, right when I was joining, they were publishing a paper. I think it ended up in maybe cell or nature. And they were basically showing that there's a specific. group of microbes within the gut that facilitate the production of a lipid amide that's basically serving as an endoconabinoid. And if you have this group of bugs, is it P-EA by chance? It was oleamide. Oh, good. Yeah, excellent. Yeah. That's a very important one. Yep. So they

basically found if you had, I think it was a group of bifidobacteria actually, specific subset of bifidobacteria in the gut. Oh, I got a subpoena about that. Yeah. Great. Yeah. So this was in, this was in rodents, but I think they're moving on to human studies. But anyway, they showed that if you had these bugs making allamide, and then you have these animals exercising, they're more likely to self-select exercising in the future because apparently this endocannabinoid can help to trigger the dopamine response to exercise, and you have that reward mechanism in place,

and the animals that were depleted of this subset of bacteria didn't self-select exercise in the future, and because they didn't have this dopamine reward, and then they provided the allamide back as a supplement, and it restored the dopamine response. So it's like there are really interesting things going on inside of our bodies naturally from the bacteria or from our own cells that are involving these pathways as well. And so I think it's a really interesting interface of like what nature can provide

and what our own bodies can synthesize to create different benefits for the system as a whole. It's such an important point because they, that entire ECS, the endocannabinoid system, has been horribly suppressed for, for reference. one of the most common G-protein-coupled receptors in the human body is the CB1 receptor. All right. So this is one of the most common – 25% of all drugs hit like G-protein-coubled receptors, and the most common one of the human body is illegal. Right?

It gives you a sense of, like, how much they've distorted what's taught in medical school, right? There's very few – today there's a few, but maybe 10 years ago. Almost no medical school was taught about the endokinabinoid system. Like, doctors weren't even aware that this system existed, that we had endogenous compounds that hit it. And now you're bringing in microbiomes. It's incredibly, you know, an important topic. But, yeah, there are a lot of them, and a lot of people tend to think of cannabinoids

as just THC, which is a big, that's success of the media trying to scare you about cannabis, that this one compound on there happens to be psychoactive. But there's a hundred other cannabinoids that aren't. You've probably heard of CBD. Many people probably taken CBD. And CBD, great, that's out, has a lot of functionality to it. But what's been in the pipeline, in fact, if anyone comes to CanMed, you'll see what's in sort of the cannabinoid pipeline. There are all the acid forms of the cannabinoids, which aren't psychoactive, even THCA isn't psychoactive until you heat it.

And when you put that acid group on there, it changes the bioavailability of the compounds. Oftentimes there are more bioavailable when there's the acidic form there. Sometimes also changes the receptor profiles that they hit. After CBD, people started playing around with CBG, which is cannabigeral. That's the precursor to both CBD and THC. The plant makes CBG first and then it gets folded into either THC or CBD. A third compound it can be folded into is cannabacromine. And not as much as known about cannabacromine.

It's being used. It has some similar properties of CBG. It's an anzolytic. It's helpful for sleep. It fights against MRSA. It has some good properties for acne. You can probably hit like chat TBT is pretty good at spelling out a lot of these differences between the cannabinoids.

We're now finding all of these other cannabinoids that have a longer or shorter carbon tail on them. When they're shorter, they're less psychoactive. When they're longer, like there's a THCV, which has got only three carbons on the side chain. And that one is known to suppress appetite. So there's some papers that came out recently showing like a 10% drop in BMI, when the people went on THCV for 90 days.

So here's something that could tackle Ozempic, right? Maybe it's not dropping people's weight as much as those Zempic, but again, it's not coming with bone loss and blindness and all these other issues. If you add two carbons to that tail on THC, it turns into THCP, which is like 30 times more psychoactive. And that's what's being found in a lot of these hemp stores. They're spraying. The plant makes, there's only been a couple cultivars where they can find

sub percentages of that made. So they're synthesizing it instead and spraying it onto hemp and claiming it was made by the plant to try and get it through overstayed lines. And the DEA hasn't really, not that I'm a big fan of the DEA hyper-regulating this, but the patients and the consumers don't know that they're consuming something that's 30 times more potent. I mean, that can get you in trouble. And so it's really more of a fraud issue that they're supplying these compounds with synthesized in a lab, and it's not well characterized as to whether the synthesis is pure, whether there's any background side products and the reactions, all the stuff. So the varins are the ones that have shorter tails. So CBDV and THV are both exciting

cannabinoins that have come out because they do different things in CBD and THC themselves. I think CBDV is being looked at an epilepsy. It looks like it has a better profile than just CBD alone. So anyway, that's probably like a dozen, a dozen of them that are, they're actively being studied today that we know something about. There's been a bit of a focus on those carbon compounds, 21 carbons in these cannabinoids, because they're lipid soluble and they get through the blood brain barrier. And you get different biochemistry when you're dealing with lipid soluble drugs than water soluble drugs. There's a host of other compounds in the plant, which are known as the flavons, the flavonoids, the canned flavon one and two being looked at in cancer. These are more

water soluble and the conneuronic acid, which they're finding in the leaves. So there's, it's a big, it's a bouquet, if you will, it's a pharmaceutical, you know, factory, if you will, of compounds that have had a, they've been well studied used in the human population for thousands of years. So the admi tox side of going down this pathway is, that's the number one thing that will drop you in a lot of clinical trials is you can't, you can't get through the admi talk side of it. But we have good confidence with the admi tox that's in cannabis, because humans have been using it and consuming it for so many damn years that it's unlikely any one of these compounds is lethal.

It's kind of gone through that selective process, the breeding process already, where we've somewhat co-habitated with this thing. And that field will quickly bring you into other plants. It will bring you into fungi like psilocybin. And we do a lot of work with psilocybin as well, sequencing the genomes of those salosophy speak uvensis to find out the pathways that make the entourage that's in those it's not just about psilocybin they make four or five other compounds as well tritamines that have different properties in psilocybin so each one of these genomes you can you know you can crack you can begin to look at the

pathways that make the compounds and all the side products they make and usually you find that all the side products are just as therapeutic as the one that's known for its recreational use they just have slightly different affinities for different serotonin receptors or what have you so I think there's a lot we can learn by sequencing medicinal genomes and putting the information public so that it can it can pull the entire sort of nutraceutical market forward, if you will, without having this lording control at the FDA over what drugs make it to market. Yeah, I love that. And I love that you mentioned like the entourage and their entourage effect.

And it's something I think about also in the context of food. And Jack always talks about how food is a light, a barcode of the light environment it was grown in and depending on that light environment, you're getting different micro and macronutrient ratios, minerals, cofactors, everything like this that are all coming together to create something that provides both energy and information to the body so the body knows what to do with it. And I think in the context of like cannabis, for example, anybody who's taken like a THC isolate, like an edible, for example, or even just, you know, some sort of a THC isolate versus a full spectrum with turpines and all the good stuff in there, the effects feel quite different.

And even like turpenes by themselves. So like I've taken limine by itself is also quite energizing and like stimulating in like a very positive way. And so I think the turpines are really interesting. And also thinking about the light biology here. And it's something I want to look into in the lab. But looking at like the absorption and emission spectra of these different molecules. And that has, of course, has implications about the growing environment. Right.

So if you're not growing outdoors, if you're going indoors and there's no UV light, now these molecules that could have potentially been carrying some UV photons into the body, let's say, maybe don't have access to that because their ring structures didn't ever get, you know, exposed to UV light during the growing conditions. I think it's super interesting. Yeah, we've totally bastardized this by when they've quote unquote legalized it, everyone has to grow it indoors. The light structure is totally different now. And that has created a total mess of the microbiomes of the plants as well because when you grow indoors, you try to start off like in a sterile environment. Like everything's clean, right? But it's not really because the seed itself has all types of microbes in it.

And then the soil you bring in or the hydro you bring, eventually this boy in a bubble gets infected by something. And it's not like a full-blown natural infection. It's a very niche, one-species dominating infection, which creates all types of havoc on indoor grows. So indoor grows actually have, you would think they'd be really clean, but they have a really hard time staying sterile and dealing with many of the microbial populations that they're tested for. So oftentimes outdoor growing ends up being cleaner because you have natural pests out there. You'll hear of indoor grows getting like aphid infestions. And that just doesn't happen outside because there's ladybugs, right? And they're predators around.

So the really good growers have to have these like IPM programs in place where they try to recapitulate as much of the outdoor environment as they can inside without getting pesticides and all the other things that they get tested for in the mix. but even the pesticides are hard for them to deal with because they've made the mistake in some cases of using drywall. And drywall is like this chalk system that absorbs pesticides and it breathes them back out when the humidity fluctuates inside the growth. So it is a – I like your analogy on the barcode of the light that's in there because I do think that plays a role in the cannabis like cannabinoid and turpene profile that these plants are generating. You can take the same cloned genetics where we know it's the identical genetics and separate the environments and grow them and get different expression. Now, usually you don't get a dramatic change in that maybe the cannaboid ratios, like if your plant's going to produce 20 to 1 THC to CBD or vice versa, it's unlike you're ever going to get that switch based on environmental because there are some really hard genetics to that.

But the terpine profiles are very responsive to the environment. Like those do change quite dramatically. In fact, there's some study showing if you spray plants with antibiotics and wipe out the microbiome, the turpene profile completely shifts. So the turpene profile really is a communication, the chemical communication layer with the microbiome on the plant. Yeah, I mean, oh, sorry. I was just going to say it's making me think of an analogy between like identical twins and you put them in completely different environments.

And sure, they're going to look the same, but there's going to be a lot different about them over time, especially. Yeah, yeah, indeed. And that's the exciting thing about working the cannabis field and any plant field is that you can make clones of things, right? It's something that's very easy to do. It doesn't require any sort of genetic triple lundies to do. You can cut cannabis plants, put them in a little bit of plant hormone, and they'll reroute, and you have genetic clones. There may be some mosaicism in that process that affects it, but they're predominantly, you're dealing, you've kind of taken out that one major variable. But this impact on the people that eat them or consume them, I think is very important.

That goes back to that. I think we had a conversation about this offline that David Sinclair paper that talked about xenohormosis and how when you stress plants, they produce a different secondary metabolite profile that's meant to signal to the seed transmitters that they're to prepare for caloric restriction. It tends to dial right into the rapamycin pathway. So that, hey, there's the environment shifting. I'm going to produce things that signal the people who are going to spread my seeds to hold on to them tightly, right?

Because they may encounter starvation. So that, that I think is helpful in cancer as well. Like a lot of people are making, you know, cannibate oils for cancer. And, you know, if they're Warburg cancers, you might need a different one than if they're not. Because the whole Warburg effect isn't necessarily driving every cancer. But to the extent that it is, you want something that's going to zero in the mitochondria and alter ATP production to try and get that back in line. And that might require a different set of cannabinoids than what you'd use for something that's not believed to be of that ideology.

Yep. And now that you're mentioning that, I mean, there's so many different ways to get cannabinoids into the body. You have vaporizing. You have smoking. You have topicals. You have tinctures. I'm sure there's others as well. And it's making me also think of, I've heard, you speak on other podcasts, but it's maybe good to mention it here that a lot of the, like, the pesticide contamination in vapes, for example, and there was that whole thing with vitamin E acetate and popcorn, you were like debunking it. I want to talk about that a second? Yeah, so before the pandemic, there was this the valley crisis, which was, which was blamed on vitamin the acetate. And so that was the CDC move. So always second guess it. What's Rosetta, is her last

name? Is her last name? I think it is. I may have to forward you the name. I sometimes fumble her last name, but she's done some really interesting work looking at the evalic crisis. And if you remember, the avaliate crisis happened right before the COVID pandemic. And one of the signatures was ground glass capacities in the lungs, which sounds just like COVID. And it also, what she pointed out is if you look at the epidemiology of it, it followed this, this Gombards curve. That, you know, if you remember early on the pandemic, there's many epidemiologists that were pointing out that this is what pandemics look like. They have this sort of pandemic curve described by Gompers. there's a noble laureate Michael was Michael's last name at Stanford that was that was Michael Levin was all over this

and and she saw that fit inside the evaluate this so she's immediately going to this has got to be another coronavirus maybe it's the precursor of what actually was released or another who knows another coronavirus and not that it was just a coronavirus but that the vapes may have been painting the target for those who got really sick because there is more inflammation the lungs with some of these vapes And it wasn't relegated to just THC. There were nicotine pens that were in the mix as well. And what stood out to us in the cannabis field is that vitamin E acetate has been in vat pens for 10 years.

Why did this show up now? Was there a form of vitamin E acetate that was doing this? And other researchers had pointed out a person to follow on Twitter is mass blank, who's done some work in this area, showing that your own body when it gets going through some type of inflammation can create its own endogenous vitamin e-acetate. And that the, the CDC trying to pin it on that was not facing that data. The fact that that's not a signature for, yeah, the pens may have it, but you may be reading that in the tissue and it may be endogously generated in the process of inflammation.

It's like fireman at the fire. The firemen didn't start the fire. They were just. Exactly. Yeah. Yeah. So there's a lot of reasons to believe there may have been a coronavirus involved in, in and not that vaping is off the hook.

But there's other people in the lab space. And a lot of the people who are in the cannabis testing labs, and they kept bringing up pesticides. Like there are so many damn pesticides in these things that are getting used. What invariably happens is the state will put out a list of like 60 pesticides you need to test for. And it's the 61st one that people move on to use.

And so it's this game of cat and mouse. I think the last paper I saw had 327 pesticides being screened up in Canada. And the black market had like 92% contamination in the tested market at like 6% contamination, but there's still some in the tested market. And those things can enrich in the extraction process. When you go in rich for cannabinoins, you might move the flour from 20% to 60% or 70% in the oil, but some of the pesticides can go from parts per million to parts per thousand. The process of extraction selectively purifies some of those molecules,

some of those molecules more effectively than the cannabinoids. And so even though there's still a parts per thousand, they can be very potent at those levels. And the one that's, the one that's probably would be most frightening to mitochondriac like yourself is Michael butanol. That thing turns into hydrogen cyanide when you heat it. And that's one of those common fungicides used in the cannabis growing community. It's outlawed in many states. So you tend to find it more in the hemp products that get, they don't make it through state testing. And so the dumping ground becomes a hemp industry. So be careful what you smoke from the hemp side of things because the pesticide, the pesticide screens come. Whenever people screen that market,

they're loaded with pesticides. And if you go through pesticides, they're mostly neurological agents, right? They're usually things that are meant to, like, screw up the neurological system of insects, and they claim they have very little effect on humans at those dosages. But once you get involved with vape pens, they're no longer at those dosages. They're jacked up the higher concentrations, and they can cause all types of havoc. Now, that's a separate issue that people end up blaming the activity of THC for all this neurological activity because they say, hey, this person smoked cannabis or a vapeat pen that was made from cannabis. They never in those studies go, very rarely, they ever chemotype and do a chemical analysis in the pen. They just say,

hey, it's a THC pen. So THC must cause schizophrenia, right? And it's like, no, it's probably the pesticides that are coming along that you're smoking at high concentrations, causing hydrogen cyanide that could be causing your schizophrenic break. And that's the quality of science that you find in the cannabis field is it's often that simplistic. Like they look at, since it's illegal, it's hard for them to do these controlled studies. They just say, we collected a thousand cannabis users and we compared to the people who don't use. But they have no idea what the hell they're consuming on the cannabis side to make those correlations. And so it just stacks all this yellow journalism against the compounds in that plan. Yeah, you're making me also think of like

round up glyphosate and the shikkimate pathway. So it's one of its main targets. And you know, that's claimed to not impact human cells because of that. But I'm thinking there's more bacteria in the body than human cells. And so we're taking something that's affecting them. We're also affecting our human cells indirectly via the microbiome, basically. So I always think it's just so short-sighted to think about things in that way. I mean, isn't there good enough evidence now that it's impact on mitochondria or is it still, are they still trying to back out of that?

I can never keep up. But, I mean, in my mind, it's, I'm going to stay as far away as possible from, it for sure. Yeah, I thought Steffie Sneff did some interesting work on that with deuterium and the impact of glyphosate on the mitochondria. But it's, I confess enough being totally up to speed on that either. But yeah, it's another pesticide that fortunately we don't have Roundup in cannabis yet. Someone has filed a patent on Roundup Ready Cannabis.

I don't know of the extent that it's actually being used. The industry is, I think, fairly adverse to that activity, but it's not. to say that someone won't try and sneak it in there. Right. And those pesticides are primarily, they're using both indoor and outdoor grows or? They are. Yeah. And the indoor ones sometimes are more enriched because they can't get rid of them. They tend to get stuck in the drywall and everything else. So they're usually in the indoor environment, they do a grow and afterwards they bug bomb it. And that bug bombing is, you know, the plants aren't around when that's happening. They're just trying to just kill any of the bugs that might be creeping around

on the walls, but the walls absorb some of those bug bombs and oftentimes breathe them back off when the humidity changes and the plants get in there again. So they have to be really careful about using them. Now, there's a, there's a list of ones that they're not allowed to use and some that they can that are deemless harmful. But the, you know, the state, at least the state tested cannabis facilities and the dispensaries, I mean, check with your state. We have some of this on our website as to what the regs are each state. But in a lot of states, they are, testing for like at least 100 of these things. And whenever studies are done looking at what's in those markets versus what's in the black market, it's always cleaner in the state market,

but it's not perfect because the state market isn't heavily as heavily policed as you might imagine. And a lot of the users aren't really aware of this problem. You know, they just assume, hey, I got a dispensary, it's better than the black market. And so they don't, they may not ask for a certificate of analysis to prove that it's actually been tested for. But the, uh, the, uh, It's getting better. You'll see a couple of studies from Page. What is your name? Page St. John has done some interesting work at the LA Times.

And then Tiffany DeVitt did some really interesting thing. If you want to scare yourself, read hemp hoax.com. They'll show you all the crap that they're finding in the hemp market. That's become the dumping ground for the stuff that can't get through the state labs. But the really weird economic dynamic going on here is that the hemp market is ironically banked. And the cannabis industry that does safety testing is unbanked. And so just the last three years, the hemp market went from nothing into being bigger than the cannabis market. So all of the growth in the cannabis industry in the last three years has really gone into

this market that has that is banked but doesn't do any safety testing on stuff. And now we're just starting to get some backlash where kids are getting these like 200 milligram gummies and parents are flipping out over the fact that they bought them at a gas station. And I think I just read that Texas is going to, you know, go pro, you know, full bore prohibition again. So it's, it's a bit of a, they call it red state hemp because a lot of the red states that haven't legalized cannabis have this problem. And the reaction isn't to legalize cannabis. It's to actually, you know, double down on probation. Yeah, it's like going to make the problem worse. I mean, I'm thinking of like the loopholes like Delta 8, for example, or like these slight modifications you can

make to make something legal in the head shop. And then as soon as that becomes illegal, they find a new one to like, you know, push into the head shop. And it's just this vicious cycle as long as it's illegal. Yeah. And the crazy thing is the, the remnants of the drug war keep this going. Like kids in schools are tested for Delta 9. Yeah. So they're incentivized to use, you know, HHC, which is, we don't know as much about HHC. It might be can. That might be a fine cannabinoid. I don't know. But it's like no one's studying that. And, And so once they make AJP illegal, they'll move on to something else that the test won't hit. All right.

So the prohibition that still exists on Delta 9, which is a really fairly safe compound, we understand it. Yes, you don't want to be, you know, taking chronic amounts of this your entire life, but it can be helpful for replacing alcohol or, you know, for pain or for sleep. But every time they prohibit that, they just push people into using these drugs that are like, you know, Jesse Pinkman bathtub gin that was made last week. You don't really know what it is. and it could have a totally different talks profile. So it's funny that people's response to it is that they see that going on in the head shops

and they say, we told you legalization was a bad idea. Like, ban it all again. Oh, go backwards. You're getting the wrong message. It's that you have one area that's banked and one area that's not banked. So all the business is going to flow to the banked region. And that bank market is right now incentivized to make compounds that don't hit drug tests. I remember once in high school I had some like K2 spice situation from like a gas.

Oh, you're crazy. It was like a straight psychedelic. I felt like I was on acid, but like the most paranoid trip in my life. It was so weird. It was weird. It actually looked like everything was like outlined in a black sharpie. And I was like sitting in a forest like so paranoid that somebody was going to find me. Oh, God.

I've never done it. But that's the thing is I prefer psychedelics. I don't have any paranoia. And I am one of those people where T.HC. like it hits that paranoia bone of mine. Me too. I'm very sensitive to it and I end up, I play with a lot of the other cannabinoids, but THC,

I can only talk in very small, very small amounts. Yeah, I'm actually the same exact way. I've been totally paranoid about, about, I've been paranoid about that concept of someone actually giving me spice. Oh, yeah,

no, exactly. What about CBN? I don't think you talked about it, but is that... The CBN is an oxidized product. And so oxidation occurs in the plant ages. And so the plant doesn't make CBN, But if you take a THC and oxidize it, you can get CBN.

It has been attributed to people having better sleep. However, there's a really good researcher out of Israel, Dedié Mieri, who has gone through this. And it's turned out there's two other oxidized cannabinoids that are underappreciated that CBD is just a canary and a coal mine for. So if you have CBN, it's usually assigned that these other cannabinoids exist. Right. He's called them Go to Sleep 1 and Go to Sleep 2.

GST 1 and 2. that he presents on. And he's isolated those. And he's been doing studies of those on mice and on humans right now. So it's a good marker. Like if you see CBN, it's likely that those other compounds are there because they are made at trace amounts. And once they get oxidized, they're more potent than CBN.

But I know a lot of people who get CBN gummies and they swear by them that they help them sleep and it works. But it can't have some psychoactive. If you take it during the day, I've heard people say it's not, it's not, it's not like CBD where it's, it's very difficult for you to sense any psychoactivity. I have a, I think so, I think the idea of psychoactivity needs to be kind of revisited. There are, they are, CBN is an anzeolytic. And I think for people who have anxiety that take CBD as an anzeolytic, that elation of, like, the relief from anxiety actually for them is euphoric, uh, slightly euphoric. not like THC, but so the language around psychoactivity, we're very careful with in the cannabis space because there are things that are psychoactive, but not, you know, that have a neurological impact,

but don't necessarily give you the high. Right. And even the high in THC is something that you can regulate with pregnant alone. Like if you give people pregnant alone, the high goes away. And the way they monitor this in mice is with these maze studies. And so there's there's two pathways off of the CB1 receptor when you hit it. There's there's a Cox 2 pathway and then there's a Pregnolone pathway. The Cox 2 pathway is more related to the short-term memory loss.

And you can you can blunt that with ibuprofen or other Cox 2 inhibitors like CBD. So people who lose their keys if you're taking THC and you think you're getting short-term memory loss, ibuprofen or CBD should blunt that. Blunt is the wrong term. but and the people who don't like the psychoactivity, some people will use certain turpenes that you potentially limit this. And like Beta Carotheline is one of them that's in Black Pepper, but pregnant alone has been shown in some science papers that like it shuts down that pathway. So they're not, they're different pathways that get triggered inside the cell that result of some of these, that result of some of these different symptoms that people report with THC.

Well, that's interesting. So if somebody's having a bad time, they could use Pregnitalone to help alleviate that? Yeah, I don't know how to administer it. And the study that they did in mice, I can't remember if it was IV, and I don't know how well that goes to the GI. So that's a good question. Jack might know, a physician might know if they've given Pregnantalone the different routes of administration for it. But I do know a lot of people who use will take beta carapolin capsules to try to as a reversal of TSC. That's interesting. It's kind of, it's reminding me of like the trip, like you can use Xanax as a trip killer for psychedelics.

Oh, yeah. Yeah. Yeah. Yeah. That's interesting. So for the cancer patients, are there specific products or modalities or like roots of administration that have, you've seen to be more optimal than others? Or is that still kind of flushing out?

So the oils seem to be the best route of administration for that now. That only works to some extent if they're not having. sometimes the nausea and the vomiting, we catch you, you have to deal with with vaporization because they can't keep the drugs down and you don't know how much they're taking. I've gone through that with my father who had prostate cancer and we had to use when his, you know, the problem with his traditional, you know, Western medicine course here was that he was having nausea and vomiting. And so they gave him casadex, which has a number one side effect of nausea and vomiting, right?

Right. And so, you know, you're stuck there as a patient in a complete, Quagmire, am I getting better or am I getting worse? Because the drugs you're giving me mimic the symptoms of the disease. How do I know psychologically it just wears on you? All right. So we went in and addressed that first. It's like, we're going to get rid of your nausea and vomiting with cannabinoids.

And then we're going to see whether, you know, this Cacidics actually does anything. And that works like a charm. All of his energy was back. He was eating like, you know, full salmon dishes before when he couldn't keep applesauce down. It completely reversed the nausea and the catchia. So you need both. You need THC and CBD. There's differences between the feeling of nausea and the actual vomiting.

I know they're linked in most people's minds, but they're different pathways. And each of those compounds have target them differently. So we were giving him very low amounts of THC because it was kind of a novice user. And it was interesting in his case when the, so his PSA was up at like 170. It was already met it out to the bones. So he had tumors everywhere. And we were putting him on about 30 milligrams of CBD, 30 milligrams of CBG, and 30 milligrams of CBDA. So three of those oils. We get those oils from like those epilepsy companies that make a lot of these nice oils. I think Charlotte's Webb is one and Miriam's Hope is another.

But they've been into business for a very long time making epilepsy, making oils for kids. So they've been, they've been queued by a lot of different labs. And then we're doing that three times a day. So that's a high dose. We didn't start in a kind of inch your way up over a week, getting up to those levels. So close to 100 milligrams of different cannabinoids of CBD, CBDA and CBG three times a day. All of his nausea went away and was able to eat. His PSA dropped to six.

And when his PSA dropped to six, his, he started getting high. And that was something we didn't really expect. And I think what happens is if you read through literature, prostate cancer cells express a lot of cannabinoid receptors. I think they're PC1 cells or PC3 cells. They express high numbers of cannabinoid receptors. So if he had a lot of those over his body, they're soaking up probably all these cannabinoids. The tumors go away.

Now there's no, there's no mop. And THC started getting to his brain. We were only giving him like five milligrams of THC at night just so help him sleep. but once his PSA started drop, he was getting stoned by it and was like, all right, I'm going to back off on all of this stuff. And we should have just backed him off the THC and left the maintenance dose and the other things. And then I think when it lasted about four years where he was sort of, I wouldn't say totally disease-free, but comfort, you know, comfortable and living and able to move around, drive around and live his life. They had to completely remove all the

cannabinoids when they wanted to replace his pacemaker because his pace. was not MRI compatible. That was a surgery. And the anesthesiologist didn't know how the stuff was going to react. So he's like, just dry him out for a couple days beforehand. We'll go through surgery. And then you can put him back on afterwards. So he came out of that surgery with vomiting, screaming, coming back.

Then the hospital couldn't contain it. And we finally told the nurses, we have something we can use to get rid of this. and first asked him if they had THC, like Grinob and all, the prescribed stuff, and they didn't have it. We gave it to him in 30 minutes. He was up walking, ready to leave the hospital, and all the nurses came running. Like, what did you give him? We need, we have nothing that could stop that. And we want to know what it is.

They started taking pictures of all the bottles. Wow. The doctors didn't ask a thing, but the nurses were like, yeah, that's important. We got to know what that is so we can help others. And so that's when the therapy started to fall apart for him. is we went through that sort of bleed out of him using those things. And we were doing sequencing of his bloodstream periodically and monitoring the mutation that he had. He had a particular mutation of his prostate tumor. That was a K-601-e variant in shit. What gene was that in? It's a

B-Raff. And so that we could see going down in the blood over time as well. And then he got a P-53 mutation after that time, that period where we pulled them off all these things. They were also playing around with other chemos at that time as well, which may have played a role. But once the P53 thing came into view, Dana Farber kind of freaked out and was like, all right, we have to accelerate. We got to drop everything on this thing. And then thrombosinoppedia showed up and it got out of hand pretty fast. So, you know, we don't have a good control here. I don't know that he would have been, you would have been able to survive all this on only cannabinoids because it was cannabinoid supplemented with what the sort of standard regimen hormone therapy was,

which was very bizarre to me because that hormone therapy is really meant for people that have androgen receptor, like 90% of prostate cancer is an antigen receptor mutation, right? And he didn't have one. He had what looked like a melanoma mutation. But they're like, we have to start with the, it's kind of like, you know, they won't let you get an MRI unless you get an X-ray. Yes, it's the insurance middleman. Yeah, exactly.

And you're like, wait a minute. minute. We just did all the sequencing that shows that's not where we're starting from. We should start over here on AKT inhibitors, right? And they're like, no, we have to go through doing cassidex and rule all these things out, and then we can graduate, torture the patient with nausea and vomiting along the way, and then maybe we'll consider the sequencing that you guys did. So it's a little bit frustrating. I definitely open my eyes to like the world of cancer and cancer of therapeutics is dreadful. And that the rules go out the window with terminal care. I think there's even odd conflicts that can occur with physicians and what they prescribe, and there's

these regimens on certain cancers where they have to rule you through a torturous protocol and rule things out before you can get to what you really need. But I have not, I've met very few people who have not been at least gotten prophylact, or I should say, not prophylactic care, but dealing with the symptoms of cancer, cannabinoids work. Like there's, I've heard this from everybody that when they have pain, nausea, and they can't sleep and need to eat, the cannabinoids, you know, alleviate a lot of that pain. And you don't have to get on morphine drips that get you constipated and run you down a wreck.

He never, even having bone meds, he never got a morphine drip. So it was, we got the pain under control with, with just the cannabinoids. But whether they actually shrink the tumors where there's evidence for this in some cases, but I don't think we fully understand, like which tumors need which cannabinoids. Right. like the glial blastomas. We have people, some people report very low dosages that work. Other people are using really high dosages that work.

That's still an unknown domain. I think what's exciting about them is that there isn't this risk of overdose. So you can't experiment with a broad range of dosages. And the running advice in the field is go, you know, start low and go slow and ramp them up until you're comfortable. And your body, when your body's comfortable, you know, you're at the right dose. Do not try to exceed that to try to fight cancer that you can't feel. Like it's really, your body will tell you when you have the right dosage of these and leave it at that dose for as long as you feel necessary and you start to see other signatures of the disease

disappear. If there's other biomarkers you're tracking, you should see those, watch those in concert with the dose that you're at. Speaking of cancer treatments that are kind of taboo among centralized medicine, I'm thinking of Dr. Macchus' work with ivermectin, fendazole. I'm very interested in all that work. I don't, I'm reading on it. I have no experience with it myself. I'm not a treating physician, but I've been reading about all the case studies.

And I did, I dug into some of the literature there. I was intrigued in that the ivermectin looks like it actually blocks SP40 from getting into the nucleus. Okay, that could be interesting. and then fenben, and I think they're replacing it with another fenbent version of the drug, that's a little bit better. But that thing stops, I think, microtubule formation so that fast-dividing cells have a hard time dividing. And I believe there's even some Brachau-1 interactions in P53 interactions from Ivermectin or fenbent.

I can't remember which one. But it made sense that's something that would help if this vaccine-based turbocancer thing is a result of any of this DNA contamination or is a result of the spike protein inhibiting P53, it made sense that those pathways should be considered. And the drugs, it doesn't seem like those drugs are, like cannabinoids, you have a large window, dosing window. Like, it's not like you're threading a needle between toxicity and therapy with those drugs. Like you are with cisplatin, a lot of the other cancer drugs. So it seems like it's completely worth investigating and worth a try.

I've seen other people say, ah, it doesn't work. And of course, if you put them down that path of hope and they don't take the other drugs, you're actually killing them, you know, you get in all those bizarre,

zero sum fallacy arguments, I think of people who don't want to consider it. But I hope to see more physicians, you know, experiment with those in cancer. Because right now, Macchus is under a lot of fire. And, you know, he's, they're going after his bank accounts and everything else.

and just be good to see some more replication of others, you know, others having success. And he's at least very good at publishing a lot, putting forward a lot of the papers that are coming out. So it's not just him. He's just been an amplifier of it, I say. Yep. But I'd like to get more input than that. In fact, those are areas that I wish we had those tools back when my father was going through this, because those may have helped him in other ways, hitting other pathways of cannabinoes can't touch. Totally.

Yeah. And we know also there's some data showing that Ivermectin can help activate autophagy, which in combination of other things can help on the cancer front to help slow down growth and glucose metabolism and all those things. But speaking of, you know, this is maybe a good time to start talking about like the plasmids and the Sv40 promoter and such. So do you want to talk a little bit about how you even ended up stumbling upon this issue, like that SV40 promoter was present in the Pfizer jobs?

And I heard somebody say that there could be some in the Modena Jabs. Do you want to update us on that as well? Oh, yeah. So I haven't found any of the Madera Jabs. That was coming from, I think, Chacharbardi's work. And I think that's an artifact from it gets into some of the weeds of how DNA sequencers behave. When we're sequencing a lot of samples on DNA sequencers, we tend to put DNA barcodes on them to sequence them. Because the sequencers put out like terabases of information in one like $20,000 run.

So what happens is you get 100 samples you want to put onto one run. You got to barcode them somehow. And the way we barcode with Ingenomics is we take a piece, like an eight base pair piece of sequence and glue it to that library that we're going to sequence. And when we sequence that as the first eight bases, we can say, okay, that's an index, that's sample one. That's a barcode that says it's sample two, sample three, so on. So the problem with some of these sequencers is that they can have a barcode misreading rate of a ground 1%. So 1% of the reads that the reading is barcode one get miscalled as barcode two, and suddenly you have what looks like chocolate in the peanut butter.

And I think that's what caused the issue with what Chakabardi was looking at. It wasn't his data. He was reading data from another laboratory and going through it. And the methods weren't really clear on how they handled the barcoding. So he just wasn't attuned to that. But so in that case, yeah, you technically can find some SV40 and some of those Moderna samples from the Orion at all paper. But when I've really tried to scrutinize those, I think that's actually a sequencing artifact from barcoding. So I've not yet seen credible

evidence. And we've done QPCR and hundreds of vials now that there is SV40 in the modernas. Doesn't mean they won't use in the future, but it's not there now. So all right, how did I find this stuff? I was sequencing doing RNA sequencing of cannabis plants as they're being infected by hoplatan viroid. That's an RNA viroid. And in doing this, you have to extract RNA and sequence it. And one day, that process was coming back. So usually when you do that, you get sequence coverage across the genome over all the genes. And you get all these gaps of sequence where there are no genes. So it's a great way of painting on the genome where all the genes are as you read the RNA and then map it to the genome and you can see where all the genes are.

one day our informatics team came back saying look this last run you did the reads aren't concentrated on the genes it's just it looks like whole genome shotgun something screwed up in your pipeline you need a control spike in a control RNA and just prove to us that the um the beads you have that are capturing the RNA are doing their job and if that RNA comes through then we'll know we'll be able to pinpoint where in the pipeline something's broken so it's like that's a great idea uh I don't have a an RNA handy except for these RNAs someone sent me that their vaccines, they have a polytale, I'll use those. Would that work? And they're like, yeah, it's perfect. You know, pharmaceutical grade, spike it in. So I do that. And it comes back and I'm like, so what's broken? And they're like, well, your RNA came through, but so did all this other plasma DNA.

We don't know what this is. Did you put that in there? And I'm like, no, no, that's got a spike sequence in the plasma. And it's got SV4. Oh, wait a minute. That's their expression there. and I was like, oh shit, this is the problem. I didn't want to inherit.

So immediately I was like, oh, this is such a headache because I know I have to, I can't hide it. I got to put it out. But if I put it out and I put out sloppily, I'm going to be drawn and quartered. So I asked the team, okay, why don't we just go and measure this every way we can in the lab? What do we have? We can measure with Oxford Nanopore. We did that, which we sequenced it with another sequencer. We did it with alumina. We did RNA sequencing. We did RNAs. We erased all the RNA and sequenced it to prove it wasn't like some artifact of the RNA. We read it through an Agilent Bioanilizer. We ran it through a nanodrop. We ran it through QBCR every which way to Sunday with DENases and RNAases. And lo and behold, it's a way higher copy number than anyone would imagine. So reference points here. A good reference point. You probably got a PCR test or someone in your audience may have gotten a PCR.

test for COVID, and it probably stopped calling you positive in around 35 or 40 CTs. And this thing comes in at around 15 CTs. So for those not familiar with that offset, that's a 20 CT offset. That's a million-fold more DNA that is, as a contaminant, is being injected into you with L&Ps than what they're scraping out of the outside of your body in your nose for viruses. So for them to have a hyper concern over a replicatable virus that is a million full lower concentrations than a replicatable plasmid that's a million times more concentrated in LNP's and being injected, is complete idiocy. Like, they cannot defend this.

And the way that they try to defend it is they say the plasmus not replication competent because you chewed it up. I love them to prove that because when we've boyed Pfizer about this and the health candidate about this, they have no assay for the length of the molecules that are in there. So they don't know how well it's chewed up. You know, when we've done Oxford Nanopor sequencing on it, we get like 3,000 base per fragments that come out, reads that come out of like when we just do like 800 reads. So if I do 8,000 or 800,000 reads, I'll find one that's 7kB, that's replication competent,

I'm sure of it. And how much these things vary lots of lot. There's got to be one that's replication competent that's in some of these files. I don't know that's in all of them. They are trying to erase it. But the way that they're erasing this DNA, is is acidide. They're not using the right enzymes to get rid of this DNA. It's a solvable problem.

And just the mere fact that there's more of a problem in Pfizer than there is in Moderna proves to you that someone, someone in the group's being lazy. Yeah. And it's not a small difference. Like I think,

I think Madonna is probably 10 foot lower than Pfizer. And that's even given the fact that the Moderna dose is like double the dose of Yeah, exactly. Yeah. Yeah, they're like triple the dose. So yeah. Yeah, Madurta actually has patents out there that describe this problem.

They actually invented a new purification method because they're so concerned about it. Their patents are like, this stuff is oncogenic. It can do insurational immunogenesis, so we have to do a really good job getting rid of it. And so they come up with some new method for getting rid of it. And clearly, they're doing a better job than Pfizer. But you can put the data in front of these regulators being like, look, you've got one manufacturer in here that's like 10-fold lower than the other. and you're you're trying to claim that this is the it's acceptable because one one group one group is has has ten full more than the other like why is it acceptable if you if it can be done one way why can't

be done for everything and they're they're not very they're not very well versed in this stuff so the reason this is happening is when you have RNA inside of a vial that has the DNA it was made from that RNA is hybridized that DNA is it's it's it's That's the synthesis process, right? An RNA polymerase goes through and copies the DNA and makes one strand of it RNA. You have RNA hybridized DNA. That is thermodynamically more stable than DNA hybridized DNA. Just for folks who don't understand the nucleic acid chemistry here, RNA sticks to DNA stronger than DNA does.

So these RNA-DNA-hybrids, the enzymes don't know how to erase, at least some enzymes. D-NAS 1 does not erase RNA-D-D-Nabrites. So the region of the spike sequence, that's the region that's not getting destroyed. which is why we think it might be related to the longevity of spike being expressed. Because that's a hundredfold higher concentration than the other part of the plasmid that the DNA is double-stranded. There isn't any RNA, and it shoes that up really readily. But they let pharma pick a PCR assay that targeted the part of the plasmid the enzyme can kill.

Very sneaky. And the part that actually is 100-fold higher in concentration, they had an assay to measure that to prove that the spike sequence was inserted in the plasmid, but they refused to use that to quantitate the DNA because they know the answer it's going to give them. Wow. So this stuff is circulating, and you can use a different nucleus to get rid of it. That does process RNA-DNA hybrids, but they're not using it.

So there's a known way to solve the problem. They're a hundredfold over, and there's other manufacturers out there that have the problem better addressed, but not perfectly. and all of this DNA contamination is happening in an environment where now we have lipid nanoparticles present that bring it right to cells. All of the boundaries and regulations they have and we can accept 10 nanograms of DNA if you inject it. That's all because it's injecting it like naked into your arm, which has DNA system to chew it all up. But once you put an L&P in there, that's the reason the MRNA platform works or supposedly works.

That's what delivers it to the cell and it's dragging all the DNA with it. So now Farmer likes to run around and be like, you've never proven that this inserts in anyone's genome. So we're going to now shove it into babies, right? The burden's on you to prove that our stuff integrates. And we're like, no, no, no. Integration is like, yeah, that's a horrible thing if it happens. But the moment you put DNA into the cytosol of a cell, you trigger an interleukin response.

You trigger a Cigasting pathway. You trigger cancer. Like you can't repeatedly hit cells with cytosolic DNA. and not make the cell think it's infected with a virus. So what it's going to do is it's either going to trigger apatosis and destruction by the immune system or it's going to go into oncogenesis. And it's to start growing rapidly. And there's papers from Kwan and others that describe this.

So the insult isn't whether it messes with your genome. Of course, that would be horrifying if we find it. And there's people working on that. It's a harder problem to solve. the insult is the moment you flooded cells with cytosolic DNA, you've thrown off the immune system. And that can be a contributor to cancer. So they don't want to talk about any of this. And it's they've been running around saying you eat DNA all the time.

Don't worry about it. DNA's in tomatoes. You're eating tomato. You're eating DNA right now. That's so disingenuous. It's like how, it's an insult to the intelligence of the American people that like, oh, yeah, eating drugs is the same as injecting them. I mean, is that why we have people all over with heroin needles in their arms all over the streets? I mean, it's, it's asinine that they, they're, they're floating these gas lights that I suspect, I guess some people are still buying or I don't actually, I don't even know how many people still believe in these things.

I just know people are forced to take them. That's the stage that we're at right now is that the kids, the kids are getting, it's getting forced under the kids. I don't know the other adults that are willing to take them. Gosh, yeah, and I remember actually funny enough when the jabs rolled out, I was at Princeton still, and everybody was, first of all, just so excited to line up and so excited to get it first. And Pfizer was seen as like the good one. Like, everybody wanted Pfizer at school and like, oh, not Moderna, Pfizer, please. I don't know how that happens. I guess they have a bigger marketing budget than Moderna maybe. It's odd. You know, a good person to chat on that topic is, have you spoken to Jessica Rose yet? No, but I've heard her on a few podcasts. She's great. Yeah, she's got a good sense of the adverse events. And so I don't know that there's substantially more or less for Moderna or Pfizer. It's hard to untangle because, you know, Moderna has more RNA, which is a problem in itself and different LMPs than Pfizer. So you're getting like triple the dose there. So the fact that they may have less DNA, but you end up tripling the dose is getting closer to being similar. But still, I think in total dose by dose, you'll get less DNA. contamination with Moderna. They have more double-stranded RNA, though, from my assessment of the two-term vaccines,

and that has its own, like, stimulatory pathway and the toll receptors that could wreak havoc. And then the Pfizer stuff, though, I've seen from, what is Marion? I think it's Marian Latterat did some of this work, where she looked at the onset of the turbocancers and was finding that Pfizer had a faster time to death in those cancer patients than Materna, but equal amounts of cancer between the two of them. So they both can be oncogenic, but Pfizer seemed to have a faster expiration, if you will, the way it was termed in that. So there are different, there, there's a lot of things wrong with these things. I think if you get rid of all the DNA, it's not going to solve the problem. So we're not trying to pin everything on

that, but the DNA is just one of these like traceable markers that we have a hard time tracing the NLMPs. We have a hard time tracing a lot of the other components in these things. But the DNA is something we can amplify from single cells. And it's a forensic marker for their, for their mistakes. So it's something that can be measured in a decentralized manner, like PCR is everywhere. You can do, you can do PCR in your basement, right? So if they can run PCR in parking lots to track COVID, they should be able to run PCR to track this contaminant in all the patients that have biopsies that have questions about them. There's others out there that are looking at spike as well, which is important because there are

cases where we're seeing spike out there, like 700 days, like we saw in that Yale study. Bruce Patterson's lab is probably the pioneers of that. They actually had data on that long before Yale. And I think in-cell DX, they're building tools to look for viral spike versus vaccine spike because they can differentiate them. But yeah, we've run into some biopsies where we can barely see the DNA, but there's shitloads of And so I don't know what that means. I don't know where the spike's coming from and why it's still there.

But it's maybe it's getting traffic from some other cells. We haven't sequenced. But we can't just look at the DNA alone. It's only one part of the story. Yeah. And isn't it the case that Pfizer left the fact that they used an SV40 promoter out of the patent that they did? Yeah. So there's a submission to the EMA.

And there's guidelines at the FDA and the WHO where you have to disclose every open reading frame of the plasmid and every promoter. and they hid SV40 from them. And I say hid because I know they did it. And that when you load up their sequence into commercial plasma annotation software, the first thing it annotates is SV40 because it's one of the most common biotech tools for hyper-expressing a protein. Right? It's just if any of you are familiar with plasmid work, it's like, you know, M-13 sites or multiple cloning sites.

These are sort of the common units that are in plasmids, antibiotic resistance genes. And so these tools will readily annotate that there's a Kenomysin resistance gene here. There's a T7 promoter here. There's a CMV promoter over there, and there's an SV40 thing over here. So their plasmine map got annotated by something that mysteriously erased the most commonly annotated region of a plasmid. So someone had to manually remove it. There's no other explanation for that. There's no way a software tool would have annotated the Kenamycin resistance gene and omitted its promoter.

That's not possible from a software standpoint. someone manually deleted it, handed it into the FDA, so the FDA wouldn't be aware of it. And then, because had they been aware of that was in there, they would have realized that's the mammalian promoter. You've got a vaccine with a plasmid that can now replicate in humans. You don't need that. Mederna doesn't have it. Why do you need it? All you need is something that replicates in a coli because you're manufacturing the psilis.

So make sure there's nothing in your plasmid that could replicate it if it ever got into a human host. Now, that part is actually a bit frightening because there's, there's now papers from Beck in Seattle who showed that the vaccine plasmid they were working on, which had an SV40 promoter in it, it was called PCNA3.1. That's one of the most common plasmids used to study spike protein in parts of this virus. These guys were studying nucleocapsin. Turned out the whole lab got infected with the thing and it got outside the lab. Had that been spike, they could have been responsible for spikeopathy spreading out, you know, from their lab. But that's the artifact of having mammalian promoters in there.

It was coupled with a bacterial one as well. So we could replicate in both bacterial and in, and, so they had an SP40 origin of replication and a bacterial origin of replication. That means it's a shuttle vector. You can replicate it in a coli and of a million cells. And they were hypothesizing that this must have been replicating an coli in their laboratory, and someone got it on their hands, and a coli loves their skin. So it got all over their nasal cavity.

and now they're picking it up in COVID tests and all the people in and in and outside the laboratory. Wow. So they need to redefine gain of function research to, like they got to put some control on these shuttle vectors that can go, they can bounce between a coli and humans that are carrying these viruses that these toxic viral peptides. But that's effectively where Pfizer's vaccine came from. It looks like it looks like a PC, a PC DNA 3.1 plasmid that they got from their gene therapy department. and they didn't bother to rip the mammalian origin or replication out or the SV40 components out and just ran with it into production and now it's in the vials getting into patients and we have another SV40 mess in our hands like we have with the poliovirus.

Now it's not the full virus but it's some of the parts of that virus that allow the DNA to replicate mammalian cells. It's got an aggressive promoter that anything that DNA lands in front of them in the genome that's going to hyper express. It's got a nuclear localization signal in it and it's also got this hypermutability element in it. So there's papers out there showing that SV40 enhancer is a hypermutability element. It encourages mutagenesis and DNA that's near it. Wow. So there's all these components to it that are just a train wreck, even without it having the T-anogen in it. So that's what they try to deflect on

as saying, look, we don't have the T-anogen in there. The tumor antigen is what causes tumors, right? So we don't have the tumor antigen in that. It's like, no, I don't think you understand how viruses behave. Like the tumors can be caused without the tumor antigen if they insert in the wrong place or they just trigger the sea gas sting pathway. So it's very, very sloppy molecular biology that they're leaning on to try to gaslight people. Like physicians in the industry, you know, love them, but they don't have this level of detail on like how these plasmids work. I've worked with the Human Genome Project. We built tools to purify like 20 million plasmids. Like I live, eat, and breathe these damn things. Each one of these components in these plasmids has a

distinct function inside of a cell. They're designed and they're engineered into these, these, these, these biotech vectors for very specific purposes. And the, the pieces they have in there are gene therapy components. There's just no question about that. And they left them in there. You think it was laziness? That would be a kind way to describe it. Yeah. Is that, okay, maybe it's just lazy incompetence race to market. But when I saw that they started buying cancer companies, like a year into the pandemic, C-Gen, $42 billion. dollars in cash dropped another one was trillium trillium was targeting blood cancers in particular which is what's happening with this um i start to question whether that was it really laziness

or was it like we have no liability here let's create a market after a market which is how will how will anyone ever trace this back to us you know they'll be able to say uh well you found some sv40 here, but, you know, SV40's, it's been around since polio, you know, sorry about that one, too. But how do you know it's ours? I mean, people are running around PCRing for SV40 in these biopsies, and we're finding it on occasion, but that does raise the question, were they vaccinated with the polio virus? How do you know it's theirs, right? And so there's a little bit of an out for them in that regard. Now, we do have ways we can figure out it's theirs. We see spike. It's then, right? The spike is not from polio. That is, and the spike sequence is so uniquely theirs. It's a smoking

gun fingerprint that it came to Pfizer and Moderna, and we can differentiate those. But when we get things back that just have SV40 and those are missing, it's a little bit more of a, okay, we can't. We've narrowed it down to one pharmaceutical asshole, but not which one. Right. So are the tumors with the SV40 only from people who are old enough to have received the polio vaccine with the contamination? Well, that's a good question that I'm not the best person to ask, but when I have read into SV40, it appears it was spreading beyond the people who were vaccinated. So when they ran the polio vaccine and you got the full SV40 virus, it would then express and shed. And so even the people who were not vaccinated were getting it. And that is one of the reasons why I think that debate still

rages on today. If you put SV40 inside of mammalian hosts, they get tumors. When you try to find a split in a demographic where vaxed versus unvaxed, you can't find it because it's shedding. And so you don't get a clean separation of who got cancer or doesn't get cancer because some of the vaccinated gave it to the unvaccinated. Right. That makes sense. What do you think about shedding with regards to the current mRNA vaccines? It's so Pierre Corey has a good threat on that. I been reading his work on that and Western was the Midwestern doctor, I think. They think it's happening. I want to find some molecular tools to prove it. They've gotten clinical arguments for why it's happening, like the menstruation occurring with women in your proximity. I mean,

they've got a lot of good arguments why it's happening. What I've always been trying to find is what is the molecular mechanism? Because if you had shedding of just spike through exosomes, let's say. You would think it'd be such a low dose that it wouldn't matter and then maybe you'd only see it in hypersensitized people because there are people out there, they're very sensitive to spike and they get near it and they flare up with rashes and have you. And so we have to be cognizant of the fact that maybe a low dose can trigger those people. But I always assumed it'd have to be something replication competent.

Like if the plasmids were moving in exosomes into patients, that would explain it. That, okay, you only need one to get in and then take some. off, right? But I don't have proof of that. I've only seen this spreading event happen in Seattle to be like, well, it happened with the backbone that Pfizer's using. The vector they have in that Seattle study is pretty close to what Pfizer has. It's got many of the same components. It's just nucleocaps is in there instead. And that thing replicated throughout a population and spread from the lab and out. So if there's any full-length plasmid in there from, and it may not be in every vial. Maybe it's in some minority of the vials that are really bad. They didn't digest well.

and then that thing gets out and spreads amongst the community, then that could explain it because the exosome data is you breathe out exosomes. So your body, when this thing gets into you, the cells want to get rid of it. So they package it up in exosomes and just it's like the garbage collector. Get it out of here. They send it out. And then your body starts exhaling nose and it comes to your skin too out of your sebaceous glands and your skin.

And that's one way we can get contact, perhaps exposure for this. So, you know, the jury is still out. I haven't seen like a hard paper proving like, all right, this RNA went from this person to that person or this DNA went from here to here. But the fact that it's persisting for so long in some patients and then we've got all that all the work that Corey and this Midwestern position put together showing that these are all the signs that it's not hormonal and that's there's actually something related to the vaccine that's moving around. Lees me believe it's happening at some extent. It's only going to get worse if they do these self-amplifying RNAs. Oh yeah. I want to

talk about that. Is there any precedent for having plasmids released from the body via exosomes, like in other contexts or not that you know of? That's a good question. I would assume that they would get moved because they're small enough to move. There is evidence of DNA traveling in exosomes, out of doubt. In fact, this is the basis why they think the MRI is ending up in breast milk. So there's a couple studies from Hannah at all that look at breast milk. And that's a bit of a paper to read with caution, like just put your DEI filters on because they talk about pregnant people in that thing. And so they, but they also try to claim that this is a minimal amount getting getting the breast milk, don't worry about it. But when you look at the limit of detection,

their QPCR assay, it's like at 40,000 copies or something. It's 400,000 copies. It's horrendous. It's the least sensitive PCR essay I've ever seen. It should be down to 10 copies. And so they have this really like blind PCR reaction going in saying, oh, look, we only find so many nanograms and below that we can't detect it. And it's like, well, that's because your law is orders of magnitude too high. You're an idiot. If you, if you account for the fact that you could pick up 10 molecules with a normal PCR reaction, you're feeding these kids pretty much a human, if you weight adjust their weight and the amount of milk they're getting, you could argue they're going to have a full vaccine dose orally taken within a couple

days of feeding. And those, now people will say, so what it's going in your gut, you're eating it, but it's coming in breast milk, which are extracellular vesicles. Those are exosomes. those are transfection vesicles. So everything your breasts are feeding to the child is getting transfected into their mouth in their throats. And that's how the children build immune systems through their GI. So it's, and these extracellular vesicles survive the stomach. So they get to your intestines, which is part of the reason, part of the mechanism of

how your mother passes immunity to the child. So for them to be like your GI is going to destroy this stuff and they're picking it up in extracellular vessel vesicles, these EVs, means that they're lying. Like, they're totally lying about that story because everyone in that field knows that that is a communication channel to move immunity to your child, is through breast milk. And whatever you're, if you're packaging the MRI molecules into those things and the DNA, that's getting into the kit. And there was a study, I think it was, who was the first author of this thing? It came up very recently where they showed it getting through, through placenta and into the newborn in mice. Wow. And expressing

spike protein and they can detect the MRNA and the spike protein in the newborn, like seven or 10 days later. So, yeah, when it comes to shedding, it's clearly shedding if you consider placental transfer. That's clearly a shedding event. It's clearly shedding in breast milk. Now, the question is, what is the dose people are getting through skin and through exhaled exosomes? That's the question mark that I think has not been quantitative very well.

Right. And especially also as it relates to like adverse events, whether. whether it's from shedding or from directly receiving the jab. I think, you know, we have no idea the implications won five, 10 years down the line, right? Because they're only looking at, you know, a certain period of time. And there could be many different effects that they have plausible deniability for, of course. But, you know, they could show up down the road. Like maybe we're shaving years off people's lives.

Who knows? I think we are. I mean, if you look at the Japanese study from Kaibo at all, their life expectancy is decayed for the first time since like Hiroshima. I mean, it's, it's, it's that, the graph that they show is absolutely horrific. They have had more excess mortality than the tsunami and Hiroshima combined. Wow. Since these went in place. Now, it's not old cancer, but it's, it's like thrombotic events and acute re-failure, a bunch of things.

I think the cancer is only like maybe 5 to 7% of the excess mortality, but it's still, it's still risen. And they're all in cancers they didn't have before. Like, it was fascinating about the papers, they show, the cancer's pre-vaccination were of these flavors and then afterwards they shift to being like ovarian lymph. I think there was prostate in there as well. So the profile of the cancer types they had before and after vaccination program shift and the age demographic goes down. So it's nice. The reason that paper is pretty clear that this is not the virus is because they got so many goddamn vaccines. They got like 123 million vaccines. It was something.

something like they got, for every person that got infected with the, with the virus, they took nine vaccines. Wow. Yeah. I mean, think of the economics of that. You're taking nine of these things to prevent a coronavirus infection. And so, yeah, the coronavirus infections are hard for them to gauge on like how actually deadly were they because they had such a high toxic burden of vaccines. There's no control group. No. Other than the tight window, there's one window where, you know, the pandemic is occurring prior to the vaccination getting in there. It's a very tiny window, but almost all of the adverse events are temporally related to after the vaccination window. So if you take that paper and you plug it into a chat GPT and feed it, like I've done this,

I have a substack on this, and you feed it with a bunch of papers. If you feed the paper initially in a chap ETPD, you'd be like, well, this is not really fit Bradford Hill criteria for causation because X, Y, and Z, it's correlated, right? And then you give it like five more paper, It will change from being safe and effective language to, holy shit, you need to pull these off the market. Oh my gosh. That's amazing. Yeah, you can watch it. You can watch ChatsyPT go through the logic of being, you know, being red-pilled on this thing. Like, okay, in light of those papers, this is the problem. And they need to, they need an emergency recall right now. Wow. Well, actually, speaking of Japan, so when I was out Rescue the Republic, I think it was in October of last year, that was the same day that there were these like riots or protests. against the self-replicating MRI jabs. Do you want to briefly talk about the difference between

those versus the current? Yeah. So those are a nightmare. I mean, it's a really bad idea. They're trying to make the claim that we need a smaller dose of the RNA to get in and make a hell of a lot more protein. So we can make these safer by lowering the dose kind of thing. And they've got no evidence to need the high dose that they have now and that the dose is the problem. It's arguably the the protein that they're expressing and the transfection that they're doing, it's the problem. But they use some encephalitis viruses, components of them, and RDRP gene to do this. It's an RNA polymerase, an RNA-dependent RNA polymerase that basically will help replicate the virus once the plasmid once it gets in.

The problem with this is that that sequence signal that it uses to make that polymerase is in other viruses out there, other EEVs that exist. There's some in South America. There's some in North America. And that means if you get a co-infection of someone who's vaccinated that also has those viruses, you don't know what the hell is going to happen. It's very likely that that vaccine is going to trigger those other viral infections to go crazy because you basically have a signal for the virus to replicate that vaccine

component whenever it's present with one of those other viruses. And there's a lot of these other viruses out there, these other EEVs. So I think it's a reckless. It's as reckless as like Bill Gates trying to use mosquitoes to spread drugs, you know. Or it's just they're way over their skis. It's hubristic that they think they, that this is a good idea. It's about patents. It's about them. The academics are all cheerleading this because they're probably on the payroll of the patent state that that's involved in this. And it is, it's out of control. That's, that's a horrible idea, particularly if they're doing this for, for respiratory viruses, which are treatable. Yeah. It's also making me think of, I don't remember his name, but a couple months ago, he was

coming out saying, you know, in the future, maybe the near future, we're going to have these targeted vaccines against certain cancers like MRI platform or whatever. Do you remember who it was? Oh, God, that was Larry Ellison, I think. That's right. Yes. Yeah. Yeah, yeah, database guy. Yeah, I mean, it's, he's not, he's clearly not aware the fact that these things are causing cancer. So, you know, coming, it's like, yeah, we're, we got cisplatin. We're going to use cisplatin to prevent cancer. You know, it's, it's, these are mutagens, if you will. I mean, they're not direct mutagens.

They haven't done a good, they haven't done a lot of work to study the genotoxicity of these things. But there's, the investment at the NIH would be far better focused on. looking at all of these other off-label drugs that have wide therapeutic indices, like iburemectin and fenbann and cannabinoids, and even psilocybin. I've seen work on that, like solving depression. Terminal cancer depression sets patients down a horrible outcome path, right? Once they're depressed, they're out. So there's been great work at Johns Hopkins looking at psilocybin for rescuing people from

terminal cancer depression, and they often have better outcomes. We've seen that with a couple case studies down at CanMed, where people used high doses of psilocybin and cannabis oils and eliminated the triple negative breast cancer in six months. Like incredible stories like that that need to be investigated. But, you know, that's a money machine thing. And granted, Larry Ellison was supposed to be the money machine for that or maybe SoftBank was the money machine for that project.

But I don't have high hopes that it's going to go anywhere. These are billionaires that don't know if the first thing about what they're trying to get done and are trying to throw money at the project to get in front of the president. and hopefully get some type of government program that, that, you know, put some wind behind their sales, I think. But, yeah, there are some, I'm not going to throw the entire MRNA thing under the bus. Like, there are some diseases where it might make sense. If you have cancer and it's terminal and this is your only shot, then, okay, that makes sense.

Respiratory viruses, the risk ratio is just not there. But there, I mean, there is a case. And so Hatter is one disease where they use short RNA. which are you can synthesize those cleanly without any DNA. There's like microRNAs, right? And when they infuse those, they infuse them over six hours with an immunosuppressant. So totally different route of administration, different synthesis process, and the terminal disease.

Okay. That's different story, right? There's other cases where they've used lentivirus plasmids to treat, they take your bone marrow cells out. And Duncan et al. has a paper that's in the New England general medicine. You take your bone marrow cells out. You treat them with lentilvary plasmas.

They do integrate. they intend to integrate these things. They integrate it like a thousand times per genome. And when that happens, 10% of the patients get cancer. But they're willing to take that risk because they have a lifespan of 20 years if they don't do something. Right. All right. So, you know, these are very, this is where this gene therapy stuff was, was like designed and marketed for.

It was not meant to like, let's take this as a replacement for ibuprofen or whatever. zinc or whatever you might use for a cold. They're trying to use this, because the reason they want to go to that market is it can hit everybody. Yeah, exactly. When you get into these rare diseases, it's like, well, we don't have enough patients. Now we have to charge a million dollars of therapy. So, you know, we've got to find a way to get this into cold patients. Yeah, exactly. And I'm also thinking I have some friends and loved ones who work in pharma. And one of the companies, I won't say who, is working on a pan-coronavirus vaccine, which is, insane because I think, I mean, my opinion on viruses, it's like, especially coronaviruses,

they're a very staple part of like the microbiome of nature, like of natural environments. They're extremely common. And then most of the time, they're not causing issues. You know, sometimes they do. But usually they're pretty, eight percent viral, you know. Exactly. And so, I mean, I personally see viruses as like primary drivers of evolution and kind of like little thumb drives that can come in and give you some upgrades about like what's going on

in the environment, let's say. to think that we like in our hubris that we should somehow make our immune system, you know, think of these things as pathogens when they're actually, you know, serving probably a really important function. And the fact that they don't really cause severe disease, it's just like, what are we actually doing here? It's like you said, we're just creating a market for everybody. That's a very good point that the assumed pathogenicity of viruses is, it's funny that they, how they've done this. There's a couple, this may help people kind of break out of the spell, right? There's a couple lies that they feed into this.

One is this, all viruses are bad, right? But we're going to use a viral vector to cure your. Yeah. The other one is, you know, well, you shouldn't give out antibiotics to everybody because you'll breed antibiotic resistance in bacteria. But when it comes to viruses, we're going to vaccinate everybody with a narrow vaccine, even the viruses mutate faster than bacteria. Right?

Like, like, hello. This is bio 101. Like, they're violating all of these rules to try to, fit their pharmaceutical industry into this, into this narrative. But I agree with you in that, like, so here's an interesting evolutionary hole that was filled just this last year by Andy Fires Group. They found these things called obelisks, right? So for those not familiar with the evolution of these molecules, viroids are circular pieces of RNA that are short, usually like 250 letters, maybe 300 letters long. And they are self, they don't code for any DNA.

or any proteins, I'm sorry. They're just RNA, and they, being an RNA molecule, that means that they're a ribosine. They can catalytically fold and perform reactions inside of cells that for some reason the cells propagate them. And in the case in the cannabis, sometimes the viroids are really pathogenic. I mean, the ones that we track are, because there's an economic motive to track the ones that are pathogenic, but there's probably a hundred we don't know about that are non-pathogenic and may even be beneficial. We don't track those because no one cares yet until we can figure out. a reason for them to improve the yield in the plant. So what Andy Fires Group found was that this missing link between viroids and this thing

that's driving me nuts up here, let me turn my monitor off because I think it's flashing on your screen. The evolutionary link between viroids and viruses was like, okay, well, where is the circular RNA molecule that codes for at least a protein? Because we're going from this leap from a thyroid, which has no protein coat. doesn't code for any proteins, but is a catalytic ribazine. Then the next leap is a capsid-enclosed viral genome. There's got to be something that is codes for some protein, but doesn't have a capsid. Where is it? Right. And so they bioinformatically went looking through all the RNA data they can find

in NCBI and found these rod-shaped RNAs known that they called obelisks that do code for one or two genes. They're a couple, like a thousand letters long. They're hair pinned, and they code for one or two genes that that that that that I don't know what they forgot what they code for but they they're important in transmitting this actual replicating this actual virus they were only found in the oral microbiomes of healthy patients wow right so you're like okay the evolutionary link between viroids and viruses is a beneficial pathogen if you want to call it a pathogen beneficial thyroid in in the oral microbiome of of and they're they believe they're replicated inside of the bacteria. So yeah, we painted all these viruses as, you know, in this Hollywood

manner of outbreak and, you know, spread fear and we're running a test and quarantine everybody. But the majority of them are probably, you know, mutualistic or providing some type of role we don't fully understand. And I think it does bring us back to this. How do you keep your immune system in equilibrium and hominostasis. So I think these viruses really only get you when your immune system's out of whack, low vitamin D in the wintertime, whatever. There's seasonality to them. And otherwise, they're probably playing some role we don't appreciate that's beneficial. Totally. I totally agree. And also this, I mean, kind of to circle back to the idea of like having a narrow band MRNA platform. Immediately, like as a molecular biologist myself, I was like,

this doesn't make any sense because if we're just targeting specific proteins of this virus, of course that's going to drive viral evolution. Like they're going to create escape variants. Like, this seems like common sense. So what is going on here? On top of that, they threw in mutagens. They threw in there. They threw in. And now there's a whole branch of the chronic virus tree that they've admitted is molnupirivir-induced mutations because they have a certain C-2-T mutation rate that's different than the virus. And they're like, that's us. We did that. Is Molotipiravir the one that failed the aims test? I would be surprised. surprised because I think that's the one that actually affects the mitochondria replication.

Yes. Yes. Yeah. Yeah, I know there was one that failed ams test. And I was like, again, this is just coming back to there's more bacteria than human cells in the body. So what are we doing? Yeah. Yeah.

That one I was shocked they got away with. And it didn't look like it had a whole lot of benefit. And then you're going to add a mutagenesis agent in there. You're going to guarantee, I mean, it's a great one to punch for pharma if they're that smart that, hey, let's convince them of a mutagenesis. drug on top of a vaccine program that's narrowly targeted and we'll just have a new conveyor belt of new vaccines every single chasing every single strain out there and when that doesn't work we'll throw in Paxlovid. Paxlovid has this problem of rebound. Anyone who knows what rebound is means the virus is sticking around for more replication cycles so there's going to get more natural mutation

rate going on. One thing after another they used made everything worse but then more money. Right. And then there's this talk of like wanting to convert the entire schedule over to MRNA and my head just explodes. Yeah, yeah, yeah, yeah, that's, that's, that's, that's, that's, that's, that's, that's, that's, that's, that's, get, get, get, get your kids the hell out. I mean, at least, at least the removal of the department of education may, may remove some of the centralization of that type of, there, there isn't one, one organization where you could demand vaccine mandates from the, you know, from the head of the government down, but, um, sadly, I don't think removing that's going to change. I think a lot of that

zeitgeist is buried in the, in the, in the parents associations and a lot of the schools, you know, that they've got the Karens that are yelling at all the unvaccinated to get their kids vaccinated. Yep, exactly. And meanwhile, I mean, they're just trusting the science, right? Like, they're not educated on this. They're just parroting whatever their favorite talking headset. And yeah, it's just very frustrating. But at the same time, I do feel like there's a lot of shifts happening, conversations being had around these things that used to be kind of taboo to talk about, which is a good thing. And in that way, I'm so thankful for the work that you're doing. I know we've gone quite long time, so I want to be mindful of your time. But this was an incredible conversation. I'm so glad

that we could do it. Yeah, indeed. And I'm glad to put it on a positive note. There are this decentralization technologies here. And that's the message I think we want to get across is that the, obviously the media got captured, the journals got captured. Everything, pharma's got, they've captured government, right? But people are awake to this now. If there's one thing that happened as a benefit of the pandemic is that a hell of a lot of conspiracy. has suddenly got credibility. And people are starting to realize they're being lied to. And decentralization is the term I'm now hearing be thrown around by politicians.

So there's an awareness that we need to do this. And it does have to boil down to the money system. The monetary system needs to get decentralized. Once that gets decentralized, it's going to be harder for capture to occur in all these other places. And just by fixing that one thing, it will start to trickle out and infuse a decentralized mindset, I think, in every other industry. It just may take another decade or so.

But I've never seen more people aware of this issue since COVID. Prior to this, you tell people that, oh, yeah, there's scientific censorship on cannabis. They'd be like, yeah, I go smoke on their joint, you know. It's on your head. And then COVID happens, and you can be like, see, I told you, first time. Yes. People were realizing, like, yeah, you're right. Yeah, it is a problem. And this drug war isn't just about drugs that get you high. It's a drug war against anything as cheap, generic that can leave you free of the medical system.

Yeah. And actually, speaking of drugs that get you high, I heard there's some research going on to try to figure out a way to make psychedelics not psychoactive, but still somehow in part there are benefits. And I'm just thinking somehow they're missing the point that there's like something going on within the psyche that's changing, that's giving the benefits. Yeah, yeah. There's a good debate on that field. I don't have a firm opinion. Great. Let people explore that. So they're looking for 5HT, you know, serotonin to a agonist that don't trigger the psychedelic effect and sometimes get other serotonin receptors. And but there may be a therapy benefit.

Do you think those other receptors? I just don't know that you're going to get this radical, like the most impressive thing about psilocybin is that you can take treatment resistant depression patients and 75% of them, you can basically eliminate the depression. in two or three therapy sessions and it's done, right? It's not lifelong SSRIs and you might shoot up a school, right? It is a complete revolution that feels, which is one reason why I don't think it's going to continue to get banned in various places

because the farm industry is going to find a way to demonize it, like, you know, kids are getting high or whatever. So Florida is talking about banning the spores again, which is like, you know, retrograde again. And so they're going to continue to incite fear from the recreational use, misuse, if you will, standpoint, so that they can demonize it for getting looked at in where it's going to wipe out their SSRI market.

That's how they do. That's how they play this game. And unfortunately, we just don't have anything else like that. And that's a revolutionary compound. I'm of the opinion that you're thinking. I don't think you get that type of rewiring of the brain without some psychedelic experience. I think there's something to that.

But we'll see where the science falls out on that later in the future. I've not found a control compound that's necessarily, maybe it's origination. Maybe it's Bayo-Sysine, these other triptomines that are really close to psilocybin, but don't have psychological experiences. But I don't have a, I don't know if anyone who's synthesizing those or making those at levels that could, where that study could be done. But yes, there are some exciting startups that are in that space. I think Saibin's one of them and a couple others that are pursuing derivatives of

psilocybin that may not have as much of a psychedelic experience that can perhaps hit other depression markets. But I'm skeptical until seeing otherwise. Yeah, like there could be some neuroplasticity benefits or something like this. The other insidious thing about the SSRIs is if you're on them, you can't take psychedelics. They don't work. Yeah, well, that's another thing about the folks that are tracking methylene blue is keep an eye on that because methylene blue is an MOAI. And that may that may make the trip last a hell of a lot longer or push you into sort of a serotonin syndrome situation. So I don't know that it's wise to mix methylene blue with with those things. But yeah, there's a lot to be learned, I think, on that front and how to, I know a lot of

people who mix them, they do mix harming with psychedelics. I mean, right, that's the, that's the, how ayahuasca works, is there's an MOA involved, but it's more of a natural DMT that prevents the breakdown of. And I know people mixing niacin and lines main, a couple other things to try to change the behavior of Solisim. Yeah. I think it's really interesting to think about the, and a lot of of the ancient and like more shamanic cultures will combine different plants together and have this incredible wisdom around the interactions without having to know the exact chemicals involved. It's pretty awesome. It's amazing. How do they figure that out? How do you mix two different chemical? I mean, there has to be a lot of experimentation in depth, it seems like.

Well, actually, it's pretty cool, but I don't remember who I heard say this, but somebody had visited and was speaking to one of the medicine guides down there, and they were saying how, you know, basically there's two plants that you need to combine to make ayahuasca. One has the MAOI and one has the DMT that are in like completely different parts of the rainforest. So like, and the way that they described it is that the plants told them where to find them, which is crazy, right? But like, hey, I'm not going to argue. I mean, it's very possible.

lot we don't understand. Yeah, I know. It's like, have you, have you, have you, have you, have you, um, listened into those telepathy tapes? No, but I heard Kai on Joe Rogan's podcast. So I'm like tangentially familiar. Yeah, yeah. But it's amazing. I'm as new to as you are, but I hear that and that's where my head goes. Is okay, that's probably figured out how to make ayahuasca. Yes, it's incredible. I mean, this is the beauty of the decentralized approach is like, like, we can study these things and we can, like, do it in a way that's not going to like rape and pillage the rainforest or like actually respecting the culture and just making some understanding that then can be applied to Western

culture to make us more healthy and happy and more functional. We certainly need to be more open-minded about that stuff. You know, where has this pillar of science led us where we only trust the white lab coats and Fauci and we shut everything else down, right? Yeah, it's crazy. It's anti-scientific, really. It is. Yeah.

Anyway, Kevin, thank you so much for your time. This was extremely fun. Do you want to briefly just tell people where they can find you your Substack and also include links to everything? Okay. So I'm on, I'm on X as under my name, Kevin McCarney, but most of my writing is done in substack. So you can find, so the substack thing is under Nipedalactones. That's the compound that's in catnip, cat person. But, and sometimes it comes up under anandamide as well, which is in it, and we were speaking about that earlier.

It's one of the endocannabinoids. So you'll find a lot of stuff on there about, you know, The cannabis work I do and the vaccine stuff that we stumbled into on substack. Only so much if it can go on Twitter because Twitter's, you know, it's not perfectly uncensored yet. And then our work at medicinal genomics, you can find. We make a lot of genomic tools for the cannabis space and the slospi space for helping people, make, you know, breed better plants and clean plants. And then I think the last one is, oh, KenMed.

Yeah, we have a conference every year. Scientific Conference. This year's down in Puerto Rico. it's June just before the Bitcoin conference in Prague. I'll be at both. So the one in Puerto Rico, I think, starts on the 16th of June and goes to maybe the 20th. And then I'll be out at the Prague meeting,

the Bitcoin Prague meeting on the 21st. Awesome. Thank you so much. This was so fun. Hopefully we can chat again, you know, offline. I'm going to be up in New England area like sometime during the summer too. So you might be away at your conferences. But anyway, it would be great to connect sometime.

Well, let me know. We're up in Marblehead. So if you make it to the Boston area, we're not too far. great sounds good we'll have a great day thank you so much thank you for the time appreciate it take care bye