Jeffrey Smith: Hi everyone, this is Jeffrey Smith and we have doctors, John Gilday and Dr. Martin Katz. And we have yet another way that glyphosate can kill you. Thank you doctors. Although that's not the main reason why we're here. We are going to talk about yet another way the glyphosate disables one of the fundamental foundations for our health. But we're not going to just leave you in the lurch and say, there you go. Jeff. Disease, destruction and despair. You're on your own. No, because these guys have figured out a way to help reverse or prevent that situation. So welcome doctors.

Jeffrey Smith: Thank you so much. Thank you so much for having us. Really happy to be here. We're sharing this news now.

Jeffrey Smith: You're going to be talking about something that glyphosate's doing and thank you for doing research on glyphosate and you're going to be talking about a supplement and the name of the supplement is Brock elite. Like what? Like an elite level of broccoli, Brock hyphen elite and for everyone, uh, we have everyone, we have arranged a discount for everyone. Um, so you can go to the end of this or we should have some information online so that if you like said, okay, I don't have time for this. I like to get it. Please take advantage of the discount because part of it also supports our work in educating people in the world. Um, and broccoli, you know, people have been talking about broccoli and the benefits of broccoli, and you have a very specific, unique thing about broccoli that you, John put together as genius, that that makes it more potent than, than any other, well one available in the United States. And we'll talk about that. But let's, let's start just by naming what it is in broccoli [inaudible] that you're going to be introducing as a protectorate, uh, so we can get that established and get that out of the way. And then we're going to jump into one of my favorite topics is how glyphosate is bad.

John Gildea: Yeah, absolutely. So the active ingredient in broccoli is called sulforaphane. And for the longest time, the literature is begging, researchers to come up with a stabilized version of that. And it's actually written in a bunch of papers. We need a stabilized version of sulforaphane. So, um, I took that call when I had a very good friend that was in need of it and figured out how to stabilize it. And that act of form of it is very bioavailable and that's sort of the summary of, of, of the invention.

Jeffrey Smith: So let's be clear that, sulforaphane is the subject of quite a number of research studies. Uh, do you have any idea of how many, research studies? I mean,

John Gildea: So in directly talking about, sulforaphane, it's, around 3000 papers and, uh, uh, indirectly through, uh, broccoli sprouts and eating broccoli, um, closer to 6,000.

Jeffrey Smith: So there's a lot of the research is done on sulforaphane that shows, and we could talk about this a little later, 39 different disorders and diseases. And many of these are the common ones that everyone knows and many of them, common ones that are specifically caused or exacerbated by GMOs and Roundup based on, or we could say based on the evidence that we've collected, they're linked. And we know that sulforaphane has a ability to help in those areas. Um, but what did they actually test? Did they test stable for sulforaphane? What is it that they tested that that is now not available? Accepted broccoli?

Martin Katz: No, I'll take that one. Or you can start out home jump.

John Gildea: Yeah. So the, um, Johns Hopkins has a whole center that produces this, the sulforaphane that's used in these papers. It's a very expensive process. It's made from, from, broccoli sprouts. And that is what's used in all of these papers. But so the sulforaphane using those papers is not available to the public. So that's the difference.

Jeffrey Smith: Ah, this is an interesting thing, right? You see a lot of practitioners and selling a broccoli sprout concentrate or whatever, but it's not actually what they use to test. What is it that they are selling?

John Gildea: So the, the, the precursor molecule is called glucoraphanin that is stable. And so, um, that's also sort of the issue is that it has to be converted by an enzyme and that conversion is very variable and, uh, only a percentage of, of the precursor molecule is able to be converted to so forth and so.

Martin Katz: And clinically and clinically, that's where we got interested in it because it seems in the literature that the people who struggle the most to convert that glucoraphanin, that precursor molecule to self, your Fein the active molecule, um, are the ones who are most ill, most sick or having the most problems. And so the people who are maybe healthier have a healthier microbiome, have more enzyme activity, do better. But you know, when, when you're dealing clinically with a sick patient, you want that, you want to know that they're getting the product or the molecule, the phytonutrient that is working. And that's what we were after.

Jeffrey Smith: Well, just about to talk about the glyphosate thing. So I'm telling, I'm letting y'all know it's just about to happen, but I don't, I don't know. Tell me what percentage of the, uh, Mr. G is transferred into the Mr. S. We're going to use those names. Um, what percentage is transferred is converted through the enzymes as a range. So we understand how effective it is to, to take the precursor.

Martin Katz: I think there is a study done out of Johns Hopkins on that very uh, topic and the, I think the average was about 10% anywhere from 10 to 40%, but the average was closer to 10%. So it wasn't a very high percentage. But if you're well you got a chance of getting up into the 40% range.

Jeffrey Smith: and so you guys have developed a way to stabilize or you particularly John to develop the way to stabilized sulforaphane, which means that it's 100% available, which is more like the stuff that Johns Hopkins was testing that is like if you look at it, we'll read the list later about some of these diseases so people can see, Oh yeah, I want to prevent that or I want to influence that. That means that yours is much more alight, much more aligned with the research.

Martin Katz: Yeah. I mean these guys have a Johns Hopkins, they'd been studying sulforaphane since the late nineties. And so they are very keenly aware of how to make this product freeze it and then have a very high self urethane product available. And that product is not inexpensive. So, um, it's uh, it's great that John was able to, um, formulate this product and have it be available at a, at a more much more reasonable price, uh, to people who can definitely benefit.

Jeffrey Smith:  Alright, everybody, of course I wanted to get that. I want him to get that across because like some people would say, Oh yeah, I know that broccoli helps. I take a supplement that has broccoli in it. It talks about sulforaphane. and I, I'm fine with it. What I wanted to point out that you guys actually have a breakthrough. You actually have something that's unique and you created it because you were contacted John by someone who had a sick friend who was looking for it. And you know, it's used in things like cancer and whatnot, but it's used in a way that's not as effective, especially for people who are sick because they're not going to convert it. All right. Having said that, let's dive into one of my favorite topics. Let's talk about what's happening with glyphosate in the body. Um, so why don't you share the latest research. I know you guys did two sets of research and we'll cover both. And we had a previous, uh, webinars. So we're gonna cover the new stuff now. So the people that saw the previous webinar, they'll cap, they'll get the, the, the update. And for everyone else, we'll just go through everything else that we covered so that they don't have to look at two different webinars. Okay. So tell us about what,

Martin Katz: yeah. So I think, um, what's, it's going to be really important to give a little bit of background here because what we're looking at is not incredibly well understood. And so what we're going to be looking at is something called a gap junction. Now, many of you know about the importance of glyphosate disrupting tight junctions. Tight junctions are really what holds the cells together. So there's a barrier between the outside world and the inside world. Gap junctions are what the cells use to communicate. And this is extremely important and extremely exciting because these cell, this is the one way or the only way that we currently know that the cells do that. Whether you're talking about nerve cells, whether you're talking about macrophages or the immune system, there's very few cells that don't have gap junctions. Most cells in your body have these gap junctions.

Martin Katz:
So there's communication and we all know that if you don't communicate bad things happen. It's in the Bible and Babylon. It's a in your home, if you're not communicating with your spouse, with your kids, you know, lack of communication really has a significant effect on your environment. And you can see that we don't see is what's happening in the body if the communication fails. But this is where these gap junctions play such a critical role in being able to communicate. Um, so electrical impulses, cat ions, a reactive oxygen species and how to deal with them or mostly antioxidants. These cells can really communicate that need. So if one sells in need and can lean on another cell. And so what's important to also important to understand is the cells will have different types of gap junctions depending on where they are. So that communication is different and important.

Martin Katz:  So, you know, France, they speak French and in America, we speak American and uh, it's very important to be able to speak French to person who only understands French. It's very important to be able to stay in English if you speak English. Um, you know, if you're talking to a Russian, you don't understand it, it's going to be a lot more difficult to get the point across. And so these gap junctions are incredibly well designed to be able to understand where they are, what is needed, what's needed of them. So in things like wound healing on the skin, these cells are just, cells are coming into repair, but they don't know they need to be a skin cell. And they form that gap junction, those proteins very specific to the style cell lines start communicating and you get immune, you get wound healing, you get immune regulation.

Martin Katz: And if the is not doing very well, you get this induced apoptosis. So these gap junctions are...

Jeffrey Smith: Apoptosis, you mean cell suicide? The cell dies.

Martin Katz: Yeah. Which is really important. If a cell needs to be gone, it needs to be gone if there's too much DNA damage or what have you. So all of these things are incredibly important and this is where the, the cell communication clinically for me, um, is so important. So we, when we went to John and said, John, what is the effect, uh, that you see on these hexomers? So these proteins get together and form these, um, these little pores, these little tunnels to get the cells communicating. So you see the gray line there, that's one cell membrane and then there's an extracellular space there. That's between the cells and the other cells getting together, creating it's polymer of proteins to come together and start communicating. And um, that open communication again needs to be continued. And needs is an, again, is imperative to the health of the cell. Um, and so we went to John and said, "John, what do you see? What can you see with glyphosate?" And that's when he's brilliance again kicks in.

Jeffrey Smith: Well let me, let me stop you. Cause I, I mean I imagine that if these gap junctions are, make the difference between cells acting individually and cells acting as a community, as a system, then they're involved in absolutely everything. I mean it's like putting headphones and, and um, completely blocking everyone's senses and having to walk around separately versus acting as a community that nothing acts as a system unless there's commuter cellular communication. Um, what's, I would imagine an extreme example of lack of intracellular communication would be cancer.

Martin Katz: Absolutely.

Jeffrey Smith: And so is it, is it true? Have you figured out, have they figured out that gap junctions fail for and, and when the, in the case of tumors and cancer,

Martin Katz:  Yes. And there is specific, um, these proteins are named based on how much they weigh. And so there's different connexins that have these different numbers associated with them. And there are studies out there in liver, colon, prostate that show if there's a lack of these, what are called connexin 43s or connexin 40s or whatever number you have associated with that specific connexin. If there is a lack of a viability of that gap junction, that there is cancer. And then if you restore that, ability to communicate, you see less cancer.

Jeffrey Smith: This is amazing because you know, cancer, you know, the cells grow separately. They don't remember they are part of the organism and they can destroy the organism as they grow because of that, because of the lack of communication, because the lack of total intelligence, they act independently. And this, this is critical. So I would imagine as we're about to see, if glyphosate is a probable human carcinogen and it is a definite animal carcinogen according to the international agency for research on cancer, then this may be a way that, if it messes up the gap junctions to cause cancer and probably many other diseases are linked to gap junction failure. Do we have a list of those diseases that are linked to gap junction failure?

Martin Katz: I think we're, I think, you know, people are starting to study, I think there's 1500 studies now on gap junctions, maybe a little more if you put into pub med connexins or gap junctions, you see quite a few studies and you know, I think there's been a huge interest in these things. I think there are a lot of diseases that are associated with these gap junctions from cataracts to cancer. So deafness as these congenital deafness. There's association with problems with connections. So there's a wide variety of diseases out there that have been shown to be connected to connexins.

Jeffrey Smith: All right. Now that means that, we've been looking for different ways that glyphosate damages the health. You know, the microbiome, minerals, the mitochondria act in, um, the, the neurotransmitters, the hormones, the Geno toxicity, oxidative stress. All these different things are fundamental to health. And now we have yet another level. It's incredible how horrible this molecule is in that it finds its way to damage the foundation. So John, tell us what you found in terms of applying glyphosate. I imagine we're now operating in a Petri dish with cells to be able to see whether these, these six proteins are open and communicating or shut down and isolated.

John Gildea: Yeah, so the, the study that I endeavored upon was, uh, using a professional cell line that's very good at making gap junctions. And this is a, uh, kidney cell line. And, the famous cell line called MDC-K. And, they form gap junctions quickly. And so to just to cut to the chase, you can measure gap junction activity. Now, I'll explain that second. But what you can see is that if you put vehicle on, and that's generally what you compare to a drug is you have to resuspend a drug or glyphosate in something. And so vehicle is the same thing minus the drug.

Jeffrey Smith: So in other words, a substrate, it could be a serum of some sort.

Jeffrey Smith: Yes. The carrier molecule, the delivering molecule. And so when I compare that to glyphosate, glyphosate reduces the ability for, um, gap junctions to, uh, transport. In this case, a fluorescent molecule between two cells. And interestingly, I wasn't expecting this actually, was that when we put broccoli on the cells, the gap junction activity, uh, went up 50%, um, and then was able to block completely block the ill effects of glyphosate. So the, the data was very clear. Um, it took me a number of times to actually get the assay to work, but once it did work, the data was very clear.

Jeffrey Smith: So let's, I mean, first of all, congratulations. This is completely pioneering stuff. Um, what was the percentage drop, from the normal functioning of these kidney cells in terms of their ability to communicate when you put the glyphosate in, what was the percent?

John Gildea: 50%.

Jeffrey Smith: So there's a 50% drop, um, which is devastating because this means that the ability of the sales to communicate, at least in this model. So we have to understand, you know, science doesn't want to overstate. And so let's just be, be respectful of the boundaries. This was not only human, it was on human cells though, right?

John Gildea: Uh, this was actually canine cells. I use this, that's cell line as a model.

Jeffrey Smith:  And they're well known as a model to be used that can be extrapolated and it was in a Petri dish and it wasn't in a body. So there's, we don't know. Now another question is how much glyphosate did you use or did you use Roundup versus glyphosate or did you use an amount that was what we could expect to be exposed to?

John Gildea: Yeah, so the, the amount of glyphosate used, uh, on this, uh, particular model was 100 micrograms per milliliter. And that would be, um, the amount found in a very high, uh, glyphosate containing food. Like soy has been measured that high

Jeffrey Smith: Oats probably, hummus, Navy beans, mung beans, the highest levels, the highest levels. Um, so that, that means that if you take that amount, then before that food gets dissipated, then it's at that full concentration and it's interacting with cells at that level. So that's something that we can say is environmentally relevant. Is it, am I, am I tracking writes about it? Said, it's when the food is still intact and the glyphosate's all there before it's been, um, diluted. Then it's at that level, then you test it.

John Gildea: Yeah, we were trying to estimate the uh, the amount of of uh, uh, glyphosate that would be introduced to a cell and it's, it's, it's on the high end for sure because we were trying to see an effect. Um, but in this case, uh, it was a very fast, so we were only introducing it for like 30 minutes before we saw an effect. So it was actually very fast too. So.

Jeffrey Smith: So first of all, before we go anywhere else, this can be a mechanism for cancer. Glyphosate, this could be a, one of the reason ... just yet another, I mean, there's so many ways that that glyphosate can lead to cancer and we can talk about that another time. But this is yet another one because if it cuts off the ability of the cell to communicate on the cell, acts independently, it as its own, it doesn't do apoptosis. It doesn't die. It just continues to be to live into, to multiply. And that's the definition, sort of cancer and tumors.

Martin Katz: Again, if you're, if you're a cell, you're not doing that well and you're relying on your neighbor to help you out, whichw e do. If we forget the butter, we go next door, the olive oil, we cooking and we go next door. That's not happening now. So the cell is going to get sicker and sicker. It's going to, you know, close. It's now closed itself off, uh, because of what's glyphosate has done possibly. And then you have this propagation because the DNAs damage and you have this propagation to tumor.

John Gildea: So this, particular cell line, um, their gap junctions are mostly made up with one called connexin 43 and that's actually a tumor suppressor. So if you lose connexin 43 activity, you become cancerous. This particular assay would be an equivalent to a tumor suppressor assay.

Jeffrey Smith: Do we know which type of, of tumor or type of cancer that it would be suppressing? Or is it all?

John Gildea: In this model? We would assume that it would be a kidney cancer.

Martin Katz: I'm pretty sure it's also being shown in a prostate and liver as well.

Jeffrey Smith: All right. So now how will you put the glyphosate, any that you probably put it in before to see what the effects were and after to see if there was rebound. Let's start with the before. So when you put the, we put the BrocElite in. Was there, was the amount of activity of the gap junctions, was it increased by itself just from the BrocElite?

John Gildea: Yes.

Jeffrey Smith: How much? Pretty dramatic?

John Gildea: Yeah, so it was a 50% increase when we added, an amount of BrocElite that we basically we'll show later in the study that, will actually get to the cell when you eat a normal amount of BrocElite. So two micromole, two micromoles is the amount used in this assay and that's the amount that actually gets to your cells.

Jeffrey Smith:  And then when you added the glyphosate after you had previously added the BrocElite, where did it go down to?

John Gildea Ah, back. Completely to, to the beginning level.

Jeffrey Smith: The baseline.

John Gildea: No change from baseline.

Jeffrey Smith: So in other words, as far as gap junctions go, if you have BrocElite, if you're the Petri dish and you're eating BrocElite and then you had, then the glyphosate comes. It's as if you didn't have the BrocElite. Yes. And you have the glyphosate, they kind of neutralize yup. Sort of like agree to disagree and they walk away. So, right. All right. So now what if a cell has already been depressed? By the gap junkers by glyphosate application.

Jeffrey Smith: Did you ever add the broccoli afterwards to see if he can puppet it back up?

John Gildea: Oh, those are longer term studies that I'm, I wasn't able to technically do because of the dye that I was using. Um, over time ends up getting sequestered inside the cell and can't go through the gap junction. So that was just sort of a byproduct of the assay I used was, I couldn't look longer than the hour.

Jeffrey Smith: All right. Okay. So I want to say at this point, before we go into the 39, uh, different diseases of disorders, I'm already very interested in this product because a, I don't want my gap junctions to be closed when they're supposed to be open. Uh, and I think now there is an opening and closing that happens. And so there must be some times when the cell is supposed to be having closed gap junctions. When is that?

John Gildea: I think in most of the cases it's when you're repairing something, um, in the instance of, um, a wound repair where you have, uh, say EGF (epidermal growth factor). Uh, so it's a normal factor that allows for cell growth. Um, so if you have, you have to repair a tissue and make more cells to repair that cell, um, then that EGF turns off gap junctions. So it's not sequestering your neighbor. It can act as an individual and start growing even though it's completely normal growth.

Jeffrey Smith: All right? So when it grows what it needs to proliferate and grow, then it gets shut off. It's interesting, you know, that of course leads to the question again of tumors and whatnot. They're in, in the early study in 1998 done by Dr Arpad Pusztai who was testing figuring out the, the safety protocol for GMOs. Um, he found incidentally that there was potentially precancerous cell growth in the digestive track. Uh, and it wasn't glyphosate based but it could this, this whole thing. It'd be very interesting to test with GMOs to see if you put at a GMO. So that, I'm going to ask you if you can get around to that at some point to see if the GMO without the glyphosate also affects the gap junctions and if that might be one of the mechanisms for this, the cell growth. All right. Now in our previous webinar as right before I go to this next question, is there anything else you want to say about gap junctions? Is there any more pictures you want to show and walk us through? Because I, I'm, I think we have a pretty good idea that we want ourselves to communicate before we go on. Why don't you take it from here and then we can jump to the next finding.

John Gildea: Yeah. So just to describe the, the assay I developed, um, in order to test this, it's a little bit technical, but you can, I think it's easy enough to understand is that I took the cells, um, they're basically in a very small dish. Um, and then I load it with a, uh, a dye called Calcein. And this dye is very small and it can go through a gap junction. So I load up the cells and then I take a very powerful, um, basically, uh, very strong light source and I bleached the center. And in this picture that's showing up here, I show that area in red. And so I bleached that center area and then do a time lapse afterwards. And then at the time zero, you can see this, the fluorescence in the very center of that image is low. And then over 10 minute period the dye is leaking from the adjacent cells into the cells that are in the center. And then that's shown in the very far right hand side image as a digital, um, some traction. So the picture on a pixel by pixel basis at 10 minutes minus zero minutes shows up in the final panel. They're saying that the dye is going up over time and then I quantitate it per cell.

Jeffrey Smith: You know, it's so interesting, um, John that what we have here is we've seen in other research that glyphosate can, it can reduce the tight junctions causing gaps so we can create leakiness between the cells and in this case it creates tightness on the cell membrane without the proper leakiness or exchange of information. Um, it's fascinating.

John Gildea:  I know that it's certainly seems, um, backwards in that it's stopping the leaking between cells and that's also detrimental. So it is, it is kind of a conundrum

Jeffrey Smith: Yes. All right, so I cut you off in the middle cause you were giving the basic, uh, that was that 10 minutes that die. So under what conditions was that happening?

Martin Katz: Well, it's interesting, just real quick on that there's, there is a maybe a um, parallel, there's a combination here cause tight junctions have a problem with zonulin. And what's interesting about these, um, connexins is there is a part of the protein that has the zonulin occludens as well. So they may be um, a combination here that works for both.

Jeffrey Smith: So make it as important mechanism. So the zonulin is related to the tight junctions gap junctions as well. And zonulin is definitely imply implicated in terms of glyphosate.

John Gildea: Alright. And you had said earlier that uh, there was some evidence about um, actin disruption and both gap junctions and tight junctions are associated with the actin.

Jeffrey Smith: This is very interesting. Yeah. Actin that's actin as like a mechanism mental. How would you describe the role of actin. We've seen um, I was talking to what research you would described it, how it destroys the active structure and he talked about actin in an interesting way. You just share this is another yet another reason why we should not eat glyphosate. Can you tell us what life, what actin is?

John Gildea: So the way, and at least in this system is a very well behaved. All right.

John Gildea: Um, epithelial cell will have a ring of actin that goes around the inside of the cell that holds it. It's structure intact so the cell will stay tall and stay, polarized and the gap junctions and the tight junctions are, soldered to that to keep it structure. And if you just assemble the actin filaments, both the tight junction and gap junctions will degrade.

Jeffrey Smith: Yeah. So actin enzyme might be some part of the mechanism so that, that's for you to find out John, get back to work, but not yet. Is there anything else you just showed us, uh, an example where you used the dye and the bleach, was that under normal conditions or was that with broccoli or was that with glyphosate? We'd probably have to go back to see the differences.

John Gildea: That particular one was, was with a vehicle. So just, uh, that was a normal condition. So with broccoli, you would seem a higher amount in that final panel. There would be more transfer in the glyphosate panel. You would?

Jeffrey Smith:  I barely see any. Okay. All right. That gives an idea. Thank you for this incredible experience. I mean, I think about how to create an analogy and it's like the actin is the structure of the house and then these windows are what you can use and the little holes in the walls of the sales or the are what, what allows you to communicate with your neighbors and also to hear the loud speaker. So there's a loud speaker going saying what you, what you just supposed to do. So you have a system wide information, then you can talk directly to your, to your neighbor through the window. And when that shut off it's like, Oh my God, I'm alone. And then when the actin is destroyed, boom, the house is falling in. So this is very interesting to, to, to pick it up here from, you know, you're going to destroy the structure of your house and your ability to communicate with your neighbor and to hear the messaging from the overall structure. So now there was another thing that, another piece of research that you did that we talked about before. You may have some additional pieces and that is something called Nrf-2. Now we're going to explain that what that is. So people don't have to memorize what Nrf-2 is, what does it do and what does glyphosate do to it? And then we could also talk about what broccoli does to protect.

Martin Katz: Yeah. So Nrf-2, clinically just an incredibly important factor. So when you're looking at disease processes, we are now familiar with this chronic disease stay we have in this country where we have this overwhelming problem with increasing oxidative stress and inflammation. So we have this wonderful molecule called the Nrf-2, which is in kept in the cell cytoplasm attached to a molecule. And when you get certain stresses, Nrf-2 dissociate from what's called KEAP1 goes to your DNA and says, "Hey, DNA, we need help. We need to be producing more antioxidants." And you Nrf-2 turns on about 200 genes called antioxidant response element to be able to deal with these stressors. And, what were I'm excited to say is that it's sulforaphane is the strongest phytonutrient that we know of single phytonutrient that turns on Nrf-2 in the cell. Um, which then allows it to go down to the DNA and say, boys, let's wake up and make some, some goodness here to help the cell out.

Jeffrey Smith: Does the Nrf-2 communicate with the DNA or is it the like standing at the cage and it opens it up and says, okay, you know, after him. So give me exactly what it, what is it the Nrf-2 does.

Martin Katz: So the likely does directly communicate with the DNA to increase this

Jeffrey Smith: Oh, okay. So it's basically tells the DNA to turn on and so the turn, so that means that the DNA then produces a bunch of proteins, uh, that are then used to fix the situation. That's exactly right. nation whenever, and sulforaphane is the number one promoter of Nrf-2, to get into, to engage the DNA. That's correct. That's impressive. So let's if, if, if, if for example, Nrf-2 was not doing its job, what would it be? What would be the outcome there if Nrf-2 was suppressed?

Martin Katz: So that's where we're seeing, um, so much chronic disease because, well what you have is a, a molecule, this molecule, which again is asking the system to help out. So what you see, John and I were talking about this earlier, you have these oxidants - say hydroxyl groups that are creating damage in the DNA or in the golgi apparatus or in some form of the cell. And if it gets closer to the cell membrane, it may cause lipoxygenases. If it causes further damages you make peroxidases. And then if you've made further damage, you get these nitric oxide substances that don't do well. Those two together are lethal for the cell magnifies.

Jeffrey Smith:  I'm just thinking of Lord of the Rings. And you have the, the, the bad guys coming in and they, they break through the first or the first barrier and then they break through the next barrier. And if they get to the inner chamber, they, they take the King and that's it. All right, so this is, so we have these, these walls, there's different levels where the bad guys are coming in the orcs or whatever. And the, if the Nrf-2 is not functioning, then it's as if the King never sends the army. It never engages the defenses. Is that, that'd be a fair, right?

Martin Katz:  We, well, we love your last example of that where you go with the coast guard, you got the Marines or the Army, you know, you all these guys working together, Air Force to, compliment each other, whether you're talking about a sea approach, an air approach, a land approach. You've got these guys coming in from different directions, but if you don't have the Nrf-2, while, gosh, the Marines just didn't show up, or you know, Air Force just didn't show up. And so the other air force on the bad guys team is gonna destroy your, your guys on the ground. Um, and so, Nrf-2 is producing this incredible array as you see here of these proteins. And, um, molecules that are helping to deal with it on numerous different fronts to help to deal with these insults. And so if you don't have that, you may not be able to deal with an insult that that gets through and again destroys your King.

Jeffrey Smith: So this means that if your Nrf-2 is suppressed, you are much less likely to stop an intruder from causing a disease. Now I imagine that the list of diseases that a suppressed Nrf-2 could generate is rather long. Are there certain diseases that are unrelated to Nrf-2 where if the Nrf-2 was suppressed, you would not expect that particular disease? I mean, can you identify any of them or are they all kind of like, maybe I put you on the spot here.

Martin Katz:  I would go with "No", make it easy.

Jeffrey Smith: What's interesting is, you know, we've talked about so many times, our glyphosate is so damaging to the fundamentals, the foundations of health. And they're like, if you talk about how it can mess up the gut bacteria experts say, yeah, there's problems with gut bacteria can lead to most diseases. It can create inflammation, lead to most diseases. It can block the ability to absorb minerals, most diseases. Here's another one. Okay. We just dealt with the gap junctions. Yeah. Most diseases. And here's another one, Nrf-2 most diseases. But I'm jumping ahead because we haven't yet said what glyphosate does, but I know because I did this webinar before, if anyone watched it. So will tell us about, give us the news about what happens when you applied glyphosate to cells to the Nrf-2.

John Gildea: Yes. So, so in the case of a model for detoxification, we use a cell called Hep-G2 is the liver cell. And as you probably know, liver does, the bulwark of, of detoxification in the body, even though every cell in the body does do detox. So we put glyphosate again, same concentration, a hundred micrograms per milliliter, for a short period of time. And it reduced Nrf-2 expression by 30%. Um, which is very bad.

Jeffrey Smith:  That sounds very bad. Now in the case of the detoxification, I know that I've talked to scientists who talk about the possibility of glyphosate damaging the P four 50 cytochrome pathway, which those enzymes are used in the liver to detox. And then if you, I've said this before, that if you can't detox out of liver, that means all the other toxins that are in the liver that are normally detox through that pathway can become amplified. So glyphosate becomes the King of the toxins because it's like, Oh, it's like it, it, it stops the cops from arresting the criminals or it allows the criminals to come out of jail. And so they all do the damage. They all do the damage and there's no way to usher them out of the body. But you're saying it's actually worse than that because Nrf-2 is not just a mechanism that's used to clean the liver, but it's used to clean every single cell. If there's junk, if there's damage in each cell and it's not being, if the waste products, if the, if the, if the toxins are not leaving, then we can become toxic, not just in the liver but throughout the body with a reduction in the ability in Nrf-2. Activity.

John Gildea: Yeah, that's exactly right. It's going to make every meal that you eat that's not perfectly clean that much more dangerous.

Jeffrey Smith:  Well, thank God everyone ... everyone listening to this is eating perfectly clean. But sometimes they have to believe sometimes for those that are occasionally breathing, this might be important for you. Right. All right, so now here comes the magic question, which I know you have been waiting to share and some people are, what happens with BrocElite?

John Gildea:  Yeah, so putting, BrocElite on these cells, very similar to our first gap junction study is it doubles the activity. So Nrf-2 add a dose, that can be achieved in the body, uh, doubles the Nrf-2 activities. So, um, we both looked at Nrf-2 and a downstream molecule and both of them went up. And, if you add both of them together, it's still higher.

Jeffrey Smith:  Both glyphosate and BrocElite?

John Gildea:  Yes. Together it's even higher than nothing.

Jeffrey Smith: So what is the, how much higher does it get when there's no glyphosate? How much higher does it get when there is glyphosate?

John Gildea:  I forget what the exact number is, but it's something like 70 or 80% higher with sulforaphane and it's 50% more than 50% higher with glyphosate and sulforaphane.

Jeffrey Smith:  So the, so the sulforaphane is saying "Na-na-na-na" and, I'm, making it better. Glyphosate comes and says, sorry, sorry. I'm making it better when you can't do much. Yeah. That's for, first of all, this is amazing because now we can detox better throughout the body. Um, and by having the BrocElite in there, even if we don't have glyphosate, and hopefully a lot of the people listening have removed glyphosate to a very large extent from their diet. It's hard to say, it'll be 100% given it's around the environment. But then we get to start to clean out other stuff with more efficiency.

John Gildea:  Right. And our next, um, piece of data to, to sort of jump to something I've been sort of itching to, to share for a while is there's not much activity, uh, evidence that sulforaphane actually activates Nrf-2 in a human at the cellular level. Um, but I figured out a way to, test that and, um, using cells that line, um, your mouth called buccal cells. So they're easy to access. You can just swipe them with a, Q-Tip, yeah. With a swab. And so I took those cells and then took those cells and put them into a Petri dish for a short period of time and added pure sulforaphane to them. And then I also, had the pill go into the same person and showed that in two hours I got the same induction, actually in the cells of the mouth, using, uh, broccoli pills, a normal dose of broccoli pills. And to our surprise, it was equivalent to 5 micromole of sulforaphane which is higher than it's been, measured in, in the body so far,

Jeffrey Smith: Let me, let me unwrap that because I, I, I know that some people are, are wondering exactly what that means. And let me see if I got it. When you take this swab and you put it in the Petri dish and you put the BrocElite in, it increases the Nrf-2. Correct by how much?

John Gildea:  It looks like a double.

Jeffrey Smith:  Alright, so doubles Nrf-2 just by putting the BrocElite, but for others, you give them a pill, you don't open the pill in the mouth, you give until it bypasses the mouth goes into the system, systemically comes back to all cells, we assume because now you're just taking a random random location of the cell in the mouth and then you check that and lo and behold, how much increase in Nrf-2 at that point it's doubled. It's doubled again. So whether you put it directly in the Petri dish or you give it to the human, which I actually prefer as a method of tradition. So you give it to the human and all of a sudden the amount of Nrf-2 is increased in the cells. This is spectacular news. I did not know this. So you've been waiting to tell, you've been holding onto this one, John.

John Gildea:  Yeah. I knew you were going to like that one.

Jeffrey Smith:  That actually says a lot to me. Now. What did you mean by 5 micromoles? You're saying that the amount of sulforaphane that end.

John Gildea:  Directly on the cell.

Jeffrey Smith:  So you were able to check the amount of, by putting, giving the BrocElite, you know, how much you were guessing that a certain amount of sulforaphane would end up in the cell, but it actually was more than you predicted.

John Gildea: Yes.

Jeffrey Smith: Wow.

John Gildea:
So in the in vitro study, I used pure sulforaphane so I could compare our product to it. And so, um, I did a couple of different doses, but basically what I'm showing here is that, um, five micromoles sulforaphane produced, directly on the cells was equivalent to two pills of BrocElite that you take orally. And the highest amount of sulforaphane measured in blood is in between one and two micromoles. So we're getting an effect that's actually higher than the, than the clinical studies.

Jeffrey Smith:  Wow. So all the stuff that John Hopkins did with their high expensive frozen stuff, you're actually surpassing it.

John Gildea:  Correct.

Jeffrey Smith:  This is really cool. Now is that mean that it's because even though they've been able to stay to stabilize it or use it for short term, then it starts to disintegrate or degrade as it's taken in and yours are stable through the whole process?

John Gildea:  Hmm. If I had to guess at a mechanism, I think it's because we're not just using sulforaphane, um, that we have by accident stabilized at least two other isothiocyanates in that come from, the, that's in the product. So PEITC and AITC and two other. Um, so, um, sulforaphane like molecules that we know work somewhat synergistically with, with sulforaphane, so that's probably the reason why

Jeffrey Smith:  I like those accidents John. I like that. All right. So, um, sometimes I forget my BrocElite. I have to admit that I didn't have some today. I'm going to have some this afternoon. All right. Um, I want to share some of these, some of the study results of the 39. Now I don't want to cut you off cause you've probably prepared some more slides for us. Is there anything else you want to share before I get to pretend that I know what I'm talking about? Because I've looked at once in one summary and it's just a, it's so exciting to see so many diseases and disorders that are related to eating GMOs and Roundup that have been to get better or reverse in some way with sulforaphane. Because if you can show that sulforaphane is reversing or protecting against two main areas where glyphosate does damage, it gives the possibility that these are the ways that glyphosate are, is causing those diseases or is exacerbating those diseases. So it's exciting for me and it's also exciting to figure out, you know, it's, it's exciting to, because people who have those disorders get hope and have a way that they can participate in their own experiment. So I want to go into that 39 that list of 39 do you all want to share any pictures first?

Martin Katz:  I think we're good at, you know what I mean? Succinctly. I think what you're, what you've shared is very important that, you know, the cell is designed in a specific way to be functional, to be able to communicate, to be able to deal with the oxidants. And if that's broken down, you're gonna see diseases over a period of time. There's only so much we can do to combat that. And if we're not avoiding or we're not doing something, unfortunately, you know, we're going to be dealing with diseases and illnesses and you know, I, as a physician, that's not what I want to be doing. I want to be telling people that they're healthy.How they can continue to support their health. How they can continue to be healthy so that they can play with their kids, they can play with their grandkids, they can travel, they can, you know, thrive help.

Martin Katz: Ultimately so do you know, diagnosing people with disease is really not what I want to be doing as a physician. And so being able to deliver something to our loved ones, to our, um, clients loved ones and themselves is a delight for us and really why we started this company in the first place. And so being able to support cellular communication and being able to support the cell and it's need for balancing this redox, again, oxidative stress versus being able to deal with that is just incredibly important. So thank you for giving us a platform to do that.

Jeffrey Smith:  And I also thought it out and thank you. I mean I love the story that, that, that prompted, you were there as very close a person in your life that was sick and you decided to use the tools of your profession and your, your training to help one person. And that is awesome. That is awesome. As the promote is the driver for that. And then discovering that, yeah, you actually discover something that no one else had discovered before. So here's my, here's my, I like lists by the way. So I want to just, I'm going to go through this list really quickly. These are the things that there's a, there was a summary on online of the sulforaphane. Sulforaphane benefits based on the peer reviewed literature, and I'm going to just mention the names of the benefits or the, that it helps.

Jeffrey Smith: Um, and now we can understand that if it promotes, if it's a single largest promoter of the Nrf-2, if it's basically, you know, sounding the horn and allowing all the air force and the Marines or, or Gandalf's army to, to go in there, then it's, that's the one way. And if it's allowing the cells to communicate so that they're functioning as a community and not boarded up the water, boarded up the windows and operating individually, that's obviously another way. Okay. Promotes detoxification, obviously combats cancer. Obviously you've talked about, here's some ones that are not so obvious. Lowering cholesterol, heart, cardiovascular disease, obesity, diabetes, immune system. It's antiviral, bacterial and fungal protects the skin that combats inflammation, combats depression and anxiety. It restores cognitive function, protects the brain, Parkinson's, Alzheimer's, Huntington's seizures, schizophrenia, substance abuse, autism. There's a very good research that I've looked at with the autism showing these symptoms improving and I think it's a very popular, um, a compound or popular supplement in the autistic community, GI injury and inflammation, which is the number one reported damaging effect of GMOs and Roundup.

Jeffrey Smith:  According to our research, I H pylori liver function, health damage from pollution, airway inflammation and asthma in auto, auto info, auto-immune inflammation, pain, bone formation, arthritis, muscle damage, muscular dystrophy, kidneys, hair growth, alcohol tolerance, um, beneficial and pregnancy offspring, health eyes were almost done, uh, against keloids, whatever that is, bladder dysfunction and children with HTPs, whatever that is, that's the 39. Now that means that it's fundamental. That means that it is a basic, a basic promoter of health. And I think we've seen in your research, John, the two ways that it does, and I'm sure there's other ways as well. And the two ways that I'm particularly interested are the ways that glyphosate moves us in the wrong direction. So I'm, I'm very grateful for both of you for doing the research and not just the positive research on BrocElite and sulforaphane and it stabilized form, but also the research on glyphosate. So that, that's the excuse that I need to get it to all the people listening now because they know they want to detox, rebuild and repair from having been exposed in the past and from the continued exposure that may happen even through the air and the water, even if they're eating a hundred percent organic diet.

Martin Katz: Yeah. And Jeffrey, let's just remind people that the absence of disease is not necessarily wellness, you know, so I often have people come in without the diagnosis and they're like, wow. And you know, they just finished a cigarette out in the parking lot or they're overweight and they just haven't been diagnosed with the disease. So, so again, these cellular pathways are incredible. Make sure that they're intact so that you don't get diseases as well. We don't want, we don't want people end up with diseases. We want to, uh, prevent that ultimately.