 Okay, looks like we are. Got it. Glide streams. Hey everybody, on this Friday afternoon, we're just popping in not for a formal, long lecture like you usually get with Bob Miller and I. That's coming. So stay tuned. We actually decided this was such an important topic that we wanted to jump on spontaneously this afternoon and just do an introduction because I think some of you may relate to this and you will want to for sure tune in for the full lecture and information on INOS. And of course, I'll let Bob talk about that in a minute here. But it will be coming on Friday, October 29th. We'll be live at 4 p.m. Mountain, 5 p.m. Central, 6 p.m. Eastern, or if you're on the Pacific Coast, it'll be 3 p.m. So mark your calendars because this will be really a big breakthrough. And again, I was just telling Bob right before we got on. I've had so many ahas in my own health. My job I've learned is to be the guinea pig. And I learned through experience. And so finally, when I kind of got that after the cancer and the Crohn's and the mold, I've just learned to accept that I'm going to be the guinea pig for all of you. And I go through experiences and I learned some really fascinating things. So this all started on while this whole month I've had some mold hits. A dear friend of mine is remediating and brought over some laundry and a few things to when they didn't have any laundry access. And so every time that there would be this exposure, and I think the underlying root was ketomium, this really nasty mold, I would have these mold hits pretty much all this month, two or three times a month, I've been having or two or three times a week, I've been having these and they will just knock me out. And when I started checking my blood pressure, I realized I was running 80 to 85 over 50 to 55, which is really not compatible with standing upright. So it's no wonder what I would happen after these. And again, we'll talk about a few details today, but I'll frame it with my story is I would literally just fall asleep. And it's interesting because for five years, I've known ketomium is a really nasty mold, not only for many of you listening, but for me. And I literally nicknamed it the narcoleptic mold, because I would be like sleeping beauty just down. If I got an exposure, I would be, I could be walking on the concrete sidewalk, I could be at work, I could be at home. And I'm like, I must lay down now, I cannot even keep my eyes open. And again, some of you listening can probably relate. And I joked because narcolepsy is that you know, you fall asleep within seconds, you could be standing up. And that's how it felt to me. And for many, many years, I've been trying to figure out what is the mechanism as it inducing low blood sugar, low blood pressure is it, there's got to be some mechanism here. And this most recent episode was one of the worst. It was actually last week on Tuesday. And I had it in conjunction with IVIG, which made everything worse. And we'll talk about some of the other triggers. But literally for 24 hours, I was sleeping, I had gotten a great night's sleep, I woke up, I was kind of disoriented after the mold exposure. And, and then that whole day, I would wake up for five or 10 minutes and then just lay back and like deep, deep sleep. And then I'd wake up again. And the funny thing I was telling some of my friends, that every time I'd wake up, I'd be like, Okay, I wonder what's going on in my vascular system. I wonder what, like I would literally be thinking through the pathways and trying to figure out what was going on. And Bob and I have been talking, and he really helped me put this together. After that episode, as we talked, and we were back and forth texting frantically, because we're like, What about this? What about this? And some of those, what about you'll hear today? And you will hear in depth on the 29th of October, because this pathway, as Bob will share, is probably underlying a lot of the complex chronic issues for people. And I'll just spill it in a nutshell. And then I'm going to kind of turn it over to Bob and now pepper in some of my experiences with what made it better and what made it worse. The bottom line is INOS regulates nitric oxide production. And nitric oxide is a vasodilator. So many of my patients actually want to produce more of it because they feel better with exercise they feel. So there's a lot of people who don't produce enough of it. And this helps with, as you can imagine, lung capacity, oxygenation, tissues, cardiovascular, workout potential, you feel better, you feel more blood flow to your periphery and to your tissues. It even helps erectile function and sexual performance. So this is a really big deal, this nitric oxide. However, on the other side of the coin, as there's always two sides, there are people like me who produce too much. And again, I'm going to let Bob talk about this in just a moment. But the thing there, as you can imagine, all of a sudden, if I have other factors, which I'll tell you some of the things I found that were contributing that I was doing, and a mold exposure, which mold is one of the potent inducers of nitric oxide, then you have this vascular collapse. And literally, I was almost like someone who would be septic or in septic shock, shock where they're in fact, one of my doctor friends said, Jill, 80 over 50, that's criteria for sepsis. Are you sure you're okay? And I was like in between falling asleep, I was I knew I was not okay, but I also knew enough to be, you know, I'll figure this out and I'll be okay. So after I figured it out and did some interventions, I'm back to normal. I still believe if I got a mold hit, I'd probably feel similar. I have to be very careful. But this is a big aha. And I am so excited to share it with you today, because I think some of you listening will feel the aha as well. So that with that introduction, Bob, let's turn it over to you to share a little bit about this pathway that you're looking into and how it affects so many other things in our body. Absolutely. I'm so excited about this of all the things that I've just looked at over the years. This might be the most exciting. And let's make it a goal and intention that the next time you get a mold hit, you don't even notice. Yes. And I promise guys, if I figure this out, I will share everything I've learned with you, because I know a lot of you who struggle with POTS, postural orthostatic tachycardia, some of these vascular kinds of issues. I think it may be related to this pathway. I do believe so. I'm going to do a quick screen share here. Oh, and let me get you to a screen. There you go. Do that. Okay. Let's see. We're going to grab the screen here. Okay. There we go. You should see the slides now, I believe. Okay. I'd first like to say that let's look at the title here. The title is The Carnahan Reaction. So this is the official launch of the Carnahan Reaction. And the reason we're calling that is because this is what the pattern is that we saw here in Dr. Jill. So let's give you the cliff notes here. And as Dr. Jill said, in October, we're going to give you, I can imagine Dr. Jill, we're probably going to go two hours, probably on that one. I can't wait. You guys must tune in or tune into the recording. And thank you, Bob. I just think it's hilarious that we're calling it this. And yet, like, gosh, if I had to suffer for science, then at least we get something named after us. Absolutely. 100 years from now, people will be studying about this, Dr. Jill. All right. I've used this slide before. The 3D chess game played underwater. It's very complex. And you did an excellent review there. And that is that nitric oxide is very much needed. So I don't want to make this sound all bad. It is considered the miracle molecule. It's just two atoms, nitrogen and oxygen. It's very significant, crucial to your well-being. It's a vasodilator, as you mentioned. It stimulates the brain, helps men with erectile function and impedance, as you talked about. Powerful signaling molecule. I mean, we could do probably several webinars on just the benefits of nitric oxide. I don't want to make this sound like it's bad. Well, Bob, I want to mention that's why, to me, this was such a big deal because I have been touting the benefits of nitric oxide to my patients for years. And we use it in clinical practice. We use precursors. We use beats. We use arginine. We'll talk about those. But what I didn't know was, whoa, could too much of a good thing go the other way? I never had the concept that this could go the other way. But as we were talking about some of the snips, the first question was, does this up-regulate function or down-regulate? And again, I'll let you describe all that. But it was fascinating to me to think, okay, something that's really good for me and for everyone else can be too much of a good thing. And in hindsight, I never do well with beets or beet juice. I don't do well with arginine. So it's interesting. We'll talk about that. But I kind of intuitively knew that something here was not right for me. Absolutely. That's why I often talk about Goldilocks and the Three Bears. It can be too hot, too cold, a little too much. 1998, Nobel Prize. I mean, if you Google that, you'll see the pictures. And if you Google nitric oxide and Nobel Prize, you'll see all kinds of websites. You'll see probably dozens of formulas to boost your nitric oxide, telling you all the benefits of it. And clearly that's true. And I'm not going to read these, but these are all the beneficial effects of nitric oxide. And absolutely all true. However, as you said, sometimes there can be too much of a good thing. Now, what I'd like to show everybody here is an interesting chart that we made up that shows how this nitric oxide works. So the one that's the good nitric oxide is your enos, your endothelial nitric oxide. Now, the way it's made is there's a substance called BH4, tetrahydrobaroptin. And we're going to keep coming back to this. And it combines with an amino acid called l-arginine, oxygen, heme, NADPH. And by the way, I would encourage people to watch the video we did some time ago back on NADPH and the NADPH steel, because that probably plays into this as well. Then we make our good nitric oxide. However, the BH4, after it donates what it needs to to make the nitric oxide, turns into BH2, dihydrobaroptin. We then need to take this BH2 and turn it back into BH4. These purple ovals here are enzymes that do that. If we don't convert this BH2 back to BH4, something very strange happens. The enos enzyme that's supposed to make the nitric oxide makes a nasty free radical called superoxide. A nasty, nasty free radical. That superoxide will combine with nitric oxide, chew it up, and make something called peroxy nitrite. And by the way, we did a whole video on peroxy nitrite. And that peroxy nitrite, by the way, the chemical symbol really is, oh no, suppresses BH4. And we're on one little merry-go-round here. Now that's what happens with the enos. Now what a miracle with the body is, I never ceased to be astonished. There's an enzyme called NOS2, or inducible nitric oxide. So the NOS3 makes little amounts of nitric oxide for the vasodilation. NOS2 is like the army. It says we've got a foreign invader here. We've got to take care of this foreign invader. It makes massive amounts of nitric oxide. McKay Ripley, who you had on before, talks about nitric oxide. He calls this the gatling gun of nitric oxide. Makes a boatload of it, kills bacteria, virus, fungus, parasites. Is this a good thing? Absolutely, unless it's excessive. Then we have tissue damage and organ dysfunction, and it hurts us. So what happens if we are continually making all this massive amounts of nitric oxide? We deplete our BH4, tetrahydrobaroptin. So now this guy runs, but rather than making the nitric oxide, or maybe in addition to, we make more superoxide. This is a bad boy. Makes the peroxide nitride. If we don't have enough superoxide, dismutase the antioxidant. We then have more of this, and even if we do, we make hydrogen peroxide that if we don't have enough glutathione and thryodoxin and catalase, we make what are called hydroxyl radicals that are again inflammatory. So there's a lot that can go wrong here. Now clearly, this is a good thing in animal studies. If they knock this out, the animal dies of infection. But I know you and I are both on the same page on this. We have done a lot of things in the environment that's really throwing a monkey wrench into things. When we do our long version, we're going to talk about how aluminum, mercury, BPA, that's your plastics that's now polluting the entire world, electromagnetic fields. By the way, we did a video on EMF, high fructose corn syrup. I am stunned how bad this is. I mean, we knew it wasn't good, but I'm going to show you a moment why it's worse than we thought. And Bob, most of that is contaminated with glyphosate, which is on this list too, right? And also, it seems in some processing, let's get some mercury in it. Gluten, and then of course, I don't have the glyphosate on here, but it's on another map. Chlorine and iron overload. So I believe we did a video on iron overload. I think we did. We did. And I'll be sure to include links. I didn't mention the beginning. If you guys want to find all the videos, they are now on iTunes. So Dr. Jill Live is an iTunes podcast. Listen, subscribe, please leave your reviews, and also YouTube, so you can find these all. They're all free. So if you want to listen to more with Bob, he is some of the most used. He is the most popular guest. He has the most views. So go back. We have four or five already done. And Bob, I want to comment on that because years ago I was a swimmer. I almost did college level swimming. And after I started getting mold exposure, I had to stop swimming because the chlorine would bother me so much. So once again, that probably played into it. And as you'll probably mention, I'm a carrier for hemochromatosis, which means I have iron overload. So it's kind of like the perfect storm. Absolutely. Absolutely. So here we have this, you know, we have this ionos enzyme that's supposed to be our friend being our enemy. Now, I'm going to pull in another map here, very similar, but it just shows, you know, again, some of those other things. And it just focuses on the, on the NOS2. And here you see the glyphosate and lipopolysaccharides. Now, also you'll note that interleukin-6, and by the way, I encourage everybody to watch our video on interleukin-6. I think like 5,000 people have listened to that so far. That stimulates NOx, makes more mass cells in histamine. We have a video on histamine. And guess what histamine does? Stimulates ionos. And then just a quick note on high fructose corn syrup. There's a very important enzyme called SIRT1 that supports ionos, supports superoxide disputase, inhibits NAD-peach oxidase, we have a video on that, and inhibits NF Kappa B that stimulates ionos. So when anyone has mutations in SIRT1, they're at a disadvantage. But if you're eating high fructose corn syrup, which is everywhere, you'll also inhibit SIRT1. So that is the, the cliff notes. And just one little thing here yet, and that is that aluminum inhibits the enzyme that takes the BH2 to the BH4. And there's something called the eryocycle that clears ammonia. Ammonia inhibits BH4. Yes, and we have patients who have high ammonia as well, so. And many of these people are inflamed. This was a new piece of news. I don't think I had a chance to pass on to you. Ammonia stimulates the arginine transport. Wow. So then that makes more arginine, more ionos, more inflammation. Wow. We'll just briefly mention that we're going to this in the next webinar. But l-arginine is important, but it's a non-essential amino acid. And if we get too much of it, it feeds the ionos. And then you can tell us later about how taking lysine helped with your situation because you cut back on the l-arginine. So there is what's happening. I believe that multiple environmental factors that we weren't exposed to 30 to 50 years ago, high fructose corn syrup only came around in the 70s and 80s, glyphosate relatively new, EMF relatively new, using the glyphosate on the wheat, relatively new. So I believe this is possibly why we're seeing so many conditions. And we're not going to get into them today. But it's kind of like the who's who list of conditions related to upregulation of ionos. We're still researching. We'll have that whole list by October. But it is an extensive list of problems created by excess ionos. Now, here is, drum roll please, the Carnahan reaction. So we may play around with this language a little bit, but for the most part, gain of functions, mutations in NOS2. Now let me explain what that is. We have our genetics and we inherit our genes from our parents, mother and father at the moment of conception. And we can have what are called genetic mutations. Most of the time, mutations make the enzyme less active. Like people have heard of MTHFR, where you don't put enough methyl groups on your folate. Most mutations are lacking function. The enzyme does less. There's a couple of them that are gain of function, meaning that the enzyme works more aggressively when it's mutated. So gain of function means that the enzyme works even faster than normal. So gain of function mutations in ionos, along with environmental and endogenous, in other words, internal things that stimulate NOS2 creates inflammation from the excess nitric oxide, inflammation from superoxide when we get that NOS on coupling, and the depletion of BH4. By the way, BH4 is also needed to make serotonin and dopamine. Yes, I was going to mention that because I love those neurotransmitters. And you can really cycle through. And if you're out of that, you're not going to create those neurotransmitters. So it can affect sleep, or it can affect all kinds of other things we need for mood and sleep, and drive, and ambition, and that. And I love, Bob, I just want to let people know, like, this is really where Bob's work has, as I mean, we've just a few months ago, when we first started talking about this, the question was, is this a gain of function, increase production, or decrease? And with his work, it kind of confirming. And I remember our very first conversation, I was like, gosh, because we had looked at my genetics specifically. And I thought, I remember, I don't do well on beats, and I don't do well on. So I had the suspicion it was a gain in function, but kudos to you for kind of solving the riddle here and putting it all together. And what's great is by October, you'll know even more about this cycle. Oh, absolutely. This is going to be our focus. And we'll have more information on it by October. I'm planning a spring conference for doctors or anyone who wants to attend, probably a three-day conference. And this is all we're going to talk about. We're going to talk about this for three days, because I think it's that significant. Okay, here it is. This is the RS number, like if somebody's done 23 in mere any other genetic testing, this is it. Mind-blowing, 4.73 times increased INOS expression. Wow. Wow. That's a big deal. Yeah. Then this other one that ends in 18, increased INOS activity. So involved with Crohn's disease. Anyone on audio, click the slide back once. I'm just going to read those, because if you're hearing it, and for some reason on this slide, so the RS277-9249, and then go to your next slide, and the RS229-7518. So for some reason, you don't have the video here. I want you to be sure and have access to those RS numbers. Sure. And if they just look up those RS numbers, it's the A allele. That's the one that's the increased on the 18, and it's the A allele on both of them. So if you've got A as one or A as both, you've got heterozygous or homozygous mutation on there. Now, what I've done here, again, I've listed the environmental factors, and then internally, histamine, mast cells, ammonia, lipopolysaccharides. And Bob, go back one slide on that last RS. I wanted to point out, yeah, right there. Okay. So you've said very early onset Crohn's disease, also colitis and IBD. We were talking about this earlier, but as you may or may not know from my history, 20 years ago, I was diagnosed after breast cancer with Crohn's disease. And once again, along with many other factors, there's no doubt in my mind, I also have a gene called NOD2, which is high risk of Crohn. So there's other things that play into this, but I believe this INOS was also playing into my diagnosis of Crohn's disease. I'm sure it was A factor, yes. So I think we mentioned everything except the mole. And we mentioned the glyphosate. And then if you've got high histamine, mast cells, ammonia, or lipopolysaccharide, guaranteed in October, there's probably going to be three columns here. Yes. As we continue the research. Now, you're very brave putting your mutations out there on the internet. So Dr. Jill has carrier status on the HFE H63D. I'm sure people have heard of hemochromatosis. That's usually when people have a homozygous on here or two. But the literature shows this causes you to absorb a little bit more iron. Incredibly common in people with English, Irish, and Ashkenazi Jewish background. Very, very common. Yes. I see. And interesting, Bob, a lot of docs aren't checking this routinely. I always check iron ferritin, transparent, all of the labs on every new patient. And then if there's some concern about iron being borderline, or if I find some funny things happening that I don't quite understand, I will check the hemochromatosis gene. So if you're wondering about this, even though these are genetics, you'd need to go with Bob or 23andMe or one of those companies, you can actually have your doctor check your iron and check your hemochromatosis status on a regular lab. And particularly if you're of English, Irish, or Ashkenazi Jewish background. And interestingly, I think we spoke about this, that this was actually beneficial during times of famine. So during times of famine, people who had this actually did better. Then hemoxygenase, we didn't talk about this whole lot, but hemoxygenase makes something called bilirubin and biliverdin, and the biliverdin inhibits the ionase. So if you've got mutations on here, your creation of that biliverdin may not be as robust. Now here's what makes the Carnahan reaction, the Carnahan reaction. Those ones we talked about, mother and father, mother and father. And you can see that this number over here is how many times this happens out of 49,000 people. So my software has 49,000 people and that generally are doing this because they're not doing too well. So I would suspect this is lower among the general population. So even among not well people, 3.9% have this, 9.9% have this. The odds of both pretty low. So this is why we're calling this the Carnahan reaction. And I've only seen one other person with both of them homozygous. Of course, we've only been looking at it for maybe six, eight weeks, but I'm sure more will come up. Now we talked about that you need to recycle your BH2 to your BH4. And there's an enzyme dihydrofolate reductase. And that is what does that. That is what takes the folate. And by the way, when we speak in October, we're going to have the entire pathway of BH4 production made. And then we are going to be looking at all of the SNPs that may further impede the DHFR. So you were kind of set up here with the perfect storm, my friend. You had all this up regulation of INOS, then you had some iron pushing it a little bit, maybe not recycling the BH2 to BH4 very well. And then all those other environmental things that you did. So all of those are moving together. Now I'm not going to go through this. This is for our October or maybe even the June. But these are all the mutations that could be related to excess INOS. It's quite the list. This is your nitric oxide or superoxide dismutase. This is superoxide dismutase. NERF2 keep one. I think we spoke about this in one of our talks, how this makes your antioxidants. Kit and NOx can make more mass cells. These are the genes that clear the histamine that we spoke about in one of our talks. CERT1 huge, as we said, supports SOD, NAS3. Here's the urea cycle for ammonia. And all of these genes are related to the BH4 production recycling. I believe you need to look at all of these to get a good look at what's going on. In October, we're going to delve in each of these just a little bit so people can understand. So now you can see why it's the 3D chess game played underwater. And there isn't just one snip here that's the problem. And I was going to share just because as we talked, then I was like, okay, let me do some interventions and see if this works. And it really did. So I was taking, because of that mold exposure, I've always known I don't do great with recycling glutathione. I think a GSTP1, maybe, and maybe another one. And there's other things we won't go into that today. But bottom line is I have, it's the Goldilocks again with the glutathione a little bit. It's okay. Too much does not do well. But I had been resilient in doing well. So with this new mold hits, I took a lot more glutathione. That was actually contributing to oxidize glutathione and making as Bob showed earlier that pathway worse. I've always known for probably 20 years, I do really well on lysine. And I do know that that will inhibit viral replication like Epstein-Barr. So that's the reason I was taking it. But when we realized this would inhibit arginine in this pathway, I took triple the dose and pretty quickly noticed some improvement on that. VIP, any of you knowing the Shoemaker protocol or working with VIP at all, I learned five years ago with my bad mold exposure, I had recovered fairly well. And I was like, okay, it's time to try some VIP. This was maybe a year into my mold exposure. I didn't know why, but I did not do well. Now I know why because VIP actually up regulates arginine in the same pathway. And on the notes to me, I had been on VIP off and on again, because I've been doing better after the mold exposures. And I think that VIP made my hypotension even worse. It's known to be a vasodilator. So lysine, VIP, glutathione too much. And again, these things are all good things. One of the other things that wasn't really interesting, I went about a week after my exposure and got a huge blood draw, which was 40 tubes of blood. So it was kind of like a therapeutic phlebotomy. And I felt so good. Most people 40 tubes of blood, they'd be like, I'm depleted. Me? No. And I've noticed that too, Bob. No surprise. Years and years and years of getting blood draws. I always feel better. And I get a lot of tubes sometimes because I'm looking at all these pathways. So that could be a clue that you have iron overload, because you feel better after you give blood, even 40 tubes of blood. So those were a few of the things that I kind of based on our conversation. For me personally, this is not medical advice. But it really helped me. And I feel like this pathway was a big aha. So Bob, thank you for sharing. And I am so excited because I know in the next month or so you're going to have even more information. Please comment, share this with your friends, because we'd love to have a big group live on the 29th with us with your questions and answers or questions. And we'll have hopefully answers. Any last comments, Bob? Because this is big. Well, I think I just take a word you said this is big. Everyone talks about the benefits of nitric oxide. All true. And I don't want to emphasize that the nitric oxide is not bad. It's our friend. But when it's up regulated by the INOS and environmental factors and genetic factors, it can turn on us to plead our BH4 and be rather disastrous. And as I'm doing my health coaching here at TEO Life, I'm just noticing that so many people that I was stuck with before, you know, we made marginal little improvements here and there. And I'll go back and look and it's like, wow, this is their issue. It could be behind many, many things that no one is noticing. And, you know, our goal here at the Research Institute is to make a contribution to humanity. That's what we want to do. So if getting the word out about the Carnahan reaction and it is helpful to a lot of people that just makes us happy that people are getting well because of this. And again, it all goes back to environmental toxins. One final note, I just have a suspicion that this up-regulation at one point in mankind's history may have been beneficial. If someone was living in parasites or virus or something, that up-regulation probably gave them the immune strength they needed to fight off the pathogen. But like many things, now today with all these environmental factors pushing it even harder, it's now to our detriment. So I hope somebody found this helpful and maybe there's somebody listening who says, I need to take a look at this and see if that's what's going on with me. Yeah, so stay tuned. We'll be back. And Bob, just publicly thank you because this is one of those things for months and years. I had these crashes, like we said, in our epilepsy. I'm like, what is happening? I've been studying, trying to figure out, and I really think this is at the root. So stay tuned, Bob. Thank you for your gift to humanity. We will have all kinds of information about your conference about where to find you. But before we go, where can people find you and find more information? Okay, sure. My clinic where we do the health coaching is Tree of Life Health, www.tolhealth.com. That's T is in Tom, O is in Oscar, L is in Larry, health.com. And if there's any practitioners who would like to do any of our work, dna-supplementation.com, tell us that you saw this on Dr. Jill. In October, we're going to have a special announcement so the doctors take a class from us. They'll get a discount because you referred them. So we'll have that coupon code and everything in place in October for people who want to take our certification course. So if anyone feels like they'd like to look at this, we'll be glad to help them out. Awesome. Bob, thank you. Look forward to talking more in October, October 29. Take care. And by then, I'm hoping you just laugh at mold. I know, right? Nothing. All right, take care, my friend. Take care, my friend.