 Hey, Dr. Ken Brown, we're live and I am so excited to, I know we've met before, but this is the first time we've actually really got to have a good conversation. I always, I often have friends on here and now hopefully we'll become friends because I really like you already. I always love, I mean, you know a little bit of my story, we might talk a little bit about that today, but I have had quite the experience with gastroenterologist and to me, there's like this very binary, like the ones that kind of say diet might have something to do with anything or the ones that are like, nope, diet has nothing to do with anything in your gut. So that's how I divide you guys up. And so I am so excited about, we're gonna kind of go where things lead us today, have some ideas, have some questions for you. Just housekeeping guys, I am so glad that you're here to listen to us. Please feel free to share with your friends. I think this will be a great, relevant topic. And if you need any more information about me, you can visit my website, just jillcarnihan.com for newsletter, all kinds of free resources. So let's jump in and I wanna introduce you first, Dr. Brown, and then we will get started. So Dr. Ken Brown received his medical degree from University of Nebraska Medical School and completed his fellowship in gastroenterology in San Antonio, Texas. He's board certified gastroenterologist and has been in practice over 15 years with a clinical focus on inflammatory bowel disease and irritable bowel syndrome. And many of you know, I am a 18 year survivor now of Crohn's disease and I have my own story with that. So super excited to talk to Dr. Brown today. He declared his mission is to bridge the gap between medical and natural science. One of the things we both share and have so much passion about is the science. I love to be on the cutting edge of what's possible with healing and health and use natural methods whenever possible. But we both really agree, we've gotta use good science and as we're doing these interventions, we've gotta actually track the data because the only way the next generation of doctors will do anything different is if we use great science. So I love that he's a fellow scientist like me but also open-minded enough to look at what's out there because what we're fed in the traditional medical journals is great but there's so much more. He was talking about a Mendeley account, I've got one too and so we dive into this and like look for it because what's amazing, Dr. Ken, I know you've seen this is there's a lot of research out there that we don't get taught in medical school that our colleagues aren't reading. I'd love to hear your take on that just a little bit because the research is there if we really dig sometimes. Oh, absolutely. And first of all, Dr. Jill Carnahan, my goodness, the unicorn doctor that I've been supposed to meet for years, every time I go to a meeting, somebody's like, how do you and Jill not know each other? I mean, and then there's a couple of times where we met in passing where you had a mutual, where we had a mutual friend. And they're like, oh, Ken, you need to meet Jill. And I was just like, yeah, we're, you know, and she's, yeah, I'm doing this also. Here we get finally get to do this across the country on a Zoom. So, we're finally meeting. I know, I'm fully excited, I mean, Jill. And you hold a very special place in my heart because you carry two of my favorite diagnoses, Crohn's and Celiac disease. So. Yeah, and so interesting about that. Cause again, now you're knowing a little bit of the functional piece. So I had cancer at 25, aggressive breast cancer within three drug chemotherapy, one of which was Cytoxin, which you probably know how it affects the gut. And there's some studies in mice that I found after the fact that show that perhaps the one of the mechanisms that it actually induces its response to the immune system to cancer is by creating a more permeable gut. So, and I was undiagnosed, silent Celiac before all of this. So can you just have the wheels turning in your head how this might have been possible to take someone NOD2 gene for Crohn's? So super high risk for this basically abnormal response to a normal microbiome, throw in any drug that creates a leaky gut, throw in an undiagnosed Celiac on a high gluten diet. Does that not make perfect sense to you of how it all happened? It makes perfect sense. And I actually read a little bit of your story. I think I've read some of your blogs and stuff when you were actually describing this. So I have a couple of quick questions. So you were raised on a farm, where was the farm? Central Illinois, right smack dab in the middle of atrazine exposure and organophosphates and endocrine disruptors and yes. So you gotta remember I'm from Nebraska, where the lymphoma belt. So if you draw a lymphoma, the incidence of lymphoma right across Nebraska and Iowa. So that's that whole exactly what you're talking about. University of Nebraska was the first institution to start doing autologous stem cell transplant because they had to. So many of the community were actually showing up with these blood-borne disorders. So there clearly is something about these chemicals. It's undeniable when I heard farm, I forgot to look where you were on the Midwest right there. There it is. And shocking that you went to a gastroenterologist as a third year med student. I mean, any of us that have been med students, that's a stressful time. I mean, that's bad enough right there. And then you're having these issues and you get diagnosed with ovarian cancer. A breast cancer. Breast, I'm sorry, breast, that's right. Breast cancer. And then it was insult to injury, Crohn's. Plus the celiac. I mean, your epigenetic environment really predisposed you. It's like what we know now, it's like you need to move from here and go to wherever. Some, Boulder, Colorado, perhaps. Totally. And you know what's funny, Ken, like looking back, I didn't know any of the, like I didn't understand this until I learned functionalism and then wanted to dive into the solving though. Like why did this happen? Just not that I never said why me. I more took it as a really cool mystery to solve. But I wanted to understand so that if I could prevent some person down the line from experiencing what I did. So my mother in utero, I think there was probably exposure there because at 25, you're gonna have cells that start to divide and rapidly do bad things, probably like five or 10 years old. And I actually had precautious puberty, breast-bud development at five years old. The pediatrician told my mom. Five? Yeah, five years old. Told my mom, oh, no big deal. Just it'll go away. Like there was no idea that those endocrine disruptors were probably either in utero affecting me through my mother's bloodstream and placenta or early, early in my infancy getting that exposure. We had well water. So who knows what kind of stuff we're leaking into that. Yeah, so to me it's like the perfect storm. And if you look at my dad's, I'm starting to write my memoir now. And if you look at my dad's journals of the chemicals they used in 1976, the year I was born, it lists like an endocrine disrupting nightmare. It's literally the top, it's atrazine, which is known to cause ambiguous genitalia and the frogs that get exposed to this. And then- What do they use atrazine for? It's for corn to control. It's an herbicide to control the weeds on corn, but it's a known, like it's banned in Europe. It's banned everywhere. And if you could pick up a map, you talk about Nebraska. If you look at atrazine and where the locations are, the hottest spot of red is exactly where I grew up in central Illinois. Oh my goodness. Yeah, so I totally agree with you. How does- So when you were growing up and when you went to med, where'd you go to medical school? Loyola University in Chicago. Oh yeah, great school. So where the doctors discussing the fact, because when I went to med school, that was the thing that they actually discussed was, look, we're getting way more lymphoma and leukemia than any place in the country. And they were pretty open about talking about it. Yeah, so I was, you know, M&M case grand rounds with the surgical residents. They would have morbidity, mortality, and they'd discuss the cases. So I was on as a case because I was the youngest woman ever diagnosed at that time in 19, or 2001 with breast cancer. So nowadays, it's actually way more common. Women in their 20s, even 16 and 18, which is so sad. But at that time I was 25 and in Loyola with this huge university system, I was literally their youngest patient that had ever been diagnosed with breast cancer. So I was kind of- Isn't that crazy? Yeah. A year ago, a whole study came out where millennials now have a significantly increased risk of colon cancer, more so than their parents. So they're having colon cancer in their parents not having it. It's the first generation ever to proceed there. The increased risk is now more in millennials. And I'm finding as a gastroenterologist, I'm finding more polyps and more pre-cancerous lesions like baritisophagus and such in the millennial population. So when you say now it's not that uncommon, that's a scary statement you just said. That's super scary. It's so scary because I remember like, I mean, it was such an anomaly at 25. And then since then I've heard and I think I've told this in part of my story, but when I was diagnosed, I was in a young woman's group and it was considered women under 40. There was about a half a dozen or a dozen of us. And I was the only one of that group that survived. Like Ken, I mean, it's a miracle, but all of those women in that group have passed because of the breast cancer. Oh my goodness. That is, you know, a tremendous story that you have and I'm so glad that your book is coming out. It's ready to be published. Any more hurdles to go through? It is in written, so it'll be like here, Kelly. Yeah, it's in the word in the middle of it. Well, I love to know, you know, you said inflammatory bowel is one of your favorite things. I'd love to know from this perspective of etiologies and things, what are some of the things that what are your thoughts? What have you seen in the literature? Does my story make sense to what you've seen? Oh, it does, totally. And when you sit there and say that I took a chemotherapeutic agent that disrupted the intestinal barrier, so I have to walk a very fine line with my colleagues because I think that when I, like many people that have this ah-ha moment where they say, wait a minute, like, you know, do you think diet has any role in this? And the doctor says, no, nothing. And you just get up and just walk out and be like, well, you're not my doctor. And then if you want to start, you know, when you become very passionate about something, there is an emotional response that happens with people. And I've seen this in the functional medicine community where somebody will really change their life. And you know, there's people that have become phenomenal spokespeople because they figured something out. I'm a little bit unique in that I didn't really have this health problem. I was doing pharmaceutical research and saw a health need and went, I think I can figure that out. So when you look at these guys that are making a big difference, like Chris Cressor and Rob Wolf, they had to find this to help their own health. And then they've allowed, they've taught everybody else about it, which is awesome. But when the second you said that this is a cytotoxic agent that disrupts the intestinal barrier, well, then what you've done is you've broken down your first line of defense for everything else. And the tight junction, so I always kind of joke about it, that the tight junction, so we know that our gastrointestinal system, all right, so obviously I'm a little heavily weighted towards the GI system, but I believe that all health begins and ends in the gut because you take in the outside environment and your body has to figure out, is this good, is this bad, is this a nutrient? This looks like a nutrient, but it's cloaked in a pesticide or whatever, all these other things. So what happens is you take in something and it has both bacteria and viruses and so on and you're in the small bowel, you have these tight junctions, these cells that are very, very held tightly together and when my patients would come to me and they'd be like, tell me, what's your thoughts on leaky gut? They use the term leaky gut. Terrible term, right? I mean, from a science perspective. Yeah, it's only a terrible term because it's a political thing and so then if they were to do this and I say, and I'm like, let me tell you what I think about it and then I would say it, and they'd be like, oh, you're the first doctor that didn't just say that's BS, it doesn't exist. And then if I talked to my colleagues about that, hey, what's your thoughts on leaky gut? They're like, oh, it's BS, it doesn't exist. Hey, and then I worded a little bit different. I'm like, hey, what are your thoughts about an inflammatory process leading to intestinal permeability that perhaps are like, hmm, that's interesting. What do you mean by that? I'm like, well, think about it. You have a dendrite that reaches up and samples the outside world, brings it to your immune system and says, what do we do with this? And they're like, that makes sense. And I'm like, now imagine if you grab gliadin and you're a celiac person, then it hands it to the B cell that the B cell goes, oh, this is bad, let's fight this. And then they mobilize it. So it's almost like a political thing where if you just kind of word it in a non-doctor Google way, in a way that seems a little more sciencey than my colleagues accept it, because there's so much science, so much on intestinal permeability slash leaky gut where we know that turns on your immune system. And when your immune system gets fired up, then it's revved up. And that's when you set yourself up for autoimmune disease like celiac and Crohn's. Makes so much sense. And I agree with you, if I'm talking to patients, they like the term leaky gut, it makes sense. But I still like intestinal permeability. I like to talk about occludin, zonulin, tight junctions, because that's really where the science is. And we have a lot of data to support what we're saying. And again, it's our immune system is our protective force. So it's not that it's doing what it's supposed to do. But when we have an absence of tight junctions and things like a corn antigen or a gliadin antigen leak through and the immune system starts to respond in a way that's inappropriate, it's also this load internally, this endotoxemia that happens. And again, we can do a whole talk on LPS endotoxemia because that is where so much of the chronic illness that we see even heart disease, diabetes, risk for COVID types of things are happening. And if you look at the cytokine response, it's the exact same mirror image of what we're seeing with COVID-19. All disease is because of inflammation and you can track it back, some sort of inflammation, heart disease, dementia, all this other stuff. So inflammation. So something, one of the coolest quotes ever, I heard Alessio Fasano give a lecture one time and he's the Godfather of Pediatric Celiac Disease and he was discussing the tight junction. And he said that it is well-known in biology that the more complex something is in our body, the more important it is. And then he did this huge slide about exactly what you're talking about, the occludons, how zonulin affects us and this and this and this. And so what I tell my patients is the way that the internet describes Leaky Gut is, and I've done this in lectures where there's like an open fence and sheep are just running right through it. They're like, Dr. Oz and company are describing how it's just chunks of meat are flying in. And then on the medical side, it's just a doctor with his head in the sand. He's like, they don't wanna hear anything. It's cognitive dissonance. Well, the reality is that there's PhDs looking at just so many things in this and how it interacts. And it's so complex that it's that important is how I take it. Yeah, and I deal a lot like one of my other topics I talk about environmental toxicity, toxic load, all these exposures that affect our membranes and our permeability. And even, I mean, we can look at mitochondria, we can look at brain. And so you could technically in lay terms call it leaky brain, leaky mitochondria. It's all inflammation, right? Dr. Brown, I mean, really at the core, it's how do we describe inflammation and the processes that disrupt our cells, our cell integrity on all levels. But what's interesting to me as we talk about environmental toxicity, people think about, oh, maybe mercury fillings in their mouth if they get too much heavy metal or if they're getting mold in their environment or some other toxin chemicals from the farm. But the interesting thing is in the gut level, you can get endotoxemia. You can basically toxic overload from within if you have a barrier dysfunction and you have excess bacteria like small intestinal bacterial overgrowth and those toxins that are being produced by the bacteria go into the bloodstream and it goes right to the liver and the enteropathic recirculation happens. And this overload can actually happen from within the body. What's your thoughts on that? Oh, I'm just like, oh my gosh, this is awesome. You know your stuff. That's what I'm thinking right now. So you said something leaky got leaky brain. So let's get back to the science really quick on this where somebody says, oh leaky brain now. In my Mendeley account, I've got several articles where people have taken, scientists have taken, I should say people scientists have taken intestinal tissue and they have shown the permeability using different sized molecules. So they can say, okay, look, it's impermeable. So they radio label and it's super complex and it's really cool, but it's all done in a lab. And then they expose the intestinal tissue to LPS, lipopolysaccharides. Or then they do different tissues with different levels of inflammatory cytokines. And they were able to show very clearly that you end up with these huge gaps and then these large Dalton molecules fall through. It's like, oh, okay, well, leaky gut, there it is. These guys took it one step further. They took human blood brain barrier and put it through the exact same process. The exact same thing happened. So the term leaky brain truly is leaky brain. If your gut is inflamed, then you can have a permeable blood brain barrier. So my typical patient that I will see, and as a functional medicine doctor, you get the people that are very frustrated or I'm gonna assume you get the people because this is at least in Texas. The people tend to start out traditional medicine, they go functional medicine and then they eventually find somebody in between where I have to do some procedures and things like that and we can talk and I have the ability to start certain drugs for things like that. So when people come in, they will have an episode, five years ago, I was perfectly fine doc and then something happened. What happened? I went through this really bad divorce or I was treated for a really bad sinusitis and I took two weeks of antibiotics and I've never been right since or I got gastroenteritis when I traveled to another country and then they come back and that is a very classic story of the motility chains that kind of leads to some sort of SIBO situation and that's where I did my research 10 years ago before SIBO was even a term. So I'm very, I said that you have two of my top five diseases and one is SIBO, two is the IVS because I can read diagnosis, then it's CELAC, then crumbs. So just know that you're in the top five, Jill. You're in the top five. And then that's SIBO and IVS too, so it's kind of all, but it makes sense, right? So yeah, oh yeah. I'm gonna send you, I'm gonna- It's SIBO. You need to get some sort of certificate, like, you know. Just check, check, check. You get like a level. You're like a level 10 gastroenterology disease. Honorary, like, yeah. But it's interesting, because you probably had this also where one of the things is a patient will come to see me as a gastroenterologist and not expect these questions and I'll be like, oh, okay. Hey, tell me about this. Do you feel like you have a brain fog and they'll lean forward like, yes? Like, have you noticed that your mood has changed at all? More anxious, more depressed, and they're like, yes, I thought I was going crazy. And then you start discussing the brain-gut access, brain-gut permeability, possibly is it through lymphatic, is it through the vagus nerve, all these other things, but the brain-gut interaction is the key there. So the thing that really gets people bent out of shape is that they're talking about their gut, but they don't feel right in their brain. And that's where I think functional medicine got way ahead of traditional medicine where you started looking at both at the same time. Yeah, gosh, I love that. And I remember, and you probably have read this too, so correct me if I speak wrong, but they had mice where they put them under stress and that was like having them swim in a water container and they had them cut vagus nerve in some of the mice and not cut the vagus nerve in the others. And they pretreated the ones with an intact vagus nerve with lactobacillus aromnosus. And they had a less high stress response in that stressful environment by pretreating with a probiotic. So they were proving that there was some action of the probiotic on the vagus nerve in the brain connection. And I was like, wow, now this is where it's at. And then again, the severed vagus nerve, there was no beneficial effect by pretreating with that specific strain of probiotic. Fascinating, isn't it? No, it's so fascinating. And I hope my, I have a graduate student, good friend Angie Cook, who I think is on this Facebook live right now and she's populating my Mendeley account all the time. And I think we're up to close to 17,000 journal articles on very specific topics. This isn't just random, this is specifically, and what we're getting really into right now is the science of motility and vagal nerve innovation. I've got, I have somebody that I've developed a relationship with in Sweden, who unfortunately went through a fecal microbial transplant and it turned on certain epigenetic genes, specifically Ehlers Danlos. And she started having alopecia aureata. She started having these issues and she did it for irritable bowel. So now we're backtracking. And those two, they've been in contact. So I've got this young woman in Sweden who's clearly very intelligent, but is trying to save her life. And my friend here in Dallas, who's super smart and has access to these articles, and they're sending me stuff. And I'm like, I don't have the bandwidth to read this right now, but you two seem like you're killing it. And they're about ready to figure out how to mitigate the vagus nerve so that we can change this whole thing. Cause it may come down to Cedakolin and this whole interaction. And we may be missing this whole ability to say, okay, look, this could be a motility thing. And Angie's gonna come on my podcast and we're just gonna do a whole thing on motility because it's super sciency and we're missing that. We're missing the fact that maybe that's what we should be focused on. I love this. And I will be listening because one of the things I see with the IBSC that I treat and I would love to know your statistics, but I have read that somewhere between 65 and 80% of IBS is SIBO underlined. Is that percentage about right? Or is it more or less than that? I'm sorry, 65 to 80% of IBS symptoms are often are due to small intestinal bacterial overgrowth. Oh my, so now you're getting into the argument of data. So let me just tell you a little bit about my background in case somebody doesn't know. So when I tell the story, I keep forgetting that I get older because I always say it's like five years ago. I know me too. And now I'm like, wait a minute. I think it's 15 years ago now. Yeah. So I was doing pharmaceutical research with, so in my, I have a private clinical practice. I saw that I'm like, wow, wait a minute, these pharmaceutical companies are paying quite a bit of money to do this research. So I started a very, very small research division in my office, hired my research manager, Brandy, who moved from Iowa. Keep that in mind. She moved from Iowa. It's a kind of an interesting story, something about breaking up with a fiance and moving down and regardless, I hired her and she showed up because she had no training, anything. It was like a friend of a friend kind of thing. It's just weird how fate sort of starts kicking in at some point. And she was working for me as a medical assistant. And I saw that there's these research studies. Somebody called me up to do, to be the physician on a research study. I was like, well, I would like to do it. I want to get into research. So I started doing pharmaceutical research for these big companies and typical stuff, phase three trial, then Zifaxon, have you ever heard of that before? Oh yeah. So Mark Pimentel, I went to a dinner and he came to talk about something else. And then him and I sat afterwards and talked and he goes, this is nuts. He's like, I got a mouse lab very similar to what you're talking about. He was like, if I put them under stress in various ways, animal in front of them, things like that. He was 20% of those mice end up with irritable bowel syndrome. And so that's where Zifaxon started was it was those animal models and they started a large nationwide study. I'm brand new to research. And my little office, me and Brandy, ended up being the leading enrolling site in the country. So this kind of shows the community level versus the Johns Hopkins, Cedar Sinai, Harvard, all these other places. Why do I know that I was leading enrolling site? Because that was one of my first clinical trials and the FDA audited me and that was not fun. And I found out later, you never wanna be the top guy because they will audit that person. Oh boy. Yeah, so it was a learning experience. But basically what we learned was, we're in there, we're doing irritable bowel and that's when Mark was like, look, you know, the belief is that where you land, irritable bowel syndrome, in my opinion, is a trash can diagnosis. So if you say, how many people actually have an IBS? I'm gonna say zero. How many people have SIBO? I don't know, a lot. How many people have gluten intolerance? I don't know, a lot. How many people have motility disorders? A lot. To me, it just doesn't exist. So I was the leading enrolling site for an IBSD study and yet I never label anybody IBS. Because once you do... Totally. It's the Rome criteria that it's just... Yeah. I kind of think of chronic fatigue or fibromyalgia. All these are similar. They're just a label that tells us where we're going on the map. It doesn't give us any real information about what's the root cause. Well, how many people have you treated and that had IBS and fibromyalgia or even rosacea or even interstitial cystitis? And you're like, oh, that all gets better. Yes. Yes. And the studies prove it, right? I always tell you rosacea, there's, you know, oh, this is great. So motility. I love this topic and I want to know, I know you've developed a product. I want to hear about that because motility for me as a treating, if when I'm treating SIBO, this is the bane of SIBO, the migrating motor complex and how do you actually get that to go? What's the deal? Just like we talked about Vegas nerve, whether it's that or some other thing. And I've got all kinds of things that I try, but I feel like that's usually the reason why it recurs and it's the hardest thing to get reverse. So I'd love to know your thoughts on motility, migrating motor complex, even the Pimentel's autoimmune hypothesis with the vignette in that. Any thoughts on all of that? That's a lot to... Yeah, absolutely. So the reason why we developed Atrantil is because while I was doing the research with Dr. Pimentel, he, him and I got in a long conversation where he was describing how well the problem is is that we will never be able to help the bloated constipated person because Zifaxin does not work on the type of bacteria or kingdom now, Archaobacter, that actually produces the gas which is causing all these problems, which is methane. And so it was, I mean, this is years ago, years ago. So like, nobody's even thinking SIBO yet or anything. And so I wrote on my whiteboard in my office, I just wrote methane. And Brandy from Iowa who had this whole other life and just kind of came down and I just hired her as a friend of a friend. She goes, oh, that's funny. When I was, she went to, she was a lawyer and she said that when she goes, when we were doing policy writing for a senator in Iowa, they were trying to mandate that farmers put in certain food products to decrease methane production for the greenhouse effect. And I just went, what? I'm like, I need all that data. And I just saw that Burger King is doing a publicity run where they're trying to say that they're gonna decrease methane production in cattle by the last four months of feeding the cattle lemongrass leaves to decrease methane production, which of course we know lemongrass has polyphenols in it. So Burger King is now trying to do this high road of ozone protection. Well, that's where this all came from. So yeah, it was the aha moment of a bloated cow. And Dr. Pimentel saying, okay, Zyphactin's gonna be approved by the FDA for IBS with diarrhea, but we'll never help the bloated constipated person. And now that we know that the bloated constipated person is producing methane, what can we do to take away the archaeabacter and decrease that? So we spent the next several years looking at all this literature and figured out that three polyphenols, peppermint, horse chest, that extract, and Kebracho had been widely studied in various parts of the country. And they had never actually realized that if they put all three together, it would probably be the ultimate product because we've been contacted by the cattle society about trying to produce something for feeds. And I'm like, it kind of took it from you guys, but okay. Wow. So- Well, it's the corollary, I'm just gonna mention really quick, all the mold studies come from livestock because when the mold affects the feeds, it affects production. There's a lot more studies on the effects on cows and pigs than on humans. So back to you, but I understand this because they take that seriously, it's a financial, and there's no politics with cows and pigs. Like there is- That's exactly it. There's no opinions, there's no politics. It's just figure out how to get it fixed. Yes. That's it. So you start realizing that it's food products and you start realizing that, well, wow, we take in polyphenols all the time and then you start going down. So that's how we ended up developing our trontile specifically to treat the bloated, constipated person. So when you look at the motility aspect of it, we initially thought that, let's use methane as an example. Methane gas, when it's produced by the archaospecies, what it does is it takes in the hydrogen gas produced by other bacteria and uses a carbon backbone that carbon backbone could be CO2 produced by fungi, which is another little side road over here. But basically the methane, what it'll do is we thought initially that it paralyzed everything. And then what has now been shown through pig studies and things like that, looking at the ilium is that it does this discoordinated contraction. It doesn't move like a peristalsis. It just goes like this. And so that's how come people are like, ah, I'm uncomfortable. I feel like I have a bowling ball in me. And that's where the motility happens. So what you're describing is how do we get that migrating motor complex? When you go to bed at night, every 60 to 90 minutes you need this housekeeping phenomenon where your small intestine moves everything into the colon so that you can keep that whole area clean. And that's the big dilemma. When Dr. Pimentel was doing his original research, he always used Zelnorm, a 5-HT-4 agonist. Zelnorm at night, two milligrams. And when he went for FDA approval, you can't do that. It's one drug, one indication, you go all in on it and they spent like $50 million to get that indication. And then they sold for $14 billion to Synergy about two years after they got it. That's the scope of what Big Pharma is after. So what I like to do, this is my little tricks to do this and we're looking at more motility. And the motility is kind of the new thing because I think that we're missing a few aspects. I think that we need to increase different products that we can talk about a little bit later but things that will stimulate acetylcholine, things that will stimulate the vagus nerve, we're looking at butyrate, we're looking at things like that where if you can get it, so it's viable and absorbed. But little tricks, so like tributyrin, I'm trying out right now because it's a stable form of butyrate. I'm trying out. I just thought that I thought this is gonna be big. Have you had any success so far? Is it pretty new, the tributyrin? It's new and it's funny because I had, this is how science-y we are. If I find something, I'm like, I'm gonna try this version, you try that version. So Angie's trying this version, I'm trying this version. I don't have the issue, so I'm just trying to make sure I don't have any side effects first. And then I'll try, I mean, I basically try everything on myself. You can go to YouTube and see that I had a colonoscopy on myself wide awake just so that I can tell my patients that, yes. I've done it. Erythromycin at night and now Xenon's back. So I'm using a little Xenon. Yeah. Is that the prokalamide or is that a difference? No, prokalamide is different. That is motegrity. So Xenon is the one that got pulled off the market. I like that a little bit better just because we've got more experience with it. Prokalamide is motegrity, which is very similar. Similar mechanism though, right? Similar mechanism, correct. Yeah. And so you take that when you go to sleep because the theory is that some people, many of them may have an autoimmune process where it's anti-vinculin antibodies. The way I describe it to my patients, if you were to think about it, you can get sick or you can get infected by a bacteria and your body recognizes it and it goes, oh, so if you've got a, if you've got a antibody, which is built to attack an antigen that let's say looks like this. So in other words, what happens is a bacteria comes in and your body reaches up, goes, oh, this is bad. It goes back. It tells soldiers to find something. Okay, we're gonna go kill this guy. But then we have to remember the adaptive immunity is that we're gonna remember and we're gonna hand this off to a cell that's gonna remember what this looks like. So next time you get salmonella or something like that, hence a vaccine, hence all the other things that we're talking about right now during the pandemic, then if something looks like this, then there's an antibody that can run up and go, nope, you're done and just gets rid of it. Yeah. Problem is, is that in about 20% of the people, this looks a little bit like my finger. And then so those antibodies that are looking for the bacteria antigen go, oh, you look a lot like that guy I'm supposed to kill. So it neutralizes it. Well, this is the anti-vinculin antibody and these vinculin and anti-CDTB antibodies, bottom line are this. If you can imagine that if you've got an electrical or cell phone towers where I want to send a message from point A to point B and point B to point C, point D and that's what happens because that's what happens in our bodies everywhere. Well, in a percentage of people, for some reason there's an antibody. So it goes from point A and or tries to go to point B and there's an antibody there and it stops. So it blocks the migrating motor complex by giving a medication that forces it to keep going. That's the goal. Dr. Pimentel is looking at treating it as an autoimmune disease and doing immunosuppressants, which gets back to the Crohn's. Don't use diet, don't do this, just take this biologic kind of thing. So it may be a little bit more traditional medicine in the way that he's kind of looking at it, but so. If we can figure out puzzles, I'm all for that too. Like I have no problem with even immune modulating drugs and severe Crohn's, I will not touch that but I still want to look for root cause. So I love this because we take great medicine, great science, but we push the envelope and say, what else, what else, why? Like we ask the questions, right? Yeah, and maybe you did this through your traditional training as well, but it's, when we launched Autron Teal, I was too close to it, way too close to it. I mean, I spent 10 years working on it. I do this thing, it's my first business venture. I avoided a few potential disasters when I was launching cause you realize that there's a lot of sharks out there that are very good businessmen and they're just got, I'm like, we need to get this out here. We need to do this. So you get really close to it. And one of the things that happened was that, we did two clinical trials, we were published and you just run into the doctors saying, oh, haven't heard of it, whatever. And now you realize why drug companies spend so much money to do all this stuff. So I got a little jaded in the whole, just here, I'm giving you science, can you read it? Can you do this? Can you look it up? And so then I kind of, the pendulum swung the exact opposite way where I was like, I'm not going to just try something because a nice rep is showing up and saying, look at this pretty graph that we did. Right. And so the science is there, that's the thing. Yeah. So the science on everything, if your listeners are there going, hey, I want to know what's your real thoughts on, oh, CBD is a great one. What's your real thoughts on CBD? Holy cow. There's so much studies out there, so many, but because they're not funded, right now I'm working with some Argentinian scientists that have discovered, well, we've all kind of known about this, but they're the first ones that got it passed to the Ministry of Health. They're actually doing a COVID-19 randomized trial on these same molecules, these tannins that we have in our trontile because they've got data for it and they've got to prove that they're Ministry of Health. So he sent me the protocol and I'm like, wow. So I called my hospital and I was like, look, I would like to see what would happen as a healthy gut can protect us from this viral pandemic. And my hospital system, which is a for-profit hospital system across the country, was like, we're fast tracking stuff like this, we want to do this, submit this. Yeah, but here's the kicker. Then we contacted our attorney and he said, oh, yeah, no, don't do that because you're gonna have to file an IND, which is an investigational new drug, you're gonna have to go through the FDA. So all of a sudden the idea of doing studies has become very cumbersome. Yes. And unfortunately, even in the United States, unfortunately there's many people that need, that make a living by doing studies that are funded by the NIH or funded by pharmaceutical companies and trying to think outside the box where you can't find any funding because possibly there's real, oh, the name's slipping me right now, but there's a motility agent, Domperidone, sorry, Domperidone. Yes. But is in Canada, but nobody's gonna do it here because it's already generic. So nobody's gonna do the study on it because it costs money. And yet it works. So it's still one of those that I like to get, I get a compounder from Canada for patients still into the radar. So you mentioned virus, like risk of viruses in the gut and I just saw study in Europe because again, it's harder to get it done on bovine immune globulins and COVID and they're studying that because that makes sense that passively can potentially bind viruses in H. pylori and some of these things as a whole nother topic, but I'd like to know your take on viral risk and gut SIBO or IBS or some of these types of labels that your patients are, our patients might have. What do you think is the connection there? Oh my gosh. So when the pandemic first started, the governor shut down the state, which ended up being probably one of the best things that could have happened to me because I had nothing to do. Like I couldn't do, like there was no telemedicine, there was nothing because we didn't have the platform to do it yet. I wasn't doing any procedures. And so I just, just got, we just got deep dive into the preprints and all this other stuff. And we, on our podcast, Get Check Project, we did a whole COVID series and everything that we said back in March is now talked about now because you're taking the time to read but it's hours and hours of reading. So shocking what's happened now is that China is now moving from a pharmaceutical aspect to treat it to a natural aspect because they're realizing that mother nature actually has a better chance of getting rid of it than an isolated molecule from a drug. So a great example would be, and I'll get to the whole concept of your risk after you get health. But a great example is that when you isolate, so the way that the virus works is it attaches to the ACE2 receptor or we're talking about SARS-CoV-2 ACE2 receptor through a furan protein mechanism as well which makes it even more bindable. And so the first thing it has to do is has to attach. Once it attaches, then it gets into the cell and once it's into the cell, then it hijacks the ribosome and starts producing its own RNA and then the RNA becomes bigger and then the cells go and they explode and there you go. Then now you've got a full-on infection. So that's the process. So everybody's trying to figure out what part of the process can we stop? So hydroxychloroquine came in and said, oh, it's a zinc ionophore and what process that stops is once it binds to the cell and tries to get into the cell, it blocks the replication. And then people said, okay, we have to block the cytokine storm. So we're gonna try and do that with various things. And then now the big push is, oh, let's do the protease inhibitor. The protease inhibitor is the very first step. Does the virus attach to the H2 receptor? So looking at this, we've got studies now and once one scientist breaks the barrier, then there's all these validation studies by other people going, trying to disprove it or prove it, bottom line is they're gonna get published. This is their job. They've got labs, they can do this. So they've got all these studies now of M docking protein showing that the effect and the strength that the virus combined to a cell and they compared it to all different kinds of drugs. So one group out of Egypt looked at this and they compared it to 10,000 different products. And what they found is that polyphenols and specifically horse chestnut work as a protease inhibitor stronger than even the protease inhibitors that we've been using for AIDS. So then another group came out and said, okay, well, you found these molecules. Let's put 26 of these polyphenols up against three different protease inhibitors in Diffavir and Remdesivir. They all have the VIR thing. And they showed at least in vitro that it's more powerful as an anti-protease inhibitor. So it's a little bit frustrating to be looking at the data and going, are we really going to charge patients $7,000 a month? Which is why I love that the Argentinians are using the data. So we've been meeting with them. Well, they actually supply our cabracho. So we work with our scientists. There's nothing like being on a Zoom call with 30 scientists around the world. And they're all PhDs. Oh, that's amazing. Oh, so cool. You know what? You know the whole thing of you always want to be the stupidest person in the room? Yeah, this is like... Well, you're the stupidest person on a worldwide Zoom. It is intimidating. Wow. Yeah, it was really cool. And you're just like, and one of the scientists. So, bottom line is, talking about viral issues, I do believe that there are natural solutions. I do know that we've got science on these large stable polyphenols because that's what's being studied right now. There may be other things, but the Chinese are doing it, the Italians are doing it, the Spaniards, the Argentinians, and the Germans have all looked extensively at this. So getting back to your question of, we're in a pandemic, what happens with the gut? So if there is SIBO or anything like that. So we know, we just got done talking about the immunity and the gut. The problem is that when you have a compromised intestine, that virus, we know that 50% of people that have COVID-19 actually can have gastrointestinal symptoms. And we know that the majority of those people tend to, if they get admitted, tend to have more severe disease. So we know that there is a way that the virus can infect the intestine. It binds to the ACE2 receptor. We also know that now we're seeing other manifestations of the disease like people are describing as COVID brain. We're seeing young people have strokes, we're seeing young people have residual, what they call COVID brain. There's new data to show exactly what we were just talking about. It makes total sense that if you compromise your intestinal barrier, you're allowing your immune system to kick in, you've got your enteric nervous system and it can just hand it off to the great highway, the Vegas Nerve, and you go up and so you have all these people going, we don't understand why all these organs are being affected. I'm like, I do. Me too. It fits. Yeah, and then part of the problem is, and this is the thing that I worry about, my SIBO people and my Crohn's and anybody, is that when your immune system slightly revved up, you are predisposed to a cytokine storm. And this is not my opinion. I mean, I got an article on article on article to actually explain it. And so if 50% of the cases are having GI issues and those tend to have worse outcomes, we know that the worst outcomes are related to the other issues. We're now seeing the thrombotic effects and all these other issues. So if we were to, I'm gonna back it up a little bit and say, okay, Jill, we know that people that are older have more disease. We know that people that have obesity, hypertension and diabetes have a greater risk of having this. Then you can take it back one step further and say, hey, wait a minute, what about that article in 2006 where it showed that as we age, we have more incidence of dysbiosis, meaning a narrowing of the microbial diversity. Those with diabetes, obesity and hypertension all have a change in the microbiome. So it's, which comes first, chicken or the egg? Are we saying, oh, if you have this, or should we treat the gut? And maybe that will help with these other things. I love that you're talking about this because I've seen, I've taught and just like you, a lot on the data with LPS endotoxemia and the literature, thousands and thousands of studies on hypertension, diabetes, insulin resistance, obesity, like literally the same. And then if you look at LPS induction of the HLA response and the same, it's the exact same cytokine, the exact same profile. So like you said, my thought is this is priming. Someone's already primed, they're producing those things. And so it just gets, it's already ready to go basically, right? It's like the Happy Meal, it's like ready to go and you just give it a little shove with that virus. But that's perfect, right? Exactly. And so it's interesting that I had patients that I'm actually writing letters. I'm like, because now when this, now when Texas reopened and people are like, I don't really want to go back to work, am I at risk? And I'm like, I believe you're at risk. If there's, if you are a, if you have COPD, you're at risk. You've got chronic bronchitis, you're at risk. Nobody thinks anything of that. Oh, it's a respiratory disease. But if 50% of the cases also have gastrointestinal system, wait a minute, that means it's also a gastrointestinal disease. And we know that you can shed this virus in your stool for weeks after doing all these things. We know that 85% of the people will have anosmia or meaning that they're gonna lose their lack of smell and their lack of taste. And so I had a patient today that I was gonna do endoscopy and colonoscopy on. Just small talk, I was like, yeah, I'm like, how are you, how's it going with COVID? He's like, man, I'm not worried. I'm like, why? He's like, I'm 100% convinced I had it in January. And I'm meeting so many patients. And there's a lot of conventions that were happening like the electronic show in Vegas. And we've got so many IT people here. So many of my patients are like, man, I got deathly ill in early February. Through negative, I asked one question. How was your sense of taste and smell? You know, that's weird because I lost like 15 pounds and it was good. I just want to eat. I totally agree. And I've seen the same thing, like almost even December through there and I'm like, yep, you likely had it. And I don't really trust. I think our antibody response to this RNA is not accurate. So I don't know that the testing, I've seen a lot of negative tests that I think are 100% clinical diagnoses of this. So couldn't agree more. Oh my gosh, yeah. I don't want to get this into a whole COVID. I know, like we can talk with this. But how about this? Okay, so I had a patient that got tested for COVID on Wednesday because they were gonna have a procedure on Friday, got a procedure on Friday and then I was on call over the weekend, not my patient, it was a colleague's patient. Got a call on Sunday and they said, yeah, patient of your colleagues, you're on call is here with a fever of 103. And we think that she may have a pneumonia or whatever I was like, okay, are you guys worried about COVID? They're like, no, she's COVID negative. Okay, so she gets admitted and she's treated for 24 hours and they say, yeah, you're doing better. It's basically a community acquired pneumonia, you're fine. Send her home, she comes back 24 hours later, they test her again and she's COVID negative and she gets admitted, but now she's got a CRP of like insane amount, a C-reactive protein of just like insanely high for somebody that isn't doing, if Crohn's patient has a CRP of 12, I'm concerned, this was like 40, wait a minute, lymphocytes were down, like everything about this. Infectious disease shows up, tests her again and she's positive. So she had, was that three negatives and a positive in a span of about four days. So you can't just completely hang your head on these tests. I couldn't agree more. Oh my gosh, Dr. Brown, this has been so, so fun. We have to do this again. Maybe we can do it on your podcast. I'll have you on here again. But I wanted to just end, first of all, I'll make sure links to your podcast are here and on the YouTube channel. And then of course, your website, we'll get all that there for everybody. So Atra and Till, we briefly talked about this, but what would be indications for use for this? Cause I've used it in my clinical practice, had great success. I love that you have that product out there. I do want people to know about this. So tell us, let's end with a little bit on Atra and Till. A little bit with Atra and Till and I do want to at least, I think it, I think we owe it to your listeners to talk about what you're taking right now, what I'm taking right now and why. Atra and Till really quick, we developed it for essentially anybody with bloating, abdominal discomfort, irritable bowel-like symptoms. And so if you have bloating, change of bowel habits and abdominal discomfort, Atra and Till is a natural, all natural polyphenol supplement that is NSF certified, meaning that if you're an athlete, you can take it. And we have shown that four out of five people will get better with this. So we've got clinical data to back it. And we know that the polyphenols in it are probably very good for you overall as an anti-aging, anti-inflammatory, so on and so on. So it's my baby, very proud of it. Just more proud that we're, we can maybe be part of a solution going forward. So that's kind of cool. So that's Atra and Till. We'll just go take a look at ATR and TIL. We could have all another podcast as to how to start a business and doing this. And we could bring Michael Lovitch on and he could critique all the potholes that we've stepped on to get to this point, but we're still here and we're doing well. So it is cool, yeah. So let me ask you, what supplements are you on right now? What supplements are you on for your brain gut health and for your pandemic supplements? Yeah, so it's so funny because patients will complain. Now I really do try to keep their list down, but whenever they complain, I pull out my little packet of 40 pills twice a day. Okay, you know what? I feel great. I perform optimally and I have a great quote, Ken. I learned this when I would take two bags on a weekend with a blender and an air filter. I said, it's okay to be high maintenance if you're high performance. So that's kind of, right? I'm like, I love it. I don't mind because I perform at a high level. I don't mind that, but back to pills. So I take all the basic nutrients and I don't do well in multi. So I tend to take C by itself, zinc by itself. I have hypochlorhydria as you can imagine. So I need the minerals. I need loads of mag, loads of calcium, loads of zinc, and of course, HCl with my meals. I actually take prescription pancreatic enzymes because I also, as you can imagine, have complete pancreatic exocrine insufficiency. So I take creatinine at the doses you would probably be shocked. I would not at all. In fact, just yesterday, me and my partner who's a pancreas expert because my regular host, Eric, is actually, he's right over with you. He's mountain biking right now in Colorado. So my partner, Stuart Ackerman, who's a pancreas specialist, we did a whole show on this yesterday on exocrine pancreatic insufficiency and it's linked to Crohn's disease and celiac. Yes, yes, because I will tell me what you thought. Keep going, but it's so fun because I think the villus atrophy will send a signal to the pancreas and shut it down. So I almost always see when there's some villus damage, you have this pancreatic response. I don't know the mechanism. I don't know the studies, but I just see it. Would you say that's true? Oh yeah, 100% extra pancreatic issues, believe it or not, are diabetes, celiac, Crohn's, because you can actually develop a type two autoimmune pancreatitis with Crohn's. And then I see it with SIBO because, and they see it, the mechanism for SIBO still eludes me a little bit other than the fact that we do say that the bacteria could digest things, but I use pancreatic enzymes a lot. Quick question for you that I've been looking, this is the holy grail for my answer. I've asked the drug companies, I've asked the natural companies, these drugs cost so much money, or at least they bill them to the pharmaceutical industry. And Dr. Ackerman's response to me was, it's all a dosing issue, but every company has a digestive enzyme. There's really only two or three pharmaceutical companies and they spend a lot of money and it costs a lot of money. Those are from pigs or from cows, porcine or bovine. So when you have somebody who says, I want to take natural digestive enzymes, what's your response? Oh, okay, and I might be wrong, so I love your opinion, but here's what I say. Basically we have plant-based enzymes, they're made on aspergillus. So if we have someone with a big mold or fungus issue, those are not the best and they're very weak. They're kind of like your day-to-day kiddos, adults, everybody could take them pretty safely, they're not very strong. I don't use those except, I definitely don't use those with a case of pancreatic insufficiency. Then we have pancreatin over the counter. It starts at around 9,000 a cap and most of the ones you find over the counter are 9,000 units of lipase per cap, but no higher. The prescription then have two advantages. Number one, they can go as high as 36,000 units of lipase per cap. So you can get four caps of the over the counter per cap and I take five per meal, which means I would need five times four, 20 caps of the over the counter pancreatin that we would see from our nutraceutical company. So I need a lot more there's no way I'm gonna take 20 pills. The other thing is they're acid resistant and I will tell you, I find that the prescription Zenpep Creon et cetera actually work better for someone like me. And then I look at pancreatic elastase and if it's below 100, I start to think more severe and start on the pancreatic prescription and they tend to work better. If they're below 50 like me, they definitely need prescription because that acid resistance, when you take it with HCL, you're gonna neutralize it, but the way it's geared to open in the duodenum instead of the stomach, it works better. What's your thoughts? I'd love to know. That's exactly it. I was, I wanted the, because the, I'll say that the nutraceutical companies say that it's just as good, but I like the idea that it's built off of aspergillus. So a mold thing is that's one thing. Dr. Ackerman's response was exactly like yours, which is just a dose thing. And then I'm like, well, if it's a dose thing, can't you just concentrate on a natural way? I only say this because I've had patients that don't have insurance and they're looking at, they're looking at $5,000 a month on pancreatic enzymes. So I'm trying to find that, trying to bridge that gap of, okay, we know that we can do this over here. We know that they're acid resistant. Why can't we do it? Is there somebody that can, that can concentrate these in a better way in a plant based way? It's just something. That's the work on that because I have the same problem. And I just feel like it's maybe like 50 to 80% as effective, but you don't get as good of a response for the severe, especially below 100 of pancreatic elastase. It's really hard to get the good response. And I know for me, it was a game changer. And then you talk about SIBO-CIFO. For me, that was a game changer because if you've undigested food going into the duodenum, you can't get rid of the SIBO-CIFO until you fix the digestion. So to me, it was like, once I fixed the hypochlorhydria and the pancreatic insufficiency, my SIBO-CIFO was a thing of the past just for the fact that I was actually digesting and breaking down food in the small bowel. For sure. So I think that there's some component of SIBO-CIFO, both. And I don't actually distinguish the two. I call it the multibiome. So I just think it's a multibiome and they just, they interact in this beautiful, sometimes a beautiful dance, sometimes a mean little mosh pit in your duodenum where they're fighting in there. But if they're in their colon and they're being in their multibiome and swimming through. So yeah, I think that enzymes, something about that I met with a pancreatic expert. Actually, my physician assistant went to a dinner and she came back all excited because they flew in some pancreatic expert and she said that SIBO does something that basically deactivates pancreatic enzymes. And she doesn't really understand why, but she uses, she gets referred a lot of steateria, a lot of vitamin B12 deficiency and they're all sent to her for pancreatic stuff. And she realizes, well, it's SIBO, but then she started asking why also. So my question is why does it deactivate it? Do the bacteria, who knows? Let's look at that and talk next time because I'm totally, I see it too, but I don't know the why. And I think there's some interaction with the villi even with SIBO, but I don't know the answer to that. One thing you ask of what I take, I do take chronic doses of low dose antimicrobial herbs because from my history, I need that suppressive dose. So I take caprylic acid, olive leaf, a few very gentle things. I've taken nautrantil and I love it. I don't really have the methane issue, but I just really like your, I love your product. I gotta send you some of these articles where that whole concept of that, so when you take these other smaller phenolic compounds, meaning like everybody's out there and they're purchasing whatever course it's in or they're purchasing, you know, turmeric and things. I did not realize that the science of polyphenols, these molecules are so big that they have all these other little Lego pieces in them and your body breaks them down. And so those, we have gone through the process of manufacturing these in a more expensive way when really if you take, and this comes back to how, okay, so postbiotics, we mentioned that briefly with the whole postbiotics, now it's become a field of study in pharmaceutical industry. So pharmaceutical industry goes, oh, look, urolithin A works as a mitophagy agent, mitophagy agent, meaning it tells old and sick and dying cells, you know, the mitochondria to go away. So now they're trying to tease out and I've been talking to a couple of scientists. They're like, yeah, the new science is how do we pharmacologically produce these molecules so that we can get the patent and we see it over and over again. It's just sort of like you can't, you can't perform better than mother nature. Give the whole plant the whole molecule, let your body figure out what it wants to do. Any other supplements? Cause I got, I got one that you're missing. You gotta get on. Okay. Well, there's a lot. I mean, I have fish oil. I have Gamalinoleic acid. I take B12 injection, of course, as you can imagine vitamin D and then I do NAC, vitamin C, acetylalkarnitine, which is acetylcholine precursor. Love that cause I'm all about. Yeah. I gotta start. I tell me, tell me that one again. Acetylalkarnitine, so it's a precursor of acetylcholine. So that's the best who are very cerebral and analytical. Ooh, it's my favorite because it'll, Well, that one I'm curious about because now we're talking about acetylcholine. We're talking about the big, right? All right, Angie, if you're listening, that's our new thing. We got to start looking up. Yeah. What about you? I mean, there's a few more, but that's the majority of them. Basically all of those except for acetylalkarnitine and you're missing the important one. You got to be on Sulfuraphane. You've had a history of breast cancer. Yes. I, I do. I have a bottle back there from Michael and I started it a month ago when he sent it. So that good stuff. Awesome. Broccolite. Yeah. Broccolite, I was so excited when I got hooked up with those guys, David and company and they are sciencey, they're PhD. It is so awesome that they, they stick the money where their mouth is. They developed this product. He developed it for his wife who had breast cancer. And when you, you got to have those two guys on. I mean, those two and his PhD is slipping my mind. I'm so embarrassed right now, but they're, it's all science. It is so cool. Yeah. And they'll actually, he actually has a lab where when they were developing it, that he could check his NRF2 level, which is the, which is the pathway that gets turned on. So the only other thing that I would add is broccoli. And then I do melatonin for the potential of the cytokine storm. Right now there are studies going on where they're randomizing people, healthcare workers to get melatonin or no melatonin during this COVID crisis. So that's kind of a hedge mud bet kind of thing. But acetyl L-Chronetine, I'm going to check that out. Awesome. Oh my gosh. Dr. Ken Brown, this has been so fun and such a delight to meet you. It's no wonder people said we'd get along well. So thank you for your time. I'm sorry we went over, but hopefully everybody enjoyed it as much as we did. Cause I sure enjoyed talking to you. Thank you so much. Absolutely, Jill. This is awesome. I have a feeling this will not be the last time we talk. Yeah. Me too. We'll have a great afternoon. We'll talk soon.