How Can Biofilm Trigger MCAS

We're just letting everybody join. We're going to talk about mast cell activation, uh, and how it relates to what I see with biofilm and breast implants. Let everybody hop on here. Takes a few minutes to get everything loaded up. Make sure and share this if you know someone who's experienced chronic inflammation, what you think is a lot of allergy symptoms, histamine release. Um, unexplained symptoms, been to a bunch of different doctors, really no answers. This might be something that, uh, they'd be interested in. Oh, hi Cindy! All right, this is for you. We are going to try to lay some, uh, important information down, trying to make it as clear as possible. Hey, Miss Chelsea, wave to Miss Chelsea. She's our lead detox practitioner at my group, Chelsea Ward Wellness. I'll give her a wave. You don't have any sound. Why don't you have sound? All right, everybody do a sound check. Somebody said there's no sound. I'm not talking, but you should be hearing, uh, music in the background. They can hear me on TikTok. How about Instagram? You have sound. Okay, who was that? Let me see. Roberta underscore N88, uh, maybe go in and out, um, see if there's a problem with settings on your phone. Everybody else has got it. Excellent, Butterfly. So we like to hear it. Somebody just joined whose handle is Pumpkin Butt. All right, there you have it, Pumpkin Butt just joined. Love that. Now, hey, share this. You may or may not know somebody, um, with implants, but you may probably know somebody with MCAS or chronic inflammation or histamine release. Somebody gets sick after they eat, somebody has symptoms that can't be explained. This might be just the thing that will help them. I tried to get some, uh, well, we'll talk about it. Y'all need to share this, get it out there. Come on. Some kind of warning. Hold on. Goodness gracious, sorry, too many phones on my desk. All right. Hey, Kim. Hi, Miss Joy from back in the day. This Joy's in Elm Grove. I'm trying to remember where that is, Joy, and I can't. I'm getting old now. It's been a while since I've been in Milwaukee. I haven't been back since, uh, Oh, I went back for a funeral. I'm trying to remember when that was. It's the only time I've been back. Hey Roberta, go to drrobscircle.com. All right. Anybody who can't hear me, go into my live, uh, on my private network. We're going there anywhere. You can watch it there. All right, keep sharing this around. We're gonna give a talk, Charisma, and then everybody can get, uh, their question answered in my live community. I want to start in a minute. Thank you. Who is Butterfly? Is that one of my patients? That's awesome though, I'm glad you did so well. Hi Karen from Chicago. Used to enjoy going to Chicago quite a bit. Used to live in Milwaukee. All right, keep spreading the word. It said my site isn't secure. That's cute. Uh, you probably just need to go, uh, you may have something that's, um problematic on the computer. Uh, you can go to like an incognito or a private window. Roberta, you live in Austin? Do you know I'm in Austin, Roberta? And did you know that is my sister's name? She passed away from breast cancer, but Roberta is my sister's name, so We'll give this talk and try to honor her. All right, I'm gonna turn off all the music. We're gonna get rolling. Yeah, we'll take some questions, Kristen. Just go to drrobscircle.com. Okay. Oh wow, it just gets— this is like reliving my college and medical school days here. Hold on, stop. Oh, killing the music tonight. All right. All right, everybody, we're gonna get rolling. We're gonna give a talk. And then at the conclusion of the talk, we'll take some questions off of— I have Facebook up and Instagram that I can see and TikTok. And we'll see whatever questions we have in the chat., and then we'll go for live, uh, private Q&A in DrRobCircle.com. So every one of us has met a patient like this. Uh, we'll say for age purposes, she's about 41 years old. She has fatigue, she doesn't sleep much, joint pain that migrates, brain fog. She experiences a lot of flushing after she eats. Her heart races when she stands up. She's been to the rheumatologist where they said her ANA was basically close to being positive, but wasn't quite positive. She's been to the cardiology and she's had an EKG and an echocardiogram and they were normal. She's been to the GI doctor and been scoped and, and that was all clean. There was no problems, none that they could identify. And somewhere in that circuit, somebody told her it was anxiety. And kind of threatened, threatened her with Paxil. Um, so she mentioned that she has breast implants, she's worried about them. And when she brought that up, the conversation usually kind of just stalls there because the literature says there's no definite link between breast implants and autoimmune disease. And that's so far true. I think the evidence is mounting that might change that. So we'll discuss that. And over the, the next several minutes, we'll look at, you know, the background of that. And maybe the, the question that's being asked is the wrong question. We've been asking whether a device causes a specific named disease, but the tissue is telling us something different. The tissue is telling us there's a chronic low-grade bacterially driven— so bacteria are driving this immune activation, right? Right at the level of the scar tissue, which is the capsule your body makes around the implant. And the cell best positioned to translate that conversation that the tissues are having into every symptom that this woman and others are experiencing is one cell that almost nobody talks about. And what I want to walk through over the, the next several minutes and go through some of the literature is we're going to talk about how mast cells are potentially implicated in this. So let's, in this first part, let's talk about like what's happening and then at the tissue level and what's happening downstream. So Between, uh, I started doing PCR testing in 2019, and between 2019 and basically 2022, we looked back at my series and submitted, uh, with Institutional Review Board approval, 694 consecutive scar tissue specimen samples from people I explanted personally. They were tested for bacterial, fungal, and mycobacterial DNA in a CLIA-licensed lab. So what we found was 29% were positive, they had bacterial contamination. And that number, you know, does two things to me when I think of it at once. I mean, it's high. It's basically one in every 3, but it's kind of low in that some people won't be taken back by that, but to me it's very, very high. So what it means is, you know, like I said, roughly 3 out of every 10 explants I do, there is a bacterial contaminant there, but By the clinical indicators, it's not a true infection because these are DNA samples and you physically don't see any redness. The patient doesn't have fever. I don't see any signs of infection when I take them out. There's no like bad material, bad fluid. Typically there's no like draining infected material, obviously. But in that study, We found 103 unique species of bacteria across those studies, but 2 were found in the highest amounts: Staphylococcus aureus and Cutibacterium. Now, both Staphylococcus aureus and Cutibacterium actus— I'm sorry, Staphylococcus aureus, uh, we had epidermidis, Cutibacterium actus. So We'll just say if you look at like Staph epidermidis, if you look at Cutibacterium actus, those readily produce biofilm. So what's the deal with the biofilm? The biofilm can interact with your tissues, but it also protects the bacteria from being surveilled by your immune system. And that's the entire point of the biofilm. That's why traditional cultures can miss them, and that's why we went to sequencing in the first place. I was very frustrated by some negative, uh, samples that I thought were infected, and so we sampled a piece of the capsule, not, not the whole capsule, and Anybody who's done a total capsulectomy knows, you know, the disease is not going to be evenly distributed across the whole capsule. Two of the findings for that series I want to hold on to there, and they're going to matter later. First, it wasn't the device, it was the scar tissue. Second, texture did not matter. It didn't matter if they were textured or smooth. So smooth, textured saline gel, the bacteria didn't care. Second, it was the host. Patient age was the only variable that survived every model we ran. Richness tracked with age, not with hardware. Now that's a strange result if you believe this is a device problem. It is exactly what you predict if you believe that this is more of a skin bacterial problem because the skin microbiome is one of the most reliably age-dependent ecosystems that we have. Sebum production shifts at puberty, and it shifts again with hormonal change. And Cutibacterium acnes and Staphylococcus epidermidis, the two are the, the lipophilic, most robust biofilm-forming organisms that are dominated in our series. And found in really high concentrations, especially Cutibacterium acnes on the face, the neck, the shoulders, and the chest. The organism in the capsule is really coming from the patient, and which organism and how many is a function of really who that patient is. The median specimen carried 3 species. 72% carried fewer than 5. So these are small, more established, stable communities of bacteria. And that raises another question that matters. You know, the presence is not necessarily the pathology. A handful of bacteria sitting on the device could be, for the most part, you know, we would say not relevant.. But then, you know, I have to hand it off to where I trained in Indiana at Indiana University Medical Center. Dr. Mathun Sina and his group published, I think, one of the best papers about this in the world. And the mechanism shows that in their study of 178 people in 3 groups, 86 with BII symptoms, 55 implanted without symptoms, 37 with no implant at all. 3 findings, and I'll give them to you in sequence. Number 1, the biofilm burden tracks with the symptoms, and then using electron microscopy, some staining tools, there was significantly more of it in the symptomatic group. And when they typed it, Staphylococcus derma— In their study, Staph epidermidis was present in 73% of the symptomatic group, and that was versus 17% of the implanted patients without symptoms. So that is quite a difference. So the Cutibacterium agnes was the top-ranked organism in every group. That's consistent with our data as well, but Staph epidermidis was the organism that separated symptomatic from asymptomatic in their group. Number 2, and this is a A part I want you to remember: the biofilm makes a lipid. Breast adipose tissue is rich in oleic acid, which is a fatty acid, and Staph epidermidis, when it is in contact with the oleic acid, it forms a molecule, oxylipentinum. So it oxidizes the fatty acid. They proved that in culture, and then they went and found it in the tissue sample. And it was elevated in the periprosthetic tissue, so the capsule tissue of the symptomatic patients. And it was dose-dependent. As ten-hung went up, bacterial abundance went up with it. Think about what that means anatomically. The bacteria are not just sitting on the shell, they are eating kind of, if you will, on the patient's breast tissue and converting it into this oxidized lipid. Number 3, that lipid drives the immune system symptoms that we see. So the T cells get exposed to oxylipin tenohome, and that causes, through a series of reaction, what we call upregulation of other factors. And then ultimately, it leads to polarization. So when this is happening— and I won't get into the very, very specifics of all the different reactions But polarization in your immune system, especially at the macrophage level, is the problem. Now, they did more studies to show that this, um, is happening, and they could induce fatigue in an animal model from this oxylipin. So that, that last bit closes the loop, right? They identified what was happening, they found the molecule, and then in an animal model they showed the molecule causes the symptom. So the macrophage polarization is a downstream event. Like I said, the biofilm really communicates to your T cells, and then that ultimately instructs your macrophages and causes the polarization. And so now, as I first, you know, thought about it, you know, when we published our paper and shared what we think is the true incidence, which is 29% have bacterial contamination, basically 1 in 3. And this paper shows what happens when you have that bacterial contamination, especially the Cutibacterium acnes and Staph epidermidis. It's not just an association anymore. So finally, in the third dataset, which I found last summer, actually, I was researching for a talk I was giving on capsulectomies. A paper out of Denmark was fascinating to me. So it was 50 women, they had cosmetic augmentations. All undergoing explant or exchange. And the, the cases were looking at basically explant or implant exchange for what's called capsular contraction. We're not going to go into the grading because it's really subjective. But the whole point of this was they wanted to determine at the tissue level what is happening. So they did whole transcriptome RNA sequencing. Nearly 32,000 genes were looked at. 1,500 genes came back differentially expressed by capsular contracture status. And when they clustered these profiles, the samples separated, basically, by disease, not by the implant surface, not by how long it had been in, and not by rupture. Then they ran a pathway analysis, and these 3 most enriched pathways in the contracted capsule were the following: graft versus host disease, autoimmune thyroid disease, and allograft rejection, with the gene overlap above 80%. So the capsule of a woman with a capsule contracture is looking at RNA analysis, looking more like a rejected organ of an organ transplant patient. The antigen presentation, the B-cell receptor signaling, the T-cell receptor signaling, the complement cascade, all of that in addition to plasma cells are revved up, there are increased amounts. Now, the authors were surprised by this, and I was surprised by it when I read it. It makes sense to me, but I, I honestly didn't think anybody would ever be able to like identify this at the tissue level. But that's how far the science is, is coming. I think it's catching up. And they found other things upregulated. So there could be some things that are avenues for treatment in the future. There's things that have to do with fibrosis at that level that they're looking into. But in that paper, there's a sentence that like sticks, you know, and to me, like, I'm not going to forget it. I mean, to me, basically they're, they're saying you're not having a foreign body reaction. You're getting your response that's similar to organ rejection with upregulation of T-cell, B-cell, and plasma cell activity. And it makes a lot of sense because those are foreign bodies. They're not self. They can't be recognized as self. So there needs to be a lot more work done with that. I was very excited when I read the paper, and I reached out to Dr. Mathun-Sina, who had already read the paper and started a grant proposal about it. So I mean, it's, it's very exciting. I think, you know, the science is catching up, most definitely. So finally, like, we're going to go past, you know, what I've discussed that's published. And everything from here, we're going to try to help those who potentially are experiencing these things understand a little bit better what might be happening. So everything I've shown you is, you know, T-cell, B-cell, and macrophage-mediated. And you have to look at the symptoms of our patients. Now, my patients all have implants basically, and many of them already have problems with histamine. But in patients with mast cell activation syndrome, there's a lot more flushing, hives, dermatographism. They may have more problems with palpitations and what's called orthostatic intolerance, getting up and and their blood pressure dropping. They have even more problems with GI issues than my patients, and increased reactivity to all sorts of foods, new otherwise unrecognized chemical and drug sensitivities, migraines, itching. And, you know, this is a pretty broad list. And I remember the first time several years ago, we had somebody with mast cell activation syndrome hadn't really had that in my clinic, per se. And they just had a lot more sensitivity than my normal patient, who's already very sensitive. So why is that happening? Well, their tissues are a little bit different. Basically, the mast cells, if you think about it, though, obvious candidate just on anatomy alone. They're tissue resident sentinels. They have and concentrate where the connective tissue is meeting our vasculature or blood vessel system, which is in my patients where the, the scar tissue of the capsule is that's around the implant. Um, they sit there for years at a time, and they're the only immune cell that can respond within seconds with basically a preformed package or arsenal. Now, nobody in the 3 papers I described studied mast cells, but when we go back and read the Copenhagen data with mast cells in mind, 3 signals fall out of the paper that never mentions them. Number 1, interleukin-9 was among the upregulated interleukins. Interleukin-9 is involved in mast cell growth, survival, and activation factor. Its presence in a contracted capsule means there's a more of a localized signal that's supporting potentially the mast cell population. Number 2, lots of immunoglobulins, and IgE was upregulated. The authors also read Excuse me. The authors also read that as a marker of activation, there was more memory B cells, but IgE has exactly one receptor, and that receptor lives on mast cells and basophils. So local IgE class switching in a tissue full of mast cells is not really a neutral finding. And number 3, there are complement receptors 1 and 2 were upregulated. And so the complement cascade, uh, was more enriched to those patients. So mast cells are activated by the, um, anaphylatoxin C3 and C5a, completely independent of IgE. And biofilms are potent complement activators. So I know that's a lot to take in, but I showed that 1 out of 3 patients basically have biofilm in 694 consecutive explant specimens. And Mathun, Siena showed that the biofilm interacts and causes oxidation. Here in the Denmark study, they're showing that there's these upregulated factors including complement. So all of that makes sense that many of the patients I have have very different presentations and symptomology. And when someone asks why they don't do well after explant, especially if they had an explant without a capsulectomy, this is potentially not just because they had leftover biofilm or leftover ruptured material if it wasn't cleaned out. They could also have and continue to have problems with mast cell activation. Activation at the tissue level. So, I think this bears more research for sure. And I, you know, sometimes it seems like this is a new clinical entity, but it's not. If mast cells have been there, you know, the whole time, they're not like new on the scene, like why is there a big change?. And although we don't know, I don't know completely. I mean, we have some plausible explanations. The first is just recognition as a problem, mast cell activation syndrome. I've had Tanya Dempsey on my show. She's an expert in this. Overall, she said, as a construct, you know, mast cell activation is relatively young in the literature. Clinicians now are looking at more and more and more. The second, which probably is even more plausible, is since the pandemic, we see it more because potentially those mast cells were primed by the virus. And it's hard to say that's a coincidence. That's a priming event, basically. So the third, I think I see a lot because I see more of a cumulative load on toxicity burden testing with microplastics, PFAS, herbicide and pesticide exposure, um, ultra-processed diets. I see tons of glyphosate. So I have the largest toxicity burden burden, uh, testing audit on patients with breast implants in the world by far. And in the first 500 tests on audit, the number one, um, finding on toxicity was BPA. Number 2 was glyphosate. Number 3 was aflatoxin. So you got, um, BPA from plastics, you got, uh, glyphosate and you got a mycotoxin from mold. So, you know, if you're putting all these inputs in, the mast cells are integrators. They don't respond to just one input. They respond to the sum. And so the more you bombard them, the more they become leaky. That's a problem. And the fourth is a genetic substrate, hereditary, Alpha trypticemia, the TP-SAB1 duplication is present in a minority of the population. It lowers the activation threshold. I don't have data on that, but that's a whole different layer onto what we already know about individual variation. In my patient population, which about 83% has SNPs, so SNPs are single nucleotide polymorphisms, and those are mutations in your own genetic code. I see them most frequently in vitamin D metabolism pathways, specifically VDR and GPX. We see them in methylation pathways, and everybody's heard of MTHFR. We see them in the glucuronidation pathways with GSST and GSTP1, and we see them in the antioxidant pathways with SOD2 mutations. So all of these things make more sense in my patient population, as they're already dealing with limited detox. So the— I get asked this a lot, you know, you know, if we check different values, you know, can we tell if it's a mast cell issue? And I had Dr. Dempsey on and I want to have her back on. Hopefully I can do that again really soon in the future. I'm not going to steal how she tests because I think it's important that you hear it from her rather than me about testing for mast cell activation. Um, you know, the big thing she brought home to me is, you know, the, the degranulation is one of the four things a mast cell can do, and it's the only one we routinely test for. There's a, you know, selective release of mediators. Mast cells can shuttle, you know, different mediators out of the vesicles within the mast cell or just have wholesale degranulation. Histamine goes out, tryptase stays in the cell. Like, all these things can happen, but there can be other lipid mediator releases. And so it's a more complex story, but the mast cells on activation can synthesize eicosanoids that are fresh from arachidonic acid, like prostaglandin D2, cysteinyl leukotrienes, and, and there are a host of oxylipins, which means that the periprostatic space can contain different oxylipins because if we have bacteria creating oxylipin 10 home, and we have the mast cells creating other oxylipins. They're both lipid oxidation products. Both are immune modulatory— modulatory, I'm sorry. And if you have more oxidative stress, that's actually bad for you. You want to live in a more reduced state. I think we can all agree with that. Mast cells secrete tumor necrosis factor, interleukin-6, 4, 13, VEGF, TGF-beta,. And that's over hours to days. And that's with no granular release. So I think you get the picture that the mast cell activation syndrome is a much more complicated, you know, both prog— it overlaps, it's its own problem. It creates more issues. I have patients with POTS, there's overlap with that. I think you've heard Dr. Dempsey talk about the overlap with Ehlers-Danlos. There's all sorts of things that are going on all the time. And so I know I've been going a long time, and it's, it's kind of dense. But let me finish with some, hopefully, you know, predictions that I think will come to fruition based on what we see in the literature and what's coming down the pipe. Number one, um, if we are looking at these explantate capsules and we stain for certain things like tryptase and chymase, compare them against non-implanted breast tissue, the mass cell density in the degranulation state should be elevated, and that should correlate. So prediction 2, patients who stay symptomatic after complete capsulectomy, and they, they can exist. Everybody who explants has somebody, you know, like this. This is a person who needs more intense evaluation for muscle activation syndrome. So I know explanting, when I do a capsulectomy, I remove a big source. I remove a big stimulus. But that doesn't necessarily resolve this problem completely. And then number 3, trying to get people in a, a better position pre-op is, is what we do with the Sharp Method. And we know that's best practice. So everybody, you know, who encounters our programming, We try to get everybody prepped and drop their inflammation. Why? So things like mast cell activation, things like heavy, heavy cortisol bursts, we try to modulate them. You can't eliminate them. You're just trying to, you know, manage them better. You know, I will always kind of go for the position that a capsullectomy makes a lot of sense. To me, if you're not removing debris or infection, or in this case, a stimulus to mast cells, then you're not really relieving the patient of the entire problem. And capsulectomy is not dangerous. I would really appreciate if people don't say that anymore. Um, it's not. And a thin layer of scar tissue is not an amount of tissue that's a problem. A problem at all. So doing a total capsulectomy intact is relatively simple to do provided there is enough thickness of the capsule. So, you know, for our patients, you know, the patients, you know, scar tissue around that capsule is having a conversation with the breast tissue. They're having conversations with the implant and the biofilm. And we don't know exactly what's going on, but we're learning more and more and more. And I think, you know, it definitely is a step in the right direction, all these different papers. And we definitely owe patients like the one I mentioned in the beginning and all of our patients our attention to this and helping combat symptoms. So that is the end of the talk. I'm sorry, it's been a long time, but I'll take some questions on Instagram and TikTok. And then I will take some Facebook and YouTube if I have those. Thank you, Linda. Linda says she can hear us. Oh, Lee is asking if I do insurance-based work. I'm sorry, Lee, I stopped doing insurance and breast reconstruction and head and neck cancer reconstruction, sarcoma reconstruction. At the end of 2019. Francis, we try to do a muscle repair on every patient. Savannah, I'm sorry to hear this, but yes, if you're struggling with mast cell and SIRS, 2 years is a long time. So I would definitely look into that. Yes. If you go into the circle, you can ask us questions as well, Samantha. But yes, it would be time. All right, do I have an Instagram question? Oh, Joanna, when will MCAS reach everybody? Oh my gosh, I don't know. That's a great question. I don't know. They pretty much hide me, so I have no idea. So Christine, I have a great patient who had a really bad case of POTS that went away with explant, and I've had patients who have POTS that got better but didn't go away completely. I tend to think the difference is MCAS, and how significant is that? That's what we're going to try to learn more about, but I don't have enough patients yet to give you the best answers for that. I think it's a real problem though, Christine. All right. Why do I not have anybody on YouTube tonight? What's the deal? It's kind of weird. Usually I have some, some folks from Japan on YouTube. The Sharp Method X4 and 1. I wrote a book called The Sharp Method. It is our methodology for surgical preparation and recovery. And it really was born out of taking care of explant patients, but it was also a set of principles that we apply now to every patient, whether they're having explant augmentation for breast with fat. So fat transfer for breast augmentation. Or if they're having another treatment with us or cosmetic surgery in general. It's basically our program to create the best, if you want to think of it, health for the patient. So then we can, um, I think get patients really in a better state of health for any kind of treatment, procedure, surgery, whatever we're looking at. All right, on Facebook, Leticia says, I've had an explant 6 years ago, but not all the capsule was removed, 20% in each side. Still have symptoms. I'm thinking of going back and removing the rest. You think this is a good idea? Leticia, I've done that for several patients and they've got symptom improvement. And I, I get concerned that if you still have the same problem that you had potentially biofilm Or you could have debris in there that's reactive, or you could have what we discussed, the problem at the tissue level with mast cells. So my book is everywhere. It is on Amazon, it is on all the Audibles, it is on Apple Books, it is on my Shopify store. So if you go to drrobertwhitfieldmd.com and hit shop, go to my books, and you can get one. Thank you for considering that. Appreciate y'all. I don't know that I answered any TikTok questions tonight. No, I did answer that one. What else do we have? Tanya says she had 3 kidney stone procedures within a month and had neurologic issues since. Okay, I'm sorry to hear that. I don't know what's— why you had that. Oh yeah, I can put the link in the chat. Yeah, yeah, hold on a second, hold on. All right, I'm gonna put this in the chat on the, um, Okay, so I put the link in the chat. I believe it's showing up. I hope it is. All right. Savannah, we do have a whole detox program. Um, Chelsea Ward is my lead, uh, detox person. She's actually on Instagram right now. But we have free discovery calls and you can talk to them and set up a call with them if you just talk about the SHARP program. You guys are making me type tonight, I'll tell you. That's scary. You don't want me typing. You just want me operating, to be honest. Okay. Yes, Cindy, the recovery time depends on where the implant is. Even behind the muscle though, my patients come to the office the next day. They get a hyperbaric treatment, a lymphatic massage, red light therapy, nano therapy, and human regenerator. Yeah, Golden, that's not true. Hey, Amber. Great to see you. Idaho Care Bear, I don't have an insight into somebody in Meridian or Boise. Brooke Okachobe is my patient from— I want to say it's from Meridian. I have several people from Sun Valley, Meridian, Boise. So I haven't trained any of those folks, and I don't know them personally. So I don't— if I don't know you or didn't train you, I don't recommend you. So that's just my personal bias because I think it's very important that I have insight into how much they've done or what they do or how they approach it. I will say, if somebody explants somewhere else, you can run the Sharp method with Chelsea and Gina, my detox team, and Melinda. That is an option. We don't hold anybody, uh, you know, we want everybody to get taken care of. We just want to help as much as possible. I'm in Austin, Texas, everybody. Austin. Okay, is everybody ready to go over to the circle? Ness_Land, no, I don't require an MRI before X-Plan. I'm heading over to Dr. Rob's circle.com. All right, I'm back. I'm putting this link in, then I'm getting out of here. Had to go over there and thumb type this in a tiny little window on my stupid iPhone. So, ah, all right, all right, let me see if I can do this in TikTok. I was— I'm terrible at TikTok. Hi, Britt! You're late to the party, Britt. Come on, you guys got to be faster. You know what I gotta do is just get all this live streaming so it's so simple from my damn— um, I hope this works. Is it still live? Okay, good. I gotta make some comment here somewhere. Okay, here we go. We're moving over to Dr. Rob's circle. Oh no, it's free to join. I don't want to hear any grief. Just go join. All right, now I gotta find my circle. Oh, goodness sakes. All right, I'm gonna start ending the stream on Substack first. Sorry, Substack, you're out. And on Rumble. And on X. Nobody likes me on X. Nobody ever comments, but that's okay.