Healing Mold, CIRS, & Biotoxin Illness (Diagnosing CIRS): Episode 2

Welcome back. Once again, during this episode, we're going to talk about diagnosing chronic inflammatory response syndrome, also known as mold related illness. Dr. Jensen and I will be talking about a lot of great things of note. These are based on a blog series we have on our website. If you want to kind of get into that, please go there. Also, if this information is helpful, please, like, subscribe, follow and share this with friends. We will be doing a Q and A session at the end of this series. So what happens with all the questions you've dropped below, Will? We'll kind of compile those and answer them in one or two sessions with the goal of something being a great, great resource for people to learn about their chronic inflammatory response syndrome, if they have it. So having said that, let's begin.

All right, it's my turn. All right, so how does one's history of exposure to biotoxins play a critical role in diagnosing sirs?

I mean, there has to be exposure. I mean, by definition, there's an exposure. So. And this is where it gets kind of tricky, because exposure could be. I was in college for, you know, four years. There were patients actually with uva. He was in college for four years. The house, who grew up four years had, you know, mold issues. Didn't know, got a tick bite, and that triggered everything. So a lot of times you have to kind of go a little deeper and dig a little deeper, but there's that exposure. And sometimes it's a slow, long exposure, and sometimes it's like, hey, I went in this really super moldy place and a month. And I started feeling foggy. But that's the nuance. And a lot of times I'll have patients, I'm sure you do as well, where it's like you have to dig and dig and dig. And they're like, I never lived in a moldy house. I never had exposure. But also realizing that it's not just the water damage building, there's also these other things, you know, breast implant illness, you know, dental issues. So that's where the exposure gets a little deeper. If you're in the military, chemical exposure, pilots are exposed to a lot of petroleum biotoxins. Now, we know we didn't mention this before, but GAFOR syndrome is another chronic inflammatory response syndrome where people were getting exposed to tons of vaccines, then inhaling burning petroleum for a year. First responders to 9, 11. So all of a sudden you have to dig a little deeper than the typical. Did you grow up in a moldy building? Right. Because it's not always that clear and concise. Yeah.

And it's not mold as often as people once thought it was.

Exactly.

And this, what, 30 biotoxins that have been described in the literature, at least at the beginning, and that number is growing and it's going to continue to grow as we do more research on this. So we talked a little bit about the cluster analysis in that first video, which is just kind of a review of symptoms that go along with this. But there's this other screening tool called a visual contrast sensitivity test, or VCS test. Can you speak a little bit about that and what that means and how that's useful for patients and clinicians?

So. So this is actually, it's like retooling of an old test that's been around for decades. Originally was actually used in the military. They were seeing pilots getting exposed to diesel fuel and having seizures. And so they were like, well, what's going on? They actually use this test as a way to measure blood flow to the brain because you can actually look right through your eyeball and see the little arteries in the back of your retina. So they realized if they had this contrast, which is different colors, these little lines that go back and forth and they get closer and closer and closer. When what happens is as you have less blood flow in your brain to your eyeballs, you lose the ability to discern those really close lines. So they figured this out decades ago that, hey, petroleum diesel exposure. Hey, if we just, once we, these guys get this visual change, we'll move them off the flight line for a bit. No harm, no foul. Fast forward decades later, we actually realize now that it's also with other biotoxins, including weather damaged buildings. So the BCS test is literally a test to look inside your brain to look at the blood flow to the finest, most sensitive arteries in your body, which are in your retina vis a vis the ability to contrast these lines. It's a really, really cool test. It's very helpful. And you can actually track people. One of the cool things about it, we do a lot. I know you like fancy, you like lots of tests, but this is one of those things where it costs you close to nothing. It's the best marker, minus the C4A and all these other fancy ones for an acute biotoxin exposure. So once people, once you know someone's on track, it's like, cool. You passed your vcs. Great. You went to your buddy's house, you feel cruddy. The VCS tests positive you know, yeah, it's portable.

It's. It's for me how I give some patients ownership moving forward. Because a lot of the times the journey itself is difficult. But then the question I get as they're nearing the end is, now what? Because I can't change their genes, they're always going to be genetically susceptible. How do I live the rest of my life? Well, this is a really important tool for that reason, because once it normalizes, you're a step in the right direction. But then if you suspect, if you're not someone who develops a towel, like some patients, myself included, develop a towel. If I'm in a really sick building. I know. And some patients have, like, their headaches come back, or you had a patient whose tremor came back. And, you know, the reality is, is that not everybody has that. Use the VCS test if you have a baseline normal score and it plummets. You had an exposure, and then you can get on your binders if you weren't on them at baseline, or you can get to a lab and have your doctor order a C4A and some of these other markers we're going to talk about. So what about some physical exam findings that might suggest SIRS that you wouldn't otherwise see?

Well, there's one thing that I used to see for years before that I didn't quite know it was a marker for neuroinflammation is a fine tremor. Some people's tremor is so fine you have to put a little piece of paper on their hand and you'll see the paper kind of shake. Sometimes you'll see abnormalities and reflexes. One of the things I've noticed is actually part of the SIRS of my dysautonomic patients is what I call an adrenal pupil. Well, you'll be shining a light in their eyeball and it'll constrict down. But then it's like, that's their sympathetic. So that's their parasympathetic vasoconstriction. But then there's sympathetic fight or flights. Like, this is dangerous. And it goes back open. You can actually see the pupil struggle. Is this a safe place or is it a dangerous place? And all of a sudden, you know, this person's neurological system is they have at least a mild form of dysautonomia. There's other differences you can do between your muscles of balance. When you do a physical exam. When you do a really good neurological exam, you can actually pick up on some of their core muscles. The Weakness, like an imbalance in their body. You know, you also look for a lot of other things. When I do like a neurological exam, my patients also look for loss of sensation of pinprick, vibration sense. Some of these people will get a fine form of neuropathy, which also is where like some of the dysautonomia stuff, which you know, we're both into dysautonomia now. Another thing you can't escape, right? Yeah. When where one of the markers of that is actually type of peripheral neuropathy that's unexplained. And so you can actually pick that up, which I will in physical exam with patients when I'm doing their physical exam, external exam with actually my little pokey wheel thing. Yeah.

A couple of patients that have been diagnosed with small fiber neuropathy and are being treated for that and they're all source patients and it's just incredibly common. And these are subtle and not so subtle findings that I think a lot of people miss. And it's because most clinicians don't lay hands on patients anymore. And it's the art of the physical.

Exam is how long does it take you to do a physical exam on your patient?

It's a while if you're doing a thorough one.

Like probably at least 20 minutes. Yeah, that's like more time than most people. Even the doctor's office, it takes us to me at least that much, sometimes 30 minutes depending if I'm doing a nasaline test on the person, if I'm doing if they're my older patients who I think might have mold related dementia changes, altered cognition. I'll do smell tests and some other neurological exam things. It's you know, half an hour sometimes doing exams. So it takes some time.

All right, what about testing? What role do lab tests play in the secondary tier of diagnosing sirs and which markers are most important.

So I think this is where it gets a little tricky because when you look at the cluster analysis, you should be able to that that diagnosis is about 95% chronic inflammatory response syndrome. Then you do the VCS test and that gets you up to that 98%. So without blood testing, we're already pretty accurate with our diagnosis plus or minus the mark on. So it gets you over the edge. And this is where the whole research bent is because Shamaker, Heyman, the guys at the top are like, hey, we need to validate this. We need to show the world this is legit, this is real. It's not just, you know, so that's where the lab testing kind of helps pinch that. And you're doing basic six major labs is the HLA DRDQ test, which is a test for genetic susceptibility.

We talked about that a little bit.

Yeah, yeah. I don't do it as much as I used to because typically my patients are positive for the other labs. Unfortunately, the you don't need every biomarker.

To be positive to make diagnostic criteria.

You need three of six. And so I've just found, personally, if someone's like two of six, I might go back and do it because I really feel like they have.

I do it more now, I did it less because again, yeah, it's cost issue, insurance based, etc. But you know, if it's covered, I think it's important to know. And I have patients that have children and they're like, well, I want to know the genetic risk of if what I have so that what I potentially passed on. I get that. And, and I think that's important even if it winds up. And sometimes you get these esoteric ones like not most susceptible, not multi, not post line, but low msh. That's a really hard one because that person isn't technically, they're not necessarily not antigen presenting in a dysfunctional way, but they're at baseline, their MSH is low, which makes them susceptible to mark ons. And just in general, maybe they're not good at processing biotoxins, but in a unique way. So I just think it's kind of important. But what other ones?

So you have C4A. C3A is not technically one, but I'll throw that in there because that can help with like Lyme stuff. You want to, then you want to look for HPA axis dysregulation. So you're looking at ADH and osmolality. So that's basically is your brain holding on to fluid intracellularly. Because one of the things that happens with these patients, particularly if they're dysautonomic POTS patients, is they can, they're extra. They're basically their intracellular volume. They're dehydrated inside their cells. So they might drink lots of fluids, but it goes right through them. So they need salt. And that's where some of those patients are doing electrolyte, different electrolyte formulas, looking at the cortisol regulation, checking out cortisol and acth. Okay, again, when you have this dysregulation in your brain, your brain's on fire. The regulatory part of your brain itself. Becomes dysfunctional, which can explain a lot of people's depression. Bipolar adrenal fatigue, Right?

Yeah.

A lot of adrenal fatigue is not adrenal fatigue. It's actually HPA axis.

Yeah. It's not inherent to the adrenals.

Correct.

It's the loop. I still use that as nomenclature to help explain it to.

True.

But really I make sure in that same conversation I'm saying things like, your adrenals are not the issue. This is the feedback loop that is problematic. But for the sake of conversation, previously described as adrenal fatigue, late stage adrenal fatigue, adrenal exhaustion, et cetera. This is kind of where you are in the continuum in my mindset. And that helps them to understand a little bit better.

And then MMP9 matrix methylproteinase, it's actually a marker for white cell activation. So it's basically a cell marker for tissue inflammation on the TGF beta, which is a marker for dysregulation of your TH17, which is your Tregs. So it's a dysregulation of regulation. And that's one of the things that's just really interesting about this. Your body is this miraculously amazing mate thing that's got regulatory, regulatory, regulation upon regulation. And so ultimately what happens with chronic inflammatory response syndrome is unraveling of the regulation, of regulation, of regulation. So if you stop at the symptoms and don't go upstream a lot, like to T. Rex, for example, or to your midbrain, your HP axis, and all of a sudden, no wonder people aren't going to get treated, get better, because you have to look at these markers. Ultimately these markers aren't looked at, they're just asteroid. And it took us a long time to figure out how to interpret those. There's a bunch of second tier labs as well that sometimes I'll do leptins. Looking at antiphospholipid antibody syndrome, one of the epiphenomenas in this disease is that people will throw off sparks. Their immune system gets dysregulated, so they throw off an ana. They throw off an phospholipid antibody syndrome. They might have some infertility issues related to that. They'll throw off a thyroid antibody.

Anticardiolipin.

Yeah, exactly. They'll throw off a lot more gluten, you know, gliadin antibody. And all of a sudden now it's like they see these specialists who say you might have thyroid issues, a Hashimoto's, you might have lupus or whatever. It's literally coming from this dysregulation in their innate immune system. So I don't always order. There's like, I order a lot of the antibiotic tests because just the way I practice, but I don't necessarily order all of those deeper ones for cost issues because ultimately, when it comes down to once you get your diagnosis, you really need to work on detoxification binders.

I would add vegf, fast food endothelial growth factor. And I would add msh, which I kind of alluded to as one of those master hormones, because MSH stands for melanocyte stimulating hormone. And part of the dysregulation that Dr. Hartman's describing is as your biotoxin bucket is filling up per se day, MSH is getting suppressed. Some people have low MSH at baseline because of genetics. This is a hormone that is so important for regulation with regards to tight junctions in the gut, therefore leading to things like gut dysfunction, but also the potentiation of autoimmunity. Right. Leaky gut and a trigger, but also things like pain, things like fatigue, sleep, androgen suppression, so low testosterone, then vascular growth factor being vegf. And that's going to be hypoperfusion if it's low. And you'll see it transiently go up first, and then it peaks, plateaus, and bottoms out. And that person at baseline is tired and when they try to push themselves, they just, they're wiped for a week. And that, that kind of all feeds into that hypometabolic, I'm tired, I have brain fog state.

So you said hypometabolic and proliferative, which are very big, confusing, big confusing words. So in a layman's term, because this is key. This is like, in my mind, this is like senescent cells. This is zombie cells, which have become popular. Yeah, in my mind, that's what this is. But a more global aware. So why don't you kind of break it down? Like, what does that mean? Like this. Yeah, these.

So this was. This is newer data. And again, it goes back to. Originally, this was described as chronic inflammatory response syndrome. And so everyone just kind of assumes it means one of two things. One, I'm moldy, and two, I'm inflamed all the time. And no, you're not always moldy. And not every source case is a mold case, and many of them are not. Two, yes, you're inflamed, but in a different immunologic way. But what's uniform throughout SIRS patients is this core understanding of hypometabolism where your mitochondria flip into what's called the cell danger response. And basically, and this is work that was pioneered by Dr. Navio, which is incredible the way that he was able to describe this. But the mitochondria, the power plant of the cell making your ATP, and all the things that we learn in school, they do do that, and that's incredibly important. But they go well beyond that and how they affect the body. And if anything, they do more than we can probably give them credit for. And we're still peeling back the layers of the onion for that. And the mitochondria, in the setting of sers, flip into this cell danger response, where they actually get stuck into a hypometabolic state where you're. Essentially, the way I described is the mitochondria kind of cowering in the corner, preserving resources, not producing energy, not cloning out, which is called mitochondrial biogenesis. And therefore the system itself is kind of suffering. It's like taking the volume of your favorite song, listening to it at the volume you want to, and turning it all the way down where you can barely hear it, and that's what's happening in your body. And the body then flips into a state of what's called proliferative physiology, which is aerobic glycolysis, inefficient fuel burning in the form of burning sugar, which is not sustainable over time. That then leads to something called intracellular insulin resistance. So unlike the typical insulin resistance we see in diabetes, in the external insulin receptors, we see this internal insulin resistance in the cell and the cytosol itself, collectively leading to this state of dysfunction metabolically. And therefore, that explains why we're seeing things like fatigue and waking and brain fog and all the other things that we see follow suit. So that is really at its core of what CSRS is, this mitochondrial dysfunction.

Yeah, it's kind of interesting because in the biohacking world, the idea of senescent cells and rapamycin and fasting, all these kind of things. Interesting. Like, it's hopping up and being really popular on one side. But what kind of brought it to the more the common thinking, I guess, was with COVID with long Covid, because basically this phenomenon with monocytes where they should turn over in seven or eight days, now they're hanging out for three to five to six months, and people have these little viral particles are picking up and these little cytokine panels, and it's the same. I won't say same because we don't have the literature yet. But it seems very simple.

I want to go on the record as saying long Covid is csrs. I mean, honestly, like.

Agreed, agreed.

Seriously, like, how can you not see. If you treat SIRS patients and you understand, how can you not say that? Like, if you look at the. The multifactorial current working hypothesis for long Covid or long haulers, it's what. It's chronic inflammation, it's chronic immune dysregulation, it's mitochondrial dysfunction, it's oxidative stress. It's everything services. The only thing that's different is persistence of viral infection. But. But every surgical patient I see has, like, EBV reactivation or CMV reactivation or some other viral. So I think there's an overlap there. Statistically, the numbers sync up about 20%. So it's. I think they're one in the same. And I think, you know, anyone that's come in with that tag already, I just treat them as a service patient and they get better.

Now, I'm also throwing the mix here. A little mast cell activation.

Yeah.

Which is where Dr. Mouldings work. It's really interesting. So in Germany, 19 to 20% of the population has this. Okay. Yeah. So all of a sudden, this. This. This 20% number is popping up in chronic inflammatory response syndrome. It's popping up in the mold world. It's popping in. It's just. And it just. It just seems more than a coincidence. And that's where I think, you know, when you start thinking about, like, longer patients which have this mast cell activation syndrome. How many of our. Our mold patients are. Have some degree of mast cell activation syndrome?

It goes beyond that. Right? It goes beyond mast cell activation. Because if you are a SERS patient and your mitochondria flipped into a cell danger response, and now you're at the next step of dysregulation of transcription of those mitochondrial genes, which is kind of the next level step in SIRS is, is ultimately these pathways that get up and down regulated. And some of the pathways that get up regulated are these histamine pathways. And when they're upregulated, every nucleated cell in the body has the potential to make histamine and starts to do so in excess. And so you can block mast cells all day long, but you have to do a lot of downstream support as well, because it's not just mast cells making histamine, it's all these other cells. So you need mast cell support, you need mast cell inhibition, whether it's quercetin, oral cromolyn, or ketofin or whatever. But then you need antihistamines for downstream. You need some DAO to break histamine up and make it inert. You might need some aldehyde dehydrogenase support. You need to do a lot of different things, but ultimately it's reversal of sirs. And now all of a sudden, someone who thought they were histaminergic their whole life, and that was just who I was. Hardwired. It's better or it's gone. That's pretty profound.

And one thing I'd add in there, it's really been unique to see this, is that with the mast cell activation syndrome, to learn that your mast cells are in many ways an extension of your neuroimmune system and how that's related with stress and trauma.

Yeah.

And all of a sudden, now when you get. And this goes back to the SIRS.

World, when does my eczema flare?

When you're stressed. When you're stressed. Yes, Dr. Jinsky. Yes, it does. Right.

Come on.

And all of a sudden, now we've learned from actually the genomic testing, the genie testing through Hayman and Shoemaker, that in this proliferative stuff you talked about, there's actually a gene expression for post traumatic stress disorder, gene activation in your brain related to the mold. And all of a sudden, now we see how mast cell activation through its neuroimmune connection can now be a part of sirs. And all of a sudden. And then one of the things really interesting, that mast cells, when they leave your bone marrow, they don't leave fully differentiated. They actually go to the tissue that they eventually live in and take on the phenotype or the type, the appearance of those tissues. And if they go to inflamed tissues and they take on that inflamed phenotype. So when you start treating some of the mast cell stuff and doing some of the things you mentioned, you have to realize that these cells have to die off and the next cells come around and repopulate that area and they'll be a little less inflamed. You have to wait for them to die off. And so all of a sudden, if you flare every two months, every three months, it's going to be really hard to get that type, that expression, those mast cells that are taking on the expression of wherever they're going to. To calm down when you flare so much. And so all of a sudden, the mind, body stuff, trauma, brain retraining and avoiding triggers.

Yeah.

Become super critical, and that's where I feel like with the diagnosis aspect, it's difficult because so many people get triggered so many different ways. What are your thoughts about that as far as, like, the whole triggering phenomena and how it interacts with not just the stress, trauma part, the gut part, the mast cell part? What are you. What are some of your thoughts about them?

About how mast cells are triggered?

Well, how plays with diagnosis. Because this. This section we're talking about diagnosing sirs, Right. We went off a little off tangent because we like to do that. But how does it come back to, like, your patient who, like, either responds, starts and stops responding, gets better and gets worse?

Yeah.

You know, how does this actually for you? Like, for me, it's like, okay, I think this person's a service patient, but I'm kind of complicated by, you know, part of the. Part of the diagnosis is do they respond to therapy?

Right.

Yeah, that's part of the traditional protocol is you get someone, you remove them from the environment, you treat them, you give them binders, and they're supposed to get better, re. Expose them to get worse. Right. That's part of the traditional way this started out. Yeah. But it's kind of complicated.

Linear.

Yeah.

Yeah. So, I mean, I would agree with that. I think that ultimately the ongoing source of triggers is multifactorial is the easiest way to say it. And for one, you want to identify the obvious trigger, which is the biotoxicity. But there are triggers that they're not even aware of, so it's hard for you to be aware of those. And that requires a lot of detective work along the way. But all interwoven within this is that limbic dysfunction that you alluded to. And how that affects each individual patient is different. I mean, this goes back to whether they had childhood trauma or adult trauma or sirs at its core, in my opinion, leads to limbic dysfunction and trauma. I mean, I don't know a SIRS patient that doesn't have some degree of limit dysfunction. And when we talk about the limbic system, we're talking about this kind of midbrain, this primordial reptilian brain, the hippocampus, the amygdala, the hypothalamus. And the hippocampus is memory, and the hypothalamus is the relay sensory center for all of these endocrine loops that we're alluding to, like the stress loop and others, including thyroid and sex hormones. And then the amygdala is mood. And if this individual is hardwired into a Sympathetic fight, flight, freeze situation, then they're not going to get all the way better. They're going to be the impetus to having that improvement in their, in their clinical state. And so a lot of times, either concurrently or prior to, or you pause what you're doing to work on the limbic retraining, then you can start to move in the right direction. But I see, I see it triggering things like dysautonomia, I see it triggering things like mast cell activation. I see it triggering things like ongoing sibone gut dysfunction because of its effects on vagal tone, which affects migratory motor complex, which leads to things like sibo, which is predominantly gram negative, which means lipopolysaccharide, which is also an endotoxin which spikes your C4A. And now you think my house is moldy. And it just becomes this vicious loop. So you always have to kind of go back, you always have to see the lay of the land. And there's something that's kind of pervasive throughout which is that, that limit dysfunction and the triggering stuff.

I think because of this complexity, one of the things that makes helps us take care of patients is having relationship over time.

Yeah.

Because this is something you don't fix in three visits or four visits. You have to know the patient. You get communication with them, you see them through the hard times sometimes this is a multi year process. It's not just, you know, the three visits and I'm fixed.

Yeah.

I love it when I see those patients.

Yeah.

They're few and far between.

So rare.

Yeah.

So I mean I have a patient I've been working with for years. She's a service patient and she's done incredibly well. But then she hit a wall and we couldn't get past that wall. And it turns out that it's her car. We finally had her take it to a detailer. They pulled out the upholstery, it was full of mold. All the while, fixed her house, did this, did that, got most of the way there. We just couldn't figure it out until finally you kind of go backwards and you start asking these environmental questions again. And she was just like, what about my car? My car smells a little musty. What about your car? We should get that checked.

Let's do now with the car. How did the water damage happen in the car?

Roof.

Roof was like a sunroof thing.

Sunroofs. Sometimes it's other reasons, but that's probably the third or fourth that have had that. And their home was fine and it was Their car. And it's like it's ubiquitous. Biotoxins are everywhere. And that's not meant to scare anybody or make them agoraphobic. The reality is that this is a very treatable, manageable condition. The goal is to identify your current ongoing massive biotoxin burden. We're not looking for biotoxin free. That is unrealistic. No one's going to live in a sterile environment. This is minimal. This is what can the system handle. And as I get it balanced and better and ramp up and teach this individual how to detoxify in a better way. Despite their genetics. Genetic predisposition is just that, predisposition. But if you can control the environmental input, epigenetics, then you're, you're able to better push that patient in a positive direction and teach them how to own it along the way, which is the most important thing.

One thing I want to add in right there as well, just a little pearl for that. You mentioned the sunroof. One of the more common places where, where people's car would have issues with it is actually the discharge from the AC were blocked up.

Yeah.

And the AC will just back up and just drop, dump through the water inside the car. Obviously. Obviously flooding. If your car was flooded. And sometimes this happened, you know, 10 years ago, there's the floods down in Louisiana stuff. People's cars were flooded and they were resold back on the market used and people got exposed to them. So. So sometimes, you know, your detective work is not just your home.

Yeah.

It's also the car you're driving. The workplace you, you're at, it gets kind of, kind of deep. So. So all things diagnosed. So why don't you take us home on the diagnosing? Sirs, what are the three major takeaway points from this diagnosing? Sers. You got the labs. What would you say the three takeaway points are?

Case definition, first and foremost, which is important, you want to make sure that you're following what you should be following to make sure that you're properly treating the patient. So symptoms consistent with peer reviewed literature. So you're going to utilize the cluster analysis for that. And then you can use the VCS to kind of corroborate that screening process. And then you want biomarkers that correspond with peer reviewed literature. We described some of those and we'll go into detail more as we go and make more of these videos. And then next would be a known exposure. And so when you have those three, you're moving in the right direction. You can probably diagnose them at that point in time. And then last would be response to treatment. And so you need all four for that to be a case definition. And the reality is that if you have the genetic predisposition and known exposure and a positive cluster analysis, you're a service patient. And at that point in time, everything else is whipped cream. I mean, it's just giving you more data. But you need to start treating that patient by decreasing inflammation, priming the pump so that you can detoxify successfully, diagnosing and treating Mark ons, remediating the exposures and moving towards the end stage treatment, which is vip.

Cool. Excellent. Well, hopefully that was helpful to everybody on diagnosing Sears. So I'm super excited for our next talk. We're going to talk about the biotoxin pathway and a little bit more. Yeah, I know, Lovely. Right, so. So if you enjoyed this, you learned something from this, please, if you have questions, put them below. I'll make sure you like follow and share this so that when the information goes out there to answer the questions, you get put in the loop. Unfortunately, sometimes the stuff we put out there doesn't get shared because of the. The bots, so to speak. So make sure you do that and talk to you soon.