Episode #152: MCAS and Implants with Dr. Tania Dempsey, MD

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Hello everyone and welcome to episode number 152 of the Better Health Guy Blogcast series. Today's guest is Dr. Tanya Dempsey and the topic of the show is mast cell activation syndrome and implants. Dr. Tonya Dempsey is an expert in chronic disease, autoimmune disorders and mast cell activation syndrome. She is sought after internationally for her knowledge of chronic immune dysregulation and has attracted patients from Israel, England, Thailand and France. Dr. Dempsey utilizes integrative medicine to get to the patient's root causes of their illness. Her purpose is to understand why people get sick and to help patients understand their body and why it fails them when it does. And now my interview with Dr. Tanya Dempsey. This is our second conversation on the podcast with Dr. Tanya Dempsey. We talked about mast cell activation syndrome and bartonella in episode 106. Today we'll be talking about mast cell activation and implanted medical devices. Thanks so much for being here again, Dr. Dempsey.

Oh, it's my pleasure. Thanks for having me.

What is the difference between primary mast cell activation syndrome and secondary mast cell activation? Synd idiopathic mast cell activation syndrome. And then in your patient population, what is the split between these different types and how do you determine the type of mast cell activation that a particular patient is dealing with?

I think that's an important question that we kind of set the stage here with. Your primary mast cell activation syndrome is essentially a condition which really starts at birth or very, very early on in life. There is probably a series of mutations that occur at the level of the mast cell. It's usually one type of mutation for each individual person. They call it clonal, it's a set of genetic mutations, but it's the same in that one set of mast cells that causes it to be inappropriately activated and reactive. And in patients with primary mast cell activation syndrome, they can have over the course of their life, a series of events, triggers that can escalate their underlying primary mast cell activation syndrome. In secondary mast cell activation syndrome, these are patients who don't have the genetic predisposition, so to speak, of having mast cell activation syndrome, but they have A trigger that then causes the mast cells to go awry, causes the mast cells to react. And in some ways we say it's inappropriate, but some of it is appropriate. If there's an infection that starts the ball rolling on the mast cell activation, then that infection is going to keep the master cell going until the infection is cleared. So in secondary mast cell activation syndrome, you eliminate the trigger. You know, let's say it's an infection or a exposure or a chemical, you eliminate the trigger, and theoretically the mast cells should reset and go back to normal where they are there, ready to react appropriately. Idiopathic, I would say, is probably a combination of both. And I would say that that's probably the vast majority of what we see is that there a lot of our patient, in my population, most of them are sort of born with that predisposition. They have a history that starts very early on in life that has a sort of flavor that there's some dysfunction of the mast cells. Over time, they've had triggers that have made it worse. But there are some triggers that when eliminated, their mast cells can reset to some extent and they can definitely improve and be well for long periods of time. I think of it as really, probably, again, most of our patients have a combination.

When we think about mast cell activation syndrome and this hypervigilant immune response that leads to inflammation and many different symptoms in those patients with chronic. What portions of the triggers of mast cell activation syndrome would you say originate from outside the body versus inside the body? And what are some of the key triggers that you most commonly see in your patient population?

I think that the initial insults that happen are primarily environmental. Even if I take. When we talk about internal and we talk about an infection, an internal infection, it came from the environment, really, in my opinion, it really is the environment that is setting the stage for this. The types of things that we see are really anything that the mast cell reads as bad, foreign. It could be as simple as for people who have allergies, for instance, it could be pollen in the air, it could be more severe. And pesticides, chemicals, things that, again, we breathe in, things that can go through our skin infections, mold, mycotoxins, any kind of toxin, anything, again, that the mast cell reads as inappropriate. I think that usually starts the cycle, the vicious cycle of mast cell activation syndrome for a lot of patients. But of course, course, we can't forget that there are lots of internal signals like hormones and other things that the mast cells read as well. And often it's a perfect storm. It's A hormone disruption associated with a chemical exposure associated with, let's say, a barometric pressure change. So I have patients. The weather is changing, the storm is coming in, pressure changes, mast cells read that change. They're also for women. They're maybe in that part of the menstrual cycle where they're approaching the menses and they're maybe having a lot of stress in their life, and maybe they didn't sleep well. Then you have this perfect storm of the mast cells reading things in the environment and things internally. And that's really a recipe for disaster, unfortunately for patients.

So talking about those environmental triggers, essentially one of the things that I heard Dr. Fiohorita say was that a cell phone can actually also activate mast cells. And so I wonder, do you see electromagnetic field exposures as a trigger for mast cell activation in some of your patients?

Yeah, absolutely. And it's a real problem, and I struggle to really find solutions. There are various things that we tell patients to do. Shut their phones off at night or make sure you don't put anything electronic next to your head. There are certain tricks. There are these devices that block the transmission of the EMFs. But at the end of the day, it's a tough problem. And definitely I have patients who have that problem. I will say that most of the patients who have that problem, though, also have other triggers. It's usually not just one thing. I rarely see patients with just one trigger. Often when they have the EMF reactivity, they also have had exposure to mold. They might have had bartonella infection. There are just some key other conditions that synergize with that. It's again, like that perfect storm.

This next question is a little long. I'll just put the question out, and then I'll let you run with it. And that is with various implanted devices. There can be metals. There can be chemicals that trigger an immune response. You recently worked with Dr. Miller, Dr. Afrin, on a study that explored the crossover between mast cell activation syndrome and multiple chemical sensitivities. And I'm wondering, are these essentially the same condition? Is the activation of the mast cells a potential explanation for multiple chemical sensitivity? And then are there some people that maybe have chemical sensitivity but don't have issues with the mast cells, or maybe they just haven't been diagnosed yet?

Yeah, I mean, this is a really a critical question, because if you take the population of patients that have sensitivity and you take the population that have mast cell activation syndrome and you add it up, it's a large group of patients and you could argue that they do overlap and you can argue that the mast cells are driving force in chemical sensitivity. And that's sort of what we were trying to show in this study. Essentially we were using questionnaire and we were correlating the answers to the questionnaire. And the questionnaire is called a queasi q e e s I that Dr. Miller designed. We used the queasy and then we correlated with the diagnosis of mast cell activation syndrome in our patients. And we again wanted to see how many of our patients with mast cell activation syndrome had chemical sensitivity or toxicant induced loss of tolerance, which is how Dr. Miller refers to a tilt. And so what we are showing, right, we can't prove it, this is not that type of study. But what we are showing is that there definitely, in our opinion, looks like the mast cells are responsible for, potentially responsible for the development of chemical sensitivity, that there's a trigger, a pesticide exposure, a chemical exposure, an something implanted in the body, there's something toxic mold, etc. That triggers the mast cell. And in a subset of patients, those patients will develop this increasing sensitivity to the environment. And so the challenge we have with the study, which is still, we're still struggling to get published by the way, so it's been in review. The problem is that the medical community doesn't seem to want to accept this view, which is really unfortunate because to me it's common sense, maybe for you too, and maybe for a lot of our listeners. To me it's like, well, yeah, of course that makes sense. What I love Dr. Miller is amazing, Dr. Claudia Miller. She's really pioneered the work on chemical sensitivity and, and she is sort of now the red, you know, the light bulb goes off for her. And she said, yeah, this is what I've been seeing. This is what I've been doing for the last 20, 30 years. It makes sense that the mast cells had to be primed first. There's an initiating event and then, you know, it sort of spirals. So, you know, we hope to get this published and out there because I think it's important information for a lot of people and certainly will change how we approach treatment.

Is your working hypothesis that multiple chemical sensitivity almost always or always involves the mast cells or are there potential explanations for non mast cell associated multiple chemical sensitivity? Try that three times.

I'm not going to say it. I'll let you say it. No, well, that's the question. Our hypothesis is that that mast cell activation syndrome explains multiple chemical sensitivity. Again, hard to prove, really would need to be done, the research would have to be done in the lab. They would have to be. So there's some basic science stuff, basic bench work, and then a randomized controlled trial where you can actually try to figure out the answer to that. But from the research that we've done from the patients that we care for, plus these queasy questionnaires correlated with our data points, it seems like the link is very strong. Yeah. The question is, are there other things that could explain it? Probably. I know in medicine, Nothing is ever 100%, and so I'd be reluctant to say that this IS. MCAS is 100% of the time responsible for chemical sensitivity, but I would say that it's a large proportion. And we need to figure out the other part. What is the other reason why people have that and not have mast cell activation?

Yeah, and I think it's exciting because historically, when I've heard mcs, it was kind of more of a label. You have it. But no one really seemed to know a lot about what to do, other than maybe supporting the liver. And so if this then brings people to an understanding that they can actually do something for the patient to make their life better and minimize their suffering, I mean, I think it's incredibly exciting research, and we'll be interested to see where that leads us in the future. There are many tools that can be used to test for the presence of mast cell activation. My observation has been that none of them have really emerged as consistently helpful. That there's sample collection and transport issues and other things. When do you do the test? Do you need to challenge it first? All of those things. And so you've been at this for a while now. I'm wondering, what testing options do you find most consistently helpful in your patients with mast cell activation syndrome? And how often are you able to confirm with laboratory assays versus treating empirically based on symptoms, history, clinical presentation?

I really try not to treat patients empirically unless, you know, it's. Unless I just really have exhausted all options for getting an answer. But most of the time, the majority of the time, I will get an answer. If I can't find mast cell activation syndrome as the root, but they have symptoms that look like mast cell activation syndrome, I might go about treating some of that. I know that it's a part of their story, but I also know that if I can't prove it, there has to be something else that is either resembling MCAS or is in the secondary realm of MCAs, kind of causing the mast cells to inappropriately React, but there's a trigger that can be eliminated, and then the MCAS can be reversed. And I think that in my experience, those secondary MCAS patients are the ones that are hardest to diagnose with mcas, and that the primary MCAS patients are the ones that are, I don't want to say easier, because nothing about this is easy, but it does seem like we can get the answer more easily. I would say at least 80% of my patients I can prove with at least two markers, two mediators that they have, they have MCAs. Now, in terms of which ones are the easiest to find or which one I see most, I would say that a plasma histamine is by far the easiest thing to do, because every lab can do a plasma histamine. And so, yes, there may be some issues with transport, with temperature, but less so than other tests. So if people can start with a. With a plasma histamine and maybe a chromogranin A, which is a little bit debatable, depending on which group or consensus you kind of go towards in the MCAS world. So sort of in our world, where I live, chromogranin A is a good marker, decent marker for mast cell activation syndrome and also easy to test for. If the levels are really high, then I'll worry about neuroendocrine tumors and other things. But generally speaking, a slight elevation of the chromograninae and an elevation in histamine sometimes give me the answer. I almost never find the answer with a Tryptase. Elevated Tryptase levels often just represent a genetic issue called hereditary alpha tryptasemia. Those are people who have higher levels of Tryptase because they have more copies of the gene that makes Tryptase. But that doesn't necessarily mean they have mast cell activation syndrome. I rarely see. I have a handful of patients that have had that typical Tryptase level is low. They're in the middle of a flare. The Tryptase levels goes up, and according to the consensus one criteria really put forth by a group of. Of mast cell specialists, they really believe Tryptase. They really put their, you know, put all their. All their eggs in one basket there. And they sort of use Tryptase as the diagnostic tool. And if I did that, then really very small percentage of my patients would meet that, you know, criteria. So I check Tryptase on the chance that it will provide some information. But histamine and chromogramin A, again, pretty easy to do. You know, heparin is probably by far the Most sensitive and specific marker for mast cell activation syndrome. Heparin is an interesting chemical because it's a drug, it's a blood thinner, it's used for blood clots, but it happens to be a drug that our own mast cells can make. And when mast cells are activated, they're more likely to release heparin. The issue with heparin is that it does have to be temperature controlled. There are a variety of issues, and the lab has to be able to measure it. Very minuscule because it's not like the mast cells are making enough, like the drug proportion of things. This is a small amount. So we have a lab that has been able to measure it at very, very low levels. And when we see some amount of heparin in the blood, that also is a really, really great tool and great marker for mast cell activation syndrome. So that has actually changed my practice in the sense of I'm able to diagnose more people because of that heparin level.

That's really interesting, too, with a heparin, because I'm guessing even when you see elevations in the mast cell activation syndrome patients, that many of them simultaneously are dealing with hypercoagulation.

Yes. And while they're dealing with hypercoagulation on one end of things, they are hemorrhaging during their menses at the same time. And so it's really, really, you know, the pathways are obviously very, very complex.

Do you find it better to run the tests when someone is in the middle of a flare or to provoke it with histamine triggers, or is that not generally helpful?

I have not found it to be helpful. So I usually don't have patients do that. And even patients are worried they're taking antihistamines. They want to know if that's going to interfere with the testing. And generally speaking, doesn't usually. I'll get the answer. Most of the time, yes. On rare occasions, I have to have them stop some things. But I never provoke because the patients, by the time they've come to see me, they're so ill. I don't want to make them more ill. I just want to get some answers. And usually, again, we might have to do a few rounds of testing. We might not get it on the first shot, but persistence usually gets us the answer. And again, if I don't get the answer on two or three rounds of testing, then I'm convinced that there's more to the story. There always is more to the story. By the way, I rarely have straightforward MCAs patients that just have MCAs, they almost always have a lot of other issues, whether it's the gut, whether it's their immune system, whether it's mold, exposure, chemicals, and all that other stuff. But in those that I can't find markers on, I know that those are bigger issues for them.

Dr. Raj Patel, Dr. Talia Hale. They've talked about a correlation between MMP9 and Mast Cell activation. I'm wondering if you've seen a correlation with MMP9 as well.

On occasion, I think it can be helpful. I've moved away from doing those sirs tests that sort of. In the realm of that kind of testing, I found them to be a little bit all over the place and not necessarily helpful in the diagnosis. The same could be true for, let's say, vegf. You know, vascular endothelial growth factor, theoretically is made by the mast cell. And so, you know, you would think, well, if patients have high levels of vegf, does that mean that they have more mast cell activation? Maybe. Maybe their mast cells, their mast cells in particular, are making more vegf. But I have so many MCAS patients who have low vegf, which you can also look at and say, well, that means something too. Right. Maybe that's mold or something else. Right. So it's complicated. So these markers are helpful, but I would never diagnose anybody based on them.

Yeah. And I think some people with elevated VEG f would argue that that could happen in Bartonella as well. So to your point, it's like, okay, there's so many different factors involved. I did a podcast a couple years ago now with Dr. Lu Jean Feng, who talks about breast implant illness, about explantation. What's your experience been in terms of your chronic illness population, whether or not breast implants can be a contributor to their condition? And do breast implants potentially serve as a trigger of the mast cells?

Yeah, absolutely. And I'm thankful that there's more attention being paid to this, that the media and the general medical community is starting to accept some of this. I mean, again, to me, this is commonsensical. Everything. Everything I do is about common sense. Right. So you put something foreign into your body and your body doesn't like it. I mean, of course it doesn't like it. Right. You know, there are probably hundreds of thousands of women, maybe more, who. Who have implants who are fine. Okay. And so their immune system doesn't recognize it as bad. That's great. You know, but again, you think about it, it's a. For some, it's the silicone on the Outside, some of it is the silicone. On the inside, some of it is leaking, Some of it is mold growth, some of it is. I mean, there's probably a lot of factors, but again, there's something that's in the body that's foreign. The mast cells will see it as foreign in a subset of patients again. And if I say that MCAS is probably about 20% of the population, according to a research study out in Germany, was about 17%. That's a lot of people that have it. And so the potential for women with implants to have a worsening of their underlying immune status is pretty high. I think the mast cells are involved. I would also argue that the other parts of the immune system are going to be activated and it's problematic. And I would also just take it one step further and say we're not just talking about implant or we shouldn't just talk about implants, breast implants, because there are other implants and there are other materials that we put inside the body. Right. We use mesh for hernia surgeries and other things. Right. And I've my mess. Some of my MCAS patients have had mesh move to other parts of their body away from where it was placed. That's the mask cells, like basically pushing it out. Doesn't want it there. So really, all these things can be problematic. And I think we need to start thinking about it before we start putting these things into people's bodies.

Absolutely. Yeah. And I'm excited we're going to talk about some of those things as we continue the conversation as well, talking a little more about the breast implant situation. Talk to us about capsular contracture after breast augmentation. Is that an immune response associated with the mast cells and the fibroblasts? Is that what's essentially creating the capsule? And what are the mast cells reacting to in these implants? You touched on that a little bit. Is that the chemicals? Is that the shell of the implant, the silicone versus saline matter? What's actually happening there? But maybe in this capsular contracture. Let's talk about how that ties into this immune response.

Yeah, I mean, look, I'm not a breast surgeon, I'm not a plastic surgeon, so I'll keep it sort of basic. But I have many patients who have had that reaction, the contraction in one breast often, not the other. So there's something about why it's happening and whatnot. Maybe it's the way it was placed in that breast. Maybe it's. You know, I think about it as anything that is done to the body, even if it's a cut. Right. So a cut has to be made essentially right, to get the implant in. So you're cutting through tissue, you're cutting through cells. You're cutting. So it's not just the mast cells, but these. There are other cells that are going to react and try to heal that. That wound. And so I wonder if it's how the wound is made, how the implant is put in Again, why does it often happen on one side and not the other? I rarely have patients who have both sides. Again, these are patients that have MCAs. We've proven they've had MCAs. Again, I can't prove that the mast cells are involved in that process, but I can say that it makes sense. Sense to me that it does. And I. And I have a colleague in Canada who is a breast surgeon who is actually trying to do research on this, and I've been trying to help him and try to navigate, you know, how to figure this. This information out. Because his question is, is it mast cell activation syndrome that's causing breast implant illness? So we're not. Not just the contracture part, but just in general, you know, is that the cause of the issues? And so I think this needs to be studied. But, yeah, I would argue that an immune response to just about anything that the body reads or the masters read as foreign is going to set off an inflammatory reaction.

In a way, it's interesting. It sounds like this contracture is potentially a protective response of the body, similar to what you were talking about with. Okay, let's try to move this mesh. Let's try to get it out. Right. That it's essentially kind of walling off that foreign body so that it's maybe less of a trigger for some of these other inflammatory symptoms?

Maybe, yeah.

Do you think that stabilizing mast cells can lead to fewer complications post breast augmentation? Is there a connection that's been observed between mast cell stabilizers and the development of capsular contracture, for example?

So this is something that I would really love to study and look at. So in the patients that I'm seeing right now, they've already had the complications where they need to get the breast implants out. They have the contracture, they have breast implant bii, breast implant illness. They have something. Right. I wish I knew those patients before they had the surgery, because the question is, could we prevent any of that if their immune system is better equipped to deal with insult on it? I would argue, though, just based on the other things That I do. If a patient gets a vaccine, I have patients, they want to get the COVID vaccine, they need another vaccine. The same thing. We're putting something in the body. We use pretty aggressive mast cell targeted treatment to, to stabilize the mast cells to minimize the side effects from that. I would argue that if we could do that before the surgeries, breast implant surgery, or any other surgery, I think the outcomes will be better. In my patients who have had surgery for other reasons though, the better they go in prepared and the better their surgeon understands what they need perioperatively for their mast cells, the better their outcomes are after surgery. That I can say.

In terms of the prevalence of the development of mast cell activation or autoimmunity after these implants are placed. Do you notice any difference between silicone versus saline or does it seem to be about the same?

Yeah, I think the issue is that the COVID of the implant most of the time is silicone, and then it could be filled with saline or it could be filled with silicone. That's my understanding of it. There are other materials that go into that covering. To me, actually, it doesn't seem to make much of a difference of what's inside. I would argue that leaking of silicone when those implants leak would be probably more problematic than saline. But. But at the end of the day, it's material that shouldn't be there.

You mentioned mold associated to implants previously. So let's talk a little about fungal issues. Mold issues associated to breast implants. Have you seen that? Once the explantation has been done, is that something that's testable? Can we identify mold from these explanted implants? And then how do we think mold is getting into the implants? Is it actually in them or is it around them?

Well, it could be both. I mean, we, we have seen, you know, the problem is that again, the capsule of the, of the implant is supposed to be pretty tight, right? So it's not supposed to leak, supposed to keep the material inside. But, but there may be holes, microscopic holes. So things are leaking. As long as there's liquid material, as long as there's something that living organisms can use and attach to, you're going to get growth. I've seen it both ways. I've seen implants that have been removed that have mold inside, and I've seen it where they have mold outside. Thankfully, there are surgeons who are really interested in this and are sending the samples out for testing. And not all, unfortunately, but there are more and more and they're finding that again, it's liquid and it's going to foster growth of other things. And mold bacteria as well, not just mold can be problematic. And we've seen people be extraordinarily sick.

When people are testing for mold. Is it most commonly Aspergillus or what type of molds do we see in these implants?

Yeah, it's a good question. I mean, off the top of my head, I mean, I could probably pull up, you know, the pathology reports and tell you what has been found. But yes, Aspergillus is definitely a big one. I think we've seen Candida, certain strains of Candida on a couple. But yeah, I'm sure the potential for others is there.

I know there's some where they actually have kind of a port where they can fill them after they're implanted. And it seems like I've heard people talk about that as another potential way that certain things get inside that then can grow as well.

Correct.

Yeah. Let's talk about biofilms. So do biofilms grow around these implants? And if the answer is yes, does that potentially lead to a congregating location for many different pathogens in the body, making conditions like Lyme and co infections even more difficult to treat?

Yeah, yeah. I mean, I think biofilms really are probably the main reason, in my opinion, that so many patients continue to be sick after they've been treated for Lyme, Bartonella, mold, et cetera. So biofilms are a huge issue. And yeah, that, you know, I think about the biofilm as, you know, like a web, like a spider web. It's really sticky. Lots of things get stuck in there. And so again, anything that any insult to the body, a wound, a cut, something getting in, is going to promote an inflammatory response and that the inflammatory response is going to cause tissue that's sticky, sort of like fibroblasts and other things that again, set things up for. For pathogens to get basically stuck in and promote their growth. Of course, you'll see that with the implants.

If we look at some of your patients that have had mast cell activation that was believed to be associated with their breast implants and then they had them removed, do you commonly see reduction in their mast cell symptoms? Is that required in some of your patients to really move the needle towards health? If they're dealing with mast cell activation, breast implants, what's the kind of clinical course after explantation?

So, you know, it's sort of interesting in a large subset of my patients who have had explant surgery. They initially experience a pretty radical improvement. They really do feel like the toxins are just taken out of their body, and they do feel better, and they notice a shift. Many of them really are just so happy to have done that to get better. Having said that, I think the disappointing piece of this is that many of those women will still have some symptoms. And I think there are a few ways you have to look at it. I would argue that many of them probably had probably primary MCAs. They didn't know necessarily. They didn't correlate the symptoms they've had for years. They. You know, I can. I can think of, you know, one patient who had a lot of GI issues. Sibo had, you know, some. Some hormonal imbalances through her life. You know, there's sort of the flavor. I would call it the flavor of MCAs, but generally very healthy, right? So. So these women, you know, they're. They're, you know, overachievers, and they're. They're doing a lot of stuff, but they have these subtle health issues that are going on. And then they, you know, they have implants for a variety of reasons, and then slowly, their health starts to go down again. You know, mast cells get activated, the immune system gets activated. Some of them start having autoimmune markers show up. I've certainly seen that. All of a sudden, their ANA is positive, and then, you know, you remove it, and there's an initial reprieve. The immune system takes a deep breath, like, okay, we've gotten rid of this. The mast cells kind of calmed down a little bit. But the reality is that the mast cells were already dysfunctional before the implants, in most cases, at least in the cases that I see. And they, you know, you still have to deal with, you know, the dysfunction as a whole. But taking the implants out, taking one trigger out can be really remarkable. For some women, it's the main trigger, and then they can control everything else pretty easily. For others, it's a combination of triggers. So those patients that get their implants out, but that don't get better. I've spoken to a number of surgeons around the country who are concerned about the patients that they've explanted who don't get better. And they don't know why, because when they take the implants out, they see all these abnormalities. They know there was a problem. They. But then they want to know why the patients didn't get better. Those are the patients that we need to look at to see Whether it's possible they have mold and maybe they weren't tested for it. Maybe they're still living in a moldy environment. It's like this interaction between internal mold and external mold. They are a little bit of a mold factory themselves, but they're also breathing in air that has it. Maybe they have underlying Lyme or Bartonella. And I would argue that Bartonella is probably the biggest thing we see, sort of correlated with patients not necessarily getting better despite our best efforts.

And it's interesting, as you're talking about kind of primary and secondary mast cell activation, I know you do a lot in the world of Ehlers Danlos syndrome as well, and there's kind of that same concept, right, Those genetic Ehlers Danlos, that's kind of what we're talking about. Maybe more primary, where that's been there all along, potentially, versus more secondary or triggered by something else, like Bartonella, for example. And so it seems like there's a correlation between the mast cell activation, the Ehlers Danlos, in both of them having kind of that primary and secondary potential.

Correct.

If we think of chronic illnesses as kind of a bucket that's overflowing, triggering the mast cells, many things like mold and emf, Lyme, Bartonella, Babesia, other parasites, pesticides, chemicals, metals. I mean, this is a long list. How significant do you think the breast implants are compared to all of these other things? Does it kind of end up high on your list of potential triggers, or is it just one of many, many things that we need to explore?

Yeah, I can't say that it's the worst trigger by any means. It is. It could be the worst trigger for that patient. But I never, you know, put all my eggs in one basket. I'm never going to just look at the implants. We're going to look at all the factors. So for the individual patient, we might find that the implant is by far the most important factor that, you know, we've ruled out mold, they don't have Lyme, they don't have CO infections, they don't have other. They don't have heavy metals. So really, it does seem like the implant for them is the biggest factor that has to be dealt with and treated. But again, for me, looking at the environment both externally and internally, everything could potentially be the straw that breaks the camel's back. That's the big thing that changes the patient's life. Could be a viral infection. Patient gets a virus. They don't know what virus. Maybe it's Epstein Barr, maybe it's Something else. And then now it's years of chronic fatigue and mast cell activation and other things. So, you know, it's really based on the person's mast cells as to what is going to be worse.

So let's talk about some other types of medical implants. Let's talk about metals in things like knee replacements, hip replacements, very common. Do you see orthopedic implants as triggers for mast cell activation or other immune dysregulations? The resulting inflammation, any of the. So what can we do to support those people in need of these types of procedures?

Yeah, no, we definitely see it. And there are a number of labs that are trying to measure immune reactions to different metals. You can measure an immune reaction to titanium and nickel and some other things. And I have patients that are in need of orthopedic procedures. They need a hip replacement, knee replacement, but they're in the middle of a really bad mast cell flare. And we worry about, now we're going to introduce something else in, but they really need to have that done. And so, you know, sometimes we can look at these tests. I can't say that I have found those tests to be really a game changer. I don't think those tests are really measuring mast cell activation, but they may be measuring some other immune reactions. It could be helpful, but I guess the main thing is really just supporting their mast cells as a whole. Whole. You know, we do the best we. We can. We. If we know they have a nickel problem, you know, I'll talk to the surgeons and say, is there any implant that has less nickel there, by the way? There are no implants that have zero nickel in them, by the way. And I did some research on this or stents or other things. It's really remarkable. So it's about trying to minimize, you know, the effects. You might not be able to eliminate it. And again, better muscle support going into the surgery is going to be key.

Is this testing similar to the Melisa testing that originated with Dr. Burastechal's work?

Yes. Correct. That is one of the ways you would test.

Excellent. Are there differences in mast cell reactivity? If we're comparing, let's say a static implant that maybe does become encapsulated or have biofilms versus a more dynamic implant like a joint ventilation replacement that maybe can produce wear particles over time and become more of a systemic toxin. Do they seem to have a difference in terms of their potential as triggers for the activation of the mast cells?

I mean, I would say just, you know, sort of anecdotally and just again, from a common sense perspective, it probably makes sense that it could, but, you know, but hard, you know, hard to say. Yeah, good question.

I'm assuming then that even things like metal plates or metal or plastic screws may be used in a shoulder operation or after a broken bone or a spinal fusion. It sounds like these also have the potential to trigger the mast cells, and we need to really give that some thought in terms of how to best support that immune system when we're doing these types of procedures.

Yeah, absolutely. And to be clear, I have mast cell patient. You know, MCAS patients that have had spinal surgeries have had different. They have material in their body that's foreign. And we. We don't. We don't see necessarily correlation in those patients to. To that material and a worsening of their condition or anything else. So I just want to be clear, right? Not all MCAS patients are going to react to these materials. Not all MCAS patients are going to have a problem with breast implants. Not all MCAS patients are going to have problems around surgery. But understanding all this, obviously, and going into it prepared is better. It's better for the patient.

Let's come back to the hernia conversation and the mesh material that's often used in these scenarios. Dr. Dietrich Klinghardt, many years ago, probably 15 years ago now, he said that I had had a hernia, caused some issues, but I decided not to do anything about it because it wasn't significant, and I was concerned about this potential. And so, you know, what is the mesh made out of? My understanding is some of them are kind of almost like a plastic material. Can it be a trigger for the mast cells? And then do you have recommendations if someone needs to address a hernia? What's the least triggering way or the best way to approach that?

Yeah, I mean, listen, again, I'm not a surgeon, and this would be a great question for a surgeon who was really interested in MCAs, because then we can kind of look at it from a few different angles. I mean, again, I have MCAS patients who have had hernia surgery, have had mesh placed or mesh placed for other things, and are fine. They have no complications. And they say that was the best thing they could have done and it changed their life so that they can go on and do what they need to do. But I certainly have patients who have problems. I have patients whose mesh moves. I have patients whose mesh becomes inflamed, patients who develop chronic pelvic pain because of that mesh in that area. Both Men and women. And again, it's sort of what else can be done. I think the research does need to look at better material. I think, like in dentistry, they're always looking at better material to put in our mouth. They've got to think about better material. As far as even stents, when people have stent placement for cardiac reasons to open up arteries. Same thing with this. All these metals or plastics or whatever they're using, they have a lot of toxicity potentially associated. I do think they need to look at that. But I would also argue that even if you do the hernia surgery without mesh, and there are surgeons who are still doing that, you're still an insult to the body. There's a cut, you know, they go in, they have to close things off. That's still going to stimulate mast cells to some, to some extent. And MCAS can change how tissue heals. And so, you know, we sometimes will see patients who have keloids, you know, like scar tissue, and that scar tissue actually can become problematic. It can become painful and can be problematic, especially if it's deep, deeper in. And so my point being that you really could have an endless array of complications, but for the most part, most people do fine. You go in thinking about this in a smart way, and you hope that the things that we can do, not just pharmacologically for MCAs, but also thinking about the healing process with vitamin C or other nutrients, making sure that the patient is optimized from their health, going into any procedure is going to be ideal.

Let's talk a little more then about the dental procedures as potential triggers for mast cell activation. If we think about amalgams or composites, adhesives and glues and orthodontics or braces or dentures, do you see those as common contributors to your mast cell activation patients? And then what consideration should we give to the patient potential for activating the immune system when we're doing these types of dental procedures?

Yeah, I have quite a few patients really struggling with various dental work that they need dental appliances. Many of my patients have had to change their dental appliances. They spent thousands of dollars trying to figure out what's going to be right. Since MCAS is correlated with Ehlers Danlos CDS or hypermobility syndrome, many patients have airway issues, so they have sleep apnea. And, you know, we often will need some kind of appliance, if not a CPAP machine, which is a whole set of other issues associated with. So they have these things in their mouth that are just trying to help Them. And they yeah, they often. They often, but not always, react to the materials. And so it is a little challenging to have. You know, it's challenging to find dentists who are willing to entertain these ideas and try to find solutions. I've had patients. One of the biggest things I see with the dental stuff is really something called burning mouth syndrome. So you can get burning mouth syndrome. It does seem to be correlated with mast cell activation syndrome. I will say that I consider it a symptom of mcas. But very often patients will say that they had something in their mouth, some kind of procedure that made it worse or brought it out. For the first time. I've had patients who have had, let's say, even a crown put in. Not a major procedure. Actually. There was one patient who had. The crown itself was a composite material, but under the crown was a metal, and the metal was exposed a little bit under the crown. And again, I'm not a dentist, so I don't know all those specifics, but every time her tongue touched the metal on that crown, her mouth was on fire. I think I spoke to that dentist at least five times, if not more, and he refused to listen to me or the patient. I really had to really insist that the patient go to another dentist because he could not wrap his head around that little metal that was exposed, that was less than a millimeter, was causing the problem. It could have been the composite material, it could have been the metal. But nonetheless, it was very traumatic, actually. When the mast cells are activated in the mouth and the nerves are stimulated, the whole body is on fire. That's how patients say just that in the mouth now makes the entire nervous system, you know, activated.

It's interesting when we're thinking about things like even, you know, retainers or dental aligners or anything that could potentially lead to some reaction. And I know there are some biological dentists that will maybe use things like electrodermal screening or electroacupuncture according to Vol, or different systems of kinesiology, or autonomic response testing or something like that. Have you found any of those types of energetic testing options helpful in determining what things to use? Or are you relying on like a Clifford compatibility testing? What are you finding most helpful to potentially minimize this being another trigger in the bucket for your patients?

Yeah, I mean, I think you need to use all the tools you have. There's never going to be one process, one technique that's going to be right for everyone. People who are sort of energetically tuned in, especially if you have someone who Knows how to do the energetic testing can be very helpful. Absolutely. And I encourage people to do, again, what they feel comfortable with. What I find interesting, this is totally anecdotal, but in the MCAS world, I have not found energetic testing to be as reliable as if, let's say, I'm testing for treatment for Lyme disease or. Or something else where I could. I'm certainly not an expert, but I can use some testing, and I have practitioners and colleagues that do it. If you're trying to figure out what Herb, let's say, would work for Lyme, sometimes that energetic testing can be very, very helpful. But when it comes to mcas, trying to figure out what would work for mcas, what materials might make mcas worse, there's a lot of inconsistency, and I've had colleagues tell me that they've noticed that too, that they can't really pinpoint it the same way. I'll just throw that out there for what it's worth, you know.

And then if we think about dental implants, have you noticed differences in terms of mast cell activation? Looking at a titanium implant versus a zirconium implant, for example, do the zirconium implants seem to be less stimulating to the mast cells?

You know, so the biological dentists that I've spoken to feel that that is the case. They feel that zirconium is a better option for patients who are sensitive. So I sort of, you know, I go with what they say, and I think that makes sense to me. Titanium. We are seeing more and more reactivity to titanium, and maybe it's because it has been used for so many years in different areas of the body, whether it's in joint, in joints, or dental implants, etc. Titanium is a key metal. And so, you know, I wonder if just over time, people have become sensitized to it and are more reactive. And so with zirconium, maybe we have, you know, we won't see the same thing. It's a different type of material. The problem is, I, from what I understand, is that zirconium is not as durable, not as strong. And so the concern that some conventional dentists have is that you might wind up having to repeat that implant, whereas titanium will last longer. So it's about risk, benefit for every patient.

Do you find that some of your mast cell patients even potentially react to, let's say, titanium dioxide in supplements? Do we need to be careful about silicone dioxide and titanium dioxide and those types of fillers and binders and flow Agents and those types of things.

You bring up a really important question because really I talk about this with my patients all the time, and that's this issue of excipients. Everything we put in our body, from supplements, food, medications, et cetera, have these fillers in them. They have ingredients that are added to them. In many cases, the mast cells can react to some or many or all of them, depending on the patient. Now, I. I certainly have patients who are really not sensitive to various fillers. They're not sensitive to supplements, but they have MCAs manifesting in other ways. But yes, I would say the majority of my patients that have at least one, if not multiple things that they are sensitive to, and magnesium stearate, microcrystalline cellulose, titanium dioxide, all these things could potentially be recognized by an individual's mast cell as foreign. I think that the real important research that has to be done is to be able to look at the mutations in an individual's mast cell population and to be able to determine what that mutation does in terms of reactivity. Will we ever be able to identify that these mast cells cells are more sensitive to xyz? And then when we know that, can we target treatment better? Right. I have a dream, like I dream of this, that we're going to be able to figure out at a molecular level what patients react to, because that would take the guesswork out of a lot of this. Right. We would know. Okay, titanium is not good for that because they have this genetic mutation in their mast cell anyway. We can dream, you know.

No, but I mean, that would be amazing because. Right. They kind of do that now with T cell tests where they then take the T cells and expose them to different microbes and things and see what the reactivity of the immune system is. And so that would be tremendous if you could test various agents against a specific individual's mast cells and see what things were leading to triggering of that. So I'm sure you're going to make that happen. There is a lot of overlap between POTS EDs, mast cell activation. We talked about that in our prior podcast. Some people find themselves there dealing with these conditions after using some medications like fluoroquinolones, for example. I'm wondering what your thoughts are on the potential for fluoroquinolones to trigger mast cell activation syndrome in these patients that have been floxed. And then can other medications like antidepressants, can they trigger mast cell activation? What are some drugs that might be potential triggers in this population?

Yeah, so it can again, this goes back to the previous question about excipients and ingredients. I believe that some of the patients who have drug reactions may be reacting to a formulation of the drug and not the drug itself. And we certainly see that quite a bit. Now, I'm not talking about really severe reactions, but even still, I mean, I could argue that I've had patients be anaphylactic towards one formulation of a medication and not to another. Now, it's hard to get a patient who's been anaphylactic to one formulation the same medications tried. Again, I'm not saying we do that very often, but the point being that there can be a lot of variability because a lot of the drugs are made overseas. They're made. We don't know what goes into many of them. Even if we have an ingredient list, we don't know where those ingredients come from. I think that is a big problem. But then, yes, if we look at, let's say, the fluoroquinolones, again, I would say that most of the patients that I've seen with fluoroquinolone toxicity have had probably underlying MCAs. I can't prove they had underlying MCAs, but there's a story for it that the fluoroquinolones made worse definitely brought it out. I would argue, though, that there's almost always a genetic susceptibility to fluoroquinolone toxicity. And I understand that there's some research looking at how to sort of screen patients who might be more susceptible to the toxicity issue. So, again, it's a little bit. A little bit complicated. But I would say that fluoroquinolones are a class of drugs that I almost never prescribe because of my fear of reactions. There are probably not many other classes of drugs that I stay away from like that. So I can't say, for instance, that antidepressants, as a. As a general rule are problematic for MCAs. They can be. But I also have patients who get remarkable relief with an antidepressant for, let's say, a neurologic condition or maybe even depression. And that actually calms down the MCAs because their body's less stressed out. So, again, I can't. I can never say always or never because it's, you know, human beings, everything is variable. So I can't. I usually. I try to stay away from saying these are, you know, common drugs that are problematic and kind of really look at the patient and try to figure out what may be problematic for them.

Yeah, the whole excipient conversation is an interesting one. Because sometimes I see, you know, in the biohacking community and people that are coming out with new supplements and longevity things and they sound great. And then you read the ingredients and I think, I don't want to take titanium dioxide and silicone dioxide and all these things every day. Or you get a new pharmaceutical medication and it's in a beautiful pink and purple and turquoise capsule and you know that there's food colorings and all these other kinds of things in there. And so I think that's why it's also important to work with your practitioner, make sure that the supplement line that you're using is ideally considering those kinds of things. There are product lines like Pure Encapsulations and others that try to minimize those things as much as possible. When we're treating chronic infections or environmental toxicants like heavy metals. Do you find that in mast cell activation syndrome patients that a gentler approach might be better accepted by the body as compared to a more aggressive one that might then be triggering the mast cells even more?

Yeah, absolutely. I have so many patients who come to me after they've been treated aggressively for their underlying tick borne infection. You know, they've been on years, months, years of antibiotics. You know, they come to me, they're on three antibiotics and doing heavy duty detoxes and heavy duty supplements and herbs and they're getting worse. So their chief complaint is I'm being treated for all this, but I'm getting worse. What's going on? And I would argue that their immune system is in overdrive, their body can't handle all that. And I would argue that the symptoms they're having is not a lot of them. Sort of associate the symptoms with this condition we call Herxing or Herxheimer reaction, which is a die off reaction. And I will tell you that almost it's not hurts it, that's mast cell activation. That is, that is an inflammatory reaction to the drugs and the herbs and everything else that you're using as opposed to the die off of the bug. We're past the bug at this point. By the time the patients come to see me, it's just so much more than that. And so I do take a gentler approach. And definitely my style on this has changed over the years. Certainly was much more aggressive earlier on before I really understood mcas. Right. The more I understand mcas, the gentler I am. And what I find really fascinating is that there are plenty of patients that I have now that previously I would have treated more aggressively for their tick borne infection. But I Actually don't have to treat them for their tick borne infection. When I take care of the foundation of their body, I've worked on, I mean I've always done this, but I've worked on their gut and their nutritional status and their diet. We're setting the foundation and then we identify. Let's say they have MCAs. So I am stabilizing their mast cells, I'm reducing their mediators on reducing their cytokines and reducing inflammation. Then their immune system could deal with the underlying infections better. And so I have this one patient that about 12, 13 years old who came to me with Bartonella and Lyme and aggressive antibiotics and not getting better. And once we switched over, I mean, I don't doubt that he has all those infections. Probably still persistent in the body, but probably dormant, so to speak. Right. Quiet. But as soon as we started working on the MCAs and we found the right combination of things for his mast cells, it is just, I mean, mind blowing actually where this kid has come and the mother says, well, what do we do about this Lyme and Bartonella stuff that keeps coming up, right. I said nothing, actually, we're going to do nothing. We're going to watch it and maybe it will come out at some point and we'll be ready because his immune system and his MCAS is better controlled. So if we have to treat it, it will be easier to treat. But I really emphasize it a lot because that's one of my frustrations in the Lyme community is just, I think we have to just step back a little bit. We want, I, I'm a firm believer that those infections are important and they need to be addressed. But I think you have to address that immune system. And if MCAS is playing a role, do that first. Set the stage, then figure out what the patient needs.

Yeah, I 100% agree and I'm even surprised sometimes just people going on a low histamine diet, like sometimes 50% of their symptoms go away or what's left are significantly less significant. And so I agree this is a big piece of the puzzle. A lot of times I kind of personally have been a little concerned about getting super aggressive with heavy metal detoxification. People want to do IV DMPs and DMSA and all these kinds of things. And I think if the metals are also potential triggers of the mast cells and you're really just moving these things aggressively through the body, it seems like you can really end up shooting yourself in the foot by triggering more inflammation that then at the end of the day is going to minimize your detoxification potential. And so it's. It kind of ends up doing the opposite, I think, of what we were hoping.

Yeah, I agree. And I almost do no heavy metal detox anymore. 10 years ago I did never with IV, but. But generally really looked at it as an important factor. Now, are heavy metals problematic? Yes, they are. But to be honest, it's very hard to really detox the body of metals. It's very hard to get them out of the body. But if you can get the body just functioning better and the immune system better and the gut better and the detox pathways better overall without trying to pull. Pull things out of the system, you're going to be better off. Patient's going to be much better.

Is there any potential downside to aggressively stabilizing or quieting the mast cells in that they do do important things in the body and are intended to be there as part of our immune system? Can we over stabilize mast cells?

Yeah, that's a really great question. And that's a question that I have patients ask me quite a bit because, yeah, they are concerned. Right. It's about balance. We want to make sure that we're helping the immune system not hurting. But we have to remember that when we talk about MCAs, we're talking about mast cells that are dysfunctional, mutated, abnormal. They are not normal and they're not helping actually anything. While we're working to stabilize those mast cells to get them less reactive, we're not stopping good mast cells from working. We're stopping bad mast cells from working. Now, will you inevitably block some of the good mast cells while you do this? Yeah, you know, you might, but the truth is that, you know, we have an abundance of mast cells. It's almost impossible to control all of them or stop all of them from working. So it really works out. And in fact, I would argue that again, the patients whose mast cells are better controlled, their inappropriate mast cells are not acting as inappropriately. Overall, their immune system actually is better. They are better able to handle the stressors of daily living, the viruses and infections that they're exposed to. And that's what's fascinating to me. It's like that key, that control over that part of the immune system just automatically balances is the other part of the immune system.

So I really like that perspective because I've heard people argue on the opposite side of that as well and say, well, no, stabilizing mast cells actually has some downsides. And so I like the way that you presented that, and it makes a lot of sense. If we look at the immune system simplistically as a balance between TH1 and TH2. I tend to think of mast cell activation more of a TH2 shift. And so I'm wondering if interventions that are aimed at reducing TH2 and or supporting TH1, if that leads to improvement in mast cell activation symptoms.

Yeah, I think that's an interesting way of looking at it. And I would say probably that a lot of that is true. I have seen the opposite as well. And again, when it comes to medicine, nothing is ever 100%. So, you know, with autoimmunity, right. We always talk about, you know, the th1 or the th2 or th17. Right. We understand that there's an imbalance, but it can go both ways. And the same can hold true for MCAs. So I would say that, yes, supporting TH1 can be helpful. It's definitely something that we. That we do, but it can't. It's not going to work all the time because it's not always associated in each patient.

Have you observed patients benefiting from limbic system retraining to calm their mast cell activation tools like Annie Hopper's dynamic neural retraining system or Ash Shot Gupta's, the Gupta program. And then given that mast cell activation is a hypervigilance syndrome, does the limbic system play a role? Can we also maybe tie that in with working on the vagus nerve and parasympathetic tone and kind of calming the system down? What role do limbic system and vagus nerve play in this mast cell conversation?

Yeah, I think this is actually a really important tool or important approach with MCAS patients. And I encourage all my MCAS patients to think about how they're going to deal with stress. So that's like a conversation we have. Whether it's meditation, whether it's deep breathing, I love James Gordon's work. And belly breath. And so there's just simple tools. But then some patients definitely need a more specific program. Right. A more comprehensive program that's really targeted towards their limbic system. Again, overall, where you want to calm down their autonomic nervous system, they want to. We want to calm down their sympathetic nervous system. Right. And so there are lots of ways to do that. But these programs where there's Gupta DNRs can be very, very helpful at targeting that. That the limbic system specifically, which then obviously interacts with the autonomic nervous system. And so they're. So. I've seen, you know, incredible results. I've seen patients who have been able. Could only eat three foods. All of a sudden can eat all foods. I mean, we've seen some really amazing transformation. It's rarely going to be the key for everything. It's often not one technique, one procedure, one treatment that's going to be the thing that changes everything. It's usually a combination. But when used in combination with other things we use, I think it can be very helpful. I'm a big proponent of that, and I encourage my patients to do it. I definitely get some pushback. Not all patients feel comfortable doing. Doesn't resonate with them. And so that's actually just going to make them more stressed out. I would say that there's a fair number of patients who don't want to go down that path. And if they don't want to go down that path and do those programs, then we do sometimes look at these other vagal nerve programs or ways to. Again, we're getting at the autonomic nervous system from a. From another angle. And that can be helpful at sort of quieting. Quieting things down. So I'm a big fan of these different techniques, and it's about really making sure that it resonates with the patient and that they will get the most out of it.

Any favorite tools in that realm that you like to use?

Out of all of them, I think DNRS is probably the one that I have seen the best results with that I have. I can say that there's more defined response, but I have patients who say, oh, this has worked. This has helped. I have patients who meditate, who do belly breathing, who do other things that feel like that's. It's all helpful. But I like DNRS because it just seems more targeted, specific, methodical.

Yeah. And that's the one I have the most experience with. I did it myself for seven months, an hour, a day. I did feel like it was very helpful. But to your earlier point, it is not the only thing people need to do. And I think sometimes this gets a little confusing. I think sometimes people think that the message that Annie Hopper is sending is, well, if you're in a moldy house and you just do DNRs, everything is going to be great. That's really a misunderstanding of her teachings. Her teachings are that DNRs is done on a platform of environmental awareness. And of course, if you're living in a multiple house, you really want to fix the tiger, so to speak, before you start trying to reboot or recalibrate the limbic system and So I think your point was an important one, that there is a timing for when these things make sense and have the most potential to help. And that you still do need to consider those underlying triggers and how to address them. And this is not going to be the one solution. But I agree. I've seen it be pretty miraculous for many people.

Thank you for saying that. I think that's an important point.

Have you found tools like LDA or ldi? Low dose allergen therapy, low dose immunotherapy. Can those create more immune tolerance to some of the materials potentially that are in the various implants that we talked about? Can we modulate the immune system so that these implanted materials are potentially better tolerated?

You know, I don't have experience myself I doing LDA or ldi. We don't do that in the practice right now. I have colleagues who do it. I have patients who come to me who are doing it. And I would say anecdotally there seems to be some positive effects for some. I can't say that it's a game changer. Right? There are some things that we do that I think are game changers, like DNRs could be a game changer for the patient. It may not be, but could be. There are other interventions that we do that I could say, wow, that's a game changer. And I've just never seen lda, ldi, those types of treatments be the game changer, but for the right patient. Some of my patients have said that it was helpful, so I don't feel strongly about it.

And extending on that, how about tools like homeopathy or naet, the number pod allergies elimination technique or bioset, or other tools that are kind of getting the nervous system to be less reactive to different materials. Have you had any patients where maybe that helped to calm their MCAs, particularly associated to some of these implanted materials?

You know, my problem is that I really love all these different techniques and different ways of doing things. I love homeopathy, I love the concepts. And I think that there are patients who respond well. I have colleagues who do naet. Again, I'm fascinated by it. I think it's a great tool. I hate to say it because I really do love the concepts. I can't say that my patients are really, again, really changed by these techniques. In fact, I have one patient who's been doing NAET probably for 10 years, maybe more. And it seems like what happens is maybe she's less intolerant to some things, but then more intolerant to other things and it becomes this sort of vicious cycle because if that's all you're doing and again, you're not working on all the other factors, you know, how successful is it going to be? So I think again, with all these tools, like you said, you have to look at your triggers and you have to eliminate your triggers the best you can. And then you have to use various methods together in a gentle way to produce the best results. So my point is that, yeah, I can't say any of those are really going to be amazing for everyone.

You mentioned game changers. And so that's a good segue into my next question, which is what interventions or treatments are exciting you the most right now in the field of MCAs and what do you see as really moving the needle for your patient population?

So I'm excited about peptides and I was sort of maybe a little late to the game of peptides. A lot of people have been talking about it for years and I think it makes sense on some levels for the immune system, the number of peptides for that, for anti aging and things like that. But interestingly, again, some of this is anecdotal and we really do need more research in this area. But when I again focus on the things that are potentially making a patient's MCAS worse, then again, it can be helpful if I have a patient who has MCAS and autoimmunity and immunodeficiency. Actually that's a very common trifecta. So they have, you know, they may have common variable immune deficiency, they might have low IgG IgA. They might also because of that be more prone to having autoimmunity. And so maybe they have Crohn's, lupus, rheumatoid arthritis or some flavor or something, Hashimoto's. But they also have evidence of mast cell activation syndrome. And again, I would argue that there's some connection, connection between all of them. And so I'm working on their mast cells, maybe I'm working using anti histamines, maybe I'm using other blockers or stabilizers, working on their foundation and their diet and all that. But you know, maybe if I also focus on the other parts of their immune system that are in concert with the, with the mast cells, I can overall get them, their mast cells better. And so sometimes like using things like thymos analysis alpha and KPV and some others, what I've seen is that it's a little hit or miss. People can still react. They're still right there's still always going to be problems. Nothing is ever going to be great for every single person you start to see things. For the right patient population, these peptides could potentially make a big difference. And because my patient population is so really largely tick borne infection and mold, there's immune disruption from the infections and from the mold and mycotoxins. Again, we're working on that piece. I'm excited about how that's really affecting the MCAS part. When I started doing the peptides I was doing it for their immune system. But I wasn't so convinced that we would see the effects at the level of the mast cell yet. We're starting to see that. I have one patient, for instance, who has a lot of urticaria, hives, itching, food intolerances, et cetera. And so we have her on a lot of mast cell targeted therapy. But then we started some of these peptides very slowly, of course, one at a time, very carefully. And what's interesting is that while she gets relief from the mast cell targeted therapy, it's never 100%. It's always like a breakthrough. But now we add this other piece on and all of a sudden everything just seems to be like dampening down. That's exciting.

Do you find BPC157 helpful in your mast cell patients? And when you're using kpv, is that the oral KPV or the injectable version?

You know, the challenge is really now being able to get the injectable right. There are a lot of places that don't have it. So I've been using more oral KPV and an oral BPC157 if we can find the injectable one. There are a few pharmacies now that have it. So, you know, the BPC 157 to me is not as exciting as others have made it out to be. On paper it sounds too good to be true. In practice it's, I don't know, rarely a game changer, as I keep saying. Right. It's not, it's not usually like the thing that's going to change everything. Sometimes it does help in concert with the other things that we're doing. But thymosin alpha probably is the one that. And that's injectable and also hard to find. Seems to be the one that I've seen the biggest shift with.

Wonderful.

And also, and I'm sorry, I'll add one more thing for the ME CFS population, you know, the chronic fatigue syndrome patients anecdotally Thymus and alpha does seem to be helping the chronic the fatigue, interestingly, and I don't understand it completely.

Yeah, it's super exciting. I mean, having been in this Lyme and mold illness realm for over 20 years now, myself, I think there's newer tools, the research is accelerating, the solutions are accelerating. Like it really is an exciting, hopeful time as compared to years past. And so it's really exciting to see some of these things being available to patients. My last question is the same for every guest and that is, what are some of the key things that you do on a daily basis in support of your own health?

I am very, very in tune into my body and to what I put in my body. So a couple things I definitely watch and follow as healthy a diet as possible. Grass fed, organic. I am carnivore, so I only do eat meat and that's a topic for another conversation. But for me that's what works. I have to have some kind of activity, I have to move. And so whether it's walking or running or weights, I mean, I'm lucky that I can do that stuff. And I know a lot of listeners, you know, you know, can't exercise or don't, you know, feel well, but, but this is sort of what I've done over the years to, to get to where I am right? I've had issues and chronic issues over, you know, in the past and so I've come a long way. So I love to run, I love to walk, I love to, to be active and, and I am trying to meditate on a, on a more regular basis. That's, that's one of the goals that I set for myself. I often am pretty good about belly breathing and taking a moment, but meditation is the one thing that I always say that I have to do more of.

This has been such a great conversation, so informative. I've probably known you maybe four or five years now and what I always love is just your passion to find solutions for your patients, your passion to educate and share your knowledge with other people, people to minimize their struggle, minimize their suffering. And I just really want to thank you for not only being here today, but for everything that you do and all of the information that you share. So thank you so much, Dr. Dempsey.

Oh, thank you so much. It's very sweet. Thank you.

To learn more about Today's guest, visit DrTanya Dempsey.com that's D R Tonya T A N I A DempseY-E-M-P-S-E-Y.com Dr. Dempsey.com thanks for listening to today's episode. If you're enjoying the show, please leave a positive rating or review as doing so will help the show reach a broader audience. To follow me on Facebook, Instagram, Twitter, or Miwi, you can find me there as BetterHealthGuy. To support the show, please visit BetterHealthGuy.com to be added to my newsletter, please visit BetterHealthGuy.Com newsletters this and other shows can be found on YouTube, Apple Podcasts, Google Podcasts, Stitcher, and Spotify.

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