 Hello everybody. Good afternoon and welcome to another episode of Dr. Jill Live. So glad to have another special guest here today. I have the best job in the world when it comes to this because I get to talk to my friends and colleagues and what's really cool, the secret about these interviews is I always learn something just like you. So I will, I'm sure that from Dr. Dempsey today will learn some great things about MCAS. Before we start and before I introduce her formally, just a little bit of background. You can find me and all kinds of blog and information from the last 10 years at jillcarnahan.com. If you need any products or services, you can find those at drjilhealth.com. And you can find this episode, which is actually I think 102 and all the other ones on my YouTube channel, which is just under my name. And you can also listen in your car as you're walking or hiking or wherever you're doing activities on anywhere you listen to podcasts. So find us on Stitcher or iTunes or wherever. Today I am just absolutely honored to have a guest that I highly respect who's been publishing some amazing work. Today we're going to talk about some of those papers. She has been putting out incredible information. We were just talking right before we got on here how important now more than ever the message of functional integrative medicine. Sometimes I call it medical mystery solving because so many of you listening and so many of our patients and if you're practitioner listening, you know these are people are coming to your clinic with very, very complex chronic issues that are mysteries for the most conventional doctors. We're both trained in conventional medicine. However, what we realized is that sometimes there's more. There's more than just what we're taught. I always feel like the foundation I have in my medical training is critical to making good diagnosis and treatment and changing medicine and shifting it however there's more and today we're going to talk about more especially in the realm of MCAS which many doctors either know a little bit about mastocytosis which we were taught in medical school and today we'll go into all the differences between the different types. How do we diagnose it? How do we treat it and everything you wanted to know about MCAS. But before I start I want to introduce my guest Dr. Tanya Dempsey, a medical doctor. She's board certified by Holistic Medical Association as well. She is a received her MD degree from John Hopkins University School of Medicine in her Bachelor of Science from Cornell University. She completed her internal medicine residency at New York University Medical Center and she's currently a community staff member of Greenwich Hospital in Greenwich, Connecticut. So Lyme country, right? Which I talk about infections too out in that. Oh yeah, yeah, cover it all. Yep. In 2011 she founded Armok Integrative Medicine which has evolved into the AIM Center for Personalized Medicine, a destination practice in Purchase New York which focuses as we just said on complex multi-system diseases. And again we were both just talking about how we need more doctors and we're both passionate about training and teaching because this is an epidemic and patients are getting sicker and sicker. She has published in so many different, she's been an international speaker, writer, keynote for the International Congress on Natural Medicine in Melbourne, Australia, featured on Fox New York Times News, Readers Digest, Having Them Post, The Observer, New York Post and countless other media outlets. And I won't read all of the publications but she is a well published author. We are going to talk specifically about some of the recent papers that you published because I think the data is going to be fascinating and interesting to our listeners. So I love to start with, first of all, welcome, welcome. So glad to have you here. Thank you for having me. You're welcome. And then the second where I want to start is just your story. How did you get into functional medicine? We're both MDs, very conventionally trained and we, you know, I like you, we love our background. It's a great foundation but we've gone broader, right? We've gone wider, we've gone deeper. How did you get to where you're at now and in the integrative realm of medicine? You know, like all of us in this, in this world, in the functional medicine world, you know, we've all had our journeys. I actually have always been interested in a more holistic view on health. And I was sort of raised that way. I sort of remember back, I was a teenager and I had a pimple and my mother consulted her little vitamin Bible and said, yeah, oh, you need zinc, you know, and I would take zinc or whatever it would work. But, but my, I grew up in that sort of mindset of like, maybe there's a natural way, maybe it was the food, maybe it was something else. So I had that part of me going into medical school. What happened was I sort of found that I had to really split, you know, kind of dichotomize my, my existence. So I was living this life where I was thinking about my body and what I was putting in it and the environment and, and, you know, the nutrients. And then I was studying science and medicine and there wasn't a lot of overlap. There wasn't ability to really overlap, but I would walk around with this vitamin book in medical school and everyone would be like, so what do we take, you know? And I mean, I'm simplifying functional medicine, of course, not just my vitamins, but it's just about the fact that I was sort of that this was a secret that the way I had to think about health and, and, and lifestyle and all that. And then what we did in medical school and then training. And so when I went into training, you know, it was all about, you know, that people have high blood pressure, you put them on blood pressure medicine. I wanted to talk to them about what else was going on. I wanted to understand the links between the rest of their life, not just their lifestyle and stressors, which are obviously very, very important, but also other things that were connecting, you know, maybe they had stomach pains and maybe they all had other conditions. And I always understood that there had to be a connection, but our training was you treat that in isolation, they have stomach pain, you send them to the GI doctor, you know, you send them to all the specialists. And it started to get really, really more, more difficult to sort of confine my practice to doing that. And I started spending more time with patients. And then I would get reprimanded my bosses, you know, you're spending too much time, you're not billing enough, you know, you're not writing enough statins, you're not writing enough Lipitor. And true story, there at one point, there was, they were docking us first a dollar patient and then $10 a patient. If the patients had cholesterol over 200, they were docking our pay if our patients had cholesterol over 200. Unbelievable. I'm not making it up. Okay. That's like a true story. So that was the last straw. I said, wait a second. This is not about like, you're going to pay me to put people on cholesterol medications. I don't even know if these people need cholesterol medication, you know, there's so much more, right, beyond medication. So that was sort of the point where I was like, okay, I think I've just about had it, you know, and the more and more I was seeing this there, I was also seeing it in my own life. I was dealing with a issue with my son who developed vitamin D deficiency, really severe vitamin D deficiency, because his pediatrician told us, don't give him vitamin D. And I was trying to be this good mother who was like, I'm going to listen to the doctor. I'm not, you know, the pediatrician used to say to me, don't be the doctor, you're the mother. Okay, I won't put him on vitamins. And oh my gosh, he was severely, really, really very sick. And so it was sort of like, okay, now I get the vitamin D thing is really important. This is very important. And I started learning through my kids, myself, my patients. And then, you know, I really had to go on my own. I said, you know what, I'm going to take a risk and I'm going to start my own practice. And I did it at a time when at least in my area, every doctor was joining those big conglomerate. You know, you were going the opposite way. And I said, you know what, I got to do what's right. I don't know. I kind of opened my practice and said, I don't know how many people are really going to come to me. But this is what I believe in, you know, this is the way that I'm going to treat people. I'm going to spend time with them. I'm going to dig, going to understand the connections for them. I'm going to help on rounder health. And you know, if I see five people, okay, you know, but it obviously, you know, really, I grew and you're known in this world in our world so well and so respected. And I love that you share that story and I can so really, it was like same thing. I grew up with organic vegetables and we like, we'd go to, you know, the homeopathic stuff or those kinds of things on our home before we go to antibiotics or medication. So I kind of lived that. And then I went to the medical school environment and there's also this very masculine, like it fit in and be this kind of like strong, tough, not intuitive, not sensitive. And so I kind of like put aside my feminine, intuitive nature, which is that not that it's like male or female, but the feminine nature is more intuitive, more wise, more feeling, more gut instinct versus just the science. And I think the best world is when we blend them both, but our conventional training is so masculine, analytical driven, right? And so again, like you've discovered, I remember a little story that relates to your, your being paid for cholesterol in the hospital. I was integrated medical director at the center. And so I sat on a board with, you know, the GI director and the rheumatology director and we were all sitting in the boardroom. And the medical CEO of the hospital was saying, okay, he's doing charts of beds filled by each department. So how many beds are you feeling as a department in our hospital? How many patients are you sending to the hospital? And of course, the gastros were filling them and the cardiologists were filling them. And then there was me with integrative medicine and it was like zero. And I'm like, um, wait a second, the same thing that intuitive sense was like, this doesn't feel right because I want to keep people out of the hospital. And I'm doing really well if I'm zero, but I was actually docked as a department for not getting people filling beds in the hospital because that's what they were tracking. So both you and I kind of came up against the system that we knew like the beautiful thing about your story in mind is this intuition, our heart was like, this isn't right. This is not right. And I'm going to risk my life on doing what's right. And I'm going to take that change. I did the same thing. I started my own practice. I moved to Colorado. Same thing. I'm like, well, anybody come, can I do this? Right? So I love your story because it's so in here we are now, like we are making a difference, not only in our clinics, but in the world and our small little sector. And it's so powerful when we follow and I just as you're listening, you might not be a doctor, but you might be a mother or you might be a nurse or you might be in some profession. And I just encourage you one of this important things out of this moment in the conversation is you need to follow that intuitive part of what's right and good and right for you and not feel like what you're told is always the right thing because we both had these times where we bumped up against something that felt wrong and we changed and we took a huge risk. And here we are, right? Exactly. Exactly. Yeah. No, I think that's a powerful message. If you know something is wrong, whether it's your career or your health or whatever, you have to start listening, you know, and that was the that was the point where I was so and such a great like foundation, even as we start talking about MCAS and stuff like one of the things I think is so important for us in our practices with patients. And again, if you're listening, patients know when something's not right in their body, right? And the more we can listen and empower them to know that they can actually trust that that feeling that something's not right. Because so often they go to the doctor, they get a basic panel on liver, kidney metabolic panel, and then they get blood counts or they get thyroid. Everything's normal, right? And they're told, you're fine, go home, there's nothing wrong. And listeners comment here if you've ever heard that because I bet you many of you listening have heard you're fine, you're normal, and you know inside something's not right, right? And again, part of our message is like listening to the patients. That's a great segue because we deal with these patients who have these kind of medical mystery conditions that many doctors haven't been able to figure out or they've been other places, I'm sure by the time they get to you. Let's start with just how do you start when you're seeing a patient? What kind of questions do you ask? Where do you go? What are you seeing change in the last few years? Give us a little snapshot of kind of the complexity and what we're seeing now in the clinical practice. You know, well, I'm asking, I mean, I spend, you know, three hours more, you know, with with patients for an initial visit. So the things that you need to find out to really start to understand how their condition got to the point that it got to and what are the the triggers and the drivers of their condition. You know, I start at their mother's pregnancy if they know anything about that. I probably, and I go back even further if their mother was sick before she got pregnant. Again, if they know that some don't, you've are adopted, etc. But whatever we could find out about what what may have impacted them epigenetically or or or directly, whether it's, you know, toxin exposure, their mother lived on a farm where they use pesticides, you know, or whatever. I'm looking at all those everything in the environment. I'm looking at stressors. I'm looking at traumas of various kinds. You know, what we perceive as trauma, what one person perceives as trauma, another person may not. So it's really understanding how things impact the patient. And, you know, all kinds of exposures to infections. I mean, you know, I live and practice in the part of the country where it's an endemic area for ticks and tick-borne infections and vector board infections. And and so that always comes up. And that's something that we always, you know, I always look for. Okay, so we're looking at all the environmental issues. We're looking at stressors, traumas, things that have affected them that that you may not have realized impact them. Even things like head traumas, discussions, things like that. And then, yeah, the area of the country where they live or the area of the world where they live, you know, I would argue, and I think there's some evidence to support that, you know, there are tick-borne infections or vector-borne infections everywhere in the world. Maybe Lyme is more prevalent in my area of the country, but that's Lyme, Borrelia, Berdorferi, and there are other strains and they're all over the country and over the world. But I'm looking for exposures. Is it a tick bite? Is it a spider bite? Have they been bitten? Have they had fleas or ticks and I mean fleas and lice and other things? Because we know Bartonella, can he transmitted by many of these? I've been bitten by animals. I love that you're saying that by the way. I just want to pause because I have seen so many Bartonella spider bites or other types of things that are not ticks and maybe don't leave a rash or don't leave and I just love that you mentioned that because people out there very much thinking vector-borne infections, which is another great thing that you said, are not just ticks. And in Colorado, we're supposed to be non-endemic. We have tick-borne relapsing fever. We have soft ticks. We have the Lone Star tick. We have all kinds of ticks that do carry infections and we're seeing as long as we're testing the right way, which we can talk about in a few minutes. But love that you're asking that question because that's so important. Yeah. I think we've become short-sighted by focusing on the gear tick, transmitting Borrelia, Berdorferi, that particular strain when we know that the other strains of Lyme or tick-borne relapsing fever are transmitted by different ticks and different species and so and then a lot of these other insects or arthropods are transmitting Bartonella and maybe mosquitoes are transmitting Babesia or maybe even Bartonella. I don't know if we have the urge yet to support that. So we need to know that and then we need to know about their pets when they were growing up. We need to know that they live on a farm. Do they have exposures to being bitten by wild animals? You'll be surprised how sometimes these things are not, they don't realize it until you start asking. You go, oh yeah, I was scratched by a cat when I was five and then I had a lift node that was swollen and then or the patient that comes in and says, oh yeah, I had calf scratch fever when I was younger. So these things are, you have to draw the memory a little bit because sometimes it's, people go on and don't realize the relevance of what has happened. The doctors they've seen, the practitioners they've seen have not really paid attention to it. So it's a really, really comprehensive and I'm also looking for, we have to look at heavy metal exposures, mold exposures. I ask about where they work and where they live and even in the past, they may not be living in mold now but maybe they grew up in a moldy place and how that impacted their health over time. I love this because you're really laying the found work of what's so important is that clinical history is so powerful and often probably like you, I'll know in that clinical history very clearly what direction we need to go and I'll prove it with the labs but often a good history is taken, you will have almost your diagnosis before you do the testing, if you're really listening for those clues. Correct, exactly. Wow, what things are you seeing? I feel like with a pandemic an already shaky system has been revealed to be even more shaky and less robust for these complex chronic conditions like you and I see. What are you seeing, you know, like environmental toxicity and increase in these ticks in areas that are more populated? What things are you seeing in our world that are making this more complex and more cases of chronic illness? Is there any ideas of what might be causing some of this? Well, I think, well look, I guess I'll say basic, basic level. This has been a really stressful time, right? There have been economic issues. Obviously now there's, you know, war and people dying and people were in isolation for a long time with COVID. We have that part of it. There was a lot of depression, a lot of eating for comfort, a lot of people. People in general need other humans, maybe introverts or maybe extroverts, but in general there's something to be said about the socialization of humans and so in isolation, I think that a lot of people just a shift, right? And so I think that that promoted, you know, the wrong eating, a lot of alcohol, excessive alcohol use, increased drug use. We saw really a range of things happen during this pandemic, but then I think that a lot of people also got sick with COVID. Some who were aware they got it, they knew they had a diagnosis, but early on in the pandemic when we didn't have testing yet or we had testing, but you know, maybe it wasn't as as people weren't able to get it. I have patients who really feel that they got sick in February of 2020 before lockdown in March and that we can't prove that they had COVID, but they feel that that was the essentially the straw that broke the camel's back, that they, their health declined at that point. And I would argue that much of what we're seeing in terms of the increase in chronic disease is linked to mass cell activation syndrome on some level. And so of course it's hard because, you know, that's the lens that I see things through, right? But there's no question that infections like COVID will trigger mass cells to activate even in normal people who don't have mass activation syndrome. And so I think a lot of people had some underlying dysfunction that they didn't know about, at least in my position. What's interesting, 100% on this, because I'm seeing that. And I think that this far is because it was so prevalent and so virulent as far as contagiousness. A lot of people that maybe haven't been exposed to tick-borne or vector-borne infections were exposed to COVID. And so that they've, let's go just to the basics because you wrote a paper on how to diagnose mass cell activation syndrome. So tell us, tell for listeners who aren't super familiar, my listeners probably have heard of this, what is it? Why is it different from mastocytosis? How do you, you know, present? Tell us a little bit about the basics of mass cell activation. Sure, sure. The paper is called Diagnosis of Mass Cell Activation Syndrome, a global consensus two. And consensus two is because there are papers that refer to a slightly different way of diagnosing mass cell activation syndrome. And so we kind of call that consensus one. And really what we're talking about is what we understand is that mastocytosis is rare. It's a cancer, essentially, of the mast cell. It's a lot of mast cells growing and they're also activated. So patients with mastocytosis can still have the symptoms of the activation. But mass cell activation syndrome is basically they have, people have normal mast cells a normal number of mast cells, but they're not normal. They're very, very reactive. And, you know, why that happens, you know, there are lots of theories to that. But, you know, what I would say is that there's some people who are born with completely normal mast cells. And those mast cells when they get COVID, or if they get another virus or Lyme disease, or whatever, they will activate. But then when the infection, the trigger, taking care of, they go back to baseline. Patients with mast cell activation syndrome have abnormal mast cells that develop pretty young. Usually patients with MCAS have signs of it in childhood. Generally, usually before, you know, they're 21, usually there's already evidence. But they may still not be, they may not be that sick. And they may be, you know, their symptoms whites and white and so they're fine. They don't think about it. And then over time, there are these additional triggers that bring it out. And when mast cells are dysfunctional, they are sometimes reacting, they're reacting, even when there's nothing to react to. They are releasing chemicals. Part of how mast cells work is that they release these chemicals that are supposed to fight the environment. But in fighting and releasing these chemicals, they're also damaging wherever they are in our own body. Backfires is very inflammatory. And so over time, people who have under mast cell activation syndrome can have these triggers that can bring it out. And I would argue that for some patients with COVID, they had something, then they got, they had it. They had MCAS, they didn't know it. Yes. They had COVID, they got COVID. And then it was the trigger that brought it out completely. So anyway, back to the paper. So what we were looking at, the reason we publish this paper, because there's just really so much really uncertainty about or differences in terms of how people look at, look at how to diagnose patients who have these symptoms. It is a multi-system sort of disorder. It can affect every organ in the body. And that's the thing about mast cells. They are everywhere, every organ, but they're not in the blood, generally. They are produced in the bone marrow. They're white blood cells. And they go from the bone marrow and they go into the tissues, they go into the lungs and to the skin and everywhere they're supposed to go. And that's where they develop. And so symptom can range, you know, basically every part of their body. So if you have patients who have multi-system symptoms, they have what looks like activation or release of these chemicals, which we're going to talk about, then you can look towards making this diagnosis. So our concern was, the reason we published this paper is that this other group, which I have a lot of respect for, put a lot of stock into measuring one particular mediator that mast cells produce. And that is triptase. Yes. Okay. I love this where you're going, because I agree more, which is why it's so important. And I get asked this all the time, you know, even, you know, doctors who are studying this, no, it's hard to understand, but I think that the easiest way to think about it is this. Mast cells make triptase, all mast cells make triptase. So if you have mastocytosis, you have a lot of mast cells, you'll have a lot of triptase. Because again, if all mast cells make them, and there are a lot of that, there's going to be a lot of triptase. In mast cell activation syndrome, it's the same number of mast cells, they're normal numbers, but they're just activated. So activation doesn't necessarily make more triptase. So there's a small subset of patients who will have a mast cell reaction and will see an elevation triptase. And they'll meet the criteria that was put forth by this consensus one group. You have to have a specific rise in triptase. And then you can say, oh, you see, you have a reaction. And so you have mast cell activation syndrome, but the vast majority of patients will not see a rise in triptase. And they will have normal triptase at baseline. And so so many people then will be misdiagnosed or under diagnosed, if we just rely on triptase. The other, there's another condition that also causes increased number of increased level of triptase. And it's called HAT, or hereditary alpha tryptocemia. It's a genetic and very easy genetic test. You can, you can check the number of copies of this gene that makes triptase. And that could be, they could still have mast cell activation syndrome too. But what we did in this article is really outline things you should think about in terms of diagnosing patients. The general themes of mast cell activation syndrome, which is you could have allergic disease, you could not, or some kind of allergic phenomena, inflammation generally, and abnormal growth and development. I think of things like increased cysts or nodules or things like that. It's more complex than that, but I'm simplifying it. And then if you have this, then you, these are, this is the way that we approach our patients who have mast cell activation syndrome. And we're saying that sure, test triptase because sometimes it will give you information. If it's too high, you got to rule out the hereditary issue and you got to rule out mastocytosis. But let's look at all these other things that we can measure to help make the diagnosis. And that's what we looked out in this article. And I think it's a helpful outline for people either to bring to their practitioners, their, you know, their doctors and to say, look, can you read this and ask me for this? Or for practitioners to actually read and get some more clarity on what they can do to try to help to make the diagnosis. Yeah, I love what you've framed because this is again, some of the stuff we talked about in medical school, we've taught in this very narrow box, the box is great, but there's often a spectrum of illness and these things that don't, they don't fit into a neat tidy boxing, yet our patients are still suffering and they still fit the general criteria. And I've heard in clinical practice and I'm assuming your paper often like the clinical symptoms that they fit and then if you intervene and they get better, is that part of your diagnosis in this paper as well? Yeah, that's because that's often I mean, granted that we do, I do the labs just like you do. And once while we find and there's other markers too, do you want to name some of the other markers that are commonly tested? Sure. You know, really the number one, the most sensitive and specific marker is heparin, but it has to be measured in a specific lab. So heparin is a blood thinner, but it's made by mast cells in the body in microscopic amounts. And, but it is, if it can be measured correctly, we have a lab that we're using right now that I think is really good at picking it up. A lot of labs will measure heparin because people are getting heparin as a drug, so they have to, they have to measure it at very, very small quantities. But heparin is by far one of the best. You see an elevated heparin. There's no other reason why they have an elevated heparin, unless they're taking it. And you can imagine if they have elevated heparin the types of symptoms that they may have. So if they're a woman and they're having heavy periods and excessive bleeding, you can say, oh, maybe the mast cells in the uterus are producing excess amount of heparin causing more bleeding. Right? So I think that's like a really, really important marker. But then, you know, we measure something called n-methyl histamine, which is a metabolite of histamine in the urine. We'll measure histamine in the urine, we'll measure leukotrienes and prostaglandins. And so there are not more things that can be done in the urine. There's some that can be done in the blood. And, you know, sometimes we have to do a couple of rounds of it. You know, I might get a heparin level. I might get a histamine level. I like to have two markers to make a diagnosis. So while I'm waiting and while we're still not sure, yeah, I'll start some simple things to get start getting people better, because sometimes it's going to be hard to make the official diagnosis. Yeah. And again, I am not the expert like you, but I have found in clinical practice, they need multiple things to get it controlled in general. Generally, one thing will not, you know, calm the system down enough. So this tends to be a multi-level from herbs and supplements and course it in and meds. And so we really go the gamut in getting these people controlled. Now, one thing you mentioned that I just have curiosity about it, you mentioned n-methyl histamine in the urine, which I measure as well. But is that a better marker than serum? Because it feels like serum would go up and down and you'd miss it. Whereas urine, you'd collect and you'd see the body. Am I just making that up? Or is that true that you're getting a better like over time measure of the histamine versus blood or am I? It's a great question. And the problem is that n-methyl histamine is a really, it's thermolabial. So it's very sensitive to heat. Yes. It's very quickly, it quickly dissipates. Okay. So take their urine with ice to the lab, right? Like it's that important. Right. Yeah. That's right. But think about this. So the patients run everything properly. They're refrigerating every sample. They're, you know, they're doing everything to keep it, you know, cold. And so the measures can be, you know, the mediators can be measured. But then it gets to the lab and it sits on the shelf in the lab. We had, we had a patient who told us this, you know, she did everything right. And she handed it over to the lab and the lab like took, took the container out and left it on the counter. Yeah. That's it. It's gone, you know? Yeah, exactly. The problem is like to assure that that sample was taken care of. What I find is that the n-methyl histamine, unfortunately, is not one that I, that I see, all of them are hard to see in the urine because they're hard, you're hard to control all the, all those variables. Exactly. Like you said, because I totally get that. Okay. The other thing I thought about was how does IgE play into this? Like at eosinophils, IgE, those aren't mast cells, but they are related. Is there a relation to elevated IgE or elevated eosinophils and mast cell are those two separate issues? No. So I think there's a subset of patients who have more allergic disease. And so to be clear though, there are patients who have allergic symptoms with mast cell activation syndrome, but they've been to the allergist and they're told that you're not allergic to anything. Yes. Okay. And you're like, yeah, okay, you're not allergic, but the mast cells are still reacting to those things, but not through IgE, which is the allergy immunoglobulin. But there's a subset of patients. I do have a subset of m-test patients who do have allergy as well. Yeah. And, and allergy is a mast cell disorder, but they have allergy plus other stomach issues. It's how allergy is the umbrella, right? And the mast cells are one thing under the umbrella, but there's other things under that umbrella of allergies that can be. I actually think the opposite. I think MCAS, or I think that mast cells, and I think allergy is one. Got it. And I think there's MCAS, which can include allergy, but doesn't have to include allergy. That's kind of how I think about it. And, and so we're going to be patients who have elevated IgE. They really do have allergy to certain things, but they also have dysfunctional mast cells that are also reacting to other things. Got it. Got it. This is a great conversation, by the way, because I know patients all the time. And so thank you for clarifying. Good. I think this is confusing. And I, and I have to say that I've talked to allergists who understand this either. So, so, you know, you can definitely have high IgE levels and MCAS, but you can also have low IgE levels. Now, mast cells also, they have a couple of jobs. They have a few, actually more than a couple. They have a few jobs. They release mediators. They, they also have conversations with other cells in the body and one of the cells that they often interact with are the eosinophils. And so there's a subset of patients who are more prone to an increased level of eosinophilia, increased level of eosinophils. They can have eosinophilic esophagitis, so EOE in the esophagus. They may have it in the blood. They may have, you know, other manifestations. So I can't say, I mean, no one studied it, you know, precisely to say that EOE is MCAS or eosinophilia is MCAS, but I would argue, clinically, that very many of those patients who have eosinophilic problems often have, when, when, when, you know, diagnosed have underlying mast cell dysfunction. And so I have patients who have EOE who have done incredible amount of work with their GI doctor. They take the proton pump inhibitors. Sometimes they change their diet, but yeah, and then I see them and they're not getting better. And sometimes they've done steroids. And I said, all right, let's figure out why these eosinophils are, are still reacting like this. There must be a trigger for the eosinophils. And so one trigger is mast cells. So we work on their diet, we work on the diagnosis, we work on the mast cell. Do you mean a low histamine diet or any other things that would be common to obviously probably gluten-free, dairy-free, low histamine? Is that the basic there that? Basic and not always low histamine, because that one, that's a whole other thing to talk about, because I think there's some discrepancies in different low histamine diets. I think that histamine is not always the issue for a lot of people. You know, if mast cells make over a thousand mediators, this means one, it may not. So, but, but that may be. I mean, I think it's very individualized, but from an eosinophilic perspective, right? So I may be targeting their mast cells and, and, and I have certainly patients who I have found the right MCAS protocol and their EOE disappears. And it's like amazing. The GI doctor like thinks something they did and, and it's really, you know, work with the MCAS. But of course, you know, with eosinophils, you always have to think about parasites and there are other things that. Exactly. I love that you've seen that. I love that you've seen that because what I've seen, and I, that's what I kind of want to ask you, what your experience is, there's people with zero IgE, like they actually have, there's a new paper on an immune deficiency that's considered just IgE, right? And I was like, oh, because we know about IgG and IgA, but that's actually a new category of the immune deficiency, but they still have mast cell issues, right? So what you said could be true because the IgE is zero and yet they still present with mast cell issues. My own personal experience was after the mold exposure, I got so sick. And then when I started taking binders, I had hives and all kinds of mast cell symptoms head to toe, because I was just going too quickly. So totally get this. What are triggers? So we talked about, obviously, usually there's this genetic predisposition where people are born more prone to this, because you could have someone with massive triggers and not get it because they're just stable, their muscles are more stable. This goes back to infection stuff. What would you say the most common, maybe top five or six or 10 or whatever things that you see most commonly triggering mast cell activation, like infections or toxins or? Yeah, absolutely. I mean, I would say mold is number one. Yeah, totally agree with you there. I mean, you know, I had my own mold exposure and issues. And so I can say that there's no question that there's a mold problem in this world in this country. There's not a lot of understanding. Too many people are living in conditions that are really, really disease promoting, really, really sick. So mold for sure. And we say mold, it's not an infection, but it can be. So some patients who are exposed to mold are sick because of the toxins, the mycotoxins. But I've certainly had patients who are sick with the actual mold, like get infestation, let's say of aspergillus, they get aspergillosis. So it could be both. But so mold is a big trigger, let's just say. I would say from an infection perspective, and again, it may be because I have a very skewed view and maybe it's the patients I'm seeing, but Bartonella is number one, two, three, four, five, you know, along with mold. And I think that the issue with Bartonella is that because it's transmitted by so many different things, it's not like Lyme that has to come from a tick. I think it is very pervasive. It can be found. The map of where Bartonella is found is, you know, everywhere, like sub-Saharan Africa, you know, everywhere. So you imagine that that's going to lead to a lot of cases and a lot of cases that we're going to see of chronically ill patients. So Bartonella and many of those Bartonella patients also have co-infections. So it's interesting, right in the Lyme world, they talk about Lyme and co-infections. I talk about Bartonella and Bartonella's co-infections. So sometimes there's Lyme there, sometimes there's something else. I love that you're saying that because I see that in clinical practice too. And so I think one more in our own little, you know, spheres were like, is it just me that's seeing this? But I would just say over and over and over again, Bartonella rises to the top as one of the biggest things with, and with mold and MCAS and these whole layered mixes that people get that they get really, really sick. And I would agree with you. I think it's more prevalent in Lyme. Like it really is a big deal by far. And I think the more we're testing, the more I'm understanding that if you think about where Bartonella goes when you get infected, it actually goes to the red blood cells. And Babesia lives in the red blood cells. And they actually have a symbiotic relationship. So my understanding is that Babesia can cause the iron to sort of, I forgot the word I'm looking for, but it basically forces the iron out of the red blood cell. And Bartonella basically eats iron, uses iron for metabolism. So what I'm finding is that the more Bartonella I'm finding, the more Babesia I'm seeing as well with it. But I think the top layer, I think the thing that's really making them sick, it's both. You've got to deal with both. But I think Bartonella ultimately is the problem, but Babesia is complicating their illness, I think. I might change my mind. I totally agree. And again, it's fun to talk to you because I'm seeing this too and yet I'm always like, is this just me or the same thing that Babesia Bartonella is so common and so and hard to treat? It's not an easy, these are not, you know, just get better in three months kind of. Wow, this is such great information. What about your paper on chemicals and MCAS? Let's just transition a little of that because you wrote another paper on and give me the title, give us the title of that one. And let's talk about what the kind of main findings there were for your main work. This is mass cell activation may explain many cases of chemical intolerance. And it was, we published it with, with Dr. Larry Affron and Claudia Miller, who is really a pioneer in the chemical intolerance tilt, toxic and induce loss of tolerance world. That's her, that's her thing. And so what we did for this paper, I mean, we had a hypothesis that, that chemical intolerance may be due to MCAS, that MCAS may be the driver. But no one's really published on, no one's really looked at it. It's sort of common physical to me, but we really need to publish it and get the information out there. And so hopefully you can, you know, go beyond, we can improve it. So what we did for this study is we had our patients fill out a questionnaire that's been validated. Claudia Miller has developed this questionnaire called the QEESI. It's a 50 question questionnaire. People can find it online. And I think if they go to tiltresearch.org, they could take the test themselves. I encourage everyone to take the test. Actually, it's so, so. And if you're listening, I'm going to get the links. I will post them. So if you're listening, wherever you're listening, we'll be sure you include all these links plus to your research, your website. So just don't worry. If you're listening in your car, you'll have access to whatever you need. So keep going. So there's a lot of information. Yeah, there's a lot of information. That website real quick. And then the QEESI test is the name of the, the questionnaire, right? Right. So it's tiltresearch.org. I think QEESI might, they may have their own website now too, I think. So anyway, QEESI is the questionnaire. There is a, a breathing questionnaire called the breezy, B-R-E-E-S-I. And the breezy is three questions. And it's pretty, it's sort of a, it's a nice sort of overview. It's very clear if you take breezy test and you answer at least one question as a yes. Have you been exposed to paint, you know, do, are you sensitive to paint fumes, tobacco, gasoline? You know, there are a bunch of these questions. And if you answer yes to any of them, the recommendation is that you go on and do the QEESI. In our practice, we just said, look, our patients are already sick. We know that they're, a lot of them are chemically sensitive. So let's just give them the QEESI and see what happened. So what we did was we took their QEESIs and we matched them up with their diagnosis. So if they had a nasal activation syndrome and they had a positive QEESI, a high score on the QEESI, we were looking at, at the numbers there, like what is the correlation between a positive MCAS diagnosis and a positive QEESI? And we found, yeah, large percentage of our patients clearly had that. You can have, we think, we don't know because we haven't proven this yet. Could you have chemical intolerance and not have MCAS? I guess it's possible. I, you know, I can't say that all those patients have MCAS yet because we haven't proven it. This was our hypothesis and we have a theory and we're supporting our theory, but we don't know 100% yet. And I would argue that you can have MCAS and not have chemical intolerance. And I have patients who, you know, they may be sensitive to some things, but they really are not profoundly sensitive. You know, I have MCAS patients who come in with perfume on. And I think, well, that's crazy, but you know, that doesn't bother them, right? But there are other things that obviously they're reacting to. So, but anyway, so, so I think this paper though is one step further in understanding why patients get to the point that they get to. So we know that some people are chemically intolerant. Some people are sensitive to EMFs. Some people are sensitive to noise and sound. And so we start to understand the mechanism. What we want to understand is why, what is it about the now, we think it's mastal driven. And so what is that process that leads to that? So that's kind of what the paper cover. Yeah, that's what this is so exciting, because I am not a researcher, but I have such appreciation and admiration for you putting out these papers, because this is where again, we need to take medicine, just bring the data. We know we see what we start with is observation, right? Which is what you're saying we saw this and we thought maybe there's a connection. So then let's start to look at the connection and write the papers and then continue to prove it out. So thank you for all that you're doing there. There is one other paper I want to mention before I let you go that you've talked about is the post HPV vaccine and what you're finding. You share just a little bit about that. Yeah, this was a case series. Okay. Again, based on our observation, and look, I'll say this, that you know, one of the things that was really important to me, once I was sort of in the functional medicine world and treating patients, it became very clear that we need to publish. I feel really strongly about that. And especially when Dr. Affron joined my practice, because he's a researcher and because he's coming from that academic background, I think that the two of us sort of saw this opportunity. We have to get this information out there. Otherwise, we're existing in our own worlds. You know that, right? We practice and do our things and we notice these things. We hear other people noticing them, but we need to convince the greater medical community, because we can't help all the patients. So we need to treat others. And so I think publishing is a really great way. So that was my little segue. I'm really excited to be doing this. I didn't think I would be doing this, but I am and I'm so excited. So anyway, in this paper on HPV, on the HPV vaccine, what we have found, there are some literature already to support this, that there's an increased risk of POTS, postural or the static tachycardia syndrome after the HPV vaccine. And so there's, you know, people are studying that and trying to understand that. And so what we're starting to understand in our practice is that POTS is very much related to MCAS in a subset of patients. So can you have POTS and not MCAS? Yes. I think there are patients who really don't have MCAS and they have, let's say, an autoimmune driven POTS, but a fear number have an overlap of mass activation, postural or the static cardiac syndrome. And I'll say EDS may be the trifecta that kind of poses the loop. So if our hypothesis is that many POTS patients have MCAS and the HPV vaccine was causing POTS, what if really what was happening was that the HPV was actually exacerbating underlying MCAS. So the key is that it's not causing MCAS, but that, like I mentioned with COVID, it's a trigger that brings that underlying susceptibility. And so what we found in our case series is that many of these patients who presented with POTS and then finally we diagnosed them with MCAS, if you go back in their history, it's very clear that they had signs of something early on, they had the vaccine and whether it was the first one or after the third one, they went on to develop POTS and significant disability and then finally we were able to put it together and they had MCAS. So this is sort of bringing to light the fact that there may be something specific about the HPV vaccine. Maybe we can generalize this to other vaccines. It's not anti-vax, very much pro-vaccine, but it's about trying to understand individuality in medicine. It's always about you need this, right? And I would argue, yes, I think that to prevent HPV related cancers is very, very important. I love seeing that because I so agree and I think of it as like, I've always told patients, I completely believe vaccines have a place, I am 100% behind them. But if you take a very large population with any intervention, you're going to reveal, it's almost like I always relate it to a cardiac stress test. You have a 65-year-old male walking along, they're fine with no symptoms, no problem. You put them on the treadmill and maximize their output or their cardiac output and all of a sudden you reveal a deficit that was, they were walking around with underlying, right? You reveal something that was hidden that could have caused death in that person. Same thing as we're talking about here, you have this massive population, most people are totally fine, but when you stress them with an adjuvant or something else, all of a sudden you reveal, oh, they had MCAS or oh, they developed POT. So I love that you're clarifying because we need this. And again, we need to be able to do this in a way that's good for our populations and helpful and also know the few canaries that maybe would react to it, right? Right. So it's helping patients be recognized that these things happening to them are not because they're crazy. That Dr. Sated patients is mind blowing. But also I think that the way science has to go, medicine has to go is we have to be able to start to identify the patients who should be getting the vaccine or shouldn't be, you know, maybe there's a way, okay, or they need the vaccine and they have underlying MCAS. Can we, can we stabilize their MCAS? Can we give them muscle targeted therapy and get them ready for the vaccine? Yes. I just love this and so important work and so, so needed in all of these realms because we need the voices that are advocates for the canaries, the one in a million or one in a thousand, one in 10,000 that are going to have reactions to these interventions. So thank you for your work. I'm just imagining too as you're talking as we end here, this big map, like ideally we'd have this map and I can just see like EDS and POTS and MCAS and like someday we're going to have a map of how they all kind of fit together and maybe the genetic predispositions and I feel like with your research, thank you because you're making this map for us. You're actually helping to create a map for the new medicine, which is the medicine of personalization that goes to the individual because we're also different. There's no one size fits all. There's no N of one, right? There's no real N of one as far as this, this perfect patient that fits the criteria. So this personalized idea of medicine is really where the future of medicine is going, I believe. Yep. I couldn't agree more. Wow. I'm so delighted about this conversation. I've learned so much in it and where can people find you? Where can people find more information on the papers you published? Tell us wherever any other links that would be helpful. Sure. So I have my practice website is aimaimcenterpm.com. So it's personalized medicine. So we kind of abbreviated it. So aimcenterpm.com. I have my own website drtanyadempsey.com. Facebook is Dr. Tanya Dempsey. Instagram, I think it's Dr. Tanya Dempsey. And so we're trying to update all those places with all the stuff that we're publishing. And of course I've done a lot of, I don't have my own podcast, but I've done a lot of podcasts and we have those all available as well. So thank you. Yeah. Awesome. I will, like I said, I'll include all those links and thank you for your tireless efforts. Just so appreciative for the work that you're doing, Dr. Dempsey. Thank you. Thanks so much.