Is It Lyme or Autoimmunity? Understanding Immune Dysfunction with Dr. Chris Turnpaugh

Introduction to Lyme Bites and Dr. Turnpock 0:00

41% of the cases of post-treatment Lyme disease or ongoing symptoms from Lyme disease, 41% of those cases actually still have infection going on. So I think that's just a huge opportunity for a misdiagnosis. So, oh, you were treated, you're better, so therefore it can't be lying. The converse is true. 59% of the patients don't have ongoing disease. So 59% have similar symptoms without an ongoing infection. This is Doctor Talks. Welcome back to Lime Bites, Rebuilding Immunity, Reversing Inflammation, and Redefining Recovery.

Today, I'm bringing you something really special. As many of you know, I recently hosted the Healing Lime Summit with Dr. Tox. And during that event, I had the privilege of sitting down with Dr. Chris Turnpock. It was such an incredible interview that I knew I had to share it here with you on Lime Bites, because honestly, I don't think we could top it. In this conversation, Dr. Turnpah unpacks how chronic Lyme isn't just an infection. It can rewire immunity, trigger autoimmunity, and inflame the brain.

We dive into how stealth pathogens hide, why some patients spiral into food sensitivities, neuropsychiatric symptoms, kids developing Pan's Pandas, and most importantly, what steps can actually bring the immune system back into balance. If you're struggling with complex Lyme yourself, or if you're a practitioner treating tough autoimmune cases, this is an episode that you must not miss. This is Lime Bites. Let true healing begin. Hi, and welcome to another episode. I'm your host, Dr. Maria Hinchey.

And today we're going to talk about Lyme disease, autoimmunity, immune dysfunction, and PANS. And here to discuss this intricate topic with us is Dr. Chris Turnpah. Dr. Turnpah is a highly experienced and dedicated health care professional who balances a full-time clinical practice with leadership as a clinic supervisor for over 20 clinicians. With over 15 years of experience conducting training sessions both nationally and internationally, Dr. Turnpah is recognized as a leader in functional medicine.

Dr. Turnpah is a published author, bringing digestible information to the public consumer with his five essential pillars for optimized wellness. Dr. Turnpah brings a wealth of knowledge and expertise, offering valuable insights drawn from his extensive work in patient care, clinical supervision, and professional education.

How Functional Medicine Began 2:50

Welcome, Dr. Turnpah. It's an honor to have you here. Um, say hello to our audience and let them know how you got started in functional medicine. Okay. Well, thank you for having me and welcome everybody. So I started in functional medicine in like 1995 or 96, and I started because I had a patient who had ALS come to see me. And he asked me a very simple question that we're going back almost 30 years. And he said, what can you tell me about CoQ 10? And I said, I don't really know much about CoQ 10. He put his finger in my chest and he said, learn or quit.

Cause I'm going to die. So literally it was put in Mark York. He put his fingers learn or quit. Cause I have ALS and I'm going to die and need somebody that wants to know. So the next weekend, actually, Jeffrey Bland was speaking in New York city. So I said, wow, that was a humbling experience. So I went up. kind of caught the bug and started learning then started teaching in 15 years ago so that was how I got my foray into it. And it was a good thing because in 2003 my wife got Lyme disease and lost faculties from her neck down so she basically was a quadriplegic for a short period of time.

Um, so we found it was Lyme disease. So he, you know, I credit really Mark, uh, the person with ALS coming in and having, you know, that, that impetus to get me further on my journey and start to be more educated in this field. Yeah. And I mean, it sounds like it was a huge blessing in disguise and prepared you to be able to help your wife because there's just so much misinformation regarding Lyme and co-infections. And gosh, if you had just gotten started down the standard road that most patients do, you might not have been able to help her the way that you were able to.

Yeah, it was a huge blessing. And that was a big learning curve, which, you know, you continue to learn, you carry it through with the rest of your patients, but it becomes personal when it's your family member. Yeah, definitely. So can you give us a breakdown of kind of how and why immune dysfunction occurs with stealth infections like Lyme disease? Sure. So. I'll break it down kind of for some people this will be remedial but for some maybe they haven't heard it before. So think of your immune system having two halves.

Immune Dysfunction and Stealth Infections 5:13

One side that is kind of your ability to kill and fight things off. And one side that's more tolerant or immunotolerant. And we call those TH1 and TH2. And that's not, you know, for those that are very technical, he may say, he didn't say that right, I know, but I'm kind of dumbing it down. So think of it as a seesaw. And in the middle, there's a fulcrum, and that's called a T regulatory cell. And so the side, the TH1 side is the side that works with things called natural killer cells. And this is kind of the active part of killing stuff off.

And, and in recruiting that what's called innate immune support and then this TH1 T helper one side of the immune system. And so you want that side to be dominant during an infection is certainly an acute infection. When you get these stealth pathogens, they tend to hide out. And one of the ways they survive inside the body is they create a TH2 dominant immune response, which allows them to hide. And they're really good at this. They're kind of like bugs. And then this other side, this TH2 side, is recruiting things like antibodies and things like that.

So the bug will come out. uh, the stealth pathogen will come out. And if you think of a jet giving off flares to avoid a missile coming at it, these bugs, especially Lyme will come out and give off an Osprey or an outer outer shell protein, a kind of flare, which will then capture the antibody. So the antibody doesn't neutralize the bugs. So it's kind of like a misfire or the missile hitting the flare rather than the jet. And also gives off a, uh, uh, a chemical mediated piece that says, don't recognize me, don't see me.

It gives off a TH2 dominant situation. So they're able to remain stealth because that's in their best interest so that the immune system, this other side, this TH1 side doesn't really see it and attack it. So it kind of creates this cloaking device that keeps it hidden. Are you ready to revolutionize your approach to diagnosing and healing complex chronic inflammatory illnesses in both adults and children? The Lime Bites Symposium is your gateway to cutting-edge education, groundbreaking research, and innovative therapeutic solutions.

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So join us at Pompano Beach or virtually from anywhere. Register now at LymeBytes.com. That's L-Y-M-E-B-Y-T-E-S dot com. And so when that happens and these chronic infections cause our bodies to go into like a TH2 dominance, what are some of the things that we see in the body? What are some of the symptoms that we see? Well, a couple of things you'll see is you see this kind of intermittent or chronic immune response. You'll see that. But you'll also see a global loss of tolerance. And what do I mean by that?

You may see people that have many food allergies or can't tolerate foods, and then they don't tolerate chemicals. They have multiple chemical sensitivity. They don't tolerate much.

Symptoms of TH2 Dominance and Loss of Tolerance 9:13

These are people that even can come in and complain of like EMF sensitivity or things that are less tangible. They just don't tolerate much anymore and their world becomes smaller and smaller. They can only eat a few foods. They can't handle chemicals. They don't tolerate even lack of sleep. If they don't get enough sleep, their immune system doesn't recover. So these are the patients that have multiple, multiple problems. They're also, you know, more stress mode, so they're not going to be able to digest, so they may have bloating symptoms, or they may have gastrointestinal symptoms, chronic headaches, brain fog, they're kind of living under this cloak of just not feeling well, and it's harder to pinpoint you have one symptom with one problem.

Right. Yeah, I often say I try to explain to my patients, like, look, Lyme infects every single cell in the body. Therefore, it's going to affect every cell and every organ and organ system. And, you know, you end up with what feels like almost this, like, multi-system breakdown and failure. And, you know, it leads people to feel like they're going crazy, you know, and a lot of doctors to be like, you're a hypochondriac. Like, all of these things can't be going on, you know, inside of you at once.

And it's so true. And most of these patients, even though it's infectious origin, they may have a psychiatric component to it. And so they are many times led down to psychiatry. And there's no amount of psychiatric medication that's going to remediate an infection, right? So it's helpful to identify why this is going on. And many times it's not just a mood disorder. So even the patients we see from psychiatry, if you do a little bit more holistic evaluation, They don't just have that, they have all kinds of other things going on.

Right. And I see that all the time. And I think one of the issues too, like with the neuropsychiatric symptoms is that, you know, when you feel this way for a long time and no one's able to give you answers, I mean, that's going to create anxiety, that's going to create depression. But then, you know, we're going to talk more about pans in a minute, but like, you know, with having inflammation in your brain, like that leads to neuropsychiatric symptoms as well. So it's like a double whammy. And red flag for those people that are listening, when you have someone that's not responding to a psychiatric medication in the way that one would think that you would, that's a big red flag that something else is going on, that it's inflammatory or infectious or often both.

But Dr. Turnpott, can you also talk about how this immune dysfunction can lead to autoimmunity? Yes. when you have that infection and it burrows into your own tissue, right? So then these are my antibodies. These go after things. So they're like your attack dogs. And when a bug burrows into the tissue, say I'm burrowing into my own thyroid here, the immune system is gonna go try to attack it and go after it.

How Lyme Can Drive Autoimmunity 12:14

So now you have a combination of bug and self-tissue. That's one piece. there's a really smaller white blood cell. So the neutrophil kind of comes in and eats that bug, if you will. And then that bug has to be eaten by a bigger fish, the monocyte, which is the macrophage. And then it's taken off into the lymphatic system. If the first one, the neutrophil comes in and eats that bug, but doesn't get eaten by the bigger fish within six to eight hours, it ruptures. Now when it ruptures, it ruptures self tissue, the little fish, and it ruptures the pathogen.

So now you have what's called a debris field, or like landmines, which are a combination of self tissue, your own tissue, and a pathogenic tissue, pathogen tissue, and there's confusion. Should I attack that or should I not attack that? And so you kind of send out this signal of something's going on with a bug. I should be attacking it, but it's mixed with self tissue. So then you can develop kind of a dysregulated immune response where you're recognizing self tissue as foreign. That's one mechanism.

The other mechanism, if the, if the bug is burrowed so much in the tissue, it's going to attack self tissue even to get to the bug itself. So there's two kind of mechanisms. And the third is what we call molecular mimicry, where something looks enough like another bug, right? So this bug looks like this bug. More importantly in this situation, this bug looks enough like self-tissue that the immune system gets confused and attacks the bug and the self-tissue thinking it's the same thing. Right. Thank you for that explanation.

That was actually one of the most succinct, like simplistic explanations for autoimmunity. And I think that'll be very helpful for our listeners, especially as we transition to talking about PANS. So can you explain what PANS or basal ganglia encephalitis is kind of like set the stage before we move deeper into this conversation? Sure. So it started off being called PANDIS because it was just from strep and then that kind of grew into it's more than just from strep. It was named by Dr. Sue Suito at the National Institute of Health in charge of pediatric movement disorders.

And the first PANDIS conference was in Lake Como, Italy, which I was fortunate enough to speak with Sue Suito at with 450 providers back when they weren't sure it was a real disease. And so, and I'll kind of fast forward to the end of that conversation once I go through this. So what happens in that situation? First with pandas, if we get to the root of it, pandas is you get strep and you confuse strep with your own brain. So you're, again, you're kind of attacking strep and your body thinks your brain is also strep.

So it will attack your brain and cause an encephalitis in the brain, confusing it with strep. And many of us have heard of this condition in a different form called rheumatic fever. So when you got strep and it looked like your heart, you'd attack your heart, it would be called rheumatic fever.

What PANS and PANDAS Are 15:49

There's another condition called Sydenham's caria, which you kind of get strep and you kind of get these weird dance-like movements. Sydenham's caria is also called St. Vitie's dance. It's just another term for that. But it's That's a little bit more transient the the Sydenham's career so you kind of get this strep infection and it leads to an attack of brain or heart or kidneys or other tissues and that's that poly reactivity piece. And then we went on after the big lecture, four-day lecture, and we were sitting around the room with all these brilliant people and they said, what else do we think can cause this other than strep?

And well, we all agreed that tick-borne disease was highly probable of doing it. We agreed that some foods, if you react to foods, it can also trigger it. But what you're getting is a vector or an agent or something exogenous coming into your body. which triggers you to mistake that trigger for your own self-tissue, specifically attacking one of many different aspects of brain which will lead to that encephalitis. And it's accompanied by, it used to be a very rapid onset of a movement or a tick disorder, but it leads to a psychiatric condition that can be triggered by many infections or environmental agents And early on, the two biggest statements by parents were literally, an alien must have invaded my child because this is not my child.

And the other one was, does the hospital perform exorcisms because my child must be, have a demon inside. And so it's a really rapid change. It's very dramatic. Some of them are more mild, but the ones that really stand out are the ones where they're very, very, very intense psychiatric conditions where it's just not your child anymore. And the shame of this is these, instances and these conditions do very poorly with psychiatric medications. That's not the indicated because the mechanism of action isn't just an imbalance in neurotransmitters.

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Learn more at Lyme Core Botanicals. That's L-Y-M-E-C-O-R-E dot com. Right. And a lot of inflammation involved with it as well. And none of these medications are solving the immune dysfunction, the autoimmunity or the inflammation that's really like at the heart of all of this. Yeah, we just actually, it was yesterday, in fact, one of our other docs, Dr. Shannon Smith, He had a patient who looked like cerebral palsy, 15-year-old, and we got the lab results back yesterday. It was Bartonella, but it was severe psychiatric issues with severe movement disorders, been all the way up and down.

Of course, they thought it was psych. They were looking for things, and it was Bart. Wow. How long had he been sick for? So Shannon called me last night on his way home. He'd been sick for at least six years and misdiagnosed for six years and just continued to degenerate. Couldn't really walk down the hallway. It's terrible. Couldn't even walk down the hallway.

Basal Ganglia Encephalitis and Food Triggers 20:18

Oh, okay. So how, what is the intersection then between stealth infections and basal ganglia encephalitis? Is it, is it all so like, obviously it's autoimmune and it's inflammatory, but there's other things, right? Like, so in addition to having like the molecular mimicry, maybe with these bugs, there is also a role. Like if, um, Cerebral folate deficiency, for example, is playing a role, right? Like there's other pathology going on as well as other molecular mimicry with foods that the child might be eating as well.

Can you kind of like walk us through those two? Well, the molecular mimicry with food is similar, like the food may look enough like, so even if it was triggered by an infectious agent, you can, a food can look like the infectious agent, which can also mimic your self tissue. So these are kiddos who had a patient in Italy who the psychiatric episode happened after lunch, then in Italy, once you're admitted for psych reasons, you have to stay in for 30 days. We knew within two days, it wasn't a psychiatric condition.

It was really a food triggered condition from something that may have been happened before. So you'll predispose yourself to this. And there are several predispositions. One of them is a folate deficiency, you know, folic acid deficiency. There is a folate receptor antibody, which is sometimes you have an antibody to the type of folic acid you're taking in, which can trigger this response to gets a lot of press, but it's very rare. It is very rare. We've screened couple thousand kids and found one.

But it is out. So there are many other deficiencies. Then there are deficiencies which predispose you to this type of a reaction. Very simply, one of those is low vitamin D can predispose you to this type of reaction. And the reaction is molecular mimicry in the presence usually, I would almost say always, but let's just say usually, in the presence of inflammation. And when that inflammation, the inflammatory piece can cross the blood brain barrier and just drive inflammation in the brain. And inflammation in the brain, the brain is a combination of immune tissue and neural tissue.

And the neural tissue is kind of like an electrical circuitry. And when you add a bunch of heat or inflammation to it, it's gonna fire differently and wire differently. So there are many, predispositioning factors to having this encephalitis. And then the other piece is specifically in the basal ganglia, it's one of the most susceptible areas in the body to oxidative stress. So those little powerhouses of the cell, those little generators, those mitochondria, they're extremely susceptible to oxidative stress, probably more than anywhere else in the body.

And so any kind of oxidative stress, and this is where it can be an inflammatory response is going to cause oxidative stress. And now you have to tie in the whole world we live in, all the toxins we take in and pesticides and chemicals and the water we drink and the air we breathe and the food we eat. If it has toxicity to it, whether it be heavy metals or plastics or chemicals, they're all oxidative stressors. And so you're going to tend to affect the most sensitive areas of the body, which tend to be the basal ganglion clue.

Okay. And then if you have, you know, increased intestinal permeability and you're not able to detox and you have all of those sort of, um, additional things going on, it impacts the body and makes it even harder for you to deal with the environment. Question. So I think you were involved in a study that looked at molecular mimicry in various children with pans and pandas. Am I correct about that? And it showed certain foods were actually the biggest triggers Right. So there's the panel called the Cunningham panel, which checks for five different auto-antibodies to the brain.

We kind of overlaid four of those and some other neuro-antibodies or self-antibodies with food and saw which ones looked similar enough or which ones had that molecular mimicry. And a lot of the common foods do, one of the ones that stood out more than any was mint. So mint, I had a Pans Pans girl who had seen some big names remain nameless, but very big in the pants pandas world. She came to me and she calmed herself down with a glass or a cup of mint tea every day. And she reacted to mint, which triggered her brain reactions.

One of the things we did that was very easy was we cut mint out of her diet and her reactions calmed down. So yeah, we published that. I probably a decade ago with Dr. Viswani showing that foods tend to look the same as neural tissue. And if you have a reaction to one and the other, every time you eat the food, you're telling your body to attack your brain.

Molecular Mimicry and Common Trigger Foods 25:40

So can you share with our audience, like what maybe let's say the top three or top five foods that you found are regularly the culprits in addition to mint? Well, mint was the one that was stood out the most because I didn't suspect it was a big one. Um, some of the common ones we see like gluten, egg, dairy were big. And then there were some that stood out for like group H strap or dopamine one receptor. So, um, and I can make that available to you that maybe you can put out all the listeners so they can see the little bar graphs so they can see where everybody has what's going on.

Yeah, that would be great. Like we can put it under like your bonus section so they can actually maybe download a copy of your study and of the foods that have the highest rates of molecular mimicry. Sure. Okay. So what's your approach to treating all of this with your patients? And I'm sure we could talk about this for hours, but you know, more summary version, how do you approach a patient that has, you know, let's say pans or pandas, but really like the underlying root cause is like a tick-borne disease or Lyme?

So it's really important for us, and I don't project out to anybody else, but in our office, it's important for us, first of all, is there still a pathogenic burden? Do we still have an infection that was missed, right? So if there's 41% of the cases of post-treatment Lyme disease or ongoing symptoms from Lyme disease, 41% of those cases actually still have infection going on. So I think that's just a huge opportunity for a misdiagnosis. So, oh, you were treated, you're better. So therefore it can't be Lyme.

The converse is true. 59% of the patients don't have ongoing disease. So 59% have similar symptoms without an ongoing infection. So the first thing we want to do, so let's just say it's 50-50, flip a coin, do they still have an infection or they don't have an infection? If you're not reducing the pathogenic burden down to near zero, which I don't know that we'll ever get to zero, but near zero, then that's the first order of business is are we able to reduce that pathogenic burden down to an acceptable rate?

So do they still have an ongoing infection going on? So I think that's important. And then are they stuck in this, dysregulated state of this high TH2 and low TH1 or inability to do that. And then what would be cofactors for that? We talked about the toxicity, certainly leaky gut. You know, if we don't fix or start to repair that intestinal permeability and leaky gut, we're allowing different things to come into our body, which is going to activate our immune system. So gut has to be a paramount.

And then inflammation, including neural inflammation. So if we're not addressing the neural inflammation, that's a problem. So if they're reacting to everything, they have lost their tolerance to the world. If they're not reacting to certain foods, so again, I'm a simpleton.

Treating Infection, Inflammation, and Gut Dysfunction 28:58

If you're reacting to everything, we have to build up tolerance. If you're reacting to a few things, we have to remove the few things. But it's really challenging to say you reacted to 108 foods. So you're not going to eat these 108 foods and you're a six year old or a 10 year old or a 15 year old. That's not reality. So you take out the big nasties that are going to continuously trigger and then you build up tolerance so that you can tolerate most of the other foods. So I think it's important to build tolerance.

and take out the things that are still irritating. Make sure you don't have an ongoing infection. And also at the same time, support the body with the inflammatory cascades, reduce the inflammatory pieces and help support that overall inflammation. With that in mind, then we want to shift that pendulum back over from TH2 dominance back towards TH1 dominance or ideally neutral. So you still have that neutral approach. So there's a lot of lifestyle change that you are doing with your patients to accomplish most of this, right?

As far as education about environment and where we're all getting exposed to toxins and a lot of people not realizing it. And as far as nutrition goes, it's way, way beyond teaching someone how to just eat a healthy diet, right? We have to look at what foods are affecting that individual sitting in front of us. as well as, as taking the molecular mimicry and all of these other things, you know, into account as well. Yeah. So if certain foods are reacting to your body, like the infection, like the tick-borne disease, we want to get rid of those because every time you eat that food, you're going to have a tick-borne pathogenic response.

So that is one piece. What foods do that? The other one is what foods are irritating or leading to your leaky gut or facilitating your leaky gut. And third, then what foods are most toxic. So if you're eating foods on what we call the dirty dozen rather than the clean 15. If you're eating these foods that are highly toxic pesticide, are they wrapped in plastics? Are you getting a lot of all these chemicals and endocrine disrupting compounds in your body? So it's much more nuanced than just eat a healthy diet or just this food reacts to you.

And to your point, the patients There's a couple of things we say in the office. What will make the case fail? The case will fail if the patient doesn't have that part of their protocol or treatment plan in place because they're not going to get that relief that they want and not just from a pill. They have to get this from a lifestyle. And there have to be, my words, they have to be directionally correct, even if incomplete. So as long as we're moving in the right direction, some of the hope I give my patients is listen, it's an old phrase I think I stole from Jeffrey Bland, the solution to pollution is dilution.

So you can't just live in a bubble and say I'm not going to get any of this stuff. But as long as you're moving in the right direction, as long as you're putting less toxins in, then you're getting rid of on a daily basis if you're facilitating that detox pathway and you're reducing that toxic burden, or you're reducing that pathogenic burden, or you're reducing that inflammatory burden, that's directionally correct. Right. Yeah, I couldn't agree more. It's hard. It's, you know, I tell everyone baby steps, just we have to start and move forward.

So, um, if you had one piece of advice to give our listeners, um, who may be struggling with Lyme autoimmunity pans, pandas, or, or all of it, which, um, a lot of them may be, what would it be? Well, I think I would actually start before that. I would hope listeners would have influence because maybe they're suffering or a family member suffering, but take heart. If you are one that's not suffering yet and you haven't chose to clean up your lifestyle, you're shifting yourself, you're predisposing yourself to that TH2 side.

So if you're not eating clean, if you're not taking care of yourself, you're actually predisposing yourself to getting sick with a chronic infection. Nothing was more apparent than COVID. So people, oh, I'm kind of healthy, but not really. And COVID knocked them over the edge. So that's what I would say to everybody. The time to act, or as I say, you want to get to it before it gets to you, whatever it is. So you want to be proactive. The second piece is, first of all, there's hope. When everybody says there's no hope, there's nothing can be done.

There absolutely is hope. And to put it in perspective, we don't say we'll see how you're doing in three months. I mean, we do. But what we try to say is we're going to compare summers to summers, winters to winters and falls to falls and springs to spring. So give yourself the ability or the patience to say you're going to compare year over year results, be directionally correct. It doesn't have to be Hard and fast, day one, you have to do everything perfect, but you do need to take baby steps and you do need to know that it takes time.

You do need to know that there is hope and you do need to know that there's many clinicians like you and I out there that have supported hundreds of patients like this, thousands, that there is hope. And it's also misunderstood. So we get into several arguments with that little hospital down south of us called Johns Hopkins. You know, it's okay to be told by a healthcare provider, oh, this is this, this is that, this is that. I would say keep being your own advocate and know that there's hope. And it's multifaceted, right?

Hope, Prevention, and Patient Advocacy 34:48

So it's not just kill the bug. It's kill the bug, repair the tissue, reduce the inflammation, restore normal balance, reduce the autoimmunity, and also know that Well, I have this named autoimmune disease. There's still hope for that. And, oh, I'm just getting sicker. Well, you can't help me because I have this. All of those are really, if you break it down, a shift in the immune system. And there's lots of hope to shift it back. Yeah, there is, and lots of opportunity. And, you know, it's funny because I've treated so many patients and then, you know, it's like all of a sudden they get diagnosed with, you know, it's that diagnosis and it's like, okay, there there's an official name.

And I mean, it could be something just, you know, like, okay, well, I have pots and it's like, well, yeah. Yeah. Yeah. Have pots. Yes. You have this cluster of symptoms, you know what I mean? That has now afforded you that diagnosis, but like it doesn't change that it was your tick-borne disease that's driving the inflammation and the immune function that's resulting in that symptom or say that they get a diagnosis of MS. And in my world, a lot of times it's atypical MS because they're not meeting the diagnostic criteria because it isn't actually MS.

It's Lyme masquerading as MS causing a lot of the symptoms that makes it look like it's MS. And then you have the other subset of patients where it's like they might truly have these autoimmune diseases, but I think you can slow down the progression and a lot of times even reverse it if it's being driven by these inflammatory infections that are the root cause of it. So if we're looking at autoimmunity as this antibody attacking self, mechanistically what's driving that antibody other than self tissue.

So to your point, you have, if you can reduce the infectious driven autoimmune condition, you can ramp this down. And then you see things where different sub silos like rheumatology or neurology, they'll label something MS or they'll label it rheumatoid arthritis, but you can be seronegative rheumatoid arthritis. And so that means, yeah, the numbers aren't there like they're supposed to be, but you still have it anyway, which means I don't really know what it is, but it kind of fits this description.

And so describing something, doesn't help us usually give us a mechanistic approach as to why it's there. So again, if you have sclerotic tissue on your brain in multiple areas, we'd call it multiple sclerosis. But how does that mechanism, so what do we do for that? Like, what's the mechanism behind that? Or you have rheumatoid arthritis, but why? What's the mechanism behind that? And I think that's all of those, even if it's truly infection drives autoimmunity, infections go on, still have autoimmunity, there's still ways to dampen that response by reducing the inflammatory cascade, not continuing to trigger in maybe blind spot silos like diet and leaky gut and inflammatory processes.

I think there's a whole host of things that can be done even in the presence of a true autoimmune reaction, autoimmune disease. Absolutely. Yeah, I agree a hundred percent. So Dr. Turnpott, for our listeners, if anybody wanted to come and see you or come to one of your clinics or see one of your other clinicians, how could they reach you? Well, our website is www.turnpawhwc.com and our phone number, I believe is 717-795-9566. Awesome. Thank you so much for being here with me. True pleasure. I love getting the word out and it's a pleasure spending time with you.

I do as well. Thanks everyone at home. Thanks for listening. I hope that this truly was helpful on your journey healing from Lyme and we'll see you next time. Take care. If you'd like to hear more from Dr. Turnpah, join us at the Lime Bytes Symposium, November 14th and 15th on sunny Pompano Beach in Fort Lauderdale, Florida. If you can't make it to Florida, you can join us virtually from anywhere. Again, that's November 14th and 15th, and you can find more information at limebytes.com. That's L-Y-M-E-B-Y-T-E-S.com.

And thank you all for joining us for the Lime Bites podcast. We hope this brought you one step closer to true healing. If this helped you, share it with someone who needs to hear it too, because together we all heal. Thank you for tuning in to Doctor Talks. We hope today's episode has enlightened and inspired you on your path to optimal health. Each day is a new opportunity to make choices that empower your well-being. For more insights and strategies, subscribe to our podcast and visit our website, www.doctortalks.com.

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