Revolution Health & Wellness

Episode 81 – Lyme Disease Basics

Episode 81 - Lyme Disease Basics

Lyme Disease PodcastLyme Disease is much more common that most people think. It is estimated that 6% of the Chinese population has Lyme Disease. It is a worldwide problem.

However, most physicians do not know how to properly test for it. Even when presented with clear evidence of Lyme disease many physicians will deny it is a possiblity. Why? Why is the diagnosis so difficult? Why do so many people suffer without an accurate diagnosis?

These are the topic of this week’s podcast. Dr Edwards discussed a brief history of Lyme disease and why so many doctors miss it. This is a complex topic but we absolutely need to raise awareness!

Speaker 1: 00:00 This is Dr Chad Edwards and you’re listening to podcast number 80, one of against the grain.

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Speaker 1: 00:39 This is Dr Chad Edwards and we’re back for another edition of against the grain podcast. I’m honored to be joined by my good friend, Dr Heath. Travis, welcome. Thank you so much for having us. So we’ve been recording a couple of podcasts. You were. You’re just a a, a captive person and you couldn’t get away. And I was like, Hey, Dr. Travis, you got to come join me for this one. So thanks for joining us. You know, it’s, we’ve obviously, we’ve had some great topics and we’re going to shift gears just a little bit and talk about one that is a, is a big passion of mine that is definitely against the grain and this is my second in a series I don’t know how many will actually do on, on lyme disease, uh, but this is number number two in this series. We did one on the lab diagnosis of lyme disease.

Speaker 1: 01:30 Uh, so if you want to know, you know, you think you have lyme disease or you think you’ve been exposed or you went to your doctor and they told you you didn’t have lyme disease, then go listen to that one to find out why you may actually have it in the testing that was done for you is not reflective of what’s actually going on in your body. So we’re going to dig a little bit deeper into that today. We’re gonna talk a little bit about the history of lyme disease and where it came from and all that Kinda good stuff. So, you know, if you got anything to add by, by all means, jump, jump in. So this lyme disease, I don’t see, uh, you know, I, I had a tick bite on my leg, uh, this was a couple of years ago and called one of my good friends and she, she said, um, and I actually had a rash around it and it didn’t have any symptoms other than the rash.

Speaker 1: 02:21 I didn’t have any symptoms and so called her and I was like, you know, I’m just a little bit nervous about this. And she was like, oh, chat, I don’t know why you’re even asking the question, go and get yourself or you know, she, she called in the prescription for me and um, so I wasn’t having to treat myself and she, uh, she put me on a doxy, doxy cycling, took it for 30 days. I’m fine now. A lot of people experienced that. A lot of people will be on antibiotics for 14 to 21 days and they’ll do well. The problem is, is there’s a lot of patients that whether they get treated or not, don’t do well. So we’ll talk a little bit about that lyme disease caused by the bacteria, Borrelia Burgdorferi, another other spire, keats, tick Bourne illnesses. Uh, you know, here in Oklahoma, one that we have his story, um, which is southern tick associated rash illness, which is like another way of saying this is southern lime.

Speaker 1: 03:16 I mean, give me a break. It’s, it’s the same thing. It’s not the same thing. It’s, but it’s the same thing. It’s caused by another, uh, it’s, it’s caused by a Barellia spiral Keat, uh, we think, but it’s the bacteria that they think causes. It is Borrelia story. I, yeah, I didn’t make that up. Let that soak in for a little bit. A barellia story. I. Yep. Straight from the Oklahoma Department of Health website, the, um, and I as legit, it’s true, it’s their stuff there. But to say that we don’t have lyme disease in Oklahoma is, is really putting the blinders on and sticking our head in the sand. And that’s, that’s what it is. Again, going back straight back to the department of Health website for a Oklahoma, it says right on the website that we have isolated Borrelia Burgdorferi from ticks in this state, which means that we should have, which means that it’s very possible that we can have lyme disease in Oklahoma.

Speaker 1: 04:21 You can get a tick bite and get lyme disease in Oklahoma straight from the Department of Health website. They’ll say, although rare now again, if you go back and listen to the first in this series, you’ll understand why they think it’s rare. I think it’s more common than they think it is. And we’re working on that. We’re trying to provide the evidence to get the awareness out there to let people know and let physicians know that there’s more to this than meets the eye. So, uh, wanted to go through a little bit of history and kind of where this came from. And we’ve been dealing with lyme disease. This is not a new entity. It has been around for forever and a day. Uh, and so just to kind of illustrate that in 19, I’m sorry, 1918, 83, 123 years ago, Dr Alfred Buke walled described acrodermatitis chronic, a trophic hands, uh, which are aca, which this is a, um, is a skin issue that usually appears late in the disease late in lyme disease, usually caused by Borrelia.

Speaker 1: 05:22 Avs Lei, maybe another Borrelia, which is the other, you know, the Guarini I is the most common European line. So we were talking about one of your friends that may have been exposed to lyme. This is a worldwide problem. It is not confined to lyme, Connecticut. It’s not confined to the Great Lakes in northeast only a, this is a worldwide problem. We see it in China, we see it in Europe. It is a worldwide problem. In fact, they estimate that six percent of the Chinese population has lyme disease. Six percent a Chinese people out there. That is a huge population with lyme disease. So it’s a big problem. In 19 Oh, nine Arvada. Avs. Les described an expanding rash. It was later called Erythema chronic of migrants, which is the, the signature rash for lyme disease. The name was later changed in 1992. Remove the chronic [inaudible]. This rash is not chronic, uh, in fact it can last hours and less than 50 percent of the population depending on the study, less than 50 percent of the population that gets lyme disease has a rash.

Speaker 1: 06:29 So even though it’s part of the diagnostic criteria, according to the Idsa and um, uh, and the CDC, it is not. There are a lot of patients that get lyme disease that don’t ever recall a rash. So 1921, a arbiter of les connected the disease with joint symptoms, which we’ll talk a little bit more about in a second, uh, and possibly linked the disease to a, a, a tick bite exposure. Nineteen, 22. The disease was associated with neurologic dysfunction. So we got nerve problems associated with this. Nineteen 30. The disease was associated with psychological disorders. Things like depression, borderline personality, not borderline personality disorder, a bipolar disorder. There’s another psychiatric things that have been associated. Not saying if you have bipolar disorder that you, it was caused by lyme disease, but you know, it’s another possibility, a 1934 disease caused or a disease diseases associated with arthritic symptoms.

Speaker 1: 07:30 One of the main things that we see, uh, you know, patients will come in and you were talking about one of your friends. There’s a lot of joint issues and if you’ve got a migrating today, this knee hurts, then it’s my left elbow. And then what does that, that’s that migratory muscle and joint pain. You got to consider one of these tick Bourne illnesses as a possibility. It’s not diagnostic, but it’s a possibility. I’m 19, 65. Dr Sydney robins described an expanding circular rash and monoarthritis. In fact, he called this a specific entity called Montauk knee and this was a knee pain. And then, uh, this mono arthritis and they had this circular rash. Interestingly, it improved with penicillin. So, you know, what’s that about? Well suggestive that it’s, that it’s an infection. Nineteen 70. Dr Rudolph Scrementi is a dermatologist, published the first report on Athena chronic of migrants.

Speaker 1: 08:30 Uh, and interestingly again that responded to penicillin. Penicillin is one of those antibiotics that has, that works on cell walls spur the, the, uh, the uh, Borrelia is a spiral that has a cell wall, at least in one of its forms, which again, we’ll talk a little bit more about 1975. Pauli Murray was a mom in a, in Connecticut that were contacted the CDC and her effort plus a bunch of other moms. The CDC sent Dr Allen steere. He was a rheumatologist into the lyme, Connecticut area, uh, because of a complaint of a cluster of patients that had these swollen joints and a rash. Excuse me, he thought it was an autoimmune disorder. So you were asking about the auto autoimmune can a association. And he actually recommended that they treat it with aspirin and steroids. So in the, in 1970 or 75. In 1982, the CDC sent, or I’m sorry, the, uh, the nih sent an epidemiologist, a willy burgdorfer a into a shelter island in eastern long island, New York.

Speaker 1: 09:39 And he identified he was also a Barellia specialist. So he, he knew a lot about the barilla bacteria and he isolated this spiral that grew in these, uh, these deer ticks and black legged ticks, and he was the first to isolate Borrelia Burgdorferi and they named it after him. So hence the, hence the name of this thing. So there’s the other thing. So there’s quite a history of lyme disease. It’s, you know, obviously we, uh, we didn’t know what we were dealing with back then, but we started seeing these arthritis issues, some skin issues, uh, some things like that and um, it’s, it’s been an issue for a long time and it goes back further than that even. But those are the, uh, you know, the points that I wanted to kind of bring up. But it’s important to understand that there are a lot of different species of Barellia, you know, I mentioned to a previously, but one of the other things is, you know what, I actually mentioned three Barellia story.

Speaker 1: 10:34 I though that, that is a, that is one of the species of Barellia. It’s a tick borne illness. Uh, you’ve got my boy, you’ve got, which is a relapsing fever associated with texts. I mean, you’ve got all these different borrelia bacteria that cause all kinds of problems and interestingly, I’ve heard that ticks are the dirty needle of nature. So you know, you think about these, these texts will bite on anything that has blood, you know, go look at your dog and like pull the number of my, my dog can find a tick in a pond. I mean, we pulled so many ticks off her and just because it’s the way does not mean that there aren’t, takes out there. They, uh, they have identified ticks north of the Arctic Circle and interestingly 20 percent of those, greater than 20 percent of those are positive for Barellia Burgdorferi north of the Arctic Circle.

Speaker 1: 11:26 So you can get lyme disease north of the Arctic Circle. It’s shocking, but truly, I mean, I hit you again, like so many other topics we talk about and that I can’t make this. Uh, the Borrelia bacteria is an incredibly complex bacteria. It is the most complex genetic structure of any bacteria that think about it as a smart, as a super bacteria. It is able to do a lot of things because of the complexity of its genetic code. It adds plasmids, which that’s beyond the scope of what we can talk about in this podcast, but it adds all kinds of things that give it the ability to survive in a variety of hosts. Borrelia can survive in rodents and in birds and reptiles and in mammals and in humans, and in you take a bacteria that’s able to survive in each one of those hosts and transmit to a, to a tick, and then there’s something else that’s a, that’s a very wide margin.

Speaker 1: 12:28 I would argue most humans can’t survive that level of complexity. Um, so these are amazing bacteria and it has many different survival and adaptive mechanisms that enable it to do that. And that’s comes from that complex genetic code that it has and has the capacity to change. Interestingly, there’s two studies that illustrate this. One was in 1971, this guy named thousandfold noted that the Barilla adapt to their local environment and vectors. So if they’re in a bird, they adapt and they change versus when they’re in a rodent. So this bacteria will change. Uh, the argument that he made is this is the way that it has the ability to develop many new varieties and a quote from him. This variability could lead to new as yet unseen forms of disease. When I think it was, um, was it William Osler? I can’t remember exactly who it was, but he said if you, if you know, um, oh, good grief, that if you know syphilis, you know, medicine, syphilis, interestingly, as aspire kids similar to Borrelia, but, uh, it is an syphilis was called the great imitator.

Speaker 1: 13:48 And the, the, uh, the lyme disease bacteria is more than five times more complex in its genetic code than, uh, than syphilis, the great imitator. So you talk about the great imitator on crack, that’s what we, that’s what we have here in 1989. This is a very interesting point. And if you don’t get any other point from this then, uh, from, from this podcast than this, I think this is very important. In 1989, this got to impact her. He infected mice with Borrelia Burgdorferi and remember there’s different strains and there’s different species, but we’re talking about a specific species. And he injected the mouse, he infected the mouse with Borrelia Burgdorferi. But as he studied this, the brain isolate what they identified, where they isolated from the brain was different than the strain, the isolated from the blood. And the point was that the environment in which the bacteria live altered the gene expression of the bacteria.

Speaker 1: 14:53 And we’ve noted this, similar changes occur when Borrelia pass from the tick to the human. So that means that the bacteria in one place looks different than the bacteria and other place, same species, different strains. To illustrate the importance of strains. We’ve, you know, you’ve heard of Ecolab, so we know that equal, I live in. Everybody has it in their gut, but which is normal. But if you get eco lie, oh, one, five, seven, h seven. It causes hemolytic certain hemolytic uremic syndrome and you can die from that, so you have one that’s normal and natural and arguably healthy, and then you have one that’s fatal, same bacteria, different strain. So if you wonder about the importance of strains, look, consider an e coli o one, five, seven, eight, seven. So the different strains of Borrelia make a dramatic and profound difference. So when it comes to, and I think I talked about this a little bit in the first podcast on this, where we talk about the different strains of Borrelia, the [inaudible] one strain is what was identified from eastern Long Island New York.

Speaker 1: 16:03 That is not a human strain. It was identified from a tick. That doesn’t mean you don’t get lyme disease from it, but they identified it from a tick. We know that this bacteria can alter its expression based on its host, so it can be different in a tick than it is in human. That’d make it a different bacteria. It’s a different strain because these things changing culture, they lose plasma plasma’s, they lose pathogenicity. They changed, they very. It is very different from that, which is infecting patients. It can be very different from that switch which is infecting patients. So the B, 31, and I talked about this in the first podcast, be 31 is what the. The testing is based on. So if you go get lyme antibody testing, if you get an immutable lot, a western blot test, it’s based on the [inaudible] strain. I had a patient today that had a negative western blot based on their standard testing.

Speaker 1: 17:00 When we did an identical genics test. It was positive looking at the same parameters, but the one from the regular lab be 31 strain only. The other lab added additional strains and was was profoundly abnormal and positive for lyme disease by even CDC criteria. So wow, this train matters, but the interest in this, this is where it’s really started getting injured and interesting to me. So borrelia Burgdorferi is immune suppressive. So when we talk about, you know, the autoimmune nature, when we talk about the variety of ways this can present, Borrelia is immune suppressive. We fight these infections with our immune system. Think about these as the Ninja bacteria. I mean, that’s probably, that’s probably a really good way to say that because they suppress and evade the immune system in a remarkably a profound way. So they, this bacteria affects specific parts of our immune system, specifically the b cells and the t cells and the natural killer cells and it, it suppresses and kills the t and b cells in culture.

Speaker 1: 18:12 So in, in when we threw them out and see it in a petri dish, it suppresses and kills these, these, um, these specific parts where our immune system plus it prevents maturation of the natural killer cells. Part of the immune function is the maturation of these natural killer cells so they can identify a specific target. And, uh, and it does that by promoting, um, by suppressing a CD 56, [inaudible], 57. So in the immune cascade where we’re trying to develop a specific target against these things. These guys have become the super ninjas in, in evading this thing. Uh, they cause a defect in this part. I mean, I keep saying this over and over again, but this is just fascinating to me. They cause a defect in the B cell signaling, so part of that immune system, uh, so that the innate immune system stays active and when it stays active, it causes a whole host of things.

Speaker 1: 19:06 Sorry, I hit my wise, I’m waving my arms as I’m ranting and raving about this stuff. Uh, so when you were with this b cell signaling, you have a, an ongoing cytokine cascade. So cytokines are these immune signaling things like interleukins and cytokines are part of the inflammatory process. And so you can have this flu like symptom and into inflammation which is independent of the disease because we’re talking about the toxin that does some of this. And you have this ongoing influence. So you have this, a flu like illness, independent of the disease because of the way the Borrelia do this, but this ongoing inflammation and the Igms, one of the early antibodies that shows up after you get exposed to an antigen or a bacteria or a virus or anything or vaccine or anything else. And this ongoing inflammation. And Igm, which is by that B cell activation does not help the body in clearing the infection.

Speaker 1: 20:03 So you have this revving up of the immune system because of this b cell dysfunction in it’s signaling. So as this altered signal, it’s almost like you’re causing a fire, you know, for know for the army fort. So everybody runs to go put out the fire and they sneak in the backdoor. I mean, that’s, it’s, it’s, it’s shocking how, how interesting and complex this thing is. It’s just fascinating. And so you have an upregulation of these inflammatory cytokines, but you also have a downregulation of anti inflammatory cytokines. So, you know, Isis couldn’t come up with a better, with a better target, you know, it’s just, it’s amazing. So there’s a whole lot going on here. There’s a lot going on with uh, uh, with disease, there’s a lot of cousins, a lot of chronic problems. But so many physicians will say that it doesn’t cause a chronic infection, that you just treat it for two weeks, three weeks, and you’re good. And that’s all you need. And I’ll tell you, it’s hogwash after we come back from the break, we’ll talk more about that.

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Speaker 1: 21:36 All right guys, we’re back. We’re still here with Dr Heath Travis. Um, we are sitting here talking about a lyme disease and having a good time talking about all the, all these shocking get amazing things. I mean, I, uh, you know, as I, as I read about this stuff, it’s just like you got to be kidding me. It’s amazing. It truly is kind of like I was telling you, I had a friend that was diagnosed after being in Europe, was diagnosed a year later and it took a lot of testing, right to make it happen, right? But then we watched his joints over the course of 10 years and just go through absolute misery and pain. Right. Trying to fight this thing off. Right. But it’s really just now getting to the point where it’s manageable, right? Let’s, it’s uh, it’s rough. It is, it is. And how many patients because of the way the testing is done, the way we understand the testing or don’t understand the testing, how many patients are walking around with lyme disease or some other tick borne illness like startup story where they’re having chronic and long term implications that no one is even addressing.

Speaker 1: 22:39 I can tell you that I’m, I’m, you know, I have patients that come in and they’re like, well, why? I asked my doctor to test for this and they wouldn’t do it. I can tell you as a board certified family physician, I was not well trained and I can’t say that everybody’s that way. I don’t mean to throw darts at anyone else. I can only speak from my experience. I was not well trained in looking for, uh, these, these things I did not understand. I could have told you. Okay. Yep. Lyme disease, burlier Burgdorferi. And that was my board question and that was it. That’s all I knew. I didn’t understand the [inaudible] strain. I didn’t understand the two, uh, the two 97 strain. I didn’t understand the, the complex genomic structure of these things and how they change epitopes and all these things. So I didn’t understand that.

Speaker 1: 23:26 And you know, we as physicians are supposed to help our patients. We don’t know everything. A lot of patients think we do. Some physicians certainly act like they do a and we don’t, we don’t know everything and we have to, you know, God has a really nice way of keeping me humble on a daily basis. So, um, but we just have to stay vigilant and those kinds of things. And so some patients will say, why didn’t my doctor do this? Well, because they didn’t understand it. Um, you know, should they and I would argue yes. And one of my favorite quotes from the Bible is my people are destroyed for their lack of knowledge. I love that quote. Um, so, you know, before we talked about, uh, the number of issues with lyme disease, some of its history, what it does to just cause the immune system to implode.

Speaker 1: 24:13 And why I, I’m, I’m just gonna start calling it the Ninja, the Ninja bacteria or the Ninja disease because it’s really sneaks up on you and, and you don’t really stand a chance, sort of. So why does this thing cause a chronic infection? You know, the immune system is such that you get exposed to something, you develop an inflammatory immune response, you make antibodies against it, you kill it, it’s done. You move on. That’s the Idsa. That’s what they tell us, that this, that this happens, this, we don’t get chronic lyme disease. I would argue that we do. And I think there’s plenty of studies out there that show that we do. So how, how does this happen? Well, the first one is the, uh, we get this chronic illness and chronic disease, chronic infection because of the induction, the immune system and the way that we just described.

Speaker 1: 25:01 It’s a Ninja bacteria that is able to elude the immune system and a number of different ways. One of those is what we call epitope switching, where we are switching, uh, these, these antigens frequently and it allows the bacteria to evade the immune response. And you have some minor epitopes switching every few days. You have some major epitopes switching every few weeks. So it is, it’s very interesting how this thing can evade the immune system. The bacteria are very, very slow growing. We talked about this and the first podcast on lyme disease. They’re very slow growing, which means they culture. It’s very difficult to get a culture. They grow very slowly. I think the culture times, like 10 and a half weeks, I’m a, tend to have months, something like that. I have to go back and wasn’t my first podcast, but it’s a very slow growing bacteria. Um, the, uh, the double time and measure is measured in, in up to weeks.

Speaker 1: 25:59 Um, there are periods of this bacteria where it’s dormant and it’s considered Leighton’s where the bacteria are not dividing, but they will continue to produce toxins which causes all this immune system problem. So the bacteria, it’s not like a standard infection where you get a staph infection or a boil or a cellulitis and the bacteria constantly dividing and you give something like penicillin, which works on the cell wall of dividing cells. Uh, it doesn’t do that, so penicillin, while it can be effective, it doesn’t catch everybody and it’s because these things are very slow growing and there are periods of this dormancy and latency where they continue to produce toxins. So they’re causing problems but they’re not dividing. Then we have the ability of these things to transform into three different forms. So I mean, again, when you talk about this thing is like so ingenious how she got multiple different ways of doing this stuff, but you got three different forms of the bacteria and this is documented, this isn’t, we have electron micrographs, we have pictures of this, this isn’t like what we think it might do that we have pictures of it, that it is solid from stuff.

Speaker 1: 27:06 So the first thing is the spire keep the standard. Bacteria has a cell wall that, that spiral is one form and different kinds of antibiotics will work on that specific form, but it can also change into a cyst form. So it will wall itself off loses, I believe it loses its cell wall, uh, but it goes dormant basically into this cyst type form and a different kind of bacteria. Antibiotic is required to treat that specific form. Then we also have what’s called an l form bacteria, which is an intracellular form of the, of the bacteria. It lives within your cells. So now you have to have an antibiotic that can get within yourselves and since it doesn’t have a cell wall in the l form is a different kind of antibiotic than a penicillin. So it causes all these immune host problems with the signaling.

Speaker 1: 28:01 It’s very slow growing. It changes epitopes, it changes forms, has all kinds of problems that it can cause and it evade the immune system, which is why we can have this chronic infection. But it also has certain protective niches and these niches and things are things like ligamentous structures, connective tissues, the eye, the central nervous system, a intracellular. Each one of these, you know, when you think about, we talk about ligaments and tendons being relatively a vascular, they don’t have a good blood supply, which is why if they’re damaged, they often don’t heal well, which is, you know, that I get on the prolotherapy bandwagon with that one. And so we talked about that particular component of ligaments, tendons multiple times on multiple podcasts. Um, but it, it’s, it’s a protective niche for this where there’s not a good blood supply, can’t get the medicines in there.

Speaker 1: 28:50 Well, uh, and then the inflammatory processes is less in there as well. Um, so then the last piece of this, the what I call the coup de Gras, of, of how these things evade the immune system is what we call biofilms. So the bacteria produced this, uh, uh, call it slime. It produces this stuff which is just this, it’s not covering over the bacteria that prevent that, prevent it from being bombarded with antibiotics and you know, those kinds of things. In fact, one of the, this guy sappy said, for example, it was demonstrated that pathogenic biofilms possessed, possessed as much as 1000 times increased tolerance to antimicrobial agents, making them difficult to eradicate. So it is a dramatic and important a mill you for the bacteria to live and evade the immune system. And these things are. We think that’s one of the reasons that this has been so difficult to treat because even though we give different bacteria and we’ve been doing this for a long time, even though we give these different antibiotics for different state, all these things, we still haven’t been able to completely eradicate it in some people.

Speaker 1: 30:06 And we think that the biofilms are the reason for that at the biofilms protect the bacteria from the host immune system attack and it’s certainly the sheltered from the antibiotics, but we see these biofilms so we know that we know they exist both in vitro in a petri dish, but also in human tissue specimens where they’ve called or they’ve a biopsied something and we have these tissue specimens and we see the biofilms there as well. The biofilms will incorporate calcium and magnesium and over time, excuse me, those things will calcify and you’re the. They will form this shell. I’m almost like your ice cream where you put the stuff on. It hardens up, but informed something so hard. Bleach won’t even kill the bacteria when through that biofilm. So we’ve got a very tricky Ninja bacteria that can evade the immune system, that can trigger the immune system through a series of mechanisms that’s been around for a long time and is essentially all over the world, causing a lot of people problems and we don’t do a real good job at detecting it because of all of the issues that we talked about in the first podcast.

Speaker 1: 31:16 So, so let me ask you real quick. So for a patient, if they’re out there and they go in, what do they ask their doctor to look for to wouldn’t say, Hey, I want, this is what I want you to do. Well, if you said I want lyme disease testing, they’re going to follow the Idsa guidelines or the CDC criteria which says it’s a two step test. Um, and, and we talked about this more in depth in the first podcast, but basically they’re going to do an antibody test. And if the antibodies are positive, they will do a western blot or an immutable blot. Uh, looking for the bacteria. Now again, I’ll steer you to the first podcast on why so many do not meet criteria based on immune of lot. The short stories, they’re only looking for the [inaudible] strain. And the second thing is they eliminate two or multiple bands, but specifically to bands that are known to be very specific for Borrelia, uh, for the lyme disease because those are the two targets for the lyme.

Speaker 1: 32:22 Rick’s lyme vaccine that was pulled from the market nearly 20 years ago, over 20 years ago because of a lack of consumer use. So they didn’t know it was only out for a very short period of time. And so they eliminated virtually diagnostic bands because the vaccine would, would mix that up. So there are multiple reasons why patients with lyme may get a negative lyme test. So the short story is, you know, I hate to say it this way, if you think you have lyme disease, you need to go to a practitioner that is versed in lyme disease. Your regular doctor will probably never find it unless they understand the implications, the impact that the testing, how this thing works. And, and you’ve got to understand that lyme disease is a clinical diagnosis. It’s, and it’s based on a lot of things. A lot of patients don’t remember a tick bite, only less than if you look at the studies, less than 50 percent of the people will get a rash, um, which are two of the diagnostic criteria.

Speaker 1: 33:32 So you’ve got to put the whole picture together. And there are bands, for example, the 41 kilodalton band on a, the immutable law is only 50 percent specific to lyme disease. So you can get a positive lyme test by CDC criteria and not have lyme disease because it may be something else. It’s not necessarily specific to lyme disease that doesn’t, you probably have something else going on. So it, I mean, you have nothing. Sure. It’s just as it burlier Burgdorferi. Is this something else? So very complex illness, very complex disease, very complex testing with a whole lot of nuances. If you think you might have it, go talk to a physician, well versed in lyme disease. Perfect. So there’s a whole lot there, uh, Zary to regurgitate a whole lot of that so fast and so deep, but we got more podcasts coming online disease. So stay tuned for more. Hope you guys have a great day.

Speaker 3: 34:27 Thanks for listening to this week’s podcast with Dr Chad Edwards. Tune in next week where we’ll be going against the grain.