Lyme, Dementia, and the Tests Nobody Thinks to Run

I just had the most amazing conversation with the world's top Lyme expert, Richard Horowitz. You're going to love this episode today. I left it feeling inspired about I'm in the right place doing the right thing at the right time. Also think about this, people my age range, I'm 53 right now, about 40% of individuals in my age range are expected to develop dementia in our lifetime. And maybe, just maybe, Lyme disease might be at the base of that. We talk about a lot of great topics. This is an individual who has 40-plus years in the Lyme world, one of the first Lyme doctors. Um, an amazing conversation. I know you all are going to enjoy this as much as I did. Enjoy. Take care. Welcome back once again for another exciting episode. I am super excited to have today Richard Horowitz, probably the top Lyme expert in the world, here on Made for Health. Um, we already started talking about some really exciting stuff related to some new discoveries with Lyme and Alzheimer's, which I want to get to. But let's start with introduction first for someone who's known to our audience and then hop into setting the table for today's conversation. Dr. Rich Horowitz is a board-certified internist and medical director of the Hudson Valley Healing Arts Center, an integrative medicine center which combines both classical and complementary approaches in the treatment of Lyme disease and other tick-borne disorders. He's treated over 13,000 Lyme and tick-borne disease patients in the last 35 years. And patients coming from all over the United States, Canada, Europe, around the whole world actually. He is former assistant director of medicine of Vascular Brothers Hospital in Poughkeepsie. Poughkeepsie, there we go. I'm like, how do you say Poughkeepsie? Poughkeepsie, New York. That's how, that's what it looks like. And is one of the founding members and past presidents of ILADS, which is the International Lyme and Associated Disease Society. He's also past president of ILADEF, which is the International Lyme and Associated Disease Educational Foundation. Which is a nonprofit organization dedicated to education of healthcare professionals on tick-borne disease. Dr. Horowitz has trained hundreds of healthcare providers in diagnosing and caring for patients with Lyme disease, tick-borne illnesses, and a whole host of other things, as you're going to find out later on today, which you probably did not think were related to Lyme disease, and actually, they kind of sort of are. Amazing educator. He's dedicated his life to helping those stricken with this devastating illness, and we are super honored To have today, the one and only Dr. Richard Horowitz.

Thank you, Aaron, for the kind introduction. It's great to be here.

Yeah. So I want to set the table real quick before we hop into the conversation we were having before we started recording. Um, where are we at currently with the Lyme and tick-borne illness in America right now? I want you to set the table just so people know what is the current situation we're talking about dealing with. Lyme disease, actually this past year, at the federal government level, we actually started to acknowledge there might be something going on. So set the table for us right now. What actually are we facing? What's going on right now in the United States related to tick-borne illnesses?

So we're in the middle of a full-blown epidemic right now. In fact, every state health department is recording more and more cases. It's the largest Lyme epidemic I think we've ever had. The U.S. government basically admits to 476,000 cases per year. But interestingly enough, when they looked at Medicare rates, it was 7 times higher. So you're talking probably somewhere between at least 2 to 3 million people a year who are getting Lyme disease. And the problem, of course, is when you look at the prior statistics, BMG Global Health published about 4 years ago that 1 out of 7 people living on the planet right now has been exposed to Lyme, right? And as we'll talk about just shortly, we're not in the middle of just a Lyme epidemic, but most of the tick-borne diseases, by the way, Babesia is getting worse. We're seeing more Anaplasma cases. People are dying from Rocky Mountain spotted fever. Alpha-gal allergy has now hit over 500,000 Americans. And we're also dealing with an Alzheimer's epidemic. And I published for the first time this year in the Journal of Alzheimer's Disease Reports, the first case in a live human being linking Alzheimer's disease and the biomarkers to chronic Lyme disease. And with a 9-week oral protocol using generic antibiotics, I reversed the most sensitive and specific Alzheimer's biomarker. P-tau 217. It had never been done in the world and proved that the same 16 factors that I'm seeing causing chronic Lyme, making people ill, are also associated with Alzheimer's as well as long COVID and a whole host of other diseases we'll talk about. So yeah, some really exciting stuff for people because we're in the middle of a chronic disease epidemic and Lyme is kind of leading the way.

So, you know, it's the number I've heard this past year, you know, there's 30,000 or 40,000 cases of Lyme diagnosed Every year, and there's roughly 700,000 cases a year. So, you know, 660,000 cases are going undiagnosed. You're telling me no, 2 to 3 million a year. That's a radically different number from the radically different number that's come out this past year. What's the disparity? Like, how are we getting this so wrong?

Well, so the problem of course is, is the way the state health departments are measuring Lyme disease is 2-tiered testing. Right? So not, they're not even looking at erythema migrans rashes anymore, right? They're looking at ELISAs followed by Western blots. And initially these criteria for state health departments to epidemiologically screen the populations to make sure they had Lyme, but the numbers are much higher. And keeping in mind, Lyme is the great imitator. So when you look at the number of people with chronic fatigue syndrome, myalgic encephalomyelitis, and fibromyalgia, which together you're talking, you know, 3, 4, 5% of the US population, You're dealing with massive numbers of people right now that are having Lyme underlying a lot of their chronic illness.

I mean, I'm working with a patient right now in her 70s who had chronic fatigue fibro from 30s till she started seeing me. And just on doing the Western blot, rabid Lyme disease, after 6 months of AMBOXX, her 30-plus-year disease is gone. So it's strange to me that something like that, we don't, it's not standard. Let's do a Western blot. Like, where's the gap in the education? the knowledge and implementation of what appears to be a ridiculously common thing that when I moved back to Virginia, when I got out of the military back in 2007, I was told by my local infectious disease doctor that this thing, chronic Lyme disease, didn't exist. Like, help me understand that. Help my audience understand what appears to be a massive disparity in that regards.

So unfortunately, Lyme is a medical-political disease. It's not just a medical one. And there's been 2 sets of guidelines to diagnose Lyme disease now. And we di— by the way, it was discovered about 50 years ago by Willy Burgdorfer and Alan Steere. And so 50 years later, you know, where are we? I worked for HHS. I've worked for the government on their first round of the Tick-Borne Working Group. I was one of 7 members who worked with the CDC, the FDA, the NIH, Department of Defense. I gave them all information about how poor the testing is, that Lyme does persist in the body. I keep sending these same doctors, right? The reference articles that it is persistent. This, I can show you 700 articles on persistent Lyme, but the reason it's not gotten out there is because the IDSA guidelines from the International Disease Society of America, they're basically saying it's easy to diagnose and easy to cure. And they're using these epidemiological statistics from health departments of 2-tier testing. If you show up with a Western blot, like in your patient who And I play this game with patients called Lyme bingo. I'm not sure how you do this, but if any one of 5 numbers shows up on a Western blot or an immunoblot, the numbers are the 23 outer surface protein C, 31 outer surface protein A, 34, 39, very specific, or 83, 93. Now the Western blot, the 31 can sometimes be autoimmune disease or Epstein-Barr, although in most cases it is Lyme. But if you just play that game and don't use CDC criteria, You're gonna find a lot of these people who complain of a chronic fatiguing musculoskeletal neuropsychiatric illness. I'm tired. I'm achy. I have headaches. I can't fall asleep. I keep waking up in the middle of the night. I've got drenching sweats. My memory's terrible. I can't remember anything. I'm moody. I'm anxious. I'm depressed. These are all symptoms of chronic Lyme. And unfortunately, doctors like you and I, you know, we see patients go to 10, 20, 30 doctors before they get to us. Because the diagnostics, you know, you can't use a Western blot from a local lab that looks for one strain of Lyme when there's minimally 9 strains out there that are making people sick. There's actually 100 and 300 worldwide, just like with Bartonella. There are 18, 19 strains of this other intracellular bacteria. You can't just look for Bartonella henselae on a lab test. So, you know, doctors really need to be educated and even patients need to be. About the complexities of this. And I've been trying to teach, you know, patients and docs for a long time. It's not that complicated, but you got to understand the basics.

So to clarify what you said, just so everybody makes sure, makes sure I, as well as everybody else listening, you're saying not 3, not 5, but 1 of the 23, 31, 34, 39, 83, just 1 of those positive, you're thinking this person has, with symptoms, of course, has Lyme.

Having done a differential diagnosis and ruled out, of course, other illnesses, because you can also be exposed And taken an antibiotic for something else, right? For an unrelated issue, actually gotten over the line, but you still have antibodies that are persisting. So, but, but the way people know, by the way, and I did a study on this, we published it in the medical literature in 2017. You can go on my website, cangetbetter.com, and take the questionnaire. If people score over 63 on the questionnaire, which I call the HMQ, the Horowitz-Emsid questionnaire, and you score high and you have migratory pain, Where one day the pain is in your shoulder and 2 days later it's in your hips and 3 days later it's in your knees. There's only 6 other diseases in medicine that cause migratory pain. And I used to joke with docs that if you were at the bottom of your medical school class, you still could identify, you know, lupus, inflammatory bowel, Reiter syndrome, hepatitis, acute rheumatic fever, right? You could identify those as opposed to chronic Lyme. So yes, any of those bands, but it's best if it's on an immunoblot. Which is a recombinant DNA test from MyGenexx in California, because the 31 band, as I said, locally can occasionally be due to autoimmune disease or Epstein-Barr. But in my 42 years of clinical experience, seeing over 13,000 of these people, a 31 band, if you have it in the right clinical setting with migratory pain symptoms that come and go with good and bad days, right? Fatigue, aches and pains, especially neuropathy, right? Tingling, numbness, burning, stabbing. vibration sense that moves around the body. The only disease that causes migratory nerve pain is Lyme. There is no other disease on the planet that does it.

Yeah. And it's really interesting. I, you know, I have a patient I'm working with right now who had a, um, IGeneX test done and had 6 positive bands and they live in California. I'm in Virginia. And they decided to see the Lyme expert in California who did a Quest Lab on them, uh, 4 months later, 'cause they weren't getting better for various reasons. No bands popped up. I got the results. I'm like, did, did it go away? Your symptoms are no better. You're actually worse. Repeat the IGeneX, same bands pop back up. And so literally nothing on the Quest, you know, 6 bands on the IGeneX. And I don't think people realize that it can be that massive a disparity between a standard lab test versus a high-level test. Absolutely.

So you're dealing with at least 9 strains of Lyme that cause illness. Quest And lab core checking for one. So it's not that unusual to get a completely negative local lab test. And, you know, there, by the way, I mean, having done multiple labs over time, there's another lab called T-Lab. I use Igenex all the time and their immunoblots are great, but even T-Lab, I will do a Lyme PCR in someone who's been treated for Lyme who has not used what I'll call biofilm persister drugs that we can talk about like Dapsone. And the Lyme PCR will be positive after decades of taking regular treatments or the Babesia fish or the Bartonella fish RNA tests for these parasites or other bacteria show up. The people who have chronic Lyme, it's never usually just Lyme disease, right? I mean, I know you know that and we're just going to share it with the audience, but I describe it like someone going into a doctor's office with 16 nails in their foot saying, I have foot pain. And the doctor finds one nail, pulls it out and says, come back in a month and tell me how you're feeling. And it's like, you still got 15 nails you got to figure out. So.

Yeah.

That's the whole point, by the way, of my prior books that I published and my new one that'll be out very shortly, Ending Chronic Illness. Yeah. I mean, I describe this so people understand how to make the diagnosis, how to treat, but also how to use the model for a broad range of other illnesses.

And just for people listening, I routinely use your IMSEDS model for the symptoms as a marker for one, do you hit the criteria level? And 2, are you responding to therapy? Because doing an IJENX test on someone every 3 months gets pretty pricey pretty quick. And again, that symptom questionnaire is validated. So it's a great, great questionnaire to use. Before we started talking today, you started talking about some of your newest research you published relating Alzheimer's to Lyme disease, which I've heard about that before. I've heard about this one study where they had Alzheimer's patients and something like 80% of them, the biopsies had spirochetes, which could be from oral or whatnot. But the numbers you quoted here before we started recording were a little staggering. Could you just briefly retell everything you said before we started recording? Because that was, it was a little bit mind-blowing for me.

So the NIH last year came out with a study and you can go on and you can find it. And what they told Americans is that 42% of Americans over 55 years old are going to become demented and develop dementia with Alzheimer's disease as the years go on. So I mean, think about this number, 42%, which means roughly 4 out of 10 people listening to this podcast are expected to get, you know, demented going on after you get 55. Now the question is, and this is really astonishing, they did not come out and say, well, why is this happening? Like, why are so many people getting demented? And what I, so I published an article this year in the Journal of Alzheimer's Disease Reports. It's one of the major journals that are out there. And what I showed is, and in the past, By the way, just to be clear about the history, and this is what you were referring to, in autopsy studies of Alzheimer's patients and including Parkinson's, they would find spirochetes, Lyme spirochetes. Also, you're correct, Denticola spirochetes from the mouth, could even be H. pylori from the stomach, anything that's a spirochetal infection. They found these spirochetal infections in the brains with beta amyloid, with phosphorylated tau, and with biofilms, which is what they find in Alzheimer's. plaques, but it was always in autopsy studies. They could never prove it. So if you, for example, went to a neurologist and you showed up with an Alzheimer's biomarker like a low beta amyloid ratio, and we'll discuss this, or an elevated P-tau 217, which is the most sensitive and specific biomarker for Alzheimer's, which is what my patient had, they would say you have Alzheimer's and here's these anti-amyloid drugs like lecanemab and donanemab. But they don't really work well, right? They, there was a Cochrane study, a big review of all the literature that said, hey, you know, the amyloid's coming down, but we're really not seeing a big difference in people's symptoms. What I showed is that all 16 of the same factors that I've been publishing on for Lyme for the last decades called MSIDS, multiple systemic infectious disease syndrome, the same 16 factors we've been finding in chronic Lyme show up in Alzheimer's. And that by using the protocol that I developed for chronic Lyme, called Dapsone Combination Therapy. It's a 9-week oral generic protocol. We completely reversed P-tau 217, this sensitive, specific biomarker. It went down by 63% after 9 weeks of an oral generic protocol. Now, to put that in perspective, if you go to a neurologist diagnosed with Alzheimer's and they give you lecanemab, donanemab, those drugs lower P-tau 217 by 23% over 6 to 7 years. I lowered it by 63% in 9 weeks. Why did that happen? Because the spirochete was driving amyloid production and driving phosphorylated tau. And we've gotten into this problem in medicine where we're naming diseases, we're throwing drugs at them, right? Which it's too late. You've got to get to the root causes of why so many people are sick. And basically what this study did is it was the first ever time in the world We proved that there is a direct relationship between Borrelia burgdorferi and Alzheimer's in a live human being. Unfortunately, the neurologists have not, you know, we need a multicenter randomized placebo trial. Of course, it's one study, although I did do it for another patient recently, which I've not published. He had fatty liver, was overweight. And by the way, this patient, what's fascinating about the patient I published, sick for 15 years, had never done any antibiotics. All she did was take the 9-week Dapsone protocol, and we completely reversed her biomarkers. Right? So that's really amazing because number one, it proves that Lyme is a persistent infection. There's no other reason it would have worked. Although Dapsone, by the way, does lower inflammation in the brain. There's a biochemical pathway called NLRP3 inflammasomes. And I, and honestly, we probably need to repurpose this drug for Alzheimer's because it, it can lower inflammation in the brain independently, likely. whether you have Lyme or not. But the point being, we're not getting to the root causes of where the Alzheimer's epidemic is coming from, right? Just like why so many people have chronic fatigue syndrome or fibromyalgia, right? Or getting cancer. The cancer epidemic, younger, younger people all the time are now getting cancer. What is driving the cancer epidemic? So what I did in my new book, Ending Chronic Illness, is I basically went through cancer, cardiovascular disease, chronic fatigue. And what I discovered to my great surprise is the same 16 factors That I've been publishing on for Lyme for decades now showed up in all of these diseases, which means we have now a paradigm shift, like a new way of thinking about these illnesses that no matter what you're calling them, go to the 16-point model. Look at infections, look at toxins, look at the microbiome of the gut, look at the hormones, look at the mitochondrial dysfunction. It's stuff that you and I do, but it's basically, you know, putting it in a way that's standardized for people to think about this in, in a new way.

Yeah. And, For everybody listening here, like I did my training through the IFM and they had their model set up and then A4M had their model. But it's interesting that the IMSIDS model, it's kind of like those models expanded. And so it's interesting how, Dr. Horwitz, you kind of figured out on your own a similar type model, but you actually separated out into 16 systems, which is really kind of, I mean, to your point, pretty brilliant. And I've kind of taken all these things and put them together because the reality is, is You gotta treat people as individuals, not as, you know, you know, whatever. You're functional. No, you're integrative. No, you're chronic Lyme. It's like, it's all a big soup.

Right. And you need to be, I believe precision personalized medicine is the medicine of the future, right? All of these patients that come in, for example, I'll give you an example in the book. How many patients, you're sure the same has happened to you. They come in with fibromyalgia, right? How I didn't learn in medical school that 80 to 90% of these fibromyalgia patients have mold toxins. I didn't learn that. I discovered it on doing a deep dive in the medical literature, right? So the point being, a lot of these patients who are now coming in who say, I'm tired, I have headaches, I have brain fog, I have neuropathy, I have joint pain, muscle pain, mood disorders. They're loaded with mold toxins. They're loaded with heavy metals. They've got not one infection, but they've got Lyme disease on top of Bartonella, on top of parasites like Babesia. Their long COVID has reactivated their Epstein-Barr and their herpesvirus 6. They've got Candida overgrowth in their gut with metabolic syndrome, right? It's basically a whole host of factors that are driving inflammation. And the good news is, is that these people have been to 10, 20, 30 doctors who said, I have no answers. You apply the 16-point model, you basically run the checklist. I mean, it's really not that complicated, and you end up discovering a whole host of things causing inflammation. And, you know, we've had great success as you have getting these chronically ill patients better. So, it's exciting for people because it gives them hope. Right. That they don't have to go to doctor to doctor searching for answers, that there's a model that works for these people.

Yeah. And in the autoimmune world, we know that if you have an autoimmune disease, which, you know, depending on what you read, that's going to— it's a lot of people have autoimmune diseases or positive autoantibodies that you have to have 4 things.

Right.

And one of those things is a chronic infection of some sort. And so all of a sudden someone comes in with Hashimoto's, rheumatoid, you know, inflammatory bowel disease. I'm routinely checking infection markers, including Lyme. Actually, one patient with EOE and SIBO. And I found under the, you know, as I was working with him, this is like a 3-year process of dealing with this EOE, then the SIBO. And as things kind of, I was always checking markers, but interesting how his standard Quest Lab marker was negative, negative, negative. At year 3, it popped positive. And the thing that got him from 60 to 80, but then 80 to 100% better was actually starting to treat his Lyme disease, which actually didn't pop up on a standard test until we'd dealt with his EOE and dealt with his SIBO. And of course, he had mold. But it's really interesting. It's like an onion. You got to know which layers to peel at what point in time. And I had one patient, I mean, I think to your point, who went to a really famous Lyme clinic in DC who put most of the patients on IV Rocephin. She worked with them for about a year, came back to Richmond, wasn't any better. Come to find out she had mold. She was hypermobile, had POTS, dysautonomia, you know, which is on your list. And then as we worked with mold, literally I got to watch her titers.

Wow.

Normalize over about 2 years. 'Cause I was like, I'm not going to give you more anabolics. You failed that. And ultimately, to your point, mold biotoxins were at the underlying thing of why she wasn't able to clear her Lyme disease.

Yes. And also ivermectin, if you've been sick for years, ivermectin, as good as it is, it's only for actively growing bacteria. It's not for the biofilm persister forms, right? What I discovered when Johns Hopkins University back in roughly 2015 discovered that Borrelia was a biofilm persister bug, like TB and like leprosy. I went to the literature and I went, oh, you mean like leprosy, you need rifampin and dapsone? That's how I came up with the protocol. And I said, I wonder what happens if I add doxycycline to rifampin and dapsone, which is how they cure leprosy. And it was a home run out of the park. And that's my first study I published on it was 2016. So, you know, I've been playing with these doses of dapsone over time. It turned out it took me almost a decade to figure out How to get the dosing right. But my wife, who had been sick for 25 years with chronic Lyme, and you can read her story, by the way, she had all 16 MCITS factors. I published her in the journal Antibiotics in 2020, and it was exactly as you said. It was like peeling an onion. Once her adrenals got better, she, you know, her fatigue got better. Once I treated her hypoglycemia Candida, again, the fatigue and the brain fog got better. Then we started treating the thyroid. It got better. Then the Babesia. It was like basically peeling an onion, but she had to take 100 milligrams of Dapsone twice a day to go in remission. She tried 50 of Dapsone for a year before I knew the dose, felt great, stopped it, and was PCR positive in the blood for Lyme. Went back on Dapsone at 100, doubled the dose, 6 months, felt great, stopped it, relapsed. And then a patient of mine came in during that time and had accidentally taken a double dose of the Dapsone. And he said, oh, doc, I'm feeling terrible. I said, oh, what are you taking? Oh, I'm taking Doxy twice a day. I'm taking rifampin. I'm taking Dapsone twice a day. I said, oh, you're taking too much. Stop. Come back in a month and tell me how you're feeling. Comes back in a month and says, I feel great. He was sick for 7 years. I said, don't take anything else. He came in every 3 months and stayed in remission. And I turned to my wife and I said, sweetheart, would you like to be a medical guinea pig? I'd like you to try this dosage for 1 month. that's what she did. She's been in remission for 8 years. It's never come back despite getting COVID twice, despite getting the flu. And you and I both know that sometimes if you've knocked down the load of the bugs, but you get other viral infections or things in your body, the Lyme ends up coming out. It hasn't come out. She's in full remission.

Yeah.

So I do believe I've discovered a cure for this disease. And I did apply for an R34 NIH grant for a multicenter placebo, you know, randomized trial. Unfortunately, My grant was turned down even though it was only a quarter million dollars because the reviewers from the NIH reviewing it went, I'm trying to prove to them, by the way, that Lyme's a persistent infection. Why did they turn it down? Oh, because it's not a persistent infection. It's like, that's why I was telling you to do the study. It's like, oh my God, you people. I can't even. So I now have to reapply. But when I reapply for the grant, I'm going to include the Alzheimer's biomarkers because I'm now telling all the doctors who are seeing these Lyme patients. You need to be checking beta amyloid 42/40 ratios, P-tau 181, P-tau 217, and neurofilament light, as well as an APOE study to find out if you have the genetics for Alzheimer's. And if you do, there's a marker called glial fibrillary acidic protein, GFAP. But if you do the basic markers of beta amyloid 42/40, P-tau 181, P-tau 217, neurofilament light, What's fascinating is half of my Lyme patients were showing up with these inflammatory markers in the brain, right? So, you know, I just finished clinical practice, but now, in fact, I would advise you also, Aaron, if you're not doing it, check your Lyme patients before and after treatments to see what's happening. Because it, it, I think this is a study that desperately needs to be done because we're in the middle of an Alzheimer's epidemic.

Yeah.

And I believe that based on the studies that have been published way before I published mine this year, They showed that the rates of Alzheimer's were 10 times higher if you had spirochetes in your brain. So excuse me, I mean, somebody's got to look at this and it's probably going to be the ILADS docs and the functional medicine docs like you and I who are going to be figuring this piece out.

Well, it's interesting because that P-tau, from my memory, the P-tau 217 beta amyloid through Quest Labs, which is a lab I have in my office, I think that became available like the beginning of last year. So it's a relatively new And it became available after the beta amyloid drugs were more popular. So it's, and they're recommending, it's almost like the drug popped out. How do we justify the drug? Well, if you do this test and it's elevated, now these people go down the drug pathway. I've been using it, to be honest with you, screen patients for risk because it correlates really strongly with cerebral spinal fluid levels. But I didn't think about it being a marker for potential Lyme. See, what you're saying is this might be a marker for I don't want to say CNS Lyme, neural Lyme, but in the nervous system causing oxidative stress, which then increases beta amyloid.

Correct. That's exactly it. So, you know, they've shown in the past, as I've said, autopsy studies showed a clear relationship of spirochetes, syphilis, right? Denticola spirochetes from the mouth. They've shown it, but it had never been proven in a live human. And I did it again with another patient where I reversed his beta amyloid ratio and Similar case, had not taken antibiotics for 10, 15 years with chronic Lyme. All he did was the 9-week Dapsone protocol and his beta amyloid ratio reversed.

Yeah.

So I do believe we're right now, there is no good treatments for Alzheimer's. There just are not. This, so this study that I published, and by the way, in my new book, Ending Chronic Illness, under the ABCs of Chronic Disease Medicine, which is one of the half parts of the book. I start with A. A is for autism, ADHD, Alzheimer's, right? And I explain exactly how the 16 factors apply to Alzheimer's as well as autism. And interestingly enough, there's a biochemical pathway which you and I know called mTOR, mechanistic target of rapamycin. It applies to both autism and Alzheimer's. And I learned this by going into the literature. I'm speaking at MAPS this year in Philadelphia for the young kids. Neurofilament light, Everybody's worried about vaccines and autism. It turns out that if you measure neurofilament light in a young child, what they showed is for every picogram increase in neurofilament light, there's a 19% higher chance of getting autism. None of the pediatricians are checking this marker. I mean, or maybe there's a few, but it's not. In other words, everyone's worried about autism where the rates went from 1 in 2,500 in the 1950s to 1 to 36. When I did the MSIDS review, all 16 factors, infections, toxins, microbiome issues, leaky gut, mast cell activation, vitamin mineral deficiencies, sleep disorders, mitochondrial dysfunction, autoimmune disorders, right? All of this applied to autism. But here, if I was a parent and said, gee, what do I do now with vaccines? I would want to see whether my child has markers of inflammation. So what I did in Ending Chronic Illness is I list out a whole chapter of how do you measure inflammation? Not just CRP, not just sed rate, but, you know, VGF, a marker for whether you might have spike proteins from long COVID or Bartonella. So I explain how to measure inflammation and how if you have a young child, you can actually do these markers and figure out before they get vaccines, what is the risk? And you'll never see anyone talk about this in the social media, which is why I'm talking to you about it because, right, they just passed the law to go from 18 vaccines to 11. Why? Because they're trying to make an association with vaccines and autism. But the problem from my perspective, it's not the vaccines. It's you have a child that's loaded with toxins, loaded with infections like Bartonella. The microbiome's been thrown off from all of the toxins we have. They're loaded with inflammation. The mother may have had an infection during pregnancy, which raises risk by 40%. And now you give 'em a vaccine with aluminum, which in some cases causes autoimmune issues. But that's not the primary cause why they ended up with the autism. The problem is all of these MSIDS factors that were not identified early on. So again, I'm hoping when Ending Chronic Illness comes out, it's going to make it into the autistic population as a way of screening, looking at P-tau, right? You and I didn't learn in pediatrics that tau and neurofilament lights show up in these young kids. I didn't know that until I did a dive in the medical literature. So.

Yeah.

The model is going to apply to a broad range of chronic illnesses right now in America. 60% of Americans have one chronic illness. 25% have 2 or more. 86% of our healthcare costs are with chronic illness. 70% of the deaths are due to chronic illness. 18% of our GDP going up to 20% is chronic illness. And yet there's no model to effectively deal with chronic illness. And that's where I think my new book, Ending Chronic Illness, Is going to play a role as the paradigm shift. Like, it doesn't matter what you're naming the disease. You've got to get to these 16 root causes of where the inflammation's coming from, whether you're talking about autism, whether you're talking about Alzheimer's, whether you're talking about chronic Lyme disease, right? So it's kind of a new way of thinking about it. And I'm hoping, again, if I can get the funding for it, and I spoke to Mark Hyman about this recently, he said, because he knows Bobby Kennedy well, there's like $100 million waiting for this. Like maybe we should be doing a study on Alzheimer's and autism and chronic Lyme and chronic fatigue and fibro and long COVID and take these chronic fatiguing musculoskeletal neuropsychiatric illnesses, right? With very similar symptoms, do the 16-point MSIDS review for all of them, and then treat and see what you've got. And I guarantee you we're going to improve our healthcare in this country. I mean, and that's what I'm hoping my next stage of medicine, right? I turned 70 years old this year. It's like, Where did the 42 years of medicine go? Like, it's like, this is what I'm hoping to benefit the world and benefit the US is kind of now going into that research spaces, you know, as well as teaching and kind of moving out in that way.

You know, um, there, I know there's going to be people listening to this right now that are just heard what you said and be like, I'm not 100% convinced of that. And I would have probably said that maybe a couple of months ago, but I'm currently in the process of reviewing all the, reviewing all the lectures from this last year's A4M conference. And there's one lecture where I had a conversation, it was about beta amyloid and Alzheimer's, but the beta amyloid being the byproduct, it's basically a marker of oxidative stress. And so if you have that, it's a marker for a low intracerebral glutathione. So the point was we can actually use a form of, you know, that's a glutamyl cysteine that goes through the blood-brain barrier. But what I'm hearing, but I'm hearing now, wait a second, if someone, if I'm thinking that I need to do a beta amyloid 4240, If those are elevated, they probably have low glutathione. But the issue is, do they have a brain infection that I need to start treating? Not just give them this glutathione precursor.

That's it. And also keep in mind with beta amyloid, and you just brought it up, apart from oxidative stress, it's an antimicrobial peptide. They've known all along beta amyloid just doesn't show up in your brain for no good reason. It shows up when you have infections. Your brain is actually trying to protect your neurons from the infection and beta amyloid gets formed and it starts depositing the sticky form, the beta amyloid 42, right? So again, this has all been autopsy. This study I just published this year is the first one. Again, we do, do we need randomized multicenter controlled trials to prove this? Absolutely. But I will tell you, knowing the literature as deeply as I did with this deep dive, I'm pretty sure that probably 30 or 40% of everyone out there who's being diagnosed with Alzheimer's dementia It's going to be what I'll call Lyme MCIDs, or it will be Bartonella MCIDs. They don't have Lyme, but they may have Bartonella, right? Driving it with mold toxins and heavy metals. It's going to basically be multifactorial, right? Sources of inflammation driving the neuroinflammation in the brain. And I think that's the model we've got to be looking at because just naming the disease and throwing drugs at it is rising our healthcare costs and people are getting sicker and sicker without answers.

Yeah. I'm wondering if, you know, with Part of the beta amyloid medications, one of the major side effects, I think something like 30% of people who get the drug will get either amyloid hemocytosis or edema. If what you're saying is true, then maybe as you remove the antimicrobial peptide, you're removing the protection. And then all of a sudden now these people from these infections, they're more prone to more inflammation. And we've recognized the side effect of these drugs and yet we push them because in our conventional thinking, that's all we have. What are your thoughts about that? Me trying to connect those dots, does that seem like a plausible—

Yeah. So I think there still may be a role for some of these drugs like donanemab and mecanemab, and I'll tell you why. So in this patient that I, the second patient I did not yet write up who I reversed the beta amyloid ratio, he was loaded with mold toxins. I'm talking off the wall. And I was worried the Dapsone protocol does not work as well when mold is there because mold will affect your immune system just the way Lyme and Bartonella knock out your B cells. You get chronic variable immune deficiency. You get subclass deficiencies. People with long COVID, it knocks out their T cells, right? Natural killer cells are, they, they're exhausted. So these people have a lot of immune deficiencies. So I was, you know, concerned a little bit in this population, but I will tell you now that I've started to use Dapsone and I have, you know, a 10-year history of doing this, and I've looked at the literature, you, and this is a really interesting study. They, they looked at Alzheimer's disease in South Korea in people with leprosy who took Dapsone. And they found that the people who took Dapsone for leprosy, the Alzheimer's rates were 6 times less. When you look at the study by Dr. Lee, it was published maybe 4 or 5 years ago. This is in 4,000 people over like a 15-year period. Alzheimer's rates were 6 times higher if they did not take Dapsone because Dapsone is a neuroinflammasome inhibitor. It inhibits this basic pathway called NLRP3 inflammasomes. And we don't know whether these people in Korea ended up having Borrelia burgdorferi or not. You know, also it could have been chlamydia pneumoniae. There are other intracellular infections associated with Alzheimer's dementia. So, you know, I'm hoping in the cases where it is infections, right, this has been a hypothesis in Alzheimer's for decades, the infection amyloid P-tau hypothesis, but it's been just that. The hypothesis had never been proven in a live person until the article I published this year showing there is a direct relationship with chronic Lyme. So I, I think it's going to open up a whole host of possibilities, but let's say mold. Or heavy metals or other things cause P-tau. Well, it's possible after you treat the Lyme and the Bartonella and use these drugs like lecanemab, donanemab, it's possible you will see actually great effects by pulling out the amyloid because you've stopped the infection that was driving the amyloid production. So I think there may be a role for these drugs ultimately, but first you have to figure out, is there an active infection that's driving beta amyloid and P-tau? Right? Is mold present, right? Do we have microbiome issues with the gut-brain axis? You've still got to go through the MCIDS model to figure out where the inflammation or the downstream effects of inflammation's coming from. But I suspect if I was to do a randomized trial and use those drugs, there might actually be some usefulness for them once the infections were treated, right? They may, they might just work a lot better than they're working right now.

So let me, the NLRP3, the inflammasone, that's really interesting because we When COVID started, I remember one of the first things the Institute for Functional Medicine started talking about is the association with NLRP3 and acute COVID, et cetera, et cetera. So, and you've mentioned briefly before with Lyme, maybe some people with long COVID, it's a Lyme infection. So let's take a veer off the road here a bit. What other illnesses or diseases besides chronic fatigue fibro, besides, you know, brain fog, Alzheimer's, should people think Lyme, you know, tick-borne illness if they're seeing a patient with these symptoms? Well, a patient with these diagnoses, what other entities should people be thinking? I wonder if underlying this illness there is a tick-borne illness.

Right. So, so the illnesses normally that were, I would call Lyme the great imitator. And these are the ones that you and I have seen coming into our practice all the time. Anyone who's been diagnosed with chronic fatigue syndrome, ME, or fibromyalgia is at the top of the list because even if they initially had herpesvirus 6 or Epstein-Barr, As the initial trigger causing it along the way. That doesn't mean you still can't get bitten by a tick or get mold toxins. What we found is, yes, we did find active viral infections in some of these people. And the last chapter in Ending Chronic Illness is V is for Viruses, where I go through long COVID and how all 16 MCAS factors are associated. So chronic fatigue fibro is number one. Number 2, and I think people really need to understand this at this point, is dementia.

Dementia.

Anyone at this point whose memory concentration is off, spirochetes have been talked about like syphilis as a relationship with dementia for a century. This is not new material. It's only because of the medical, dysfunctional medical politics surrounding Lyme disease. Otherwise, I believe the Alzheimer's-Lyme connection would've been made truthfully a long time ago. Then you've got also the autistic population. Autism rates have gone, as we talked about, from 1 in 2,500 to 1 to 36. Now, when speaking to people out there, including mothers with autistic children, it's not just Lyme, but it's Bartonella. Bartonella bacteria, another intracellular persister biofilm bacteria, is showing up in a lot of these kids. Apart from the mold toxins and the heavy metals and the microbiome issues with propionic acid and mitochondrial dysfunction, it's the same 16 factors. And I found the same 16 factors in ADHD, like I can't concentrate. I have memory issues, which is why I'm on Adderall and Concerta and all of these drugs. Lyme causes memory concentration problems, as does Bartonella. So in the book, what I go through is whether you're calling it autism, ADHD, Alzheimer's, cancer, cardiovascular disease, chronic fatigue, fibro, digestive disorders, mood disorders, obsessive-compulsive, bipolar, schizophrenia, anxiety, depression, chronic viral infections, Borrelia burgdorferi, Bartonella, and these 16 MCID factors. They're underlying these chronic fatiguing musculoskeletal and cardiopulmonary diseases. So I think we need to understand we're in a full-blown Lyme epidemic, just like we're in a full-blown environmental toxin epidemic where 90% of my chronically ill patients now come in with mold toxins and evidence of heavy metals apart from glyphosate and all the other hundreds to thousands of chemicals, PFAS and everything else getting in, causing fatty liver. Right? 1/3 of the world's population has non-alcoholic steatohepatitis, fatty liver. 1/3 of the world's population due to PFAS, due to, you know, all of these environmental toxins, it causes metabolic syndrome with insulin resistance and they die with cirrhosis and liver cancer. Yet it's a silent epidemic. Then you don't hear about it. It's those type of diseases I talk about in Ending Chronic Illness. So, you know, my take at this point. You're a patient searching for answers. You use the MSIDS model if you're chronically ill. If you're a doctor, and like you and I have done for chronic disease patients, use the MSIDS. But what about a mother whose child has autism or not yet sick? Use the model to see if your child has inflammation. And if you're someone like me who's 70 years old, who, you know, God willing, I'm still in good health. What if I want to live till 108 years old? I need to know where inflammation's coming from, because as we know, there's inflammaging, Aging, inflammaging is coming from inflammation. Inflammation is underlying all— what are they seeing now with these GLP-1 agonists? 33% less heart attacks, less dementia. Why is it working? Because it's lowering inflammation. Great. But where is the inflammation coming from? And that I think is the key piece that I'm bringing out in my new book, Ending Chronic Illness, is we have to get back to basics and stop naming the disease and throwing drugs and figuring out where it's coming from. It's logical. We've been doing it as functional medicine docs, but it's not been integrated fully like in medical schools and the rest.

I want to talk about Dapsone briefly because we had a conversation maybe a year ago and I started dabbling in Dapsone a little bit. And it's a little scary. I mean, I know you told, you told me your exact words about using Dapsone to me were, I need to get some kahunas. But you said, you know, not quite that same, but, but, you know, Dapsone, walk me through using it. Because I think a lot of people on my end still, you know, hemolytic anemia and all this kind of stuff. Like, Help us understand, one, how do you start it? What do you look for? How do you prevent side effects? And what if someone has a horrible, like one of my patients actually got a horrible hemolytic anemia from it. Um, like what does, what, what could that mean? Does she have under, does she have underlying Bartonella, you know, or something like that that might be going on? Help, help walk us through Dapsone.

So, so right now for chronic Lyme disease treatments, there's only 2 persister drug regimens that have ever been published in the medical literature. Which is disulfiram, the drug that's been out there for alcoholics to stop them from drinking, as well as dapsone. So the thing about dapsone, what I think people need to realize when you look at the biochemistry of the actual drug, it is cytoprotective. I can show you the literature that shows you dapsone protects the heart. Dapsone protects the lungs. You probably don't know this study, but during the COVID pandemic in 2020, when people were dying of ARDS, acute respiratory distress syndrome, The only study that showed that people did not die of ARDS, you know, the drug they took, dapsone, 100 milligrams per day, because it stopped the NLRP3 inflammasomes and the inflammation in the lung. Dapsone protects the brain, it protects the kidneys. So first thing that people need to understand, the drug has side effects, but if you are G6PD positive, which 99.9% of people are, some people of Italian Mediterranean origin, are GCPD negative, you are going to get hemolytic anemia if you take Dapsone under those circumstances. I've only seen 3 people in 42 years who could not take Dapsone. But here's the thing about the hemolysis. For most people, it's very mild. So if you start with a hemoglobin, let's say a 15, you're going to be at a hemoglobin of 11 when you're finishing the protocol. But the way I designed the protocol is you're on 320 milligrams of folic acid. The way you reverse the side effects of anemia Is massive doses of folic acid. The way they do it, if you're a rheumatoid arthritis patient and you took too much methotrexate, they give you massive doses of folinic acid, leucovorin. So the way I designed the protocol is I found that if I give people 200 milligrams of leucovorin, if I give them 120 milligrams of L-methylfolate, 320 milligrams, I can limit the anemia in most people to 3.5 to 4 grams. And if you stay on the high-dose folic acid when you're done with dapson, Your levels will be completely back to normal within 6 to 8 weeks off the protocol. It always comes back. You do not need to do transfusions. Let's say you're a woman who's got heavy periods. You may need to stop and start the protocol if you're getting iron deficient in the middle of it, but there's always a mild hemolysis on Dapsone, but it doesn't affect the long-term results. In other words, if you have lung cancer and I say to you, I've got a chemotherapeutic regimen with radiation therapy. But I put you on cisplatin and you go through it, but you're going to have long-term chemo brain fog and neuropathy. But I'm going to put you in remission and cure your lung cancer. You go, you know something? I'll deal with the chemo brain fog and I'll deal with the neuropathy. Dapsone has no long-term side effects. None. Zero. As long as you follow the protocol and take the four probiotics that I'm advising twice a day, which is like a trillion of these high-quality probiotics, right? We haven't seen a case of C. diff. Right, in ages on this protocol. But the other side effect is methemoglobin levels go up, meaning you don't carry oxygen well in the blood. How do I reverse it? Well, methylene blue, which they're now using, by the way, for Alzheimer's at around 120 milligrams a day, because they know mitochondrial dysfunction is one of the things that relates to Alzheimer's. Methylene blue reverses the side effects of Dapsone. So does glutathione, which you mentioned. So what the way I designed the protocol, Is I use antioxidants with vitamin E, 300 to 400 I use twice a day, 2,000 of glutathione up to 3 times per day with N-acetylcysteine, which regenerates glutathione. We use Inada NADH because the enzyme that reverses methemoglobin is NADH reductase. So I decide it took me years, by the way, to figure this out, Aaron. But we've got it to the point that the average methemoglobin level is about 5 to 6%. In 2/3 of the people who go through the whole protocol. Now, you may have blue hands and blue lips. You may be slightly short of breath, but there's no danger. Dangerous methemoglobin is 45, 50, 60%. We've never seen anyone go above 23%, and that was with a 13-year-old who didn't take his methylene blue and didn't take— tell his mother. So I designed the protocol. It took me 10 years to figure out how to reverse the side effects. So let's look at the pros and cons. It's a 9-week protocol that can put people in remission for years. 50% of the people who take Dapsone, 9 weeks, who don't have active Bartonella, who don't have mold, will go into long-term remission with a 9— and that people are sick, by the way, for 10, 20, 30 years. I mean, that's amazing. So you're correct that there are side effects, but having done this in thousands of people for a decade, it is way overblown. You have to consider that untreated or improperly treated Lyme. Without using these biofilm persister forms, how many patients do you know go for hip replacements, shoulder replacements, and knee replacements when they have chronic Lyme and Bart? Why? Because it eats away at your bone and they go bone on bone. Or how many people end up with dementia diagnoses with Alzheimer's, but it was the Lyme and the Bart and the mold, right? So you've got to understand, yes, the protocol has side effects, but it took me a decade to be able to kind of figure out how to get around it. And I would only do a protocol. That I myself would take, I would never give to a patient something that I myself. So if I had chronic Lyme, I wouldn't even hesitate. But what I did in Ending Chronic Illness, and this I think answers your question, for the people that are sensitive to Dapsone, I added something under the Bs. The chapter B is for Borrelia, Babesia, Bartonella. I added a section of how to do low-dose Dapsone, how to take 25 milligrams or 50 and start and stop. So you're not getting through the protocol in 9 weeks. It might take you 6 months or 9 months, but you'll still get through the protocol because every time you stop it, even though, and the labs will always come back to normal, you're lowering the biofilm persister forms of the bacteria. So let's say you lowered 'em by 30% the first time you took Dapsone and you stop it. They're not gonna grow back. How do I know that? I've seen it. I've seen it where people stay at a certain level of health. You go back in 2 months later. Let's say you do 3 weeks of Dapsone. And, and by the way, I've had people only pulse Dapsone for 2 weeks with 6 days. They never do the 9-week protocol. They still get benefit because the way you get rid of biofilm persisting bacteria like Lyme and Bartonella is you have to pulse these regimens. You cannot give continuous antibiotics to people. It'll lower the load, but it won't get rid of it. And I think that's what Lyme docs out there really kind of need to realize now. I could have proven this to the world if they would've approved my R34 NIH grant, but they're putting me through the hoops and making me do it again. But if you ever have questions, Aaron, I will give you my private telephone. I'll give you whatever you need. I will work with you to put 10, 20, 30 patients, whatever you need. I will work with you and I'll show you the results myself. There's no reason to be scared of this regimen. Your patients will get their lives back. But I understand the concern from doctors, by the way. It gets scary looking at the anemia and methemoglobin. It's, this is all temporary stuff. And if you look at the risk benefit, everything we do in medicine is risk benefit. The benefit, it's 1,000 times more than the risk. The only risk, honestly, that you have is if a woman has a heavy period and you don't stop the Dapsone while she's, you know, bleeding out from a heavy period, or you gave Dapsone to someone who was G6PD negative and they got more hemolysis. But even then, if you keep them on high-dose folic acid, the drug is outta your body within 3 to 4 days. Right? So they're going to reverse the side effects. I have, I've had women with 6.5 hemoglobins because they came in with low MCVs because they had genetic predispositions towards it. And every day giving them high-dose folic acid, 6.5 went to 8 within 3 days. 8 went to 9.3 within another 3 days. In other words, you just keep them on the high-dose folic acid and the anemia resolves very quickly. What it comes down to, I think, is all of us who are well-meaning docs who want to get our chronically ill, you just kind of have to understand that if you look at the actual science of Dapsone, that it is cytoprotective, not hurting the body. And I can send you the articles on this. You'll be actually surprised that this drug is way more protective than most people thought about. And I think eventually it's going to be repurposed even for Alzheimer's dementia, independently of whether people have Lyme or Bartonella driving it or not, simply because it lowers inflammation in the brain. And the only reason you haven't heard of it, because nobody makes money off of it, right? It's a generic drug that's been out for 50, 60 years. So nobody's making money on it. So they're not doing studies on it, but you and I who are in the trenches looking to get our patients better, we need to be considering these types of therapies.

Yeah. So one, I'll make sure I respect your time. One last question for you here. Testing. This is where I think people are like, what's the right test? Is it, you know, is it LabCorp? Is it Quest? Is it, you Immunoblot from genetics? Is it a FISH test for Bartonella? You know, is it a PCR? Like if someone's starting out and they're like, hey, I want to do a testing on a patient, you know, what's the first, the testing initially for diagnosing Babesia bartonella and Borrelia? And then what's the follow-up testing?

You won't be able to see this well, but I've got probably 25 pages in the beginning of this book that if you have, let's say fatigue, and I put one of the differentials is Lyme. It will have underneath there all of the testing, ELISA, C6 ELISA, checking for the 3 strains, IgM, IgG immunoblot, send it to Igenex, TLAB. The book Ending Chronic Illness lays out exactly the protocols of how to do the testing, how to interpret the testing, and then how to bring it to your doctor and work with them and to get you better. So, you know, the answer is, is Medicare covers the Igenex testing, which covers 9 strains. It's completely covered. It might be a copay, but even if the only thing you did was to use an IgM-IgG immunoblot from IGEnX, because let's say your local labs were negative, you did an IFA, an immunofluorescent antibody, you've done a Western blot, you've done an ELISA, you've done a C6, you're not getting back positives. If you spent $200 to $300 for IGEnX, you'll see one of those Lyme bands that we talked about earlier when we played Lyme bingo. You'll see one of those bands show up. And by the way, Maybe one out of a hundred times it won't, and it might be tick-borne relapsing fever. It might be the cousin of Lyme disease, right? Other Borrelia miyamotoi and other ones could also look like Lyme, and it's not going to show up on classic testing. And I go through that in Ending Chronic Illness to explain also the differential diagnosis of how you also do the testing. So, you know, if the people take the questionnaire on my website on cangetbetter.com and see that they have migratory pain and score high. Odds are Lyme is going to be there. We're in the middle of an epidemic. You just can look at the book, work with your doctor with it, and it'll tell you exactly the protocols of how you order the tests and how you interpret them.

So when does the book come out and how can people learn more about you?

The book is going to be out October 13th. It's actually coming out very shortly.

October 13th.

And, and you know, what's, what's great for me is after being in medicine for 42 years, this is my gift to the world. This is my gift to the chronic disease population of all these people who came in who said, Thank you, Doc, for getting me better. It's like I'm passing on, which is what we're all supposed to do. I'm passing on to the next generation of doctors and patients what I learn so everyone can benefit from it. So you can learn more about the book and about me on my website, cangetbetter.com. I have a Medical Detective Substack that is free, no charge. Some people pay me $7 a month, but it's completely free. So it's Medical Detective. I have Facebook. I'm putting things on Facebook intermittently. It's Dr. Richard Horowitz. And Instagram is @DrRichardHorowitz. So those are probably the best social media sites, but Ending Chronic Illness from Simon Schuster, it'll be out within the next 7 or 8 weeks. I'm really excited because it's like a compilation of my work's worth and taking my life's work and moving it into this broad range of chronic illness that I'm really hoping will shift the paradigm for all these chronically ill people. Not just in America, but, you know, across the world who are looking for answers and have not been able to get them.

I'm definitely going to get a copy of your book when it comes out. And if you're up for it and willing, I'd love to talk to you afterwards after I read the book, because I have a feeling that it's going to have a lot of really cool insights in it that will tweak little ideas in my head. Because when you read books from people who spent their whole entire life doing something, there are always hidden gems that you don't have time to talk about that trigger ideas of other things you've read. So that's one of the things I like Finding the people who are experts in the fields and kind of drilling into it. 'Cause you also find gems you wouldn't find any anywhere else.

I'm happy to work with you. And again, if you'd like to do some patients together with Dapsone, holding hands, making sure they get through it, sending me, I am happy to do whatever. At this point in my life, I'm here to kind of, you know, teach and hold hands and educate and help whatever way I can. You know, my wife and I discussed that I need a life together with her after 30 years in the trenches. You know, we've been married for 30 years. She said, sweetheart, When can we have a— like I said, sweetheart, now that I got Ending Chronic Illness out there and I kind of passed on all this information, I'll be doing hopefully randomized trials, helping doctors like you and everyone else. But yes, I'm happy to help. And look, friendships also, like we get deep friendships over the years working together this way. And what's more satisfying than that when you're working together in healthcare, right? Helping others. I mean, it's, there's nothing more satisfying.

Awesome. I really appreciate your time again for showing up on the podcast, sharing your wisdom. And for everybody out there, we will get the— if you could share with me the links and stuff, I would love to share this book because we have— we're in Central Virginia where I was told there's no chronic Lyme disease and it's kind of everywhere. Oh, I know. Yeah, it's crazy. Like what I've been told by my infectious disease colleagues, but really appreciate your time. And thanks a lot.

My pleasure. Good speaking to you.