 All right, welcome everybody. I am live here with Dr. Richard Horowitz. And I am just, as I told him before we started, I am honored to have him and have his time today. He's got so much on his plate, like all of us do nowadays. And yet he is one of the docs that I have some of the greatest respect for in this field, making a difference and not only making the difference in his clinical practice and protocols, which are really revolutionary, but he's publishing on this. And this is what helps us as physicians get the change in the world that we need to prove that some of the new protocols that we're putting into place are actually effective. So I have not only the greatest respect for him as a clinician, but as a scientist. And one thing I love about you, Dr. Horowitz, and I'll read your formal bio in a minute, but I love your heart to serve. You've always struck me, I know you bring this, you know, your practice and teaching into your practice. And I love, I wanna talk to you a little bit about that and about the importance of mindfulness meditation because so many of our patients are at the edge and their limbic system is completely out of sorts. And I think it's really important for you and I to bring that to our practice and to our patients because some of them reach the limit of what medication can do. And if we don't address that piece of the mind body, it's not doing them service. So thank you for always bringing that to the clinicians that you teach and to your patients as well. You just are a great example of someone who really does things in a very holistic way and yet it has such great science behind him. So thank you. Thank you, Jill. Yeah. And we'll talk about it at the end for any physicians who are listening. He, Dr. Horowitz does a course. It'll be virtual next year. Dates will be announced and I'll let him tell us about that. But he does a great training that I did last year. I highly recommend it on the science and the state of the art of treatment of Lyme disease and co-infections. So we'll be sure and talk about that. I'm gonna introduce you real quick and then we'll dive right in. Dr. Richard Horowitz, if you don't know him is a board certified internist in private practice in Hyde Park, New York. He's medical director at the Hudson Valley Healing Arts Center. That's where we did our course and now of course it'll be virtual. An integrative center which combines both classical and complementary approaches in the treatment of Lyme disease and other tick-borne disorders. He's treated over 12,000 chronic Lyme disease patients in the last 26 years and I'm sure that's just rising every month, every year with patients from all over the US, Canada and Europe to his clinic. He's former assistant medical director at Vassar Brothers Hospital and can't pronounce it in New York. Poughkeepsie. Thank you, Poughkeepsie. I know I was there and I remember. Thank you. And one of the founding members of the past president of ILADS which is another great physician organization that teaches us how to treat Lyme disease and kind of on the cutting edge of that. He is a prolific author and if you haven't read his latest book How Can I Get Better? Excellent resource for if you're a patient. It really, really boils down some of the things about Lyme disease that you need to understand. If you're a practitioner, it's excellent too because he really references well his protocols and what he's recommending. I don't know of anyone, Dr. Horowitz who's made such a difference in the field of chronic infection and tick-borne illness. So number one, just thank you. I honor you for being here and also just for your contribution. Thank you again, Joe. You're welcome. So let's dive in. So I wanna hear first, I always find that our stories is what brings us to what we do in the passion and I wanna know if you have any story around how did you get to be where you're at now and what brought you into this as far as the passion or the drive to really treat these most complex patients? Yeah, so the story is quite interesting because I had done my medical training at the Free University of Brussels in Belgium and it was interesting. I was on wait list in US schools and my stepfather was a surgeon had studied in Europe. He told me it was great. The Free University of Brussels accepted me and I had had a lot of French courses. I took a training in Lausanne for three months before starting and it was a seven year medical program. And so I was pulled to Europe. It was just a wonderful experience and in my fourth year of medical school, I had done transcendental meditation the first couple of years because as you know with medical school it's a bit stressful. So I was meditating a couple of hours a day and it was really helpful. But around my fourth year the Tibetan Lamas had lived, believe it or not, about three blocks from where I was living in Brussels. I didn't realize this, my friend Bill told me. And I went over there to start getting teachings and that's where I met some of the teachers who instructed me on meditation and the type of practices that I'm doing now. And you know, the motivation that I have and that drive that you're talking about really it's thanks to them because when I spoke to Lamagen and Rupeshe and I asked them when I was leaving medical school, you know, what do you want me to know? What's the most important thing that I should know going out into the world? He said, Richard, the most important thing is compassion. Just put yourself in people's shoes and do for them what you would want done for yourself. Right, it's really quite simple. And you know, it's always about service, right? From that perspective and as physicians, of course, that's what we do. But when I finished my Mount Sinai training in New York City I had a choice of where to practice and one of these llamas, Colorinpeche, was teaching in Wappinger Falls which is about an hour and a half from the city from where I was doing my residency in internal medicine. And I went there and I asked, you know, what do you think about coming up? I could get meditation teachings. I'd be close to my parents in Queens. And he did what's called a mower divination and he said, oh, coming up here very good. So, you know, it's like one decision because my mother wanted to open me up an office in Bayside Queens, right? And of course, what happened is I was pulled to Hyde Park, New York, which is right of a Poughkeepsie. And at the time in 1987, I was moving into the largest Lyman-Demek area in the United States and I didn't know it. Wow. So, you know, the training that I had in Brussels was great because as an internist, it was a seven year program and I really taught, was taught how to be a medical detective. I like always joking about MD being medical detective about doing differential diagnosis. So, you know, when these patients came in with erythema migrans rashes and 75, 80% got better with antibiotics. But then of course, they're the 20 to 25% that didn't. That's when I went on the journey to start, you know, looking for answers. I went to conferences like the LDF. I met Joe Boroscano and Ken Liegner and Sam Donta and of course all the great grandfathers of Lyme who preceded me. And, you know, it just kind of started from there. Wow. And we all stand on the shoulders of someone else. I feel the same and again, I owe a lot to you, but it's so interesting because we keep perpetuating and hopefully this generation, even today, part of my goal is to teach physicians little pearls or things. And as it sounds like for you, I always say with mold and Lyme, I didn't choose them. I probably would have never chosen to treat the most complex chronic illness in the US and in the nation, in the world, but it chose me. And it sounds like in that way, it kind of acts not really accidentally, but in a way you were drawn to this area, you had to treat the people that were sick there and that's how, so thank you for that. And also thank you for the compassion that you bring. So one thing I want to talk about is there is, first of all, there's still people out there that think that this doesn't exist. And you and I in the trenches, we see this every day. It's very clear. It's clinically diagnosed with excellent test. But one question would be, why do you think the prevalence is increasing? Talk a little bit about why we're seeing more and more cases of this from your perspective. So, you know, the numbers of cases, of course, it's an estimate, right? So when the CDC years ago used to say there'd be 30,000 or 35,000 cases and multiplied by 10, 350,000, there was an article, by the way, that was just published this morning by Basant Puri and Michael Cook on the prevalence in the US and Europe. And the numbers they came up with was closer to about 450,000 cases a year in the US. And that fits with some of the studies that I've seen from the CDC. But anywhere from, you know, 45,000 to one year, a couple of years ago, almost 600,000 cases. So, you know, it varies, but that's Lyme, right? That's not talking about Ehrlichia, Anaplasma, Babesia, Bartonella, Rocky Mountain Spotted Fever, Cue Fever, Tularemia, right? We're not counting those. So then, of course, I count, for example, those with chronic fatigue fibromyalgia, which is a clinical diagnosis that has exactly the same symptoms as Lyme. That's 5% of the US population. So that's about 17 million Americans that have a chronic fatiguing, muscular-scale, you know, cognitive deficits, which includes, by the way, POTS disorder, NAMI, as you know, it's part of that protocol, and there's no test. So, of course, the question I have for people is if we have 17 million with chronic fatigue or fibromyalgia, and then over 20 million with a autoimmune disorder in the United States, 46.5 million with preclinical dementia, and Lyme has been linked. In fact, so interesting nature, just a couple of days ago, re-broth this up in an article I posted on my Facebook page, that chlamydia pneumonia, Borrelia burgdorferi and porphyrmonus gingivalis from the gums, are the three bacteria that are now showing up in Alzheimer's with the herpes viruses, and JAMA published years ago on pesticide. So, you know, how many people really have this? My best guess is it's probably a lot more than what we think, because how many people are getting tick bites? They don't see the ticks, right? The testing is unreliable. It's about a 50-50 shot with the ELISA and Western blot. So, you know, regarding that, for people who are not sure, who are listening, you know, who say, hey, I have chronic fatigue and I have good and bad days and the symptoms come and go and I have migratory joint pain, migratory muscle pain, or migratory nerve pain, tingling, numbness, burning, stabbing. That migratory pain is really the hallmark of Lyme. There's only seven diseases in medicine that cause it and most people that walk into your office or mine are not gonna have acute rheumatic fever or hepatitis or ulcerative colitis or gonococcal arthritis or writers, right? All these other differentials. So, when you've got those symptoms of migratory pain, fatigue, headaches, I can't fall asleep. I keep waking up in the middle of the night, memory concentration problems, walking into rooms, forgetting, that's really specific, right? It's the hallmark of the symptoms. And I did publish a study years ago, you know about this. It's published in the International Journal of General Medicine. We did this with Dr. Phyllis Freeman from New Paltz and Mary Alice Seterra. We looked at 1,600 people, both healthy and with Lyme and we developed a screening questionnaire which was based on Dr. Borsgano's questionnaire years ago. And for those who aren't sure if they have it, you should go online and take the questionnaire. A score more than 63 is two standard deviations above the mean. It gives you a very high likelihood you have it. And then you just send off an immunoblot to hygienics, right? Like an IgM IgG, because the immunoblot, which is their newest test in the last few years, doesn't check one strain, like questrolabcor. It doesn't check two strains like their prior Western blot, which was the B31 and the 297. Now it's checking eight strains, including abzellae and gurini and some of the European strains. It's just not checking me a motoy. You have to do a separate relapsing fever panel. But if you do that and you see a 23, OSP-C, 31, OSP-A, 34, OSP-B, 39, 83, 93. If you've got migratory pain and even one of those bands on an immunoblot, you're honing in on the diagnosis, right? So I mean, it's complicated in some ways and in other ways you could kind of simplify it, right? In my world and in yours. Yeah, so for you as a patient, if you're listening, you're like, what did we just talk about? Really simply, if you go to lab core question, you get a Western blot, which is the classic test that's easily available. And even then they usually allow for a lysis screening, which is very low sensitivity and specificity. And then they'll only go to the Western blot if that's positive. But if you get a Western blot, what would you say that's one strain? I would say it's one strain of, I would believe like Connecticut, Eastern type of Lyme viralia. And it's very, very gonna yield a low sensitivity. What you're talking about is hygienics, immunoblot, which is a much higher yield. So if you're a patient and you've said, oh, well, I was tested for Lyme and I don't have it. If you were tested by one of those conventional labs, the likelihood, is there a percentage you would guess on how the sensitivity of that one strain versus the immunoblot? You know, it would be a rough guess, but I would guess because I usually can pick up at least one of the really specific bands on an immunoblot, both, and the IgM by the way, people should know, IgM Western blots are immunoblots. Most people think are just with early Lyme. We published a study, and as did John Hopkins University with John Alcott, that a CDC positive IgM immunoblot or Western blot is seen in chronic Lyme. So, you know, if you get one of those and you take it to your doctor and they say it's a false positive because you can't possibly have an IgM in chronic disease, the answer is no, you can. And I'm not the only one who's published it. So I would suspect probably the Quest Lab Court testing maybe picks up 20 or 25% maximum. I get very high yields from my genetics, especially when you're looking at it as a clinical history. Yes, I agree. So we're looking at multiple strains, which means you're covering more of the US. And then the other thing you mentioned, I definitely want to talk about today, we could talk about it now, tick-borne relapsing fever. I am seeing massive, now that I'm testing for it, a lot of cases, and I actually feel like my most difficult clinical cases are showing up with tick-borne relapsing fever. Tell us a little bit about what is this? Why is it harder to detect? Why is there usually not a rash? And are you finding more cases of tick-borne relapsing fever? You know, we definitely are. So tick-borne relapsing fever is like a cousin of Borrelia burgdorferi, the organism that causes Lyme. And there's two types. There's soft tick relapsing fever, right? So that's Borrelia hermsi and some of the ones in the Midwest that you'd have outbreaks in Arizona that's been happening for years. But then the newer one is Borrelia miomotoi and that's hard tick relapsing fever. So they call it Borrelia miomotoi disease. Now the problem with that is you could have a Lyme-like illness and have fatigue and headaches and joint and muscle pain and cognitive issues, test negative on all the standard Lyme testing, but the reason is you don't have Lyme disease, you have a relapsing fever strain like miomotoi. So it's very important when people are listening and they're saying, you know, what tests am I supposed to do? Very important point that you wanna do a relapsing fever panel. And again, and I wanna be clear, I have no financial incentives with iGenX. They don't pay me to advertise for them. They just happen to be the best lab, in my opinion, in the United States doing this. But if you do a relapsing fever western blot through them and they also have a relapsing fever PCR panel, you'll generally find it. And is that what you're using, Jill, is that? Yes, and I'm fine, exactly. And they're really the only ones that are doing that from the MCI and the miomotoi and all the different strains. Is there maybe up to eight strains and then they have a generic that covers all the different tickworm relapsing fever strains. Yeah, I think they're actually up to 16 to 20 relapsing fever altogether. Of course, that includes the ones in Africa, like Dutoni and some of the other ones that are out there. So I wanna take a little tiny commercial break and tell you a little tiny piece of my history. And because I think some people can relate sometimes that. So I was 25, had breast cancer six months after my chemotherapy, radiation and toxic treatment. I developed Crohn's disease. Now, interestingly, and I think you'll get where I'm going with this in a minute. My Crohn's presented with cyclical fevers that was it. I didn't have gut pain. I actually didn't initially have diarrhea or bleeding. I only had cyclical fevers and granulomas. Now in hindsight, I have tested positive for the Midwest Hermitii. So the tickworm relapsing fever, Bartonella, hence why? And then also Babesia and Borrelia. So really all four of those. I suspect that my trigger for Crohn's and maybe my presentation and this is just me postulating. I have no sound evidence for N of one equals me. The chemotherapy dramatically dropped my immune system. So I had almost like an induced immune deficiency based on three toxic chemotherapeutic agents. I think I had a dormant case of Bartonella Borrelia and tickworm relapsing fever. And after the chemo, it became active and actually started to present for me as Crohn's disease. Would that make sense from what you've seen as being a postulation of how I developed Crohn's and autoimmunity? Oh, not even a doubt. Well, first of all Borrelia causes autoimmune reactions in the body as does environmental toxins as you well know, cause we're seeing it all the time. But now I would not at all be surprised because when you look at the number of people now that are coming in with that, you know, that trio of Babesia, Bartonella, Lyme. I mean, it's most of the sickest patients are all coming in with it. And of course, any immunosuppressive drug, right? I mean, they're giving dexamethasone now for COVID patients in the hospital. And my greatest fear for some of these people is if you've got a chronic Lyme patient and they're giving them high dose dexamethasone and let's say they have parasites, you're gonna start to reactivate some of those infections. That's why by the way of some exciting news I wanted to share with you and everyone is Congressman Chris Smith had me on the phone about a week ago. And there was a patient in the hospital in New Jersey who was a chronic Lyme patient with COVID. He was on a ventilator. Now this was already day like 25. He was not doing well. He was on dialysis. And he asked me, he had heard about my protocol from Pat Smith. And so I was on the phone with the hospital administrator trying to get him IV glutathione. Well, you know, fast forward, the hospital would not do it because it wasn't a drug because they didn't know how to use it. The sourcing I was getting it from, lo and behold, the patient have died. So Congressman Smith was on his way driving three and a half hours in one direction to pick up glutathione vials from me. And he had to turn around. He was so frustrated with this. And I don't even know his relationship with the family that the next day he said to me, I'm gonna get the head of HHS, Alex Azar on the phone. And I want you to speak to him about your protocol and let's see if we can get a randomized trial. So as per his word, the next day I was on the phone with the head of HHS, other doctors were on the phone also and with Congressman Smith. And they looked like they're gonna try and fast track it through the NIH. Kristen Honey was with me. We corresponded a few days ago and we're gonna try and get this through to try and get an ivermectin glutathione protocol for COVID as well as today, and I was emailing also someone that he put me in touch with to get a randomized control trial also on the double dose that's on protocol that we'll discuss today. So I'm really trying to move this ahead because as you said earlier, there are a lot of people who don't believe this, who don't believe that this is a chronic persistent illness. And the only way we're gonna convince the mainstream medical establishment, we've gotta do a randomized trial. Absolutely, and I just support you in every way. And any way that I can be a part of that, I am in because I see this as the epidemic. Now, something you mentioned earlier that I think is relevant for people who are listening, whether you're a practitioner or a patient to understand this is, I think part of the thing we're seeing is immune system suppression. So that can happen in many ways, but what I've seen over the last 10 years at least is there's much more chronic severe complex illness than there was even a decade ago. And my theory on that is our environmental toxic load, whether it's mold or whether it's heavy metals or where it's chemicals in the environment, our air quality, our food quality is all decreasing. And so our immune systems are having this onslaught of toxins that are suppressing it or like you said, steroids or immune modulating drugs. All of these things that are suppressing the immune system and these old dormant infections that in some people they could walk around if they have a very robust immune system and not be very symptomatic. Or all of a sudden the bar drops and they start to pop up. And that's what you're talking about with dexamethasone or any other exposures. Would you agree that that environmental toxic load is part of why we're seeing much more prevalence of this? Oh, not even a question. I'm convinced of it, especially with the mold. You see all these people coming in with gliotoxins, right, almost all the patients are showing up. It's an immunosuppressive toxin, right? Apart from mercury and some of these metals driving autoimmunity. I mean, at this point in the medical literature they have linked up PCBs and dioxins and plastic pesticides to autoimmune illness. So it's not really surprising. You put Borrelia on board with that, that drives autoimmunity. With these environmental toxins, why would any of us be surprised that our immune systems having a tough time keeping up, right? And we see about 70% of our patients with low adrenals. Your adrenals are low. You can't fight the infections. We check natural killer cells and T cells. We find them low in patients where we've got to use beta-glucan or transfer factors. So not even a doubt their people's immune systems are being affected. Yeah, and to me that's a perfect storm because I really believe there's still thousands of people walking around without symptoms that if you were to check they might have those spirochetes or co-infections in their body, but their immune system is robust enough to keep it in check. So there are people who are asymptomatic, but what we see in our clinic is those who have lost that ability to suppress this. And really part of the treatment is absolutely the medications. We all use the modulators of detoxification and immune system and all the other support that we use because you have to look at all this. But a big piece of this is if you can get the immune system working with you, with the protocols, that's how people recover and go into remission is their immune systems a piece of the puzzle and then all the things that we do to suppress that infection is the other piece of the puzzle. And with Lyme and Dr. Freeman and I published this a couple of years ago, we did two precision medicine papers in the Journal of Healthcare and in the International Journal of General Medicine. We found that 7% of our patients had chronic variable immune deficiency. They had low immunoglobulin G, they couldn't fight infections, subclass deficiencies, one, three of the big ones, they go up in Lyme and acute and they go down with chronic. So yeah, a lot of immune suppression that we're seeing in these patients. And I think it was 75 to 80% of our patients had subclass deficiencies from the Lyme alone because they've shown that when Borrelia invades the body and gets into your lymph nodes, it attacks the parts of your lymph node that make IgG antibodies, which is why you get the CDC positive IgM Western blots is because it's basically shifted your T cell response. So yeah, it's a big problem. So if you're a patient, now if I'm in both of us in clinical practice, I'm checking every single person I see for total IgG, IgM, IgE, IgA, and then the subclass is one through four of IgG which are critical and as you mentioned, chronically they can be elevated. Would you say the IgM is, I'm sorry, acutely elevated and then chronically more suppressed especially type one and type three? Yes, although I've also seen high IgMs in some of these patients too. I've seen it both ways. And then we like, look at myelodysplastic things and that's all negative. It's just this Lyme is causing the reactivity of the immune system. And then like you said, the gliotoxin and nicely myelophenolic acid which is another massive immunosuppression from aspergillus and penicillin. And these are literally the mold creates a toxin that causes immune suppression. So it's this perfect storm. And clearly you're seeing more mold as well. Now say you have someone with Borrelia co-infections or in a moldy home, is there an order that you treat that? Do you try to work on getting them out of the mold and then treat the Lyme or do you do it simultaneously? You know, I do a lot of it simultaneously but as you probably do too, if someone for example has leaky gut and difficulty with their GI tract, you gotta work on the GI tract first and get the liver detox pathways working. But a lot of times I can do a lot of this together. I found that oral phosphorylcholine with some liposomal glute and a little bit of clay charcoal sometimes, you know, questrin, it seems to work and get it out. But of course the problem for people is that they're still in the environment and they don't have any place to go. And that is a problem for some of the patients. Yeah, I feel like that's my most difficult clinical conundrum is having the right environmental experts to take care of their home because that's not my expertise. But I know that they can't get well if they're still living in a water damage building that's significantly affecting their immune system. So let's talk about, you mentioned the COVID and the Ivermectin trial potentially with a glutathione. And I think I recall you mentioning that you had been using glutathione, aniseal cysteine, lipoic acid, and then also Ivermectin. Is that the basics of that? Yeah, so for those of you who don't, you know, aren't up to date in all the COVID literature, I published two articles this past year on COVID-19. One was in the Journal of Respiratory Medicine case reports and it was two patients who had COVID pneumonia who were getting very sick. One almost ended up in the hospital as oxygen stats were starting to drop. And we gave them first oral and then IV glutathione and both of these patients within one hour of taking glutathione along with aniseal cysteine, which is a precursor that helps to drive glutathione production, alphalipoic acid, which also helps to regenerate intracellular glutathione. The reason I came up with this protocol is because when I was looking at the cytokines, the inflammatory molecules from COVID, they looked exactly the same as the ones I was seeing with Lyme. And you know, for the last 20-something years, we'd be blocking the switch inside the nucleus called NF Kappa B using NAC, alphalipoic acid and glute. And I thought, well, that's interesting. Let's try it in COVID. And it's worked at this point, I've treated about 30 COVID patients. Now one of my chronic Lyme patients have ended up in the hospital using this protocol. So I'm excited. And the ivermectin, it's interesting because before I started using it, we were looking at Alenia Nidazoxazide, which also had effects on previously on the SARS virus. And a lot of these antiparasitics have very good antiviral properties. There's a study in ivermectin through Leon Cayley that a large dose in culture drops the viral load by 5,000 fold within 72 hours. And they did a randomized control trial through Europe US. They found that people on ventilators, they did way better than they were on ivermectin. So that's why I'm trying to get a randomized control trial in the United States. Excellent. And you mentioned IV glutathione. Obviously, that's more effective to bypass oral and it's not well-absorbed. But have you treated patients with liposomal and oral of those three, the lipoic, or is it only IV protocols? Oh, no. Most of them actually are oral. And what was kind of funny is there are patients who I've treated and they've gotten better. And about three months ago, I got an email from family who I hadn't seen in a couple of years and the family got COVID. And they had seen the articles I published and they got glutathione, took it, and they had the same response that within an hour they felt better. Their fatigue was lifting, headaches were better, shortness of breath was better. An emergency room doctor on the front lines of New York City was disabled with COVID pneumonia and oxygen sats in the 70. Couldn't go back to work. I gave him the glutathione protocol, NAC alpha lipoic glutathione oral, not IV, with ivermectin 10 to 14 days later. He was back to work. His pneumonia completely cleared, oxygen sats got better. He sent me pictures because he was with his fiance and he was really worried. He would never be able to perform as a physician again on the front line. So I've seen it work. It's just now a question of proving it with randomized trials. Yes, and it makes sense because as you said, whether it's LPS-induced endotoxin in the gut or whether it's Lyme disease or even mold cytokine storm, these are all similar pathways. One of them IL-6 and then many, many more. So it makes, to those of us who are functionally-minded, this makes perfect sense because it's a common denominator, common to all of these inflammatory chronic infectious processes so we can apply the same types of protocols and treatments, even though it's slightly different infections that are contributing to it. So I love that that's clear. I wanna talk about- And by the way, for people that want to actually see the science behind it in the protocol, one or two days ago on my Facebook site, which is Dr. DR. Period Richard Horowitz, I posted a seven to eight page scientific document that I sent to Kristen, Honey and HHS, which was the scientific basis for using glutathione and ivermectin. So for people that wanna see it, it should just, you just have to scroll down a couple of posts that I did probably a day or two ago. You'll find the document and you can use this for yourself and bring it to your healthcare provider. You might find it be quite useful. And I will find that link and link it up. So if you're watching this or watching a recording, it will be below our Facebook Live here shortly. I'll make sure and include that link as well. One thing I wanted to explain to those listening, you and I know this well, but with Lyme, there's different forms of Lyme. And that's why the dapzone and the dysulfurin can work. Can you explain a little bit about why persisters are important? What does that mean? And why we have to treat those in order to get a cure? Sure. So for those of us who've been in the field for 30 plus years, we used to think that the reason Lyme persisted in the body was what was called cystic forms, otherwise known as L forms, S forms, cell wall deficient forms, or that they were hiding in the intracellular compartment. I mean, that was our belief up until about seven years ago. And then all of a sudden, Kim Lewis from Northeastern and Eva Shopee at the University of New Haven and Dr. Ying Zhang from John Hopkins and Stanford researchers, they all started discovering that there were biofilm forms of Lyme disease. Now, for those of you who don't know about biofilms, you do because you go to the dentist to get the plaque taken off of your teeth and that's a biofilm. And in fact, the bacteria I was talking about earlier for Alzheimer's, porfumonous gingivalis, that's what happens where you don't brush your teeth with gingivitis, it can go straight up into the brain and cause an inflammatory response. So regarding this, we sent this protocol out, we've been trying it, looking at biofilms, looking at persisters, but the persister literature, the reason I came up with it in a specifically dap zone, Ying Zhang, when he published on persisters, this is five or six years ago. We all knew that Lyme persisted, but I never thought of it in terms of, oh, it's a persister like TB, like leprosy, like a mycobacterium. It's like the light bulb went off in my head and I went, hold on, when I was doing, my residency at Mount Sinai, I was treating HIV patients all the time with mycobacterium, right tuberculosis or MAI. So I was used to using rifampin and INH and pyrozinamide in these drugs. So I really wanted to use them, but I didn't have a reason to use it up until a few years ago. So I went to the literature and I looked up, well, how do we treat, for example, leprosy? Leprosy, they use rifampin and dap zone. And I said, okay, hold on. I looked up dap zones, you know, qualities, and it's like it lowers inflammation, great, because the reason you're sick from Lyme is from inflammation. It has anti-malarial effects, oh, great, because Babisi is in most of my patients. It hits persisters, right? And it's used for autoimmune illness, which again, we see in Lyme patients. So it had like these four prongs and I said, geez, why don't I just add doxy to it in case people ever lick ya and a plasma, et cetera? I came up with doxy rifampin dap zone being the protocol. So we published several studies. Dr. Freeman and I had published two separate studies, 300 patients who did dap zone protocols up to 100 milligrams, which is the standard dose, and it worked. It helped eight major Lyme symptoms, but here was the catch. It helped most people, except when they stopped the protocol, they relapsed after a certain period of time. And as, I forget it was Louis Pasteur, someone was talking about when chance meets, you know, science at some point, some guy accidentally in my office came in and took a double dose of the dap zone. This goes back like two years ago. And he was very ill and I went, oh my God, you could have killed yourself. He came back in a month and he comes back in a month. This kid was in his 20s, sick for like seven or eight years in bed, couldn't work, couldn't go to school. He comes back a month later and he goes, Doc, I feel great. I like, I've got no symptoms. I mean, he needed IVIG for a little bit of immune deficiency. And I said, all right, hold on, don't take anything else, come back in three months. Comes back in three months, he says, I feel great. Comes back in six months, I feel great. This went on for a year until he got 16 tick bites in Maine, whole another story. Yeah, I was probably just strangling him at that point. I turned to my wife and I said, hey honey, would you like to be a guinea pig? I have a protocol, because my wife had suffered from chronic Lyme for the last 30 something years. She did the lower Dapsone and at 50 milligrams when she stopped it, she was PCR positive in the blood for Borrelia. She did a hundred, she liked it even better, but relapsed. She did the double dose Dapsone protocol almost three years ago. Her Lyme symptoms have never come back. And what's really fascinating about this is that it's an eight week oral protocol. It's eight weeks of oral generic antibiotics, doxycycline refampin and Dapsone with Plaquenol, with Nystatin, three biofilm agents, stevia, biocytin, seropeptase, probiotics for the gut obviously. But the really great news is that Eva Shopee and I and Dr. Freeman published one month before the article came out that in culture, when we looked at the doses of Dapsone and these different drugs in combination, it turned out that the higher the dose of Dapsone, the better it affected the biofilm forms of Borrelia. So these persisters are hiding in the biofilms. If you don't open up the biofilms and hit the persisters, you can't get rid of the disease. So we are on the cusp of a true possible cure. No one dared use this word for 30 to 40 years. I can use it now, we are on the cusp because it is clearly the biofilms and the persisters that was the problem. But in the study we just published, what was also important, and this was in the journal Antibiotics for people that wanna see it, maybe you can post it on your site, Jill, is that if you had active Bartonella, by Bartonella fish testing from hygienics, I think it was eight out of 40 patients were Bartonella fish or nine, they did not go into remission. They all improved 98% of the patients improved on this protocol. 45% went into long-term remission for one year or longer. 58% of the PTLDS, the post-treatment line, went into remission for a year or longer. But active Bartonella prevented full remission as did half the cases of Babesia. So take home message. You gotta go after the Babesia and Bartonella before you treat with this Dapsone protocol or my next step is to combine things like using Zithromax with Dapsone Rifampin and Doxycycline, maybe adding extra methylene blue using Pyrazinamide that I published on Bart. Like you've gotta add things on for the Bartonella because we're having a big problem treating it, but even just last week, I think the universe is favoring me on this one. There was an article published on essential oils. They talked about that if you get the right combination, like cinnamon, oregano oil, clove, peppermint, if you add these to gentamycin, which is one of the few drugs I've ever found for Bart has been effective in putting in remission, but I hate using it because of ototoxicity, renal toxicity. The essential oils lowered the MIC, the minimal inhibitory concentration. Maybe we can use gent at half the dose or a third of the dose with essential oils so you don't get the toxicity. We have a cure for Bart, right? And then we're gonna see all these people go into remission from an eight-week oral protocol. I mean, it's really, really exciting. Unbelievable. I'm just, and I'm gonna share your new research and again, we just are so grateful for you being on the cutting edge. So just to repeat what I understand, some of the triple indicellular, the hitting the Bart, the babesia is ideally done before to lower the load. And then this is kind of at the end that eight-week treatment for persisters and that's when you're getting the best results. And that's kind of what I've been doing too, is trying to really get the load down first. And then, now we didn't mention disulfurum, that's something that has been used, of course. Dapsone, it sounds like is actually more effective with less side effects potentially because it's a shorter course. I'm seeing a lot of side effects with the disulfurum, but what's your thoughts on disulfurum? Is that still- Yeah, so there's side effects with both drugs. I mean, the thing about disulfurum, the problem with the drug is the half-life is 14 days. And I have people at 62.5 milligrams once a week that hurts with this drug. I mean, it's very powerful. So right now, I'm not going past 125 or 250. Glutathione still helps when people do get herxes, but the problem, of course, is the neuropathy. And we gave it to about 150 people, five out of 150 developed neuropathy. Fortunately, most of them are reversed over time. We gave them mitochondrial support and high B vitamins, et cetera, benphotiming. They are getting better, but the problem with the drug is it's really toxic for people. I mean, the fatigue and the brain fog when they hurt, they can't go to work for days. The dapsone only has a 24-hour half-life. So if you get side effects from dapsone and you stop it, it's out of your body very quickly. And we've learned to minimize the side effects like the anemia from dapsone with just very high doses of folic acid. We've learned to minimize the methylmoglobinemia, which is when oxygen is not carried properly in the blood. It's a side effect of dapsone with methylene blue, which, lo and behold, is a drug that's been shown to be helpful for Bartonella. So, you know, it all kind of intertwines, but yeah, I mean, and by the way, I've used disulfurin and dapsone together. And there are people who swear that the combination of the two together work better for them, where for example, I couldn't get them at higher doses of dapsone, they couldn't tolerate it. I've used low doses of disulfurin with lower doses and there's definitely a synergistic effect. That's a whole nother study that needs to be done at some point in the future. Gosh, I just love, again, that you're doing the research and reading the edge on this because we need good treatments. And my experience with disulfurin is it's very good for Borrelia and Babicia, not so good for Bartonella. So we're back to that difficulty with the relapses due to Bartonella. And again, just to repeat, you're going for treating the Bartonella the best that you can before launching into one of these courses. I think it makes sense. Now, the problem is is we don't have a cure for Bart. Right, right. I mean, I've had patients, the one patient, there's a patient in Arizona treated literally for 13 years within days of stopping. She was on at least four intracellular at the same time. Mino, rifampin, pyrazinamide. She would relapse within days. At one point, I gave her Mino, Zithro, rifampin, pyrazinamide. I published on pyrazinamide for Bart about four years ago in a Bessette's patient who responded beautifully and it turned out it was Bart. My take at this point, by the way, on Bessette's, it's probably Bart and eloquent Anna with parasites. But in any case, when I added Gent, that was the only different drug she did. She's now in remission for three years and has never had to go back on antibiotics, which is why this essential oil paper that just came out may be the way to use this drug effectively and safely because I am scared to use gentamicin at this point in time. So I think I'm gonna go back to Dr. Shopey and say, or even Ed Breishwert and say, hey guys, we need to do some culture studies of these combinations with essential oils and let's see what hits Bart best and let's then bring it into the clinic and see what we've got. Yeah, and that's the beautiful thing about what you and I do and all of our colleagues out there is our conventional training is the best in the world and we're using that and we're using drugs that are very appropriate to treat these infections. But when we bring in the liver support, the detoxification support, the support for the gut, which is usually nutrient-based and we think about essential oils or biofilm disruptors which many have come into natural form like seropeptase, biocytin, NAC and others, stevia, we really get the best of both worlds and I don't think we could treat Lyme purely with one side or the other, we need this combination. Oh, absolutely, I could never do it because we need glutathione for the Herxes, we need all the massive amounts of good probiotics to keep the gut in order, but the beauty of the eight-week protocol if we can prove that this works, it's no more long-term antibiotics for Lyme disease, I mean, you're talking about still replacing the microbiome afterwards, but nothing like what we have to deal with. Exactly, and again, I do a lot of inflammatory bowel because of my history and I see a large percentage of Crohn's and Ulcerative Colitis caused by their mycobacterium species or Lyme. And so again, these things that are presenting with other, they're labels, the chronic fatigue, the fibromyalgia, all these things are labels and what we often find underneath these infections. In fact, Garth Nichols had even published on Michael Plasma Species with Crohn years ago. I mean, there's lots of these things that show up in the literature. And interestingly, that's when I first started doing triple intracellular before I knew you, and I knew you, but I hadn't taken your course and I was doing Chlorithro, Rifampin, and usually one other intracellular agent and I was getting reversal of Crohn's disease and I thought, well, we had map positive, right? So I was thinking of us treating map and then when we talked, I said, I wasn't treating map, I was probably treating Lyme and co-infections or at least both things because it's the same treatment. And you know that they found Lyme and co-infections in the GI lining. Yes. There's a gastroenterologist in New Jersey, Martin Fried, who did the biopsies years ago and proved that they were there. So yeah, they may be causing an inflammatory reaction in the gut. And from what I understand, Bartonella, granuloma, cysts, lesions, it's very good at disrupting collagen and so the granulomas in Crohn's could be very well be related to Bartonella. Absolutely, that's one that needs to be examined. That's a good point. Yeah, this is fantastic. So I'm gonna link to your articles. Is there anything else you've been working on or published recently that our listeners should know about? No, I mean, the two Dapsone articles, the one in Springer BMC and antibiotics are the two latest. I mean, in the last year, I've been quite prolific. I still work for HHS. I was on the tick-borne working group and I went down to two days a week when I started working for them. But this past year, I was on their HHS Bebezia subcommittee in Sam Telford, who's great. He and I did the chapter on Bebezia. So that's also why I'm so up on Bebezia. But I published, I think, seven or eight articles this year, one with Dr. Shaw on the use of the Bebezia fish test as being one of the best tests for finding Bebezia. So for those who are looking for Bebezia Bart, I think, again, IGNX fish testing is wonderful. I can unfortunately do Galaxy Lab in New York. They have a new PCR, their DD direct droplet PCR that looks very sensitive for multiple strains of Bart. So for those who can use Galaxy, absolutely use it. But we published an article on Lyman environmental toxins driving a lot of these chronic diseases. So yeah, I mean, there's been a lot of publications this year. I finally had time to kind of catch up one on pregnancy, showing Lyman pregnancy with Bebezia that you can treat with clindamycin and mepronazithromax in the third trimester safely. That was a case study that I published. Then Dr. Freeman and I published two COVID articles that, so yeah, it's been a prolific year and I'll send you the links for all of them so people can see. Wonderful, and I will share those. This is incredibly exciting. And again, we're so grateful for you leading the edge on this. Two quick questions. Tick-form relapsing fever, would you lump that in because it's similar in treatment if you're doing Borrelia triple undercellular that? With that, is there anything different with tick-form relapsing fever? Or is it? I don't think so. And that's of course a good question that I don't think anyone knows the answer, but I think it probably will still work, but because we don't test for it, a lot of doctors don't test for it, we don't have large studies on it, it's kind of difficult to know exactly, but I would imagine it probably does work. Yeah, and then the second thing is in my clinical experience with Bebezia really amplifies and makes these worse. Is that true, would you say that when someone has really any co-infection, but especially if Bebezia tends to make the course a little bit more difficult, a little bit more lingering long-term, what's your experience with Bebezia being in the mix? No, absolutely. I mean, Bebezia makes people three times worse. You know, it was published in JAMA by Peter Krauss in 1996 about these people getting worse. And essentially, you know, what happens with it is that these people who present with base sweats, night sweats, chills, flushing, air hunger, I can't catch my breath, right, or cough. Those are the ones obviously that have Bebezia, although by the way, I've probably seen about one in a hundred that don't even have the malarial symptoms and they still test positive. But yes, it absolutely increases the underlying severity of the illness. And that's why most of the time, I think you and I are seeing the same, it's Bebezia Lyman-Bart, they're showing up in a triad. I mean, we're also picking up Michael Plasma, Chlamydia, and the rest, but that triad specifically, and we're now looking at Tefeniquin. It's a newer drug, antimalarial. I'm just starting to test it out now for Bebezia. There's very few Bebezia treatments that have come out in the HHS tick-borne working group report we did. There's no cure for Bebezia. So we list all the treatments. I think they lower the load of the parasites, but very difficult to get rid of 100%. So we'll see if Tefeniquin has some studies and I know that Dr. L. Currie at Yale, he presented to our committee and he's got some really interesting research which I'm sworn to secrecy and can talk about. But he's probably gonna be publishing some very interesting information on drugs that you would not suspect, just like with disulfoam, you would not have suspected it hits Lyme. Same thing with Bebezia. I think he's looking at some really interesting older drugs that may have a good antimalarial effect. That's what I love about these. This is not the classical med school. We have this one line of this drug treats this and it's not that way with what we're using. And the more we think outside the box, the more I think we're going to find curative treatment regimens for Lyme and co-infections. Last little really quick fire, a PCR versus fish for Bart and Ellen, Bebezia. I've been doing both. Is this one better than the other for detecting? I'm finding the fish to be way superior. And that's been showing across the board for me. The fish testing seems to be really an excellent test for picking up Bart. That's why I published it in the recent study that we did. And by the way, for those who are listening, I just want to remind you, we did not really talk about prevention at all, but please be aware. A lot of people are not still doing tick prevention like they should. You've got to be looking at using permethrin on clothing, unless you're really chemically sensitive and using things like picoride and 20% on the skin. I've tried 5%, 10%, it doesn't work. The mosquitoes come after me like crazy because my chromothiaxides, you know, it shits like crazy. I have to agree because we don't like toxic chemicals, but in this case, the prevention is so much better than the cure. I highly recommend permethrin. I don't use deed. I mainly use picoridin at this point, 20% with that. And there'll be, you know, nuctitone, which is a citrus based soap. It's from the CDC. It's going to be released in the next couple of years and it has a very high efficacy actually for repelling ticks. So you'll be able to actually use a soap that's a tick repellent. Stay tuned because it's got a nice citrus smell and that's going to be coming out very soon. But please, I beg of everyone, you've got to be very, very careful with this because once you get this disease, I mean, yes, we're coming up with solutions after 40 years of doing this, but you don't want to get there because there are people that still die from Erlickia, Anaplasma, Rocky Mountain spotted fever, right? Absolutely. And then one last little thing, and then I want to be sure and ask where people can find you and take your course if you're a physician. In treatment, we talked about triple intracellular and some of these things you can do to reduce low. Refampin, are you going up to like 600 or more per day in those intracellular? Are you going pretty high on that? And refampin versus rifabutin, any comments on that? Yeah, that's a great question. You and I could be speaking for hours here. Maybe one day we will for all the doctors on listening. So I still stick with refampin more than refabutin for several reasons. The half-life of rifabutin is much longer. And I've seen side effects of rifabutin with lower white cell counts, platelet counts, where I don't usually see it as much with refampin. So I tend to use refampin. It's generic, the insurance companies approve it. It's like 400 bucks out of pocket to do rifabutin. But that being said, when I'm now starting to do fabart as a trial, and I don't have the results yet, I already know that regular dose refampin at 300 twice a day is just not enough. I'm now double dosing the refampin as a pulse two days a week. So for example, on a Monday, Thursday, Tuesday, Friday, I'm using 600 twice a day to try and see because we found in Dr. Shopee's studies that I did with her that refampin actually acts as a biofilm agent also. I mean, we didn't know this until we actually did the culture studies. It's possible, because we now know that Bartonella has persisters and has biofilm forms in the same way. It's possible that the higher doses may help with the biofilms, but my next step is now to try these new essential oils like cinnamon, clove, oregano, peppermint that just came out two weeks ago published to see if these are more effective for Bartonella biofilms with double dosing the refampin with like doxy, pyrazinomite, right? Starting to do the multiple intracellular. And then seeing if we can do some studies eventually in culture on Bart using lower doses of gent with the essential oils to see if it works. I think that's gonna really be the next step that's gonna move this ahead. That makes perfect sense because that's what I'm running up against you is how high can I go with the toxicity? And then last thing, malarone versus meprone, any preference on treatment of babesia? I hardly use meprone anymore. It used to be called oligold. There's resistance to it in the United States. By the way, for those who wanna learn about tick-borne disorders, I was on the first round of the HHS Tick-Borne Disease Working Group and I was the co-chair of the other tick-borne infections and co-infection subcommittee. Well, there are new reports that have now come out on the HHS 2020 site for lichia, anaplasma, rickettsial diseases, babesia. If you read the babesia piece that Sam Telfrin and I do, you'll get a complete overview of what's going on. It's got the most up-to-date literature review, so it's a really great place for people to go to get up-to-date literature, because these are some of the best scientists in the world that come together on these subcommittees to produce the reports. Fantastic, and again, I'll be sure and get those links from you and make sure everybody has those on here and then on YouTube. So where can people find you? Of course, we'll keep links to your site, but where can people find you? Find more information. So I mean, the main social media site, where I'm posting a lot these days, is Facebook, which is Dr. Period, DR. Period, Richard, I think Period Horowitz or Dr. Richard Horowitz. If you want to keep up-to-date with what I'm doing, I'm usually posting what I think is the most important literature on Facebook. I will be doing, I'm only doing this once a year. I'll be doing a virtual course for Lyman tick-borne infections. You were the last group that did it in person, and of course, we have a great time doing it, but we can only fit 40 people in that room. We can't get past. The last one, we doubled the number of attendees. I'll probably be doing it, I'm assuming in spring or early summer, probably sometime next year, and the way to learn about it is my office email, it's probably the best way, which is medical at hvhac.com. It stands for Hudson Valley Healing Arts Center. So medical at hvhac.com. If you want to learn about the course and get more information, my office staff will get me your information and we'll get you whatever you need. Perfect, and again, this will go out to practitioners, and so if you're a practitioner, I just want to give my endorsement, this is one of the best education. There's a lot of things out there, but Dr. Hurwitz, you put on a great, and you just pour out your heart and your soul and all the information, just like today, you just fit about three or four hours of information into less than an hour, and we love it, we appreciate it, and if you are a practitioner wanting to learn more, I highly recommend this course.