Research has shown that treating chronic Lyme disease with Dapsone combination therapy can significantly reduce Alzheimer's biomarkers, specifically phosphorilated tau (P-tau 217) levels, by up to 63% within 9 weeks, suggesting that chronic infections may drive neurodegenerative processes through inflammatory mechanisms rather than amyloid plaques being the primary cause of Alzheimer's disease.
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Chronic Lyme and Alzheimer's Disease
Added:We're live now. Hi everybody. Great to have you here. I am really honored. Uh one of my colleagues and a guy I really admire, Dr. Richard Horowitz, he is the world leader in Lyme disease. Uh there's a wonderful documentary that has him in there treating patients. It's really fantastic to see. And so uh great to and the timing is perfect. Uh Richard, thank you so much for joining us today.
>> Well, thank you for having me, Dale.
It's great to see you again. And um this is great time for a couple of reasons.
Uh number one, he's just published a really exciting paper uh in which and I'll let him describe it to you, but the bottom line is really showing how treating chronic lime successfully impacts biomarkers of Alzheimer's disease. It fits perfectly with what we've all been talking about for years.
Uh and now he's got a fantastic book coming out in October uh that will that you know that will uh that will he's got a copy right ending chronic illness they come out October 13th correct >> that's it >> and very excited to to see that and it goes into many chronic illnesses so I think the timing is fantastic let's start with the case study that you just published if you could tell us a little bit about how how the setup I mean how did this person come to you how did you decide that treating was going to be helpful and then looking at Alzheimer biomarkers in someone who had chronic lime.
>> Yes. You know, it was it was a little bit of um serendipity because, you know, I just finished 42 years of clinical medicine. I just actually retired for the first time. I'm moving into the research space. So, you and I hopefully will have some discussions in the future, Dale, about setting up randomized multic-center placebo trials for lime and Alzheimer's. But but the way this kind of unfolded, it was um it was really unusual because this I had very few patients in my practice who had not done dapsom combination therapy by the time I was finishing practice. And this this one woman, she was 67 years old. Um she met all the criteria for chronic lime post treatment Lyme disease syndrome. She had an EM rash that had been treated with doxycyc. Um and she had 15 years worth of symptoms. She had joint pain and what was interesting about her joint pain, she had rheumatoid factors that were positive uh which were on and off but but quite high for the last 15 years but was not rheumatoid arthritis. She was CCP negative. Uh so this was just an inflammatory marker from lime and the last year or two before I was finishing up I saw that question labc course started doing these Alzheimer's biomarkers. So I decided because I knew Eva Shoppiey's work and Judith McClosy's work from years ago where they had shown that in autopsy studies they had found bofilm uh beta amaloid and phosphorolated tow in the brains of these patients who had died with Alzheimer's or Parkinson's but nobody had ever really looked at it in live patients. So I decided to start looking at my chronic lime population.
And to my great surprise, about 50% of all of the patients that I started testing who had chronic lime, who had not finished the Dapsone protocol still had, let's say, bartinella that need to be treated or they had mold toxicity.
They were showing up with mostly, by the way, talopathies. It was mostly elevated pile 181, ptow 217. U bunch of neuroilament light was showing up. Um, and and occasionally the beta amaloid 4240 ratios were low. Um, so it it was surprising to me. Now at that point when I was seeing it, I said, "Oh, it's inflammation in the brain from lime, you know, to be expected, but I didn't realize that if someone had gone to a board-certified neurologist with these biomarkers, they would have said, "Oh, you have Alzheimer's. Here's lacanab or danmab, and you're going to go on these drugs to take amaloid out of your brain." So I decided with this patient who had had lime and and by the way what's beautiful about this case there's very few cases that are not only status postdm rash but eliza positive C6 Eliza positive um IGM western blood positive IGM uh imolot positive IGG amino positive by CDC criteria there was no way that anyone from the NIH or CDC would have looked at this case and said this is not a classic chronic lime PTLDS case. So she had had besia and bartinella, fortunately not active at the time when I was treating it. She had been exposed to Q fever, coxiella bernetti. Um she had had other inflammatory factors like metabolic syndrome. Um her B12 level at one point was a little bit low. Um she had some microbiome issues with leaky gut, intestinal hypermeability. So she had a couple of overlapping inflammatory factors, uh mineral deficiencies. Um and I said to her, listen, I'm finishing practice. you've got some joint pain.
Her cognition, by the way, was not terrible. She was meditating. She thought it was really pretty good. And I said, "Listen, I'm a little concerned.
Your pal 217 um was over two times normal. Um so the level was 33. Normal is less above 0.15." And I said, "Listen, I don't know whether Dapzone combination therapy is going to help, but I'd like to do the 9-week protocol with you." So she did it. Um and we checked her pout 217 3 months later and to my great surprise it reversed down into the normal range. It was 0.12. So we lowered it by 63% with a 9-week oral generic antibiotic protocol. And then when I checked what lacanabanab and these anti-amaloid drugs did they lowered it by 23% in 6 years I lowered it by 63% in 9 weeks. But basically the reason and and we reversed her beta amaloid right her beta amalloid ratio started getting improving but I was going after of course the hypothesis was it was the burillia which was driving the phosphorolated town now I didn't know what it was going to work I put it in the literature and then discovered it was the first time it had ever been done like I didn't even know this by the way when I was submitting the case report I now have a second case that just came in several days ago um he also reversed his beta amaloid I have to decide you'll Tell me whether you think it's worth submitting to the literature.
He was just below range at.169 >> and we treated him with dapsone and it went above range to.173. So we in we lowered his beta amalloid by like 2.3%.
His pal 181 was a bit high was.165 but interesting his pal 181 went up a little bit as did his pal 217 as the beta amalloid ratio improved. And I don't know if this is just like it's going to take a while for the pout to clear or he had five mold toxins that were literally his glyotoxins were 14 times above normal limits. The guy had non-alcoholic stato hepatitis although he lost 35 lbs and his liver functions were normal. He had metabolic syndrome but he reversed his hemoglobin A1C from 5.8 to 5.6. Um, so in other words, we went after all his inflammatory markers and they were much better. But because this is only the second case I tried this on and I'm now betting I'm like I'm betting a thousand as far as the beta amalloid, but I'm only batting 500 with the ptow. Um, you know, because we've never done this.
This is brand new. I mean, I don't know whether the ptow will eventually come down or we need to get rid of the mold.
So, it's almost like opening up a door that no one's ever opened before. It's very exciting cuz you and I have gone back and forth on this before. How much is burilia really playing a role? And it does appear it is driving amaloid in pa but again we won't know until we get a really large multic-enter placebo randomized trial and that that really is going to be the next step.
>> Yeah but you need these anecdotes to to give you support to do a trial. So I think this is really exciting because it's it's giving us new insights. You know what's interesting? All these things have to fit together and you know they you you can't have a well sometimes this sometimes that these they all must fit together and that's what this showing. So this idea that's come up over the years that the amaloid and the tow are really not the causes of the illness. They are the responders to these various insults. This again provides more clear information that here's someone that is driving their amaloid and their tow in this case with burilia and potentially other things as well. You treat them and look at I mean this dramatic improvement and how long was the span between the two pal levels when it went down 63%.
>> Um so the the first level was that it was probably about a five or a six month change. Five or six months.
>> Yeah. Because we we checked it the dapsone protocol is eight or nine weeks.
We waited three months and we repeated it and it was about the same thing with this guy who just reversed his beta amaloid. That's the second case now. Um so yeah, it's usually about three months after the dapsone was done. Right. Now you mentioned the second one actually lost some weight and we see have seen this repeatedly and we saw this in our trial where we had people who had dramatic improvements in their cognition and when you'd look at the pau the ptow actually went up and they had lost typically when you lose weight your pal goes up at least transiently. So I would check it again in a year after he's been stable for a while. We saw it again and again and again as they'd lose 20 pounds, 30 pounds etc. the PAL would bump up not down. Now part of that seems to be change in blood volume. Uh but there may be other things that work as well. So again all these different observations from people doing you know different things is going to be so helpful for all of us to understand this. Interestingly, as you were referring to in the drug trials, they had this decrease in the PTA, not dramatically, but but a decrease and yet they had no improvement in cognition.
So, there is a dis, you know, a disconnect there. In your case, you had some improvement in both, >> right? And well, and again, and keep in mind, I mean, this was the 11th study published on dapsum combination therapy in the last 10 years. 10 of them are from me. One of them is from uh Monica Ember's group where she showed that dapsone and rafamp and cured lime in the mouse model. So we have you know culture studies we have a an animal study and we have about 375 patients retrospectively but interesting the number one effect of dapsom combination therapy when we look at fatigue joint pain muscle pain neuropathy um day sweats night sweats shills besi it was always cognition cognition was always the number one effect on dapsone and as I wrote in the paper some of it we know that beta amalloid is antimicrobial I mean this goes back to now the the theory that's been out there that it's showing because it's an antimicrobial peptide and it's trying to actually protect the brain, right? But yeah, so but that's interesting. I did not know that this weight loss because my patient lost like around 40 pounds and reversed his non-alcoholic style hepatitis and metabolic syndrome, but I didn't know that that could cause the pizza to go up.
>> Absolutely. So yeah, again, I would check it again in a year.
>> So again, all these pieces coming together. So let me ask you you know years ago uh you're aware of this even you know this literature better than I do um this idea that you know is neurobiliosis a critical player in in neurological diseases like Alzheimer's and the claim from the negative side was well if you look at all comers with burilia you don't see this dramatic increase in all in Alzheimer's diagnosis on the other hand as you said mcclosy and others have said well yeah but if you look at it from the other side you're seeing pathologically there it is and there's no question you get this amaloid which is essentially sequestering whether it's herpes whether it's p gingalis whether it's borelia something else what we believe now is that this is a pre-inflammatory component so before adaptive response before the innate response you have a pre-inflammatory response which basically says I'm going to allow your brain to to continue to function. We don't want to compromise it with a lot of inflammation. So, I'm going to get away with sequestering surrounding these pathogens with amalloid and that will essentially get them out of the way. And I can and that's why, you know, people will have 20 years of amaloid in their brains and still be thinking very well.
But if they now have this this push onto the pro-inflammatory side and onto more PTA, now they start having a decrease in cognition. So again, your stuff really supports this idea that this is a response to pathogens to insults. It's not the direct it's not something that happens randomly and causing you to have Alzheimer's.
>> Right.
>> And and of course the dapsone because it goes intracellular all the theories about chlamydian pneumonia all these years. I mean if there was chlamydian pneumonia or myopplasma or other intracellular infections theoretically the dapsone protocol would have also hit it. So you know when the [clears throat] trial is done this is going to be fascinating to look at you know the viruses the bacteria the fungus the parasites to look at all of this and in fact the other thing I published in the journal article in the journal of Alzheimer's disease reports is that all 16 MSIs factors um which I had previously published for chronic lime and long COVID are now showing up in Alzheimer's and and what's the main point about my my new book of ending chronic illness is those same 16 factors when I did a deep dive in the medical literature They show up for ADD, ADHD, autism spectrum disorders, allergies and asthma, a whole bunch of autoimmune diseases from MSU uh to rheumatoid arthritis, cancer, cardiovascular disease, chronic fatigue syndrome, fibromyalgia, hormonal dysregulation, mood disorders, depression, anxiety, OCD, psychosis, uh bipolar, they all show up with the same 16 factors, which means chronic inflammation is underlying these chronic diseases, you know. So, it's it's kind of a paradigm shift of how we look at this. We can't just name the disease and throw drugs at it because our health care costs are going through the roof. And right 60% of Americans have one chronic illness and 25% of two or more. I mean, we've got to do better with these chronic illnesses and Alzheimer's. You know, McClassy's work is that there was at least a t-fold increase in Alzheimer's looking at again at this is autopsy studies when belly was present, right? So, we we considering the Alzheimer's epidemic is doubling and tripling, right? in the next couple of decades, we've got to get this study done and and really take a good hard look. Um even even repurposing Dapsone as an NLRP3 inflammosome inhibitor, right? It could be that those who don't even have Burilia driving inflammation, it may still be a very good drug because Lee from uh South Korea did that study in over 3,000 leprosy patients. He gave them rafampen and dapsone. He gave them like for 15 years. the rates of Alzheimer's were like six times less when dapsone was on board because it was looked like it was acting like an NLRP3 inflammosome inhibitor. But of course, we don't know in his study whether they had burlli or chlamydia or any other bacterial infections that the dapsone may have actually been hitting.
>> So no question that so many of these diseases are including this NLRP3 inflammosome that you mentioned. The question then is if we're going to go after that, is dapsone something that has enough side effects that you only want to do it when you've got pathogens that you're seeing or is it something that you think has few enough side effects that everybody who's got cognitive decline, any sort of biomarker increase should be thinking about including dapsone. So the the it's it's of course a great question and the reason I think it can be repurposed um and at a dose of 100 milligrams or less is I had a patient um I I've been presenting this in case studies when I've been talking to other doctors. She was roughly close to 80 years old and she didn't want to do the whole dapsone protocol and I just gave her 25 milligrams of dapsone which in my world is like homeopathic dapsone. We did it with I think one minute cycling which also has great penetration into the brain.
>> Her cognition completely improved. Um but when I stopped it after a year and a half and I looked at her barkers your pile 181 was high as was her pal 217 and I said to her listen you really got to consider doing the whole protocol but I saw even in very lowd dose dapsone and I did this for a couple of patients they basically said my cognition was perfect and these were like 80 year olds who just didn't want to herx and go through the whole protocol but 100 of dapsone which is the dose that Lee used in his study in these like 3,300 people over 15 here is if you give enough folic acid the the main side effects of dapsone is do what I call do no harm. H is herxes, A is anemia which is folic acid. R is rashes if you have a sulfur uh side effect and M is methmoglobanmia.
And a dose of 100 milligrams of dapsom which is what he used showing the rates of Alzheimer's were six times less. If you give people let's say 25 twice a day of lucavorin and lmethylolate 15 milligrams twice a day the maximum drop in hemoglobin you're going to get is probably around 2 g and at that dose of dapsone if you use lowd dose methylene blue which they're now using anyway for mitochondrial dysfunction with Alzheimer's. Right. Right. I mean the the dose they're optimizing I think was around 138 milligrams or something of methylene blue was showing it was helping some people with Alzheimer's by increasing mitochondrial. Well, methylene blue reverses the side effects of dapsone. So you could theoretically give a low dose of methylene blue with antioxidants like glutathione which reverses methmoglobin and even at 100 of dapsone you might get a methmoglobin of 4% or something but people don't even notice it. So as far as a repurposed drug, absolutely. In fact, I'm surprised nobody's even discussed this before because instead of just using arisp and amenda and you know some of the classic accetosterase inhibitors and NTA, >> why don't you use something like that is an NLRP3 inflammos inhibitor that's at least been shown in this study from South Korea over 15 years. It lowered Alzheimer's progression. I think it's a great repurposed drug that should be used. It's cheap. It's generic. And I've learned how to minimize the side effects because I've been using it in, you know, thousands of people now for the last decade. So you could easily use a hundred of dapsone or lower dose. You'd need to do a good study. Absolutely.
Without really even noticing because when you get a, you know, a one or two gram drop of hemoglobin, it's so slow people don't even notice it. Um, so yes, that that could absolutely be done going forward as a repurposed drug.
>> Yeah. I you know, I think you said the key word, which is cheap.
the people out there trying to sell you these things don't want to hear that.
They want to hear that they can make some money from it which is unfortunate.
So it looks like you this could be a a wonderful part. The armamentarium in cognitive decline and in neurodeenerative disease is growing by leaps and bounds. Everything from photobiomodulation to stem cells to peptides to you know intraasal approaches to exosome. I mean, it's amazing and getting at what is actually driving it is so interesting and so helpful. So, how long would you then keep it? So, let's say that someone responds, they do very well, whether you're giving them a hundred or whatever, uh, and their biomarkers are improving and their cognition is getting better. How long would you then recommend that they continue that therapy?
>> Well, so the beauty of DAPS combination therapy is it's a nine-week protocol. Um the last part of the protocol if you don't have active besia if you don't have active bartinella if you don't have mold toxins um in other words if you don't have the other overlapping MSIs factors driving inflammation people about 50% of people go into long-term remission with just this nineweek protocol. I mean remember it took me a decade 10 years working out the doses of dapsone to figure this out. My my wife who was sick for 25 years with lime is now 8 years in full remission. She had tried 50 of dapsone for a year. She relapsed and was PCR positive in her blood. She did a 100 of [clears throat] dapsone for 6 months. She go, "Honey, I feel great." She stopped it. She relapsed. She then did a 100 of dapsone twice a day, 200 milligrams for one month. She's now eight years in remission. Now, the reason she did so well with only one month of doubled dosone is she had done a year and a half of lower dopsone lowering down the bofilm persist forms of the bacteria.
And I've seen this in other patients like I've had pediatric patients that have done a little bit of lower dose apps for years and then her their BART fish is positive. They finally do the nineweek protocol and then they're three or four years in remission without having to do anything else. But the key for this protocol to work can't be active if there is bartinella which shows up now in 80 to 90% of our patients. You need four a minimum of four twoe pulses of highdosese dapsone combination therapy which is just 6 days of dapsone but at 400 milligs a day.
This is the dose that was needed to kill bartinella and it's based on the John Hopkins research that when you use rafampen with zithramax with methylene blue in culture it takes six days to get rid of these bofilm persistro forms of bartinella and there are now over 18 different pathogenic species of bart that are making people sick. So, you know, again, even Bart I and I spoke to G. Erlick yesterday about this. We were on a call. He was saying now in some of the autopsy studies, you can maybe confirm this. They weren't just finding lime. They were finding bartinella in the brains of some of these patients with dementia, which would not surprise me at all. It's almost like one of these hidden infections, apart from, you know, Ed Brywart who's been standing up and yelling this out, you know, for years.
We're now finding this in the majority of our chronically ill patients. And it's important to know because anyone out there diagnosed with dementia needs to be looking at not just belli burgdorfry but looking at also parasites like besia bartinella not just bartinella hensile quintana bililloiforis um in my new patient um he had bartella elizabeth right an unusual species with hens um but again he reversed his beta amaloid ratio with the nineweek dapsone um by the way I'm so happy you told me this about the weight loss because I was really racking my brains to figure about how the beta amaloid improved but the ptow went up because here his non-alcoholics theata hepatitis was better from the weight loss his metabolic syndrome was better from the weight loss right um it it was a little confus I thought maybe the mold toxins you know could have possibly been driving the ptow and of course that's something that needs to be looked into um but bartella is a big factor um but you don't need long-term dapsone the only time you would ever need longer doses of dapsone in my opinion would be if you don't have an infectious cause driving it. Now, let's say you had pesticide exposure or mold exposure driving it or microbiome issues with the wrong type. You don't have enough short- chain fatty acid bacteria. You do have mitochondrial dysfunction from all the free radical oxidative stress from just living on the planet. Um you you've got dishonomia. If you have other factors driving it that are not infectious, right, and you have then it might make sense to actually be using it longer term, but that's going to have to be determined in the longer term studies.
And I mean, I'd love for you and I to sit down. Yesterday I was on a call with Nikki Schulttech and others with G Erlick um talking about this. We need a brainstorming session to say if we're going to design a randomized trial now looking at Burellia, looking at BART, looking at these MSIs factors, uh do we just do it in a pilot study to get it off the ground? Do we do a full like I I'll be calling you for this one so you can you know give me some of your brain power on this one to tell us the best way you think to do it. I look forward to discussion that there's so much here and I think again this is taking the next chunk out of Alzheimer's and getting us closer and closer to where we can get everybody to improve. In our trial 90% of people improved 10% did not. And the 90% that improved, some of them improved a little, some of them improved a lot. Now you know Dr. Cat Tupes very well who is uh who was the PI on this study that we just finished. And one of her points was if you look at infections overall over 90% of the people that were in this trial had some infection or another and often a tick born tick related uh infection. Uh interestingly about 40% of them in our previous trial had a tick born illness.
Uh now my question for you then and I we're going to get to the question.
There are a bunch of good questions here but let me ask you why is it that you see so many times and you've alluded to it here micotoxins going with these various infections. Why do these tend to run together so frequently?
>> Um I don't well at this point I just think it has to do with our climate and and people's basements flooding. I mean I years ago when I was checking for mold toxins um I probably was not using real-time laboratory as much. We might have gotten it from Vibrant or Great Plains which by the way I can't even do Great Plains in New York but we were finding them but not with the frequency I'm finding it now. I'm now finding moltoxins in up to probably nine out of 10 patients coming in. Um and a lot of people don't know they've ever been exposed. And of course the problem is these moltoxins are you know they're mitochondrial poisons. They they poison your immune system. So think about this.
You get lime, burly, burgdorfry and bartinella which both can cause a chronic variable immune deficiency with subclass deficiencies are knocking out your B cells. Nicole Bgarth and others have shown this. Now you get long COVID.
Now you've knocked out your T- cells.
Now you have T- cell exhaustion. So now your B cells are affected. Your T- cells are affected. And now comes along miccotoxins, right? Which also are imunosuppressive. How can you expect people to get better when we have this overwhelming effect of infections and toxins driving inflammation affecting immune system? Right? So, infections and toxins are causing this immune dysfunction. And I just think it's now just living on the planet with the amount of flooding we're seeing. Look, we had mold in our home. Um, they did not close the chimney flu correctly. Um, we found black mold. Now, neither my wife and I got sick. Probably thanks to the 70 plus supplements I swallow every day. Uh, apart from maybe my genetics, but uh, no, I mean, if I showed you my kitchen counter of what I'm swallowing every day, you're going you're going for 108, right, Rich? It's like I Dale, I know too. My whole family is dead of cancer. I mean, I don't have one person left in my family. So, I'm doing everything I can to maximize, you know, my health. And if anybody wants to see what I swallow, go on my website, can get better.com, and look at the nutritional section, and you'll see just a minimum amount of what my wife and I take every day. Basically, it's blocking inflammatory pathways and opening up, you know, these detox pathways. But the mold is so common that and I did you I don't know the answer. Did you check it frequently in your study or you were not checking for the miccotoxins the same way?
>> Oh, we absolutely checked both both our previous trial and this trial.
Absolutely. And the majority of people had some exposure. And I think it does come back to what you said. We're all exposed. So, what's happening is we're getting rid of it. We're dealing with it pretty effectively most of the time. But as your immune system breaks down and if you've got genetic detox issues or acquired detox issues, you know, that that is a problem. So it is does come back to what you're saying. You've got to look at these for each person and you really have to to deal with them. And we've got now three grandsons and as I say, three grandsons and 300 viruses. So we're trying to keep the immune system in tip-top shape for seeing the grandsons. So let's go to there's some wonderful questions. First one here is from Nora and she's asking you about she said she's been 18 months of six antibiotics still not successful in knocking out her lime. So the question is now that you have retired who are the people you've you've uh you know you've taught where someone can go today and get treated someone who hasn't been treated successfully. What would you recommend for someone today?
Um, so I have a doctor training course and I've trained hundreds of doctors in my protocols, right? The the key for me for getting better from chronic lime is it basically the light bulb went on in 2015 when John Hopkins researchers like Ying Zang started discussing Brellia being a biofilm persist bacteria. Up until then we knew it persisted but we thought it was because of cell wall forms, intracellular forms, cystic forms otherwise known as cell wall deficient forms, L forms, S forms, round bodies.
But then we found out there were these bofilm persist forms. It turns out these biophilm persist forms are exactly like what you see in TB and leprosy. So how did I come up with dapsone combination therapy? It really wasn't that smart. I just looked at leprosy and said how do they cure leprosy? It's like oh it's a year of rafampid and dapsone. I looked at dapsone. It's anti-inflammatory.
Everything you get with chronic lime is from inflammation, right? Um, it gets great penetration into the brain. I don't have to use IV drugs. Um, it hits parasites like besia. It's antimmalarial. It hits autoimmune phenomenon. We we get molecular mimicry all the time with burellia with all these autoimmune markers, right? Um, so it it hit kind of all it checked all the boxes and it's a biofilm persist drug.
Um, so for someone that's not gotten better, you should go to ilads.org, or check the eyelids doctors in your area to see and find out. I'll be I'll be speaking at eyelids this year. Um and ask them, you know, to be able to treat you with Dapsone combination therapy.
Now, not all of them are doing it. Um there some of them are afraid of the side effects and they shouldn't be because all the lab abnormalities on dapsone always come back to normal. And I'm going to repeat this a second time.
The anemia always reverses. You may drop four grams of hemoglobin. you're back to where you were two to three months later as long as you stay on folic acid. Um, liver functions come down. There's no long-term side effects as long as you follow the protocol the way it's been developed and written out. So, you can't get over from my perspective, you cannot get over chronic Lyme disease or bartinella if you are not pulsing these biofilm persist drug regimens. I've tried it. I've been doing this for 42 years. It is the only thing I know of that puts people into long-term remission. And it does look like it cures a large percentage cuz my wife has had CO twice. She's had the flu. None of it's ever come back from the Lyme disease.
>> Yeah. So, one of the interesting things to me when we were studying amaloid years ago is that this, you know, if you designed something that would be an endogenous antibbofilm, you would want that EDTA metal binding effect plus the antimicrobial effect, which is a common way to go after biofilms. And so, what does amaloid do?
It binds these metals, these dvalent metals very tightly and it kills the bacteria and the viruses. So it really is a an endogenous antibbofilm agent in some sense.
>> So these things, you know, these things keep coming back again and again. All right, very interesting. Here's some questions from Margarita. Uh she says, "For patients with cognitive decline or memory impairment, what is your preferred Lyme disease workup? And are there tests you find more useful than standard CDC two-tier testing.
>> So, um the test that I like to use first line is Igenics. They have an IGM and an IGG immunolot which checks up to nine strains of borellia. Um I don't use the standard Eliza followed by a western blot or the modified two-tiered protocol. That's mostly for early lime.
Um, but the hygienic, so the way it works is I have a a validated symptom questionnaire on my website can get better.com. Just go under symptoms or questionnaire. You download the PDF and fill it out. We validated this questionnaire in 1600 people. It was done with university researchers from the State University of Newalts.
Three-line practices, 1600 people, including healthy. If you score over 63 on this questionnaire, you are two standard deviations above the mean. And the most important symptom you need to know about is migratory pain. If you have migratory joint pain, migratory muscle pain or migratory nerve pain, tingling, numbness, burning, stabbing, or sometimes a vibration sense that's moving around and you have even one Burrellia specific band on an imolot, 23 outer surface protein C, 31 outer surface protein A, 34, outer surface protein B, 39, or the 83/93.
If you're scoring high in the questionnaire with migratory pain and you've ruled out the other six diseases in medicine that cause migratory pain like lupus um writer syndrome uh inflammatory bowel um acute romatic fever hepatitis gau cockal arthritis there's only six others if you have even one bellia specific band you have chronic lime disease and and that's where I would use the dapsone protocol so someone's failed even a month of regular antibiotics I go straight to these bofilm persist drugs because they're so highly effective for lime. But again, you've got to go through the 16point mids model. Do you have besia? Do a bzzia immunolot and a besia fish. Do you have active bartinella? Do a bartinella fish from hygienics or teab. Uh do a bartella immunol. Again, checking for multiple strains. I if you look at not my prior book, how can I get better does it? But again, I have a chapter in ending chronic illness on the three Bs. And I described the dapsone protocol literally like a cookbook. Um, so that you just go to your doctor and bring it. I even did a lowd dosone protocol for those people that say, "Look, I got to stop and start." I show them how to do the lowd dose protocol. So the book is going to be out in a couple of months. You just bring it to your doctor. It's like a cookbook and it'll show you exactly how to run through the 16point model and how to do this.
>> Great. It sounds like we got a lot of good presence for doctors. That's great.
All right. And Margarita goes on to say, "What evidence do you rely on to determine whether Lyme disease is actually contributing to a patient's cognitive symptoms rather than simply being an incidental finding?" So you you're always going to do a differential diagnosis in medicine. So there are standard workups. So for example, if we've checked your B12 and your folic acid and your methylonic acid as an oult B12 marker and we've checked your thyroid functions and we've looked at heavy metal toxins, mercury, lead, arsenic, right? aluminum, things that cause cognitive issues, mold, which causes cognitive issues. You basically do a differential diagnosis. And and again, in any chronic illness, that's about page 50 or so, I have a list of all of the differential diagnoses for cognitive issues of the boxes you need to check off. So, you're always going to do a differential, but you'll find in most cases, it's never going to be one thing, right? It it can be, you know, that people have had diabetes type three, right? they've got insulin resistance and they've got slightly low B12 levels and they've got heavy metals and mold. But we still find even with all of that that usually at the top of the list that's causing the cognitive issues in my population and this is now 13,000 chronically ill people in 42 years, it's lime, it's besia, it's BART, and it's mold followed by heavy metals.
So yes, thyroid, yes, B12, yes, microbiome issues with the gut brain axis. Um, yes, mitochondrial. All of these things can affect cognition, but ultimately in my world, it's these infections and toxins that are ultimately at the top of the list that are making people sick. But but you'll find the differential diagnostic list um in ending chronic illness. It's around page 50 or 60 of the book.
>> Great. Thank you very much. Uh she goes on here to ask about uh evaluation. She says mentions UCLA. Um so asking about talking to me and so if you go through Pacific Neuroscience Institute um that's where we are uh seeing patients. U all right here's another question. This is from Tammy. U she says there are so many quote oxygen and blood cleansing type treatments. If a person could only afford to do one, which one do you feel is most valuable? Do you like IV ozone, HBOT, MHBOT, hydrogen, therapeutic plasma exchange? um EBO or other are there certain things you feel that would be better for and I realize these have different mechanisms u but are do you have a favorite among those >> so so here's the problem and you have to realize my bias I've had patients come to me who've gone to Germany and fried their brain at 106 107° some of them will be better for a while but they ultimately relapse I've had people do SOT therapy it does help some people I've still seen them relapse um I've seen people do IV ozone here.
You're using free radical oxidative stress to kill the bacteria. The problem with asking me this question is I'm a doc who's knows that we're in the middle of a worldwide epidemic where according to BMG Global Health, one out of seven people on the planet has now been exposed to to Lyme disease, right?
14.5%. And believe me, it's more.
Believe me, it's it's a lot more. It's probably at least 25%. So when you're asking me this question of whether you do hyperbaric or the rest, my problem is these things may give you temporary relief, but they will not cure a chronic persistent infection. So if you're talking about chronic lime, which is a chronic persistent infection with burilia, you either only there's only two persist drugs out there, which is dulfrum, which Ken Lner has published on through Stanford and Dapsone combination therapy, which we have 11 studies at this point. So it's not that you can't do hyperaric and get some benefit in some people. There are people who are loaded with toxins that will do plasma exchange. In those cases, you may get some help with plasma feresis. It's quite expensive. So it you have to really look at whether let's say for me I would only consider something like that. If I had had a patient who had done dapsone combination therapy and said listen I got help as most people do but I can't get over like I still have mold toxins. I think then you might want to consider plasma feresis. But my goal was in the middle of an epidemic to find a quick short oral generic protocol that anyone across the world could afford, right? And do the testing that also could be affordable. That really was my goal in my 42 years of clinical medicine. So I you understand you're speaking to someone biased because these all can help but they're not curative and that's why you're hearing a biased answer from me.
>> Yeah. No, I think what you came up is brilliant actually because there always comes back to the idea of public health.
How do you do this if it's going to be $50,000 a year for some drug that doesn't work very well? So, you know, you've got something that works quite well and is much much less expensive than that and really could be used globally uh you know, as to to help reduce the global burden of dementia, which is fantastic. Now, it's interesting. I would go back to the fact that these things have very different mechanisms. I mean, I think of HBOT and EWT as being for people where you want to get better blood flow, more oxygenation, people who have some vascular disease, people who have uh, you know, who potentially have, you know, high cholesterols or uh or sedentary lifestyles, things like that.
That's one thing. Plasma exchange very different. I think of that as being more of a detox agent for people who have high microlastics, for example. for people who have high micotoxins, those sorts of things where the goal is let's reduce the toxic burden. But as you just said, Richard, that's not going to kill your persistent Lyme disease. Um, now, but what about ozone? Do you do you tend to use ozone or not? Me, not personally.
Again, I know people that have gotten better from doing both IV ozone and different forms of it. Look o ultimately brilliant and these bugs are causing oxidative stress but on the other hand using ozone with oxidative stress will kill some of these bugs but again I've seen so many relapse or people where their veins don't function anymore because they were doing so much IVO zone they blew out their veins it's not something I could in good conscious tell people to do and I you know and even among mys group I don't think you'll ever find two doctors doing exactly the same thing so I think there is a role right hyperbaric can be very useful right in in some people with cognitive dysfunction and uh so but but it it's got to have a time and a place when you're going to the underlying inflammatory causes that after you've gotten rid of infections, you've detoxed, then maybe some of these things would be, you know, would be helpful in that population.
>> Yeah. And I always go back to what's the mechanism, what's actually driving this that you're trying to treat. And in your case, yeah, what's driving it is the pathogen and you're trying to treat that. And then the other piece is do the basics before you start adding all the new, you know, people will say, "Oh, there's some crystal I'm supposed to put on my forehead." And there's, you know, there is a lot of pseudocience out there. I don't know if you've seen the word, >> I don't know anybody that's tried that one, Dale. You should, you should share that with me at some point in time.
[laughter] >> There was one I just saw a couple of days ago that said, "The reason that there's not a single case of Alzheimer's in Israel is because of this potion I've developed. And if you just buy my potion, you can be the same and have I mean, it's so silly. Of course, there's not zero cases of Alzheimer's in Israel.
We all know that. So, in fact, we you know, we interact with some doctors who are treating Alzheimer's in Israel. So, we so there's there is a lot of pseudocience. I think we all have to be really careful of the junk that's out on some of the internet sites now.
>> Well, and and one and one thing you should know about this because of you know, there's been an attack on science.
I don't need to tell you. In fact, by the way, part of the maha movement I completely agree with is we we have a chronic epidemic problem in this country. I mean, the the autism rates have gone from 1 to 2500 to 1 to 36.
That's not just better diagnostics, right? I mean, 2 to 3% of the population is ADHD. I mean, we're really dealing with chronic illnesses. So, they're correct. They deserve something better.
And regarding this book, Ending Chronic illness, I have over 2,000 scientific references. They're putting them up on my website. they'll be available next week because there was no place in the book. It was 173 pages of scientific references which is jamanuing like top references right so everything I'm saying in ending chronic illness is backed up by hard scientific proof right and it's really important in this day and age because there's so much like what is true what is pseudocience as you're saying what do we believe you've still got to go back to hard science and what science has proven over and over now using common sense right there's things published in the medical literature I'll give you one example by the IDSA and their guidelines lines on chronic Lyme disease. They are leaving out all of the important research that bellberdorf persists and that is a biofilm persist infections and that there's overlapping factors like msids factors make they left it out because it's not politically convenient for them and it's published in guidelines. I don't agree with those guidelines but I've been in medicine long enough to know that the iides guidelines are going to say the exact opposite. Right? But you have to know how to get through the science, right? And read it and understand what is true and use your clinical expertise with your two feet on the ground and right head in the sky to know exactly what is true and what's not.
>> Yeah, it is unfortunate that sometimes the goal for best outcomes has been uh has been impacted by the goal for best incomes uh by various companies etc. So, we want to focus on the outcomes, not the incomes. And and I think that that's key. And you know, there's that wonderful documentary that you're in.
It's all about uh chronic lime and the the refusal of the of the medical system and the insurance system to believe that chronic lime is a phenomenon. When it's clear right in front of your face, it's happening all the time. Then along comes long COVID and everyone says, "Oh, sure there's long COVID, but not chronic lime." What do you mean? Of course, there's both. And there's an excellent question here from Lindsay where she asks about uh where Lindsay asks about uh COVID. Now, we're seeing and you're probably seeing the same thing. We're seeing people who get COVID and now have some cognitive decline, but we're also seeing people who get vaccinated and then have some co some decline. So again, it comes back to anything that is triggering chronic inflammation can be a contributor to cognitive decline. Are you seeing this impact the people that you're looking at with these various tickborn illnesses? Yeah, in in fact the last chapter in my new book ending chronic illness is vasa viruses and the last part is on long co I published in the journal microorganisms back two years ago that all 16 msids factors are associated with long co and what we were finding after people got covid is my hypothesis is it's not just the spike proteins that are in the endothelium that are driving VGF vascular endothelial growth factor what we were finding in a lot of these patients that got sick after COVID first of all they had low glutathione. The lungs have 140 times more glutathione in the body than anywhere else. So in that first wave of COVID um I published the first article on glutathione in April 2020 where we had we by the way we didn't have one person die in our practice from COVID because we were blocking NFCappa B using NAC alpha lipoic acid glutathione um stimulating NRF2 using a curcin tumeric broccoli seed extract sulforophane gluc and I found out afterwards that the virus has to replicate by lowering glutathione I didn't even know that when I was publishing the article so what we were finding in these long COVID cases is the VGF was from bartinella. It was reactivating because VGF is an indirect marker of bartinella. So the problem is in these long COVID cases where they get T- cell exhaustion. They now know that they're throwing off the bifidobacterium in their gut and they're getting depressed. Right? So now they're looking at like SSRIs and going, "Oh, that's a treatment for long COVID." But that's only because it was throwing off your serotonin because it's throwing off your microbiome. Or they had low adrenal function. they would give them adrenal and they would notice their energy would pick up. It's the same 16 factors in long COVID except we were seeing the T- cell exhaustion. So I was using Bruce Patterson's lab in California to look at the chemocines and cytoines. Um and and ultimately we were able to get a lot of these longcoid cases better but it wasn't just from treating viruses except when they had reactivated Epstein bar or herpes virus 6 that in those cases we had to use things of course like famcyclo or other antivirals. And by the way I discovered something interesting about these EBV reactivations which they're now showing up with autoimmune diseases like MS. I did a search and it's it's in an in chronic illness that spironolactone a drug we've been using for ages for PCOS which is now POS uh to lower testosterone uh for and they use it for blood pressure um it is a drug that is very useful for Epstein bar with percentine dipol when you combine these two drugs with a standard drug like fam cyclloe it hits the epstein bar virus at multiple points of its replication and looks like it's going to shut it down and I put these kind of tricks in my new book, Ending Chronic Illness, because we would see these people with EBV reactivations and now they know it's associated with MS, but there's nothing out there to say, well, how do we actually keep EBV in check, right? Doing a deep dive in the medical literature. I may have discovered something that's useful. I need a again randomized trials to prove it. But when you look at the biochemistry, it looks fascinating. If I had it, I would definitely be speaking to my doctor about these kind of drug combos. But that but that is the last chapter in my book vsiruses is looking at long co and how these 16 mids factors are keeping people sick.
>> Very interesting. All right. There's another one here. This is from Julie. Is taking a second generation antihistamine like zerek daily for decades contributed to developing dementia? I'm asking as a lime and mass cell activation patient who needs to take an antihistamine daily but notice it does dull the brain. Okay.
So there are two pieces here. As one is as far as drugs to increase risk for dementia that's been published. There are about 32 of them. Um, and yes, anything that is antiolineric, anti-histaminuric, those are very common ones. Of course, the benzoazipines, those are all ones that can. Some of the SSRIs, these are all ones that increase the risk for dementia. Now, Massel, I wanted to ask you about that, Richard.
when you are having your patients who you're treating them for burilia and or other tickborn illnesses um and they have significant mass cell activation syndrome what are you adding for that >> so you you have no choice in these severe mass cell patients you've got to use an H1H2 blocker like like Zerek and Pepsid by the way the way we reverse the acetyloline estate it's an interesting question although I under I was under the impression however it was more benadryil and dyen hydramine and some of these stronger first gener erations that had a much stronger effect. That's true, Dale. Yes.
>> No, no doubt. Yeah. And they have more antiolinergic effect.
>> Yeah. Um but so what we do in those patients when I have to use an H1 H2 blocker and and Singular Montalucast also excellent. Um in those kind of patients, we use PA Leoline. Um there's a product called Sunbalance, excellent for it. We use DAO, damine oxidase because these people, you've got to degrade, right, their histamine, and they're very low in their enzyme DAO.
Um, you've got to look at also the microbiome and how it's affected with leaky gut because when you have leaky gut with intestinal hypermeability that is also driving the histamine secretion with mass cell. In fact, my asthma completely got better by healing my leaky gut. Um, I'm still taking bovine imogloabbulins for it and basically avoiding like high histamine foods. My wife's migraines are gone because it was being driven by histamine and my mother-in-law at some point. Uh, but that's a whole separate issue than mass cell activation. But but the point being when someone has to take these there's a supplement I really like from or molecular called membrane which has huperazine and vinosetine and these are natural herbs that are acetyloline eststerase and they will bring up acetylcholine. So basically what I do is in someone that has to use these I actually I give them membrane. Um it's a very cheap over-the-counter supplement from orthomolelecular u that's actually a trick since you asked me about it using H1H2 blockers.
>> Right. Right.
>> Uh that's one of the tricks actually I use because of the effect of these antihistamines on brain function and and so far I mean it looks like it's been quite effective but but by the way you still have to get rid of mold. If you've got mold toxicity or lime or bart driving your mass cell activation, >> your massel activation is going to be present until you treat the infections, you treat the mold. So, like anything, you've still got to get to the underlying causes, intestinal hypermeability, lime, bart mold, because these all can be driving mass cell activation.
>> Great point. You know, there have been a few that have had CGP inhibitors like Ubelvi actually have a short-term effect. Another one that's interesting is this new one, Rep. You seen this new drug candidate, this new drug coming out, Repzedo, it hits multiple of these same sorts of uh same sorts of pathways.
I mean, it looks like it may be something. We'll see. Time will tell, but it looks very promising. So common mass cell activation. My worry is whether there is kind of subclinical intracell activation in many of these patients that we're missing as we're trying to treat these things. And again, it comes back to the nice anti-inflammatories that you're using uh along with the antimicrobials.
All right, next one here is from Roxan.
And Roxanne says, "I'm a physician on Long Island. What is PTA?
Do we check routinely with the tick panel or wait to get a positive? Can you elaborate on what physicians should order as far as markers pre-treatment with DAPSO?" And I guess sounded like she was uh going back and I don't know if you actually said PTA. She's looking at something that you were talking about markers. I think she meant PTA.
>> Yeah, PTA. This not PTA. This is PTA.
PTA 217 is that he was talking about.
>> So in if if you're on Long Island, I'm sure you're seeing your fair share of chronic life patients. So, so what I'm asking all physicians to do and I'm discussing this at every conference I'm speaking at, including I'm asking all my colleagues at this point to start checking beta amaloid 4240 ratios. I like Quest. I know I I happen to find the Quest Labs is an easy way to get them. They do it through LabCore, but I really like the the format through Quest. Get a PAL phosphorolated towel 181 phosphorolated towel pal 217 neuroilament light, which is more axonal damage, more non-specific. You can get it with high blood pressure, cholesterol, kidney disease, etc. Anemia. Um, and I would only get, and you can confirm this still, a gofibrillary acidic protein if they were APOE44 with genetic Alzheimer's. Uh, because that looks like it raises your risk uh like 10 years in the future. But I'm asking every practitioner out there who sees lime, please check these biomarkers because in my population, it was roughly half. I asked a doctor I've been training in the last year. She said it was about a third. about a third of her patients were showing up with these Alzheimer's biomarkers, which means that the the true number of patients that may be going on towards dementia from lime, it may be somewhere in the 33% to 40% range of, you know, these cases of dementia are going to be driven by infections like burilia. So, but if you're going to use dapsone, you have to check a G6PD. Um, you have to do a glucose 6 phosphate dehydrogenase to make sure people are not going to hemolyze. you want to get a baseline methogmoglobin level. Um, but if if you read my article in microorganisms 2023, I think it's September, the entire DAPsone protocol is listed. And and if I can get you an early copy of of ending chronic illness, literally, I'm not exaggerating. It's like a cookbook. Like week one, this is what you take. This is when you do the labs. Um, if they if people have to start and stop, this is how you go back on it. Please learn to use this protocol. It is the most highly effective protocol short-term I I've ever seen. But but you do want to check these biomarkers to see what you're getting. And by the way, then publish it. I mean, that's what I'm planning on doing now with with my colleagues. We've got to get this into the literature. I couldn't agree more. And this has been one of the biggest problems. People talk about it. They may present it or they may talk about it on a podcast, but they don't take the time to document and publish it. And this is what we've been doing recently. So we have now an example of posterior cortical atrophy that reversed. This was someone taken care of by by wonderful caretaker Carrie Rutland. Dr. Craig Tanio down in Florida has an amazing case of cortical basil syndrome. To my knowledge, the first one where there's documented reversal uh of the symptoms. Person did very well after being told by their doctor originally, forget it. It's over. No one's ever gotten better from this disease. uh we've got a couple of cases now of progressive super nuclear palsy that are improving. I would love to know how many of these people are going to end up having tickornne illness as one of the drivers of these degenerative conditions. These things are all coming together and we do need we need to get them out there. We need to get them published ultimately get them into trial so that we can take this to the next level and have this become part of the normal treatment part of the standard of care. So all right, even though I promised my wife I would not be doing any more medical articles after this guy just the second patient just reversed his beta amaloid with the one where the pile went up slightly. I realized I have to put this in the literature, right? I mean this this is the only way that the the field is going to move ahead.
>> Yeah. Now we had a question that disappeared here. So whoever's disappearing the questions, please put the questions back. A question disappeared here. Um that was about what about anti-amaloid antibodies? Have they ever been used in COVID or lime? I'm not aware that they've ever been used in anything except Alzheimer's disease.
However, uh the the idea of removing these things that are antimicrobial, I think in the long run, what you want to do is you want to remove all the insults first. You want to get people doing very well and then I think down the road you could then I think micro doing slowly that I think that's the the future bringing these all together. But the key is you don't want to remove the protection before you remove the need for protection. And I think that's that that's where I think that would probably not be a good thing to do. All right, here's one from Elizabeth. My brother had lyme menitis about a year ago, three months later started to develop symptoms of mythenia gravis. Our father died of Alzheimer's disease. Given this combination, should he be undergoing early evaluation for Alzheimer's? his lime was only treated with 10 days of doxycyc. Should he be treated more aggressively with dapsone now a year later? What's your sense about that? So I mean it always comes back to clinical.
So you know if your brother has a chronic fatiguing muscularkeeletal cardopulmonary neuroscychiatric illness meaning I have good and bad days. My symptoms are coming and going. I am tired. I have aches and pains. I have neuropathy tingling numbness burning stabbing vibrations moving around. My memory concentration's not working. I can't fall asleep. I keep waking up in the middle of the night. I'm walking into rooms and I don't remember why I'm there. It you've got depression, anxiety, and I don't know why. If you've got this constellation of symptoms that are seen with chronic lime, 10 days of doxycyc, especially if it's lime menitis, that is not normally the standard of care. Standard of care would have at least been 28 days. A lot of docs would have even used ibrophen sept trioxone for that 28 day period. You can cure lime when you get it early, but 10 days of doxycycan is minimal. So if if you're still finding a year later these kind of symptoms and you're doing a differential and you're ruling out other causes of it, I absolutely would, especially family history of Alzheimer's, you need to check the APOE status. You absolutely should check the Alzheimer's biomarkers. And if you did an IgenX immunolot and you still saw uh that there was positive, you know, bands on there. Um now again remember when you treat with antibiotics early on you abre areate the immune response where you may not get antibodies later on because it shuts it down so you can't rely but for example tab does a very good PCR for bellia berdorphy I actually like for the PCR I actually like tab better than ienics the hygienics I mostly do the imunolots but I would use tab to find out if he's PCR positive I would look at the immunolot fill out the questionnaire on my website can get better.com but remember it's a clinical diagnosis But um and and even spinal taps are tough because you hardly ever find the burilia active on a spinal tap. There's there's antibbody antigen complexes that form that you don't even find it most of the time. Um so if he did have symptoms consistent with lime and you've ruled out other diseases the myastinia you know we get autoimmune antibodies all the time anti-uclear antibodies rheumatoid factors anti-ganglio antibodies anti-gad 65 anti-thyroid peroxidase anti-therog we see loads of themia not so much I will tell you um but you know he would need to have things liketosis and you know classic neurological symptoms of myastthenia possibly has two different diseases of But someone like that, if it is active with lime, yes, dapsone would be of course perfect because it has great penetration into the central nervous system. But still remember, you always have to do the 16point MSIS review questions 1 and 22 on my questionnaire.
Do you have day sweats, night sweats, chills, flushing, unexplained cough, air hunger? Does he have besia which shows up in 60 to 80%. Does he have bartinella? Does he have those bartinella stretch marks, right, which you can look up in to see what they look like? Um, you've got to rule out all these overlapping causes of inflammation because the 16 points model applies to lime to longcoid to Alzheimer's. You've got to look for where the inflammation's coming from.
>> Yeah, great point. Okay, I know we're we're running up against the timing here, but I want to take what's one more from Lucy. She's asking about approach to treating Lyme disease in patients who are already taking SSRIs or SNRIs and she's mentioning here the inability to to consider methylene blue and is that okay and patients and I realize that you you mentioned you didn't say that you have to take every single person needs to take this. So the question then is what about people h how do you treat people who are already on SSRIs or SNRIs?
>> Yeah, it's it's a great question. So, first of all, I do my best to get them off of them. Um, and and that's number one. And the reason is, for example, my wife who's 8 years in remission, she did not use methylene blue. She used 2,000 milligs of glutathione three times a day to lower methmoglobin. So, be clear that the way I created this protocol, which took me 10 years of playing around with these drugs, use simetadine. Simetadine lowers methmoglobin. Um, NAC and glutathione will help lower methogmoglobin. NADH inata helps to lower meththemoglobin by one of the enzymes that lowers it down. Vitamin E will help. So there's lots this is actually in the the type protocol for dapsone. All of this is in there. So you can do the protocol without methylene blue but the problem is going to be the last week on the protocol if it's chronic lime and you're doing 4 days of highdoseseone at 400 your methmoglobin levels are going to be you know high.
Now as long as they're below 20% I will have people hang in there. dangerous is like 50 60%. I've never seen it happen.
Um, and generally if you give them 2,000 milligs of glutathione every day, you'll probably keep it low. But the reason to consider using methylene blue is methylene blue is a biofilm persist drug like dapsone. So if you look at the John Hopkins studies, methylene blue rafampen zithramax kills bartinella. So I love methylene blue because it's helping mitochondrial function. It's lowering meth hemoglobin. Um, it's hitting the bofilm pyroforms. It's doing a lot of different things when you're using it.
Could you do it without it? The answer is yes, you could. But try and get the patients off of those drugs. And you know, if you've got to use I I use things like LRA pregablin to get them to sleep. Um I I'll use other tricks. You you can't really even use Wellbutrin because it also has a little bit of that effect. Um but but I do try getting them off as best as I can for those nine weeks and then putting them right back on. Remember these tickorn infections drive depression and anxiety. So a lot of these people when the tickborn infections are treated and the mold is treated and you've addressed all the MSI factors, they don't need these SSRIs and SNRIs, right? So just keep it in mind, but you can do it with the protocol with highdose glutathione. It's just going to be a little difficult the last week on the protocol.
>> Yeah, great point. And I would go back also one question and say cat tubes had uh in the trial uh in which by the way every single one of her patients improved uh one one of them did have myastinia gravis which got much better um just doing the the right things for for that particular person. So uh certainly it does impact autoimmunity.
All right well I'm going to stop there.
We'll try to take the rest of them on Facebook. Thank you so much Dr. Richard Horowitz. Always great to talk to you.
Congratulation on the new book coming out October 13th, Ending Chronic Illness. Thank you for writing that. I'm sure it's going to be very helpful to so many of us. And congratulations on your patient in getting this published showing this 63% reduction in phosphottow with a person improving with their cognition and improving marketkedly with their Lyme disease.
This it's a new era and neurodeeneration is is uh you know neurodeeneration is going to be less of a problem going forward. So this is fantastic to see.
>> Thank you. And and by the way, the second patient that I'll probably put in the literature after doing the dapsone therapy, no more fatigue, no more joint pain, no more cognitive issues. He's 100% well clinically with the beta amalloid reversing, but again the pow going up, which again may be what you explained today. So >> yeah, may maybe better in a year. So all right, fantastic to talk to you as always, Richard. Thank you. Have a great summer and we really appreciate the discussion.
>> Okay, take care.
>> Okay, bye-bye. Bye-bye.
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