What if some people diagnosed with chronic fatigue, fibromyalgia, autoimmune disease, anxiety, or even early Alzheimer’s are actually dealing with an underlying infection that was never properly identified?
Today, I’m sharing my conversation with Dr. Richard Horowitz, a board-certified internist who has treated more than 13,000 patients with Lyme and tick-borne disease over the last four decades, many of whom had already seen countless doctors and collected diagnoses like chronic fatigue syndrome, fibromyalgia, depression, anxiety, multiple sclerosis, and early dementia before discovering Lyme may have been part of the picture.
Dr. Horowitz calls Lyme “the great imitator” because its symptoms can overlap with so many other conditions, and since 2016, Dr. Horowitz has published 11 papers on treatment approaches. In one of his latest studies, he and his colleagues explored a possible connection between Lyme disease and Alzheimer’s biomarkers, reporting major improvements in certain inflammatory and cognitive-related markers after treatment.
We discuss his broader “MSIDS” model, which looks at chronic illness through a much wider lens. Instead of looking for one single cause, the model examines multiple overlapping factors that may contribute to illness, including infections, toxins, gut dysfunction, nutrient deficiencies, sleep issues, immune imbalance, and inflammation.
Table of Contents
In this podcast, Dr. Horowitz and I discuss:
- Why Lyme disease is called “the great imitator” and how it can resemble chronic fatigue syndrome, fibromyalgia, multiple sclerosis, anxiety, depression, and Alzheimer’s disease
- The often-overlooked migratory pain that is one of the hallmark symptoms of chronic Lyme
- The Lyme symptom questionnaire, which he developed and validated on 6,400 patients
- How research from Johns Hopkins and other universities changed our understanding of Lyme as a persistent infection
- Why Dr. Horowitz began using drugs like dapsone and rifampin in Lyme treatment protocols
- His published research on dapsone combination therapy and the improvements he has observed in patients
- His recent findings on Lyme disease and Alzheimer’s biomarkers, including reductions in tau217 levels
- Dr. Horowitz’s unique MSIDS model and the many overlapping factors that may drive chronic illness
- Why chronic illness rates continue rising and what conventional medicine may still be missing
- Why Dr. Horowitz believes recovery is possible, even for patients who have been sick for years
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Transcript
Dr. Richard Horowitz: The anti-amyloid monoclonal antibodies, like lecanemab, donanemab, that are out there, they lower p-tau by about 23% over six years. We lowered it by 63% in nine weeks. The reason being, the amyloid that was being produced in the brain, so the phosphorylated tau, was coming from an infection.
Introduction: Dr. Richard Horowitz and the MSIDS Model
Ari: Hey, this is Ari. Welcome back to the Energy Blueprint podcast. With me in this episode is Dr. Richard Horowitz, who is a board-certified internist and medical director of the Hudson Valley Healing Arts Center, an integrative medical center which combines both mainstream and integrative approaches in the treatment of Lyme disease and other tick-borne disorders.
He’s treated over 13,000 Lyme and tick-borne disease patients over the last four decades, with patients coming from all over the world to his clinic. He’s advised the HHS, the New York State Department of Health, as well as governmental agencies all over the world.
His third book, titled Ending Chronic Illness, is coming out in October of this year, 2026. The broader discussion of this is, as you’ll hear in this podcast, he’s developed this framework over the last four decades of treating thousands of patients.
He’s developed this 16-point, what he calls MSIDS framework for understanding and treating chronic disease. This was originally developed in the context of Lyme disease, chronic Lyme disease, but he has now discovered and published research on the use of this model in treating other illnesses. There was a recent paper that he’ll discuss in relationship to using this model to guide the treatment of Alzheimer’s. They have some very positive results in this early pilot research.
What we’re going to talk about in this conversation is his MSIDS model, what it consists of. We’re going to talk about Lyme disease. We’re going to talk about other chronic illnesses. We’re going to talk about the gap in understanding between the conventional thinking and his MSIDS model. We’re going to talk about some practical aspects of diagnosing Lyme disease, understanding symptoms, how the symptoms overlap with other conditions like chronic fatigue syndrome, fibromyalgia, and a whole bunch of other stuff that is relevant to anybody struggling with chronic, complex disease or very unrelenting symptoms that just won’t go away and are very difficult to resolve despite trying lots of things, seeing lots of doctors, et cetera.
I hope you get a lot of value from this episode. With no further ado, enjoy this conversation with the very, very knowledgeable Dr. Richard Horowitz. Dr. Horowitz, welcome to the show. Such a pleasure to have you on.
Dr. Horowitz: Nice to meet you, too, Ari. Great to have you here.
What is Lyme Disease? "The Great Imitator"
Ari: The first thing I want to talk about is, what is Lyme disease? What is chronic Lyme? Let’s just take listeners through this from the most basic foundational understanding of what’s going on.
Dr. Horowitz: Lyme disease is a disease that you get from a tick bite. It’s mostly deer ticks, Ixodes scapularis. Lyme disease is essentially a bacteria called Borrelia burgdorferi. It gets in the body after a tick bite. The usual themes is that it takes 24 to 48 hours to get in, but I can tell you from personal experience, even within a couple of hours, my patients have reported that they’ve gotten sick.
The point being that Lyme is a great imitator. I’ve been doing this for 41 years. I’ve seen over 13,000 chronically ill patients with this disease. Most of the patients who came to see me, they weren’t even diagnosed with chronic Lyme disease. They were diagnosed with things like chronic fatigue syndrome, myalgic encephalomyelitis, fibromyalgia, some non-specific autoimmune disorder like multiple sclerosis, even Alzheimer’s dementia.
As we were just discussing before we came on, I just published an article in the Journal of Alzheimer’s Disease Reports for the first time linking Lyme disease and Alzheimer’s in a live patient.
This bacterial infection essentially makes you tired. People come in with chronic fatigue. They come in with migratory joint pain, migratory muscle pain, and migratory nerve pain. This tingling, numbing, stabbing, burning sensation, sometimes a vibration sense. They have memory concentration issues where they have word-finding problems. They walk into rooms and forget why they walked in. They can’t fall asleep. They keep waking up in the middle of the night and they don’t know why. Many are depressed and anxious.
The problem with this disease is, when you get inflammation from Lyme disease, it mimics so many different symptoms that it’s very confusing, I think, to many patients out there, as to doctors. Chronic Lyme disease is essentially the chronic form, which, by the way, it’s a big topic because it’s still debated among certain scientists whether it’s a chronic persistent infection or not. I can tell you 100% for sure, from my perspective, it absolutely is. There’s no doubt about it.
The Controversy: Why Conventional Medicine Denies Chronic Lyme
Ari: Why is there controversy about that? What is the alternative explanation if not the chronic infection?
Dr. Horowitz: There are two groups out there, the Infectious Disease Society of America, or IDSA. It’s an infectious disease group that basically says that Lyme is difficult to catch, easy to cure, and that if you’re sick after 30 days of antibiotics, we don’t really know why. We think it’s aches and pains of daily living. Maybe it’s autoimmunity. Maybe pieces of the bacteria called peptidoglycans are stuck somewhere in your body. It causes an inflammatory reaction. They call it infection-associated chronic illness, just like they do with long COVID.
The problem is that after seeing- I’ve been in this field for over four decades, we definitely get DNA positives, they are called PCR, Polymerase Chain Reaction. We get absolute proof of chronic Lyme in our patients. The reason there’s controversy is, with these two groups, they’ve looked at the scientific literature, and what they would like is a randomized multicenter placebo-controlled trial to prove that antibiotics work in this population.
The reason they don’t believe it is because going back almost 20 years, they did a randomized multicenter trial using standard drugs like Doxycycline, IV Rocephin. What they said when they were interpreting the NIH trials is that the results basically didn’t hold. In fact, the people’s memory and concentration did get better in the study by Brian Fallon from Columbia, and fatigue got better in the trial by Krupp. It’s gotten out there that it didn’t hold, they relapsed, therefore, the antibiotics don’t work.
What the research didn’t realize is that it’s only in the last 10 years we discovered from John Hopkins University that these bacteria are very specific bacteria called biofilm persister bacteria. Just like when you go to the dentist to have them take plaque off your teeth so that you’ll get a gingivitis, and they’ve now shown that porphyromonas gingivalis, the bacteria under there, can go up into the brain and cause Alzheimer’s. In a similar way, Lyme is a persister biofilm bacteria like tuberculosis, like leprosy.
What I did about 10 years ago is, once that literature came out, I looked at some of the tuberculosis and leprosy drugs that have been out forever. I had done a lot of TB treatment back in residency at Mount Sinai Hospital. This goes back like 45 years ago. I was using drugs like rifampicin, pyrazinamide, INH. I decided to try these TB drugs, specifically rifampicin and dapsone for Lyme. I added some doxycycline to it, and I published the first study in 2016. It was a home run out of the park from day one.
I did, in fact, recently apply for an NIH grant for a multicenter randomized placebo trial. The researchers who reviewed it said, “Well, we think we need a lot more information on this, but we’re going to deny the grant. Why? Because Lyme is not a persistent infection,” which is exactly what I was trying to prove in the first place doing the study.
The whole scientific literature is there. There’s probably 600, 700 articles on chronic persistence, but because of these old studies done by the NIH 20 years ago, there are certain groups that are just refusing to believe it.
Ari: Interesting. A couple of things, and you may want to address this in multiple parts because it might be complex. I know that there are some controversies around the diagnosis of Lyme and certain tests that are involved, and different practitioners favor one test versus another, and say that a particular type of testing is not valid. Then the other aspect that I want to address is, you mentioned that the symptoms of this can often manifest as chronic fatigue syndrome, fibromyalgia, vague symptoms relating to memory or brain fog, things like that.
Diagnosing Lyme vs. Chronic Fatigue Syndrome & Fibromyalgia
How does one differentiate between those conditions? Let’s say chronic fatigue syndrome versus Lyme. How would one know whether their symptoms are caused by one or the other?
Dr. Horowitz: Yes, it’s a great question. It’s an important question because we’re basically dealing with 3% to 5% of the US population with a combination of chronic fatigue, ME, and fibromyalgia. Long COVID, by the way, exactly the same symptoms; fatigue, aches and pains, neuropathy, brain fog, sleep disorders, memory concentration problems, even what’s called POTS dysautonomia. POTS stands for Postural Orthostatic Tachycardia Syndrome. It’s when a part of your nervous system that controls your blood pressure and heart rate gets affected.
Unfortunately, all of these diseases share the same symptoms. Chronic Lyme disease, fibromyalgia, chronic fatigues and ME, long COVID, they’re all chronic fatiguing, musculoskeletal, cardiopulmonary, neuropsychiatric illnesses.
The way you make the diagnosis of Lyme is that, well, first of all, if you have a bull’s-eye rash, and half of the rashes, by the way, don’t even look like bull’s-eyes, they look like spreading red rashes that could be confused with a cellulitis, spider bites, sometimes even herpes zoster shingles. If you have the classic bull’s-eye rash, which again can be 50% of the time solid, you have the diagnosis, but it has to be physician-documented. You don’t need a positive blood test because many times, people take antibiotics shortly after getting the rash, and that stops your immune system from even making antibodies.
The way you make the diagnosis is it’s a clinical diagnosis. I published back in 2017 with researchers from the State University of New York at New Paltz, Maryalice Citera and Dr. Phyllis Freeman. We published an article where we took 1,600 people from three medical practices and people who were healthy, and we validated a Lyme symptom questionnaire that I had been using. I took it originally from a questionnaire developed by a colleague of mine, Joseph Burrascano. We validated the questionnaire statistically, and it’s on my website, cangetbetter.com.
If you take this questionnaire and you score over 63 on the questionnaire, and it has symptoms like, do I have fatigue, mild, moderate, severe, do I have joint pain, muscle pain, nerve pain? If you score over 63, it means you have a very high probability of having Lyme disease. If you score in between 35 and 62, there’s a moderate probability. Under 35 to 25, it’s possible. Under 25, it’s not likely you have Lyme disease. When you take the questionnaire, it gives you a pre-test probability.
One of the ways clinically anyone can know if they have it is there’s only seven diseases in medicine where pain moves around your body. It’s called migratory pain. If you have pain in your shoulder that three days later is in your knees and four days later is in your ankles, and it’s just moving around and you can’t explain why, or you have migratory muscle pain, or migratory nerve pain, tingling, numbness, burning, stabbing sensations, or a vibration sense, which moves around, again, without reason, migratory pain is the hallmark of chronic Lyme.
There’s only six other diseases in medicine. I used to joke with doctors that unless you graduated at the bottom of your medical school class, you pretty much could figure out that this was not lupus, this was not ulcerative colitis or Crohn’s disease, this was not gonococcal arthritis, you didn’t have acute rheumatic fever, you didn’t have Reiter’s syndrome, or hepatitis. There are some basic other diseases that cause it, but very easy, in fact, to differentiate it. 95% of my patients have migratory pain.
If you’re someone listening, and you’re tired, and you have good and bad days with the symptoms come and go, and you can’t explain why your pain is moving around your body, and you do have, in fact, neuropathy, this tingling, numbness, burning, stabbing, with memory concentration problems, and your doctor has ruled out other things. They’ve checked you for thyroid disease, hypothyroidism and B12 deficiency, heavy metals, mold toxins. We find mold toxins in about 90% of our patients these days, which also, by the way, could cause pain and fatigue and memory issues. In fact, it’s an overlapping factor in a lot of our patients.
The point being, if you take this questionnaire, you score high, you have migratory pain. Then what I usually suggest is a blood test from a lab called IGENIX Laboratories in California. This particular laboratory does a test called an immunoblock that checks for nine strains of Lyme disease. The CDC, if you go on their site, they will tell you it’s a clinical diagnosis, and they want you using a set of testing called two-tier testing with an ELISA, E-L-I-S-A, followed by a Western blot.
The problem is that half of my patients will never test positive by an ELISA or a Western blot. The Lyme suppresses their immune system, as does mold toxicity, as do people with long COVID, where they get T-cell exhaustion. Then Bartonella, another bacterial infection frequently associated with Lyme, also destroys their immune system. These people are not even making antibodies. You can’t pick up antibodies in people when their immune system has been shut down. That’s part of the difficulty sometimes in picking up positive tests.
If you do get back a Western blot, and they say it’s negative, you don’t use CDC criteria to analyze it. There’s a game you can play called Lyme Bingo. What this is there are five numbers on a Western blot or an immunoblot that if any one of these numbers is positive, you have been exposed to Lyme disease. Those numbers are: 23, that stands for the outer surface protein C of Borrelia, 31, the outer surface protein A, 34, the outer surface protein B, 39, very specific, and the 83/93. If it’s a Western blot with the 31 band, you can get a false positive with Epstein-Barr or autoimmunity, but in general, these five numbers, 23, 31, 34, 39, 83/93. If you’ve got a chronic, fatiguing, muscular skeletal illness where you have memory concentration problems, sleep disorders, the pain is moving around with even one of these bands, you have Lyme disease. It’s an easy way to just explain it that, and we pick it up, by the way, that way often in our clinical practice.
The Bio-weapon Question: Was Lyme Disease Man-Made?
Ari: Fascinating stuff. That was like a tour de force of diagnosing Lyme disease. My next question might be a digression, might be a tangent, but I think it’s an important one. I’m personally interested in finding your answer because this is a topic I haven’t studied in great depth.
I have heard some rumblings over the years that Lyme disease is actually man-made, that it was originally a bio weapon. I know there’s a whole history. There’s a book, Chris Newby’s 2019 book, Bitten, that’s been written on this subject with Willy Burgdorfer, who is the scientist who discovered this bacteria, Borrelia burgdorferi. I’m curious what your take is on all of this because I know it’s controversial. It’s still in the realm of, to some extent, it’s regarded as conspiracy theory. It’s certainly not consensus, mainstream view. What is your take on this whole idea that Lyme disease comes from bio weapons accidents and that sort of thing?
Dr. Horowitz: There’s two parts when I’m going to answer that. The answer is, do I think it’s been bioengineered? The answer is absolutely yes. There’s no doubt in my mind that there were scientists, Operation Paperclip from World War II, they took Nazi scientists, they brought them over to the US, they worked on bioterrorism experiments. That is known, by the way. Chris does describe it well in her book. There’s other books out there also about it.
The issue for me is not that the government has worked on ticks and worked on bio weapons. They have. In fact, I’m fairly sure most governments in the world have probably been doing the same thing. The issue is Lyme was around way before this ever happened. Lyme’s been around for a million years or longer. If you go into amber, if you were to check ticks that are fossilized in amber, you will find things like Borrelia burgdorferi a million years ago. You will find parasites like Babesia, a frequent parasite that causes malaria symptoms in our patients. It was there a million years ago.
In Otzi, you may know this, a lot of people talked about this, Neanderthal man. They found it in this Neanderthal man 5,000 years ago. I don’t think the issue is whether Lyme was created in a lab. Borrelia burgdorferi has been around for a very long time. Did they try manipulating the genome? Yes, based on my knowledge of what happened on Plum Island. In fact, I did a Medical Detective substack. I have a substack series. I did it on this, I don’t know, maybe two or three months ago and discussed it.
From my perspective, the reason it actually doesn’t make any difference because Chris Smith in Congress, he’s actually raised a bill now for them to look at it. I know Chris Smith very well because I’ve worked with him over the years. I actually worked for HHS, boy, it’s less than a decade ago. I was on the first round of the tick-borne working group where we gave Congress recommendations where I worked with the CDC, NIH, the Department of Defense, and the FDA. I’ve worked with many people from the State University of New York. I’ve worked with our health departments in New York State. I’ve worked on their tick-borne working group.
The answer here is, it’s a very complex organism. It has about three times more DNA than most bacteria that are out there. It’s extremely complex. In either case, whether they worked on it or not, I have an answer. I believe it’s a cure. I’ve been working on this disease for 41 years. I’ve published 10 articles on dapsone combination therapy in the medical literature starting in 2016.
The 11th article that I just published was on linking Alzheimer’s and Lyme disease for the first time in the medical literature where we’ve reversed Alzheimer’s biomarkers. The most sensitive and specific Alzheimer’s biomarker is called p-tau 217. The anti-amyloid monoclonal antibodies like lecanemab, donanemab that are out there, they lower p-tau by about 23% over six years. We’ve lowered it by 63% in nine weeks. The reason being, the amyloid that was being produced in the brain, so the phosphorylated tau, was coming from an infection.
Now, that doesn’t mean that all amyloid and p-tau is coming from Lyme. There’s other bacteria that cause it. There are viruses that cause it. There are parasites. There’s fungus. Environmental toxins can cause it. The point being, it was the 11th article, and in the articles I published, including one from Tufts University that showed rifampicin and dapsone cured Lyme in the animal model, we have about 375 patients in retrospective studies, fatigue got better, joint pain got better, muscle pain got better, nerve pain got better.
Memory concentration, by the way, was the number one effect of dapsone combination therapy, which is why I’m hopeful that in what they suspect is probably 30% to 40% of Alzheimer’s cases may be due to Lyme disease. If that is proven to be true, I may have accidentally found a solution for at least some cases of Alzheimer’s disease where the bacteria is driving amyloid because in the past they found on autopsy studies of Alzheimer’s patients and Parkinson’s patients, they found biofilms, amyloid, and phosphorylated tau next to spirochetes in their brain. It shouldn’t be that surprising because Lyme disease is a spirochete like syphilis, a known cause of dementia.
Because no one had ever reversed the Alzheimer’s in a live human being, the American Academy of Neurology, if you get Alzheimer’s, never tells people to go check for Lyme disease. Well, they should because I believe it’s part of the epidemic of Alzheimer’s.
The fact is that we do have answers for this. Whether they did work on it, which I believe that they did, it doesn’t matter because once John Hopkins and Stanford University and the University of New Haven and Northeastern, all, by the way, at the same time back around 2015, 2016, once they reported that Lyme was a biofilm-persister bacteria, that was when the light bulb went off in my head and went, “Oh, that’s why the drugs never held. We needed to be using more drugs like we use in tuberculosis.”
It took me about a decade to figure out how to design this eight to nine-week oral generic protocol, no more IV drugs. I haven’t used IV drugs in years because the penetration of this regimen is so excellent into the brain.
Yes, they played around with it, but from my perspective, it doesn’t make any difference because we have an answer. I’ve tried approaching some of the researchers now who know Bobby Kennedy to see if we can get research money so that I can do, in fact, a randomized multicenter placebo trial, which is the gold standard that everyone needs to prove this.
The Startling Link Between Lyme Disease and Alzheimer's
Ari: This might be a bit of a digression, but you mentioned some of the anti-amyloid drugs in Alzheimer’s. I’ve read quite a bit about those drugs. I know that there was quite a bit of recent media attention on those drugs, maybe six months ago, eight months ago, something like that.
In the commentary I read, one of the things that they showed was that many of these drugs are highly effective at combating the development of amyloid plaques, but that it doesn’t actually translate into a reduction of symptoms or a slowing of the development of the disease itself or the symptoms associated with the disease, which is really what ultimately matters, what people care about.
Then there’s controversy around whether the amyloid plaques are a cause and a driver of the disease itself or are part of the body’s protective response to, let’s say, the spirochete bacterias or other pathogens or toxins and so on. Given that your study focused on biomarker reduction, how do you know that it is likely to translate into symptom reduction, into combating the disease itself, or did you actually measure other outcomes beyond the biomarkers?
Dr. Horowitz: No, it’s a great question. By the way, everything you mentioned before was absolutely on target. In fact, even a month ago, there was a report that came out called the Cochrane Report that said exactly what you just said. They did an analysis of all of the studies that were out there, and they said, “Yes, you’re lowering down amyloid.” It was at 23% total, 29% because the placebo went up by 6%, but it’s exactly that. It was not translating into big clinical differences.
My take on it, and this is what I published in the Journal of Alzheimer’s Disease Reports just about a month ago, is that what we found is that Lyme disease has 16 factors which make people ill. We know that in most chronic diseases, it’s due to inflammation, both in acute and in chronic illness. What I discovered in Lyme disease is that, I call them like the six rivers of inflammation that go into an ocean of inflammation, and then there’s 10 downstream effects of inflammation.
Number one is infections. Bacteria like Borrelia burgdorferi or Bartonella henselae, Chlamydia pneumoniae, also, by the way, an infection we see that’s been associated with Alzheimer’s. There are viruses like herpes virus 1, 2, herpes virus 6 and 7, Epstein-Barr, parasites like Babesia, even fungal infections. Number one on the map that drives inflammation is infections.
Number two is environmental toxins, mold, heavy metals.
Number three is the microbiome of the gut; that if you have the wrong types of bacteria in the gut that don’t produce short-chain fatty acids, you get inflammation. It’s affecting the gut-brain axis.
Number four is leaky gut with mast cell activation. You’re getting food particles or lipopolysaccharides getting across into the blood-brain barrier, making more inflammation.
Five is vitamin mineral deficiencies.
Six is sleep disorders.
Taking these six factors, and it’s like going into a doctor with 16 nails in your foot saying you have foot pain, and the doctor finds one or two nails and says, “Come back in a month and tell me how you’re feeling,” we both know that you’re still going to have pain.
These six main factors cause 10 downstream effects of inflammation, which is mitochondrial dysfunction, hormonal dysregulation. 99% of my patients have low adrenal function. Men in their 20s come in with low testosterone, and they’re coming in on shots and creams and gels without realizing it was the Lyme that was shutting down their pituitary gland, making luteinizing hormone, so they weren’t making testosterone.
We see POTS dysautonomia, low blood pressure with people passing out, just like you do with long COVID, neuropsychiatric issues, liver dysfunction, deconditioning, immune dysregulation where people get autoimmune reactions from Lyme from a bystander. It’s like your body’s trying to attack the bug, but it’s attacking your own tissues inadvertently, causing immune dysfunction.
These 16 factors that I’ve been talking about for Lyme, I just published in this Alzheimer’s journal that all 16 factors, and this is why I’m digressing for you, are associated with Alzheimer’s. When someone says, “I’ve been diagnosed with Alzheimer’s based on the beta amyloid 42/40 ratio being low, if you get that test back from Quest Laboratories, your insurance company will essentially pay for lecanemab or dinatimab, these anti-monoclonal antibodies, oftentimes without an F18 PET scan, but these are, of course, people that are cognitively impaired.
In the patient that I studied, interestingly enough, she was not complaining of a lot of cognitive issues at the time. She thought her cognition was good because she was meditating a lot, but she had a rheumatoid factor that was positive with joint pain, and she’d been sick for 15 years with no antibiotics. She decided when the p-tau 217 came back high, and by the way, she also had other factors, what I call MSIDS factors, multiple systemic infectious disease syndrome, like she had autoimmunity with these rheumatoid factors. She had heavy metals that had a key lead out of her body. She had other infections like Q fever, coxiella.
We addressed all her issues, but interestingly enough, three months after we did the Dapsone protocol and I asked her about her symptoms, not only was the joint pain much better, the rheumatoid factor that had been positive for 15 years reversed to normal, meaning the bacterial infection that was alive in her body, which was chronically persistent, now that it was shut down, the rheumatoid factors turned negative, she said to me, “I thought my memory was actually pretty good, but ever since the p-tau came down, I notice I’m a lot sharper.”
Here’s the problem, I think, for all of us as we get older. We get used to living in a certain way like, what’s normal as we’re getting old? I got a couple aches and pains. I’m missing a few things since I’m getting older. What do you want? I just turned 70 years old. It’s like, what’s normal? I don’t know what’s normal. I feel great for 70 years old. I feel like I could go on to 108.
Here’s the problem, you start getting used to symptoms and then you think, “Oh, it’s just aging.” I have had people who are 80 years old who said this to me, “Come on, Doc, I’m a little tired. I forget a word from time to time. What do you want from me?” I give them the protocol. They come back months later and they go, “Oh my god, that low back pain, for the last 10 years, it’s gone. My mind is sharp. I can’t believe it, Doc. I thought I was getting old.”
This is really tricky, Ari. I can’t tell you how many people out there. The CDC tells us 476,000 people a year, almost a half a million people a year, get Lyme. If you’re following the news, you know that this year is the worst year they have ever seen for ticks. Maine and all the states are up by at least 25% more than they’ve ever seen.
The problem is Medicare rates are seven times higher than what the CDC reports. That means if the CDC is reporting roughly a half a million cases, there may be 3 million Americans per year who are getting Lyme, and those are the ones with cognitive issues that they go to their doctor, and they get these Alzheimer’s biomarkers and they get to say, “You have Alzheimer’s, here’s your anti-amyloid antibody.”
From my perspective, I do think there’s a place, by the way, for these drugs. If you have mold toxicity or heavy metals, and they are causing amyloid and p-tau in the brain–
By the way, what’s interesting about my patient, she was A-T+. What that means is, her amyloid was not high, she just had phosphorylated tau. There’s a specific subsection of these people that have elevated p-tau but are not amyloid positive. That was my patient, and I’m finding this in a bunch of my chronic Lyme patients.
I think what we’re going to find over time when the neurologists start to check their patients is that, instead of just naming a disease, you have Alzheimer’s, here’s the drug, we approach Alzheimer’s, just like long COVID, I published in the medical literature two years ago, that all 16 MSIDS factors that I’ve seen for Lyme are associated with long COVID. Interestingly enough, in my new book, Ending Chronic Illness, I discovered that all 16 factors on the MSIDS model are associated with chronic fatigue syndrome and fibromyalgia.
What does this mean? This means that when you now go to your doctor and they’ve labeled you with a disease, what I’m basically telling the docs and the patients out there is we need a real paradigm shift in how we do chronic disease medicine, because 60% of Americans at this point have a chronic illness. 25% of Americans have at least two or more chronic illnesses. 86% of our healthcare costs are due to chronic disease. 70% of the deaths in this country are due to chronic disease. We don’t have any model to treat chronic disease.
What I found in doing a deep dive in the literature, and I’ve got roughly 2,000 scientific references backing this up, is almost every major illness I looked at in Ending Chronic Illness, not just chronic Lyme, not just long COVID, not just Alzheimer’s, but autism, spectrum disorder, ADHD, where like 3% to 4% of the population is being diagnosed with ADHD. Autism rates went from 1 to 2,500 to 1 to 36. What is that about?
The NIH is telling us that 42% of people over 55 years old are going to get demented. Somebody’s got to step back at the top of the healthcare chain and look at all this chronic disease and go, “Hold on here. What is going on that’s making so many people sick?”
My take on it, after being in the trenches for 41 years seeing 13,000 of these chronically ill people, is it’s these 16 factors. It’s the infections, it’s the microbiome, it’s the environmental toxins, it’s mitochondrial dysfunction, and it’s all going to be different from person to person. This is like where precision personalized medicine is going to take place, but we’ve got to stop just labeling the diseases and throwing drugs at it because that has not solved our chronic health problems.
My take is you’ve got to unlayer each illness into the 16 points, and that’s what I’m suggesting they do for Alzheimer’s, because you’re correct, the amyloid hypothesis has been questioned, and it’s likely, and especially in our patients– By the way, what was interesting about my patient, when her p-tau level reversed, you saw less amyloid in the brain. When they showed us the curve for amyloid, the amyloid went down when the p-tau went down, and the p-tau is actually a better marker of amyloid than it is of phosphorylated tau in the brain.
My understanding with all these sick patients coming to see me who are diagnosed with chronic fatigue syndrome, which doesn’t mean, by the way, they couldn’t have had a virus like Epstein-Barr or herpes virus 6 as the initial trigger, or they got a vaccine for COVID and the spike proteins got in there and made them ill.
What we discovered, even in long COVID, is many of these patients who had inflammation in their endothelium, there’s a marker called VEGF, Vascular Endothelial Growth Factor, those patients most of the time had Bartonella. They had another bacteria in their body that was active, that was causing the VEGF. It wasn’t just spike proteins that was making them ill, but if you had a certain amount of inflammation in your body and then you put a vaccine or you got COVID, it just created more inflammation and then it was just too much for your body to handle.
This paradigm shift that I’m talking about, I think it’s really going to be very helpful for a whole broad range of chronic illnesses. Of course, there’s a difference between association and causation. I can tell you for sure, I do have an answer for chronic Lyme. It’s very exciting that maybe this one case study, and it’s only one case study, we can’t obviously go too far with this one, but it gives us a new avenue of research, like light that now can be shown on this, like, “Hold on, there’s another way to look at Alzheimer’s. Let’s look at these 16 factors. Mold causes memory concentration problems. Maybe we should be pulling out mold and seeing what happens to amyloid and p-tau .”
It’s exciting. At this stage in my career of being in medicine for so long, it’s cool to discover things like these two epidemics are actually related to one another based on what I’ve seen, and it’s exciting.
The 16-Point MSIDS Model: A Ground-Up Approach to Healing
Ari: Yes, fascinating. A few questions on the MSIDS model. I’m curious how you would describe your development of this model. You mentioned conventional medicine doesn’t really have a model for treating complex chronic illness. You’ve developed this MSIDS model based on these 16 factors.
Would you say that your development of this was more of a top-down process, you had this theory in your head and you’ve verified it through practice, or would you say this was something that emerged organically from the bottom up as a result of working with patients, trying one approach, not getting results, looking for other factors, and over time, over thousands of patients, looking for other factors, you developed this bigger model?
Dr. Horowitz: That’s it. It was from the ground up. I had no idea about trying to design any model. I’ll give you examples. I start out in 1987. I’m moving from my internal medicine residency at Mount Sinai in New York City. I come up to the Hudson Valley. I move up to the largest Lyme endemic area in the United States at the time. I’m seeing all these patients.
A couple of years in, when I discover that people keep coming back after treatment, and I’m sending them to infectious disease doctors and rheumatologists and neurologists, and nobody knows what to do. It’s like my Tibetan teacher when I was- I’ve been a practicing Tibetan Buddhist for the last 45 years, by the way. I went to my Tibetan teacher before finishing med school. I did it in Belgium in French, by the way. It was a seven-year program. It was a whole other story, but it was fascinating and a great experience.
I went to my teacher and I said, “Lama, what do you want me to know before I become a doctor? What’s the best advice you want to give me?”
He said, “Richard, the best advice is, put yourself in people’s shoes and do for them what you would want done for yourself if you got sick.” They call it exchanging oneself with others. Basic advice, have love, want other people to be happy, compassion, relieve their suffering, basic advice.
I said, “Okay, thank you.”
Here I am now in the middle of this epidemic, no one knows what to do. I remembered his advice and I put myself in the patient’s shoes and said, “All right, I’m going to go on a journey and figure out why these people are sick.
Here’s how it goes from the bottom up. A woman in a wheelchair comes in the early 90s. She’s 35 years old. She’s paralyzed from the waist down for five years. She can’t walk. I take a medical history and she’s got drenching sweats at 35 years old. She’s not in menopause. She doesn’t have hyperthyroidism. She doesn’t have other diseases like TB or non-Hodgkin’s lymphoma that cause drenching sweats. I said to her, “This sounds like a parasite I just learned about at a conference called Babesia, but it wasn’t supposed to be in the Hudson Valley where I was living.”
We sent out the ticks from the Hudson Valley from the Institute for Ecosystem Studies. We take her blood. Lo and behold, we find Babesia. I gave her a 10-day treatment of Mepron and Zithromax. Six months later, the woman is walking out of a wheelchair and she’s now skiing.
Now, I didn’t know that parasites were making the bacterial infections worse. This is the ground-up approach that you were discussing. Next, another patient comes in. She can’t talk. Words literally will not come out of her mouth. She’s 40 years old. She’s been to Harvard. She’s been to Mass General. She’s been all over the world. They think she’s had a stroke or she’s had a migraine that affected her speech. I do questionnaires for her. We find she has Bartonella.
Now, this goes back 25 years. I gave her two intracellular drugs for Bartonella, different treatment now, but within days of doing this, she starts talking. For the first time, she had aphasia where she couldn’t talk. It’s like, “Oh, there’s other bacteria with the parasites.” Now, long COVID comes along. We see Epstein-Barr and herpes virus 6 reactivating in some of these people. We do find viruses reactivate. It’s like, “All right, now we’ve got bacteria, we’ve got viruses, we’ve got parasites.”
Then we would do microbiome studies of people’s microbiome of their guts and we’d find candida overgrowth or fungal overgrowth from other sources or mold. We realized that when we treated the candida or pulled the mold toxins out, all of a sudden their fatigue and their pain and their memory would get better.
It’s a great question. It’s a ground-up approach. What happened year by year as I kept looking as a medical detective to figure out why these people were sick, it was like, “Oh, it’s the microbiome.” “Oh, it’s the mitochondrial dysfunction.” “Oh, it’s the hormones that have been thrown off.” It was different in every person. Most people had adrenal dysfunction. Not every man who came in had low testosterones, many did.
It was an individualized personalized protocol. Because I’ve been in medicine for 41 years, it probably took me maybe the first 20 years of clinical practice to put all the pieces together. The first article I actually published on the MSIDS model was back in 2018 in the Journal of Healthcare. Interestingly enough, I talked about it for not just Lyme but other chronic illness. Then COVID comes along two years later, and the model that I was using, I applied to COVID. I published the first study in the world medical literature on using glutathione, which I’m sure you know, it detoxifies the body, but also helps with inflammation.
It turned out that not one of my patients died during the entire COVID pandemic, blocking a switch of inflammation in the nucleus called NF-κB. They took N-acetyl cysteine, a precursor of glutathione, alpha-lipoic acid, which regenerates glutathione. Not one patient died while they took turmeric, curcumin, and other things. Now, I didn’t know at the time that the COVID virus had to lower glutathione to replicate. I didn’t know that. No one did.
It turned out later on in the ICU, when people were dying of ARDS, acute respiratory distress syndrome, they looked at these people’s bloods, and they found out they had low glutathione, and you have 140 times more glutathione in your lung tissue than anywhere else. If you got COVID on the first wave, and you used up all the glutathione in your body to detoxify heavy metals and chemicals, you were going to be the kind of person that was going to likely die and have ARDS. Not one of my patients got sick.
Now, how did I protect them? Basically, looking at these inflammatory pathways and applying one model for one disease to another. Now, of course, I didn’t know at the time it was going to work. Even now with Hantavirus and Ebola virus that we’re talking about, it’s interesting that the first four inflammatory pathways that I discuss in Ending Chronic Illness that are in the MSIDS model, I discovered that there were 16 inflammatory pathways underlying these 16 factors. When we look at Hantavirus and Ebola virus, these first four pathways, NF-κB, NRF2, NLRP3 inflammasomes, prostaglandins, are very relevant to why people die from these viruses.
I’m doing substacks now, hoping that somebody’s going to pick this up. If, God forbid, we don’t get this thing under control, these will be ideas for the scientific community to look at because dapsone, interestingly enough, blocks NLRP3 inflammasomes, which is an important inflammatory pathway in these viruses. As I’ve been in medicine for over four decades, it’s fascinating to me that, as I looked at the biochemistry of inflammation and where the inflammation’s coming from and found these 16 factors in these pathways, it seems to be applying to most of these chronic diseases. I think it’s going to give us literally a new paradigm shift at chronic illness.
For example, a Crohn’s patient who came in who was on drugs for the Crohn’s disease and couldn’t get off or on a liquid diet, I gave him dapsone to lower inflammation, treated the microbiome of the gut, treated their leaky gut. They were off their Crohn’s drugs. It was the bottom-up. It was like these cases where I discovered that if I tried hard enough, these diseases that sometimes have very good medicines, and don’t get me wrong, I use medicines as much as I use nutraceuticals and natural approaches, but there’s a place for them.
We don’t just label the disease and throw drugs. We’ve just got to do a better job at unraveling it into these component parts of where the inflammation’s coming from. I think that’s going to be really the essential model going forward for Alzheimer’s, for long COVID, for many of these chronic diseases that people are suffering from.
Overcoming Biological Reductionism: Systems Biology vs. Monolithic Models
Ari: I see a couple of problems or issues when it comes to obstacles, let’s say, with widespread acceptance of this model that you’re proposing within mainstream medicine, evidence-based medicine. I’m curious if you agree with me or how you perceive this. One of the obstacles that I see is, basically, mainstream medicine, evidence-based medicine is built around biological reductionism. To some extent, you are very much speaking that language of mechanisms and NRLP3 inflammasome and NRF2 and this pathway and that pathway.
However, the nature of the model that you’re proposing becomes more expansive. It expands from a single mechanism and a single pathogen as being the cause of a disease and having a single treatment to combat this single mechanism or single pathogen to something more expansive, to something that moves away from just a pure germ theory model towards more of a terrain theory or some hybrid of the two where you are incorporating elements of the terrain, of the physiological terrain, as being a critical factor in the disease, not just the pathogen.
Because you’re developing this more expansive view, model of the disease, and moving more in the directions of systems biology rather than reductionist biology, there will be some pushback on it. The other issue that I see or obstacle that I see for widespread acceptance of this model you’re proposing is some critics might argue that it is unfalsifiable in a way.
If one or two aspects of the treatment approach don’t work, let’s say you’re targeting the gut microbiome, or let’s say you’re targeting mitochondrial dysfunction, or let’s say you give antibiotics for a particular pathogen that you identified, and let’s say you don’t get results, then you can always find something else to blame and say, “Well, it’s because there’s other of these 16 factors that we haven’t addressed yet. Maybe these weren’t the needle movers for this particular patient, but we got to address these other pieces of the puzzle.”
Again, that’s an obstacle for the typical way of thinking in evidence-based mainstream medicine, where they like single variables, single mechanisms, single pathogens, single treatments, single interventions. I’m curious how you perceive that. If you agree with me, disagree with me, how do you perceive that?
Dr. Horowitz: Oh, no, I agree with you 100%. There’s no doubt there will be some pushback. Although I think the functional medicine docs who do integrative medicine, they already do a lot of this stuff.
Ari: There’s also pushback against functional medicine. Functional medicine itself is not widely accepted within mainstream medicine.
Dr. Horowitz: Right. Although, look, as a board-certified internist who learned classical internal medicine, who’s learned to use the drugs that they give us, which, by the way, are fabulous. I have nothing against the toolbox of giving statins when they’re needed or giving migraine medicines with sumatriptan or some of the newer drugs, Ajovy, for migraines. I use them all the time. I use pharmaceuticals where I need to.
You’re correct about the germ theory and the way this developed. In the 1880s, when Kotz’s hypothesis and Pasteur was around saying, “It’s this one germ causing this one disease,” at the time, we weren’t dumping 50,000 toxins into the environment starting in the 1950s, where all of a sudden, we’ve got these environmental endocrine-disrupting chemicals getting into people’s bodies, causing havoc. At the time, I don’t think they had probably as many infections, or at least I doubt they did as we have now.
Based on my experience of 41 years in the trenches, seeing these 13,000 people, it is actually true that, let’s say, dapsone had a success rate of, let’s say, 80% in chronic Lyme disease. I spoke to people this weekend about this and many of the patients who’ve said they’ve gone into remission. My wife was sick for 25 years with chronic Lyme. She’s eight years in remission without a symptom coming back. Now, she had all 16 MSIDs factors. I had to address her migraines because she had mast cell disorder. She was eating the wrong foods, which were secreting histamine. I had to address her adrenal. She had hypothyroidism. She had sleep issues. There were mother-in-law issues with stress.
I addressed all 16, but it is true that, in my world, if someone, let’s say, does not get better from treating with dapsone for Lyme and Bartonella, most of the time, it is mold toxins and heavy metals or other things that are interfering. How do I know? Well, I treat those factors and then go back and treat with dapsone, and they do get better. There’s no doubt that genetics are going to play a role in some of these people, where you’re only going to be able to go so far. Although now, of course, with CRISPR technology, they’re looking at a whole bunch of different things. I think the way to answer the question from a traditional standpoint is that’s why I applied for an NIH R34 grant.
I put in for a randomized, multi-standard placebo-controlled trial, which is the gold standard in medicine. I was ready to prove it to the world. By the way, the one variable I was going to change was not to dapsone in one arm to a placebo and give dapsone in the other. What was going to be interesting about that, because Lyme is a biofilm persister infection, is the other drugs I used with rifampin, methylene blue, Zithromax, still has some effect on biofilms. People still may actually get help without dapsone, but we wouldn’t know that until we did the study.
You are correct that one variable is the way to do these studies. What’s going to be needed at this point, because 18% of our GDP of healthcare costs is chronic illness, and it just keeps rising, we’re going to break the bank in the next 15 years where we’re going to go broke. They can’t afford it. There has to be a paradigm shift in how we deal with chronic illness. If I was heading up the NIH and the CDC and somebody said to me, “Hey, Dr. H, we want you to design all the studies you want,” it’s exactly what you just said.
I would basically take patients with ADHD and autism and Alzheimer’s and all these different chronic illnesses, and I would look at the 16-point model, which already we know there is an association of all 16 factors with ADHD, autism, Alzheimer’s, chronic fatigue, fibro, long COVID, all 16 show up, but you are correct, there’s a difference between association and causation. That is where we’re going to need really good randomized multicenter placebo trials. I’m fine going through the usual mechanisms.
I’m enough of a scientist to recognize that we need to do these studies to prove it, but the reason I think we should do them is the model we’re using right now is just not working. Look, if you have rheumatoid arthritis and you’ve gone into TNF alpha inhibitor like etanercept, it may save your life. It may prevent some of the worst complications of rheumatoid arthritis, but it also suppresses your immune system, and in some cases, leads to reactivation of tuberculosis, or you get cancer with non-Hodgkin’s lymphoma.
It saved your life temporarily, but there are side effects of these drugs. I think there’s a place for these medications, but if it was me and I had rheumatoid arthritis, I would take, pharmaceutically, what could get me through the worst part, but then I would want a doctor to work with me on these 16 factors to say, is Lyme there? Is Spartanella there? By the way, I’ve had rheumatoid patients where methotrexate didn’t work because they came in with migratory pain, and I said, “Migratory pain is not rheumatoid arthritis. Migratory pain is Lyme disease,” but they had the marker for rheumatoid. Not just rheumatoid factors, but this marker called CCP, cyclic-citrullinated peptide.
Once I treated the Lyme, the methotrexate worked. Even in some of these autoimmune diseases where people are not getting the response they want from biologics, from these drugs, some cases, this is my experience, treating some of these underlying MSIDs factors may make the drugs work better. It doesn’t mean they may be able to come off all their drugs, but it may mean they may get a better effect profile from it with less side effects since they won’t need as many of these pharmaceuticals on board.
You’re absolutely correct, by the way. We must do good studies on this to prove it. The framework that I’m using has worked for me in clinical practice. It’s not like I have 100% success rate with patients. It is true, by the way, something you mentioned, that when part of the model didn’t work, let’s say they got through Bartonella 4 pulses with dapsone and they still were sick, we usually found the Bartonella was still active. It’s usually because they had things suppressing their immune system or other things going on.
I just recently retired after 41 years of doing this, and I’m now going into the research space so I can actually do these studies. I think that’s serving the millions from serving one-on-one makes sense to me as a clinician. No, I agree with you 100%. The studies need to be done, and they should be done. I just hope that someone at the top recognizes that we’re going in a bad direction with chronic disease in this country.
Almost two-thirds of Americans have one chronic illness. 42% of patients over 55 are getting demented. I don’t understand why someone at the top of the health food chain is not looking at this going, “Oh, my God, what’s happening here? Let’s unravel this thing and figure out through systems biology or whatever. How can we explain why this is happening?” I think the model I’m using does explain it, but give me a chance to work on the studies. Stop denying my NIH grants. I’m happy to work and do it.
The Biggest Blind Spots in Conventional Medicine
Ari: Okay. Specifically, you have this MSIDS model with these 16 factors. How would you conceptualize the gap or the biggest areas of gaps between the MSIDS model and the conventional framework as it exists now? What are maybe the top 3 or top 5 factors of the 16 in the MSIDS model that are missed by the conventional medical approach?
Dr. Horowitz: Great question. Infections and toxins, those two factors are definitely at the top of the list. In our chronically ill patients, most of those patients have parasites like Babesia. Up to 90% have Bartonella, another intracellular bacterial infection. Most doctors who go through med school, they’ve heard about Bartonella henselae, cat scratch fever. They’re not aware that there are 18 other pathogenic species of Bartonella making people ill. It causes, by the way, rheumatological symptoms with rheumatoid factors and the rest that if you went to a rheumatologist and they thought, “Oh, this looks like Lyme,” and the Lyme is negative, many times they won’t even know to look for Bartonella.
There’s no doubt in my mind that between these intracellular bacterial infections under biofilms, and Bartonella, by the way, is another biofilm-persister bacteria like Lyme, definitely reactivated viruses, HHV-6, Epstein-Barr, CMV in some people, not even a doubt. Parasites, Babesia is really common. We find it at least 80%. Then I do find a fair number of my patients with fungal overgrowth with Candida, with mold toxicity, up to five different mycotoxins showing up in 9 out of 10 patients with heavy metals. I chelated myself for heavy metals for a year and a half. I had my amalgams taken out. My levels were so off the wall. Every one of my family members has died as a different form of cancer.
I have no one left in my family. Part of my interest in looking at this model for cancer and all of these diseases is kind of like how do we create a better mousetrap to look at what this is, because I have no one left in my family, but the two factors at the top is definitely infections and toxins. After that, the microbiome of the gut, it is turning out whether you look at rheumatoid arthritis or MS or Parkinson’s or Alzheimer’s, there are really strong associations now that the prevotella, formicutes ratio, the bacterioides, these things are playing a massive role because of the gut liver axis, the gut brain axis.
When I was describing to you the six rivers of inflammation, infections, toxins, the microbiome with leaky gut, vitamin, mineral deficiencies, and sleep, it’s the same thing with Alzheimer’s. You don’t get enough sleep. You have sleep apnea. That’s going to basically increase your risk of dementia, just like type 3 diabetes, right? You’ve got insulin spikes, high glucose. It’s not one factor driving amyloid and phosphorylated tau. That’s again the problem with the model. They have all these models for Alzheimer’s of the autoimmune hypothesis, the amyloid hypothesis, the P-tau, but what no one said with the Alzheimer’s hypothesis is, where is the inflammation coming from?
What I showed in this new paper in the Journal of Alzheimer’s Disease Reports is all 16 factors are associated, but excellent question. In my world, it is ultimately the toxins and the infections and not getting to sleep with vitamin, minerals, microbiome, always at the top of the list. It doesn’t mean your hormones, like adrenals or testosterone or thyroid, can’t be affecting it. It can, or that postus autonomia, the autonomic nervous system being off. By the way, even trauma. My God, it’s at least a third of the women who’ve come to see me have had emotional, physical, and sexual trauma.
If you don’t do some form of limbic retraining and reset that part of your brain, it’s almost like your immune system says, “I don’t deserve to be well.” The mind-body connection is strong in a lot of these patients that I’ve seen. I don’t want to make it so reductionist, but since you asked the question of what are the most important factors, yes, it’s those six rivers and infections and toxins. Most of the time, even if I’ve not cleared the trauma, they’ve not done enough limbic retraining or EMDR or cognitive behavioral therapy, whatever they’re doing, or not addressed mitochondrial, once I’ve lowered the load of those toxins and gotten rid of the infections, already they will tell me they feel significantly better.
I’ve just been a perfectionist in my life that I want 100% well, not one symptom. Because I’ve been such a perfectionist, I think it’s in part probably why I’ve done as well as I have being in the trenches for so long. That’s a great question because it sounds like it’s complicated. You got all these 16 factors, but it is a couple of those factors that are driving most of the inflammation in the patients that I’ve seen.
Terrain Theory vs. Germ Theory: Why the Environment Matters
Ari: I think that this distinction between germ theory and terrain theory is also relevant here because I think when you’re dealing with an infectious disease, the standard way of thinking within mainstream medicine is identify the pathogen, have a drug, an antibiotic, or whatever antimicrobial drug that targets this particular pathogen to cure the infectious disease. There’s like a gap, there’s like something blocking within the conventional view, a connection between a infectious disease and connecting terrain to that.
Whenever you start talking about something like the gut microbiome or mitochondrial health or the person’s hormonal status or glutathione levels, I feel like within conventional medicine, that kind of terrain talk is immediately sort of discarded as being less scientific because it’s less focused on this specific pathogen and the specific intervention that targets it.
Dr. Horowitz: You’re right that there’s definitely a bias in classical medicine, but I think what I’ve been trying to do for the years, because I came out as a board-certified internist using all the tools they gave me, great for blood pressure, great for cholesterol, great for migraines. I mean, look, there’s a great bunch of pharmaceuticals, but most docs will tell you out there, when you got a chronically ill patient who comes in with chronic fatigue syndrome, fibromyalgia, long COVID, it’s like, “Oh my God, long COVID, what causes long COVID?”
I mean, most doctors don’t know that all 16 absence factors are associated with long COVID. I published it two years ago in the Journal of Microorganism. What does that mean? It means that the spike protocols that they’re doing, this detox to take out the spike proteins, you may start to get some help in some people with plasmapheresis in doing this, but ultimately, if you don’t look at the terrain and what the other bugs are that they are, and didn’t realize that Bartonella was causing some of this endothelial dysfunction while you had mold toxins, and that’s what we’re finding, by the way, in a lot of our long COVID patients, it confuses it.
I think going from the one cause, one disease model, which was appropriate in the 1800s during Pasteur’s postulate and Koch’s postulate, it was appropriate. Now that we have so many tens of thousands of environmental toxins getting in with this whole new range of infections and viruses and bacteria, I think things have changed enough over time that the reason I published so much in the medical literature is because I’m trying to bridge the gap with hard science saying, “Here are the articles backing up what I’m doing.”
Most of the doctors, by the way, who I’ve trained and I’ve trained hundreds over the years in this model, they’ve seen the results themselves. To answer your point, the only way that looking at the terrain and looking at this all at the same time, it has to be done in systems biology, basically through these randomized multi-center control trials. It has to be because that is the gold standard. That is the only way that the general medical system is going to look at it.
Just knowing how many people are getting chronically ill and what the Alzheimer’s rates are and the rates of chronic Lyme disease going up every year, I think the bells and whistles are going off enough, at least that people should have an interest in saying, “Let’s go beyond the standard models and let’s look at what else is out there that we can benefit people.” The model I’ve been using, it’s been helpful for many, many people. Many people have gotten their lives back with this model.
Ari: Are you okay on time for a couple more questions?
Dr. Horowitz: Oh, of course. I have all the time you need.
Ari: Great. I’m curious, you’ve been practicing over 40 years and I don’t know, have you been focused on Lyme that entire time or is that a more recent thing, only part of that 40 years?
Dr. Horowitz: Yes. When I came out in 1987, when I moved up to the Hudson Valley, I joked with my friend, Howie Prusak, in our third year of residency at Mount Sinai, and I did it in the city hospital at Elmhurst because my grandmother was living nearby. I’m a Queens boy, just like Mom, Donny, and Donald. When I came up to the Hudson Valley, I was trying to be a country doc. I was planning on doing blood pressure, cholesterol, diabetes. I loved internal medicine because I loved the medical detective part of you had to know a little bit about everything and figure stuff out. That always intrigued me as a doc.
It wasn’t until the early ’90s, mid-’90s that I started seeing these Lyme patients coming in with the rashes where 75% got better with antibiotics, but it was the 25%, 30% that didn’t get better, that after referring to infectious disease doctors and rheumatologists, neurologists, and no one knew what to do with them, it was like, “Okay, Lama, I remember your instructions. I’ll do my best to figure it out.” Little by little, when you start digging to figure out why people are sick, I didn’t learn functional medicine coming out of med school. I had to start taking course– I used to read Sherry Rogers’ book. She’s an old functional medicine doc.
I would take these tons of hundreds of pages and read nutritional biochemistry and try and figure this stuff out. I ended up having to learn this stuff on my own. Of course, I went to conferences over time, but it really just developed looking for answers and cures for this chronically ill patient. I’m enough of a scientist to know that I needed hard science backing this up. I wasn’t going to just say, I’ll give you a homeopathic and hope for the best, although I will say also that I’ve used homeopathics like Thuja for warts on the bottom of the foot. They have gone away, including myself.
I’ve looked at alternative medicine. I’ve used traditional Chinese medicine for years. I’ve looked at herbal therapies because years ago, we didn’t have these answers for Lyme. No, it was like I was being a board-certified internist doing a little bit of everything. When someone presented to me with a medical problem, and they weren’t getting better with standard therapies, or they were having side effects of standard therapies, it felt like my job was just to do a better job to see how I could either get them on a different drug that worked better or get them off the drugs and figure out the cure.
I never came from the point of view of like, “I can’t get you better.” It was always like, “Let me try. Let me see what I can do.” It really, as we talked about earlier, it was from the ground up. This whole thing developed where I just learned this going to conferences, reading in books, going to the medical literature. It took decades, honestly, of learning this to figure out to get to the 16-point model that I have now.
Changing Minds: What Dr. Horowitz Learned Over 40 Years
Ari: What do you think is the single biggest factor or the single most important thing in your model, your way of thinking about Lyme and chronic illness, that you have changed your mind about? Something that you believed very strongly when you were younger, maybe in the ’90s or the early 2000s, that you now believe is wrong?
Dr. Horowitz: When we were first doing Lyme in the ’90s, because we didn’t know it was a biofilm-persistent bacteria, I published the first study with a doctor called Dr. Martin Atkinson Barr on the use of Flagyl, a drug that’s been around forever. We found that our helicobacter pylori patients, the bug that causes gastritis, ulcers, and gastric cancer, when we gave them tetracycline, bismuth, and Flagyl, they had a Herxheimer reaction and was like, “What?” It turned out some of these H. pylori patients had Lyme. I discovered that Flagyl was hitting a certain form of the bacteria called the cystic forms, cell wall deficient forms, S forms, L forms. They’re called different forms.
For decades, we believed that the reason the Lyme persisted was from cell wall forms, that’s we used amoxicillin or IV Rocephin, intracellular forms, that’s we’re using doxycycline, Zithromax, or these cystic forms. Then it turned out, it’s like, based only 10 years ago, already 30 years into my career, it’s like, oh, these are biofilm-persister bacteria like leprosy. What are they used to cure leprosy? Rifampin and dapsone.
It wasn’t, by the way, so much that it was so brilliant, all I did is look at the literature and go, “Oh, they cure that disease using rifampin and dapsone. What happens when I add doxycycline to it, which hits ehrlichia, anaplasma, Rocky Mountain spotted fever, Q fever, it hits all the other tick-borne infections and Lyme, what happens?” It was a home run out of the park, but it wasn’t like I invented the whole thing. I just looked at the literature and knew where to look. Whereas we thought it was a normal bacteria, we realized after time, Lyme is not. It is a biofilm-persister bacteria.
Just like you would never think of treating TB with four weeks of antibiotics, you would always use a multi-drug regimen for it. That changed my opinion. Also, the other thing I changed is I didn’t think environmental toxins were playing that big a role years ago. I published some abstracts years ago on heavy metals and pulling out mercury and lead and found that about 25% of my chronic Lyme patients said, “Hey, my fatigue and my brain fog and my joint pain is better when you took out my mercury and lead, and it went great.”
I didn’t realize how much mold was getting in until about six, seven years ago when I started using a lab in Texas called Real-Time Laboratories. We were finding aflatoxins, gliotoxins, trichothickins, all of these immunosuppressive toxins. Then we realized that Lyme was suppressing the immune system, that 20% of my patients were immune deficient, 85% had subclass deficiencies where they couldn’t fight infections, Bartonella made it worse, then long COVID came along, and you got T-cell exhaustion.
You were talking about infections, walking outside the box, it’s like, well, these infections are basically affecting your immune system and when long COVID and mold came on top of it, your body just couldn’t fight because you need a healthy immune system to fight these bugs. It’s been little by little, I’ve given more credence to infections and toxins together. These environmental toxins are playing a massive role, just like microplastics in some people are getting into the carotids and they’re finding they have a risk of strokes and heart attacks.
In these people, where they’re finding microplastics, I didn’t give it as much due years ago with how far these toxins were driving reactive oxygen species and inflammatory pathways. I now realize that it’s this multi-systemic model that the inflammation is coming from multiple sources, but I’m giving these biofilm, persister bacteria, and mold, and some of these toxins, a lot more credence than I did maybe even 30 years ago when I was starting.
Practical Steps: What to Do If You Suspect Chronic Lyme
Ari: Fascinating. On a practical note, just to wrap up, I guess there’s two aspects to this. One is if someone suspects that they have chronic Lyme, but they can’t access a specialist, what are the highest leverages things that they can start doing? The other practical aspect of this, because of what we talked about at the beginning, the fact that these symptoms overlap with other conditions, chronic fatigue syndrome, and so on, if there are people listening to this who have many of these types of symptoms, and now maybe they’re wondering, do I have Lyme disease, could that be the cause of my symptoms, what would you say just as far as practical guidance to listeners who are in those positions?
Dr. Horowitz: There’s an organization called ILADS, the International Lyme and Associated Diseases Society. I was one of the founding members. It was 26 years ago. We were in New York City with Joe Borscano, Nick Harris, Steve Phillips, Andrea Gaito, Terry. We all sat down, and we created this organization, and at this point, we’re 26 years in the making. ILADS has a website, ilads.org, I-L-A-D-S.org, and many of the Lyme organizations, really good Lyme organizations, Bay Area Lyme. Global Lyme Alliance, gla.org. There are a lot of good Lyme organizations out there, including ilads.org.
If you are concerned that you may have Lyme disease, you should go on the websites and find a Lyme literate practitioner who understands the pros and cons of the testing. Again, you can go to my website, cangetbetter.com, and take the questionnaire just to get a pre-test probability. My prior books, Why Can’t I Get Better, How Can I Get Better, outline a bit all of the testing and what we’re doing. My new book, Ending Chronic Illness, does have a lot online, but it’s one chapter. Most of this book is actually about all these different chronic diseases, from autism to Alzheimer’s to cancer to cardiovascular disease, like how this model applies.
I do have very specific instructions, like literally a cookbook, and it’ll be out in October from Simon & Schuster, of how to work with your doctor so that– I’m available if people need to speak to me through their physicians. I stopped my consult model because I tried helping patients after I retired from clinical practice, and I started getting calls from all over the world, from Czechoslovakia and Bulgaria. It was unbelievable, the number of calls.
I’m now available to speak to doctors and help them. I’ll hold their hands and guide. These organizations are excellent resources to find doctors, and ILADS has a training program for physicians. I’ve done training for doctors. I’ll probably pick one up again soon. I would suggest you speak to a Lyme-literate doctor through ILADS.org. Speak to Global Lyme Alliance. Speak to Bay Area Lyme. Speak to some of these organizations that have a lot of experience with Lyme, and they’ll guide you in the right direction.
A Message of Hope for Chronic Illness Sufferers
Ari: Dr. Horowitz, thank you so much for coming on the podcast and sharing your amazing expertise you’ve accumulated over 40 years. The level of expertise is pretty astounding. I really appreciate you coming on. I think that this is going to serve a lot of people. The last thing is, if you want to leave our listeners with anything, if you want to direct them to follow you, to get in touch with you, or to know how their doctors can work with you, or any other final words you want to leave people with.
Dr. Horowitz: The one thing I would tell people, and I think it’s important, is many people are very discouraged with chronic illness. The people who’ve come to see me, they’ve been to 20, 30, 40 doctors before they ever got to see me. I was able to provide them with hope, and not false hope, true hope. As you said earlier, it’s not like I will ever have 100% success rate. There’s no doctor on the planet that will. What I can tell you for sure, being in the trenches for 41 years with these 13,000 chronic ill patients, is hope is real.
If you use the 16-point model, it will, in most cases, my success rate’s probably around 95%. There’s always going to be 5 out of 100 that they still have mold, the Bartonella’s still there. There are things that I’ve not been able to get to, which, by the way, some functional medicine practitioners have had luck with, whether it’s SOT therapies or certain other things out there.
The point being, I want to leave you with a message of hope that whether it’s autism or ADHD or cancer, cardiovascular, digestive diseases, chronic Lyme disease, chronic fatigue, fibro, if you look at this model that is in any chronic illness, and you work with your physician, it will give you a blueprint with over 2,000 references to go in a very scientific, step-by-step manner to try and figure out why you’re ill and what can be done. Based on my experience, there’s a real chance that your health will get better. I have many patients in long-term remissions.
Really, the message is one of hope. If you need more information, my website is cangetbetter.com. endingchronicillness.com is where you can find information on my new book. I have a medical detective subset that’s free. I don’t charge for it. People pay me $7 a month to do it, but it’s free for everyone. Every week, I’ll put out a new substack on something new in medicine. If you want to stay in touch and understand how I’m looking at science and things like Ebola, Hantavirus, just sign up for Medical Detective Substack. Facebook Dr. Richard Horowitz. I’m posting all the time. That’s usually the best way to get in touch with me and just see what I’m up to these days.
Ari: Great. Thank you so much, Dr. Horowitz. Really appreciate your time and expertise.
Dr. Horowitz: My pleasure, Ari. Thank you for having me on.
Show Notes
[00:00:00] Introduction: Dr. Richard Horowitz and the MSIDS Model
[00:03:00] What is Lyme Disease? “The Great Imitator”
[00:05:13] The Controversy: Why Conventional Medicine Denies Chronic Lyme
[00:09:20] Diagnosing Lyme vs. Chronic Fatigue Syndrome & Fibromyalgia
[00:15:49] The Bio-weapon Question: Was Lyme Disease Man-Made?
[00:22:44] The Startling Link Between Lyme Disease and Alzheimer’s
[00:35:04] The 16-Point MSIDS Model: A Ground-Up Approach to Healing
[00:43:21] Overcoming Biological Reductionism: Systems Biology vs. Monolithic Models
[00:53:05] The Biggest Blind Spots in Conventional Medicine
[00:57:47] Terrain Theory vs. Germ Theory: Why the Environment Matters
[1:04:17] Changing Minds: What Dr. Horowitz Learned Over 40 Years
[1:08:18] Practical Steps: What to Do If You Suspect Chronic Lyme
[1:11:15] A Message of Hope for Chronic Illness Sufferers
Links
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