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Rethinking Alzheimer’s: The 16 Factors That May Influence Brain Aging

Dr. Heather Sandison, ND (00:01.238)
Welcome back to the Think Well, Age Well Podcast. I am your host, Dr. Heather Sandison. And today’s guest is someone who has spent decades asking questions where many others weren’t, and helping patients who have felt they were had run out of answers, where there was nowhere else to turn. I feel very, very fortunate that I have been learning from Dr. Richard Horowitz for years. He’s a board-certified internist and internationally recognized expert on Lyme disease and chronic illness.

He is the founder and medical director of the Hudson Valley Healing Arts Center. And over the course of his career, more than 13,000 patients from around the world have sought his expertise for complex chronic conditions that have fallen through the cracks of conventional medicine. Many people know Dr. Horwitz as the author of the New York Times bestselling book, Why Can’t I Get Better? This is often referred to in my circles as the Lyme Bible.

His groundbreaking work led to the development of the MSIDS model, the Multiple Systemic Infectious Disease Syndrome Framework. And this helps clinicians understand why chronic illness is rarely just caused by one thing. And most recently, Dr. Horwich has published a remarkable paper that we’ve been talking about in my circles extensively, and it’s exploring the reversal of Alzheimer’s biomarkers in a patient with chronic Lyme disease.

using his Dapzone Combination Therapy and raising important questions about the role of these infections and in inflammation and immune dysfunction and of course cognitive decline as we age. So Dr. Horwitz, I am so delighted and privileged to have you here on the Think Well, Age Well podcast. Thank you for joining us today.

Richard Ira Horowitz (01:47.404)
No, thank you for having me, Heather. It’s good to see you again.

Dr. Heather Sandison, ND (01:50.05)
You as well. You have spent decades treating some of the most medically complex c patients that exist in the world. Literally, they are flying in from all over to see you. And I’m curious what originally drew you to Lyme disease? When so many physicians, you know, kind of throw up their hands and say this is too complicated, I’ll refer out. What made you dig in?

Richard Ira Horowitz (02:10.925)
I I wasn’t planning on becoming a Lyme doctor. That’s one of the jokes in my career is

It’s not like I turned to my mother when I was young and went, hey, guess what, Ma, I want to be a Lyme doc when I grow older. I just ended up, you know, moving when I finished my internal medicine residency at Mount Sinai in New York City. I ended up moving up to the Hudson Valley, New York, which back in 1987, and I didn’t know it at the time, was the largest Lyme endemic area in the United States. So it was simply, you know, a board certified internist, I’m here to help people. I like to think of myself now as more of a medical detective trying to figure out why people are sick. It’s actually what drove

Drew me internal medicine. But when people were coming in with rashes back in the 1980s and early 90s, we didn’t really know much about Lyme at that point. So I started on a journey to figure out why a lot of these patients who, you know, kept relapsing off antibiotics, why they got sick. And that led to a 40 plus year journey seeing over 13,000 chronically ill patients from all over the world. And I really I credit, you know, my sticking with this. Truthfully, with my spiritual teachers who I met in med school, I

I was studying with the Tibetan Buddhist Lamas when I was at the University of Brussels, and one of my teachers told me Lamagendon one right before I was leaving. I said, What do you want me to know before I go out into the world as a doctor? And he said, Richard, the most important thing is exchange yourself with others and do for them what you would want done for yourself. He said, if you do this, everything will go well. It turns out, of course, that every time these patients were coming in, they didn’t have answers. I kept looking for answers. And, you know, at one point I discovered Babesia, this parasite that was keeping

Keeping people ill, a woman in a wheelchair for five years who couldn’t walk, all of a sudden got up and walked, you know, after a few months of of therapy. another woman who couldn’t talk, she had no, she was aphasia, she had no words coming out of her mouth, went to Mass General, went to all these, nobody knew it was wrong. They said it was migraines. Turned out it was Bartonella, another, you know, intracellular bacterial infection. So the MSIDS model that you described, you know, it kind of grew from the ground up as I was just searching for answers as to why these people became ill.

Richard Ira Horowitz (04:14.564)
Now it turned out I’ve I’ve discovered that the 16-point model applies to Alzheimer’s, it applies to autism, to ADHD, in fact to most chronic diseases on the planet. And that’s the, you know, that’s the basically objective of my new book, Ending Chronic Illness, is to point out that there’s other ways of preventing, diagnosing, and treating chronic illness, not just naming the disease and throwing a drug at it.

Dr. Heather Sandison, ND (04:35.775)
Right, right. So I want to hear about that framework, but you are known as a Lime doc, and so I want to dig into this a little bit more. There’s chronic Lyme and there’s what you described, that rash that and I’d love for you to even tell us what stands for. So there’s the tick bite and a rash that comes with it, and that’s that acute phase.

And that’s recognized in conventional circles, but this chronic phase is less recognized and harder to test for, certainly harder to treat. Can you just kind of give us the synopsis of of that for a minute?

Richard Ira Horowitz (05:10.702)
Sure.

So so right now we’re having a tick explosion in the United States. If you go online, you’ll see that ER visits are up at least 25% for tick bites this year. It’s I mean, it’s a massive amount of ticks that are out there, likely from climate change, from the warming of the environment. So stands for Irithema migrants. So you’re right. I mean, the early lime rash, which half the time looks like a classic bullseye and half the time looks more like a spreading red rash, like a bacterial infection, like a cellulitis. Some people have been mistaken for.

Like herpesoster, getting shingles or getting a spider bite. Half the time it does not look like a classic bullseye. But what happens is about 75% of the cases, 80%, are going to get better with doxycycline or ammoxicillin. But about 25% and more, if you look at the literature, it even goes up to 48%, will go on to develop a chronic form of Lyme disease, which I still refer to as chronic Lyme disease, but it’s otherwise known as post-treatment Lyme disease syndrome. And so what

This is basically Brelli Berdorfry, the agent of Lyme disease, is the great imitator. So these people come in with drenching night sweats and day sweats if they have Babesia, this malaria-like parasite that gets in quite often. They have a chronic fatiguing, musculoskeletal illness with migratory joint pain, migratory muscle pain, migratory nerve pain, tingling, numbness, burning, stabbing sensations. They can have chest pain, shortness of breath, oftentimes memory concentration problems with word-finding problems.

Problems, difficulty falling asleep, waking up in the middle of the night, neuropsych symptoms, suddenly they’re depressed, they’re anxious. They even develop things like OCD, bipolar disorder, schizophrenia. So Lyme is really the great imitator, and the problem is the CDC said there was at least 476,000 cases just a year or two ago. Medicare rates are seven times higher. So we’re probably dealing with a couple of million people per year, and many of these people go on to chronic Lyme. And now

Richard Ira Horowitz (07:11.0)
we know that, you know, according to what I’ve seen, a lot of these people who’ve developed what they call chronic fatigue syndrome, myalgia concept myelitis, fibromyalgia, even some of the long COVID patients, it turned out it wasn’t just like part pieces of the virus, the spike proteins or active virus that was making them ill. It was Lyme, it was Bartonella, it was mold toxicity. All 16 MSIDS factors that we’ll discuss in Lyme today applied to long COVID. I published it a couple of years ago in the journal Microorganisms. So it’s a chronic fatigue.

Musculoskeletal neuropsychiatric illness, very prevalent, great imitator. And as you said, the testing can be negative in a lot of these patients because they become immune-suppressed. Lyme and Bartonella can suppress the immune system where you don’t make antibodies. If you’ve taken antibiotics early on in the course, it’ll abrogate your immune system to not make antibodies. And then you get long COVID, your T cells get exhausted, and then you get moltoxins like gliotoxins that suppress your immune system. And lo and behold, you get all these chronic.

patients coming in that are looking for answers.

Dr. Heather Sandison, ND (08:13.983)
You mentioned the rash, this eryth erythema migrants rash, and how it can look different. It’s not always the classic bullseye rash, but also my understanding is some people will never get a rash, or if they get a a tick bite on their scalp, they might not see the rash. It might be hidden. Also, my understanding is that it’s not just ticks, right? There are other vectors, the other insects, right? Spiders or fleas. Certainly with Bartonella, fleas come up a lot, but there’s

Richard Ira Horowitz (08:29.122)
That’s correct.

Dr. Heather Sandison, ND (08:42.411)
It it I think sometimes people pigeonhole it into I’ve never had a tick bite, so I couldn’t have lime. But there’s other ways that we can be exposed. Can you go into a little bit of that?

Richard Ira Horowitz (08:51.576)
Yeah, so

Mostly for Lyme disease, it’s usually by a tick bite, but maternal fetal transmission from the mother to child can happen. Blood transfusions will not happen for Ribrillioberdorfri, but just about every other tick-borne disorder I could mention today, whether it’s reliciosis or different tick-borne viral infections, babesiosis, Bartonella, they can be transmitted not only from mother to child, but also by blood transfusion. And even Babesia can be transmitted by solid organ transplantation. But Lyme itself.

Is mostly going to be seen from tick bites or maternal fetal transmission. And that’s tough because there we have seen parents who have transmitted congenitally Lyme to their children. Oftentimes they’re misdiagnosed, they’re told they have autism, spectrum disorder, but it’s actually congenital Lyme. BART, on the other hand, which you mentioned, BART has a huge number of vectors. And Bartonella actually looks like Lyme. It similarly causes fatigue and headaches and joint pain, muscle pain, neuropathy, memory concentration problems. So it looks like

Like Lyme, but the vectors can be ticks. There’s a European species, Bartonella Bertilesi, transmitted by Exodes Ricinous ticks. It’s still debated how much ticks are transmitting it here in the US, but fleas, cat scratches, cat bites, mosquitoes, spiders, kids, which are biting flies, even the triactomed bugs, which are some of the newer vectors on the planet right now, which are transmitting Chaga’s disease, they can transmit Bartonella.

Bartonella is a big problem. It’s it’s oftentimes misdiagnosed, but but it’s a big problem, especially in the children that develop new onsets of seizure disorders or neurocognitive issues. So the most of those vectors are mostly for Barton, not so much for Lyme disease.

Dr. Heather Sandison, ND (10:36.361)
Got it. Okay. And I I’m wanna go into this MCIDS model. So wick I want you to explain s first what it is, and then why do you feel like it’s such a big paradigm shift compared to say what you learned in medical school?

Richard Ira Horowitz (10:50.638)
Yeah.

So we learned in medical school, and I you you may have learned the same thing, but it was kind of the one cause, one disease model from Cox postulate or Pastor’s postulate that we learned. And of course, this goes back to the late 1800s when there was a bacterial infection, like you know, strep causing glomeruline nephritis or rheumatic fever. But what we find now in our chronically ill patients is there’s never one thing wrong with them. It’s like going to a doctor with 16 nails in the foot, telling the doctor you have foot pain, and if the doctor doesn’t find all the nails or finds one or two nails and says, hey, come back.

In a month and tell me how you’re feeling, we all know the patient’s not going to feel all that well. So, what I ended up discovering over time with the 16-point model is that all of these factors drive inflammation. And we know inflammation is the number one cause of all chronic disease and many of the acute diseases, also. So, where’s the inflammation coming from? So, the first main six factors on the MCIDS model, which I call rivers of inflammation going into an ocean of inflammation, is number one infections, which includes A.

A bacterial infections, like Lyme disease Bartonella, B parasitic infections, like babesiosis, C viral infections, like you can have long COVID and reactivate Epstein Bar virus or herpes virus six, or D, fungal infections, you may have a candida overgrowth in your gut or actually get fungus in your body. And as you know, they’ve even found it in the brains of Alzheimer’s patients. So number one is infections. And when you mix these infections with environmental toxins, like mole toxins and heavy metals, I mean there are

ultimately hundreds and thousands of environmental toxins getting into everyone’s bodies, but the ones I usually focus on that do a lot of the damage, and we can detox a lot of the other chemicals in detoxing mold is mostly mold and heavy metals. When you convix infections and toxins like this, you get a massive amount of inflammation in the body. And then you combine it with microbiome abnormalities in the gut. You’ve got the wrong type of bacteria. You don’t have enough short chain fatty acid bacteria to lower inflammation. The fourth

Richard Ira Horowitz (12:51.022)
Point is leaky gut with mast cell activation, where you get things like lipopolysaccharide that gets across the intestinal barrier, causes a blood-brain barrier to get leaky. You get then inflammation in the brain. So points three and four is microbiome, leaky gut, mast cell. And then the fifth and the sixth are vitamin mineral deficiencies, because your body has to detox all these chemicals and deal with the inflammation from infections. And number six, insomnia, where people just don’t fall asleep or keep waking up in the middle of the night. And that happens.

From Lyme, but even young, thin women have come in with sleep apnea. You know, men can have benign prostatic hypertrophy, women in menopause. There’s a lot of reasons why people don’t sleep. But the point being, when you combine these infections with toxins, with microbiome issues, with leaky gut and mast cell activation, with vitamin mineral deficiencies and sleep disorders, and even in sleep, you know with Alzheimer’s, the glymphatics, you need those lymphatics to take the garbage out at night, otherwise, you get these pathological proteins of pizza.

Tau and amyloid beta that accumulate, those are the six major factors on the MCIDS model, and they have downstream effects from the inflammation. So, for example, the mitochondria in your body have nothing protecting them from all this free radical oxidative stress. In Alzheimer’s, right, and what you’ve been looking at, we know mitochondrial dysfunction was one of the hypotheses, but where is it coming from? Right? So infections and toxins can drive it, but we also see hormonal dysregulation. People come in with low adrenal function, low testosterone.

Women go into early menopause. We get immune deficiency or autoimmune reactions. Because as your immune system is trying to fight Lyme borrelia, you get a lot of autoimmunity in the body with anti-nuclear antibodies and rheumatoid factors and anti gangliocides. So you combine this with deconditioning and liver issues and neuropsychological issues. It’s basically a lot of inflammation in people. And Lyme, as I said, it’s the great imitator because most of the patients who’ve come to see me over my

41 year clinical career, they were not all diagnosed with chronic Lyme. They came in with a diagnosis of long COVID or chronic fatigue syndrome, mygia concepamyelitis, fibromyalgia, you know, some of the cases of dementia that have come in, in fact, weren’t what I would call true Alzheimer’s dementia. It was Lyme induced neuroinflammation driving those biomarkers, which we’ll talk about. So in this day and age, when someone comes in with an illness, I don’t find anymore that it’s one thing making them sick. That model we learned in medical school.

Richard Ira Horowitz (15:20.548)
school is pretty much outdated. So, you know, that that’s what we’re finding is really needed to get these chronically ill patients better.

Dr. Heather Sandison, ND (15:27.597)
You know, when you have people frustrated with the conventional system and you know it takes them a long time to get in, it’s like the a pill for every ill, but that’s what’s covered by insurance. How do you help patients navigate sort of this frustration of but if but that functional medicine MSIDS type framework?

Is outside of what I can afford. And I I that I don’t mean to put that all on you, but it’s something I struggle with, right? We want to help as many people as possible with dementia, but it’s not covered by insurance. And so how do you help people square that? Is there is there an empowering message that we can leave, you know, that people can take away today around this?

Richard Ira Horowitz (16:09.39)
Sure.

So fortunately for me, almost every protocol I have published in the medical literature over the years are generic oral drugs that are covered by insurance. So for example yeah. no, and in fact, if someone comes in, I mean, I’m probably drawing like 35 vials of blood on the first visit. But fortunately, Quest Lab Corps Bioreference, the local labs cover it. People usually do not end up with bills because of the coding, right? If you if you’re coding correctly, most of the time the coding covers it. They don’t end up with big lab bills. And Dapsone combination.

Dr. Heather Sandison, ND (16:18.615)
Amazing.

Richard Ira Horowitz (16:39.888)
Therapy, which I’ve pioneered for the treatment of chronic Lyme, it’s all oral generic drugs. You go to your CVS pharmacy or whatever, it’s covered by insurance. What’s not covered is you know the probiotics for the protocols or some of the folic acid supplements I’m using or using glutathione to help protect you from Herzheimer reactions. But honestly, when you consider that most of these people have been to 10, 20, 30, 40 doctors before seeing me, I have developed these protocols in a way that they’re short, they’re fast.

I get people better and they’re out of the office so that you know we can get new people in. but it is mostly covered. But you’re you’re correct, you know, like for example, a mold test from real-time laboratories can be a few hundred dollars. It won’t over be covered, but what I find is if we give the code for mold, once the test comes back positive and they apply for their insurance, a lot of times they will get money back, but you don’t always get it up front. But fortunately, the way I’ve developed these protocols, most of the things are actually covered. so

So but you’re correct in the functional medicine space, of course, there could be a lot of tests that aren’t. The heavy metal test we’ve used most are you know in the serum, which won’t always cover it, but even the six-hour urine DMSA challenge from doctors’ data was 60, 70 bucks, you know, at the time. It was not a highly expensive test. I’d say probably the biggest issue is if you’re not a Medicare patient, getting some of the Lyme testing, like I we we can get it through the local labs again, Eliza, Western Blotz, all of the regular tick-borne infections are covered.

Dr. Heather Sandison, ND (18:00.408)
Right.

Richard Ira Horowitz (18:09.614)
again through local labs, Orlichia, Anaplasma, Babesia, Bartonella, Rocky Mountain spotted fever, Q fever, tularemia, they’re covered. But the problem is there’s so many strains of Lyme disease, we usually have to use specialized labs like IGenics. Again, they will discount them, but you know, you’ll probably pay about $300 to get you know an IgM and an IgG immunoblot. It’s not nothing, but it’s not thousands and thousands of dollars. So when I have to establish the diagnosis,

I have a questionnaire on my website, cangetbetter.com. Costs no money to fill it out. And it gives people a pretest probability of what is the likelihood you’re actually going to have Lyme disease. And if you score over 63 on this questionnaire at cangetbetter.com, it tells you, hey, I really should get tested. Now, you can get tested through the local apps, but if it comes back negative, you then really need to do some of the specialty testing. Because a lot of times we need to do fish testing, which is fluorescent in CT.

Hybridization. It’s an RNA test. Very useful for strains of Babesia and Bartonella. But if you just start with an immunoblot from hygienics, or even look at the bands on a western blot through a local lab, there’s a game I play with patients called Lime Bingo, which is if you have any one of these numbers on a Western blot or an immunoblot, bingo, you’ve been exposed to Lyme disease. And those numbers, you know, people can take notes on this is the 23 band, 23 is the outer surface protein C, the 31, the outer surface protein.

Protein A, the 34, the outer surface protein B, the 39, very specific band for Lyme, and the 83 slash 93. Now, a local Western blot, if there’s a 31, could theoretically be due to Epstein Barr and autoimmunity, but in real life, it’s it’s Lyme like 99% of the time. So

Dr. Heather Sandison, ND (19:58.582)
And forty one is super common. It comes up on absolutely everyone, but non specific, right? Yeah.

Richard Ira Horowitz (20:03.566)
Yeah. Yeah. So so th there’s ways of getting through these tests without spending a fortune. honestly I find that most of the monies that people have spent is usually before they’ve ever come in to see me because they’ve been to so many doctors getting tests trying to figure out what’s wrong with them and never got to the source.

Dr. Heather Sandison, ND (20:14.093)
You know, I what’s wrong? Yeah, and then not not being able to work, net right being a burden on their family potentially. the caregivers can’t work. It gets very expensive, not just directly paying for medical costs, but it’s like it’s all the opportunity costs. You know, I just want to take a minute to applaud you and thank you for being aware of that piece of this and for making this as accessible as possible for people because I I th th in in these circles it is hard.

It is challenging and people deserve good medicine. And so thank you for finding the ways to make the labs accessible and to make the treatments accessible as and and creating that as part of your protocols. I I really think that that increases the impact. And it’s not easy, right? It’s easier to just spend more money. So thank you.

Richard Ira Horowitz (21:02.242)
Well

Well, I I recognized early on that we were in the middle of an epidemic of tick-borne disorders. and now of course what’s really interesting is now we’re putting together the epidemic of Alzheimer’s disease and the epidemic of Lyme disease, there is maybe a you know, a reason why there’s a bridge between these two. Because as you know, they’ve talked about in the medical literature and autopsy studies for years that they would find brelliborf rye lime in the brains of Alzheimer’s patients with biofilm, with amyloid beta, with phosphorylated tau, but it was

Dr. Heather Sandison, ND (21:06.519)
Yeah.

Richard Ira Horowitz (21:32.755)
Always someone who had died in an autopsy study that had never been in a live human being. So I recognized early on this in a worldwide epidemic, I had to find a protocol that was not IV, that was oral, generic, that any person across the globe could take it. And I published it in open access journals, right? So that anyone could go read my literature. They don’t have to come to see me, you know, and get this protocol. And I’ve I’ve done medical detective substacks, which are also free to sign up, where I’ve explained these protocols.

Protocols and in my new book, Ending Chronic Illness, that’ll it’ll be out this October. I basically have a section on the three Bs, Borelia Bartonella, Babesia, where I explain these protocols like a cookbook, that anyone could pick up this book and understand how to do these protocols, that if God forbid I should not be around tomorrow, people would be able to take this book and run with it to find answers for Lyme. I mean, my wife was sick for 25 years. She’s eight years in full remission since she did the double-dosed absone protocol.

Dr. Heather Sandison, ND (22:07.863)
Congratulations.

Dr. Heather Sandison, ND (22:32.651)
That’s an incredible personal testimonial and story. that’s phenomenal. Congratulations on your book. Thank you for making this an open book. Like literally, it’s an open book about how to do this. I’m curious, as we shift the conversation into dementia and Alzheimer’s and and this this clinical case that you published around the biomarker reversal, how often do you think that these infections are only one part of a larger puzzle when it comes to

Age related memory loss.

Richard Ira Horowitz (23:04.686)
so

Based on the factors, in the article that I recently published, this was just a month ago in April in the Journal of Alzheimer’s Disease Reports, what I found is that just like I published for Lyme, that there were these 16 MSIDS factors making people ill. And in 2024, I published in the journal Microorganisms that these 16 MSIDS factors were associated with long COVID. Now I published in this journal that all 16 M-SIDS factors are associated with Alzheimer’s dementia. Now, from my perspective, what do I think are going to be the most important factors? I do think it’s multifactorial.

And you know, you can tell me your take from having been in the field for so long. But I do think it’s probably a combination of bacteria like Lyme combined with viruses, whether it’s herpes virus six, seven, eight, or herpes virus one, or you know, EBV. I do think it’s a combination of bacteria and viruses that are probably, along with these environmental toxins. Jamine Neurology was publishing years ago, they would find pesticides in the brains of people driving amyloid production. Knowing the number of hundreds and thousands of toxins getting into

People and knowing how bad these infections are, and knowing that these environmental toxins are completely destroying the microbiomes of guts, where we now don’t have that short chain fatty acid bacteria to lower inflammation, I think those first six factors on the MCIDS model that I discussed, with infections, toxins, microbiome issues, leaky gut, not getting to sleep adequately, and vitamin minerals are probably at the top of the list. But you know, if you happen to be a type three diabetic with, you know, people with high insulin spikes.

Dr. Heather Sandison, ND (24:28.343)
Training.

Richard Ira Horowitz (24:35.12)
Of course, that’s going to be a major factor if you’re one of those people. But even dysautonomia, right, was playing a role in some of these patients. Mitochondrial dysfunction is playing a role, but of course, my take is it the infections and toxins that are causing the mitochondrial dysfunction. So, you know, with these anti-amyloid drugs, you I employed them for trying to use them, but it only lowers it. In the Cochrane review that came out one week before my article got released, it basically said they’re not really changing the clinical core.

They’re lowering these biomarkers. They’re slowing it down, maybe, but we don’t really have good answers. And this is the first time. By the way, when I submitted the article, I didn’t realize I was this was the first time anyone had ever reversed PTAU 217 completely. I was completely ignorant of this when I submitted it. And then I realized, like, this is actually a big deal because the anti-amyloid drugs were lowering it by 23% over six plus years. I lowered it by 63% in nine weeks, but it’s because in my patient it was

Obviously, that the pTau was being driven, in fact, by Borelia Bergdorfry. So I do think it’s going to be multifactorial. I don’t ever think in Alzheimer’s dementia you’re going find one factor, but there might be one that is at the top of the list. Like in my patient, I treated her heavy metals, we treated her for Q fever, I indirectly treated her for BART. She had metabolic syndrome with an elevated hemoglobin A1C. So she had other factors that could have caused memory loss, but we kind of addressed it.

12 was borderline, but we addressed all these, right? So ultimately, I think in her case it was infections. But I think if we were to do, you know, thousands, thousands of patients, and this is what I hope will happen, the neurologists out there, if they were to check for all 16 MSIDS factors in their dementia cases, you know, it may turn out that there’s two or three or four factors that are the main ones driving it. But my concern with the Lyme epidemic now showing a you know relationship with the Alzheimer’s epidemic, we have to make sure that Borelia Berdorfry is not there because.

Then you may actually have a treatable cause. I mean, we won’t know until we do a multi-standard placebo-controlled randomized trial, the gold standard of medicine. This is one case study. I can’t, you know, go too far on what the implications are. But knowing that in the 375 dapsome cases I published over 10 years, the number one statistical effect was always memory concentration, word finding. It was always 70% of the people said the number one thing that got better from dapsome was memory concentration. And whether that’s

Richard Ira Horowitz (27:04.686)
Because it was an NLRP3 inflammation inhibitor lowering inflammation in the brain, which, by the way, might really be a reason to think about repurposing this drug, even if you don’t have Lyme disease. You know, maybe it’s chlamydia and pneumonia, right, that’s driving it. And maybe these same drugs will help. We won’t know until someone really takes the time to look at all 16 factors, use dapsone independently from infections like Lyme as a repurposed drug to lower neuroinflammation, and see what we have. But the beauty of it is at least.

gives hope. Like at least we have a new research. You know, I opened the door a little bit to get some light in to a, you know, to a field that really needed it.

Dr. Heather Sandison, ND (27:41.962)
Yeah. And i it was the PTAP two seventeen, that was one of the biomarkers that was reversed. It basically went from positive to negative, right? And reduced by you said sixty three percent. Right. That’s phenomenal. Were there other biomarkers that you looked at? Was there an NFL or A beta ratios? Did you look at other things?

Richard Ira Horowitz (28:03.104)
So we did. So her PTAW 181 was normal. her beta amyloid forty-two forty ratio was normal, but what was fascinating about the case, and again I learn all this while I’m going through the literature.

And the PTAW 217 came down, her beta 4240 ratios improved. So when I published the article, what it showed is that the Quest Labs has this really beautiful graphic. And you can see that the graph is going up. And you know, and for the listeners who are listening, you you want a you don’t want a low beta 42-40 amyloid ratio. It’s the 42 protein that’s the sticky form that’s really causing a lot of problems. You want it actually to go higher, and that’s what happened in our patient. It actually showed from Quest Labs.

That there was less amyloid production showing up as the PTau 217 went down. But she had a normal neurofilament light, normal PTau 181. Her initial beta amyloid 4240 ratio was normal, but improved. You could see it was actually getting better after we did the Dapsone nine-week therapy.

Dr. Heather Sandison, ND (29:01.953)
And what was your reaction when you saw that? When you saw her labs come back?

Richard Ira Horowitz (29:05.668)
I was jumping up and down for joy. I was

I mean, literally, I was like a kid in a candy store going because I didn’t know it was gonna work. You know, she was one of the few patients at the end of my 41 clinical career who had never done dapsone. And she’d been putting it off for 15 years. She had not taken any antibiotics for 15 years. so I was really excited because I real, you know, I recognized like, my God, this is such a wonderful result, but I didn’t know the full implications until I started writing up the article for review and then realized that it had never been done.

And that the Alzheimer’s Trailblazer study that they had done back, you know, four years ago in JAMA lowered it by 23% in six years, and I’m lowering it by 63% in nine weeks. It’s like, okay, you guys were trying to pull out amyloid, but maybe the reason it wasn’t always working was because Borelia Burdorferi or Chlamydia pneumonia or other bacteria were there. Now, you know, honestly, if I was a pharmaceutical company making these, I would want to do a parallel study to see how effective these drugs are.

drugs are once you start hitting Lyme. It could be that if the amyloid in PTAW is due to mold or due to heavy metals or due to these other MSIDS factors, these drugs may actually end up being much more effective than they are right now. So that’s a study that definitely needs to be done.

Dr. Heather Sandison, ND (30:23.051)
Yeah, couldn’t agree more. And I think some people hi will hear this and assume that we’re saying Alzheimer’s is caused by Lyme disease. But I think I want to make sure that we zoom out that you’re just you’re describing these MSIDS. Dr. Bredesen talks about the Bredesen 7. I my framework is the six primary level drivers, causes of neurodegenerative disease. And so I think that we wanna make sure that we put all this back into that framework. Lyme disease generally.

Has been, I think, underrepresented, particularly in conventional communities, particularly at this this chronic form, this longer form Lyme disease. And what we’re saying is that, yeah, that might be one of the primary drivers for some people of dementia, of neurodegenerative disease, because of the role of infection triggering the inflammatory process. So, okay, we’re in agreement. We’re

Richard Ira Horowitz (31:10.872)
Correct.

No, no, no, I absolutely not. I mean, if the literature says

If it’s right, that maybe a quarter of the cases, somewhere between 25% or a little higher of what’s now being diagnosed as Alzheimer’s. Because when I saw this patient with PTau, you know, by the way, I had many patients before I finished clinical practice, probably half of them were showing up with these Alzheimer’s biomarkers. so so the problem is I thought at the time, it’s Berillion, it’s other things driving, you know, these pathological proteins driving neuroinflammation. But then I realized if my patient had gone to a board certified neurologist with a high PTAu 217.

She would have been diagnosed with Alzheimer’s, not Alzheimer’s due to Lyme disease, because the American Academy of Neurology doesn’t even look for Borelli Bergdorff rye as a cause because it’s all been autopsy studies. It’s never been proven in a live human being. So, yes, I mean, clearly your framework and Dale’s framework, and even mine, they’re all, as you know, they’re all kind of synchronous. We’re all talking about the same thing. It’s only going to be a certain percentage of these cases, but it now means if you’ve been diagnosed with this, it’s at least something you know.

You need to look at because there might be a potential solution. Again, until we do a really good randomized multi-center placebo trial, we’re just not going to know.

Dr. Heather Sandison, ND (32:25.665)
Right. And I think if hopefully all of our listeners here have heard this before, but amyloid and pTau are antimicrobial, right? They are there to protect us. And so what and inflammation is also there to protect us. Now inflammation can get stuck on, just like amyloid can get stuck in the on position. pTau can get stuck in the on position. And so we want to be able to turn those off. But the way to turn them off is not to just take them out.

Not to just reduce inflammation, not to just extract the pTau or just extract the amyloid, but to ask the question of why. Why is the brain needing to protect itself? Why is there an inflammatory cascade being turned on in the first place? And so you’ve found associations between all of these 16 MSIDS factors and Alzheimer’s disease. I want, I think we’ve gone through six of them. I wanna make sure we go through the other 10, and then I’m curious.

Which are the most important ones in your mind, particularly when it comes to aging and age related memory loss?

Richard Ira Horowitz (33:27.246)
Mm-hmm. So the the the 10, so after the six rivers of inflammation, which again is infections, environmental toxins, microbiome issues with the wrong type of bacteria driving inflammation, leaky gut with mast cell activation, vitamin mineral deficiency, sleep. Those are the main six. The ten downstream effects are mitochondrial dysfunction, which you know, mitochondrial hypothesis and the amyloid hypothesis and autoimmune. There’s all these hypotheses with Alzheimer’s, but from my perspective, it’s like, well, these infections and toxins and sleep disorders drive mitochondrial dysfunction.

So that’s, you know, so that’s number seven. number eight is dysautonomia. People will get definitely POTS dysautonomia. We see immune dysregulation with immune dysfunction, where some people have chronic variable immune deficiency, but we also see a lot of autoimmunity. So immune and autoimmunity are some of these factors. We see neuropsychological issues, so neurological symptoms, psychological symptoms. the liver, it it turns out with these people who have non-alcoholic steatohepatitis, NASH, or fatty liver.

One-third, which is one-third of the world’s population, they have metabolic syndrome and insulin resistance. And we know that these blood sugar spikes with insulin will affect the brain, right? It’s it’s one of the known causes of how you can get inflammation in the brain. And then there’s people who become deconditioned over time from their illness. those are really the main factors, you know, in in the 10 downstream effects of how this affects people. and in my view, the biggest ones ultimately are going to be infections and.

Toxins, microbiome sleep, as we talked about earlier. But that doesn’t mean in an individual patient, like hormonal dysregulation, you get inflammation in the brain, it affects the hypothalamic pituitary axis, and the hormones get dysregulated. And we know with low estrogen, you go into menopause, there’s memory loss. All of this may play a role. And in some people, it may be that the hormones are playing, you know, a big role, as is dysautonomia, as is immune dysfunction, autoimmunity. I don’t think you’ll ever probably find two people that will be exactly the same.

Same, but for me, the broad brush strokes is that it’s probably going to be because in my world with chronic Lyme, when I treat the infections and toxins, that’s usually the biggest factors that get these people ill with chronic Lyme. and as I said, 70% of these people who’ve taken dapsome combination therapy for chronic Lyme say memory concentration cognition is my number one best effect of doing this drug regimen, and it’s durable. And that’s why I think it probably is going to work in the Alzheimer’s space, is because I don’t see people

Richard Ira Horowitz (35:56.829)
relapse from their cognitive issues when they’ve done dapsone, if the other MSIST factors have been adequately treated. Yeah.

Dr. Heather Sandison, ND (36:02.613)
have been addressed. You know, I hear the same thing from patients who have done the hyperthermia treatments. What are your thoughts about hyperthermia treatments for Lyme for treating

Richard Ira Horowitz (36:14.072)
You know, it’s it’s an interesting hypothesis because they found early on that if you heated up the body temperature at least 104 degrees for two hours or more, you could kill spirochetes. So I I think there’s definitely a group of people who go to Germany who do hypothermia who will get some help. But here’s my biggest problem.

Lyme and Bartonella are what are called biofilm persistro bacteria. So they go into hiding in these under these biofilms where your immune system can’t recognize them and your antibiotics don’t penetrate easily. And these persistriforms are a type of the bacteria that go into dormancy. So that’s why when you stop ivirocephan, I mean I’ve had patients take IV drugs for Lyme for a year, not with me, but with other doctors, come to see me, and within one month off the ivirocephon, the symptoms are back. It’s like, well, why didn’t iverosephon kill the bacteria?

Iburicephan does not hit these biofilm persistraforms. The way I designed the protocol is looking at the tuberculosis leprosy drugs because TB and leprosy are biofilm persistra bacteria. That’s how I came up with the idea of doing this, because they use repampin and dapsone to cure leprosy. So it wasn’t all that brilliant. All it was is, hey, I wonder what happens if I add a tetracycline to repampin and dapsone, because tetracyclines hit Erlichia, Anaplasma, Ricketzia, and it turned out it was a home run, you know, out of the park with this. So

I do think that hyperthermia has its place, but ultimately I’ve seen too many people relapse. So I think what it does is it probably lowers the load because you will knock off a certain amount of the bacteria, but ultimately, I don’t know that there’s any proof that hyperthermia is affecting the biofilm persistriforms, just like a lot of these alternative therapies, like SOT therapy. Some people, SOT therapy will shut down these bacteria for a while, but I’ve heard it comes back later on, right? Because you’re just putting

Kind of like a lock and the key to shut off the bacteria for a while. But if you understand, like TB, you need to use four drug regimens specifically for this type of bacteria. Once you understand that Lyme and Bart are a similar type of bacteria, that so I think these other therapies have a place. But from my perspective, not only are they highly expensive, you were talking about what it costs to do some of these integrative therapies, SOT therapy could be $3,000 a pop. You go to Germany, it’s $15,000.

Richard Ira Horowitz (38:30.865)
Dapsone therapy is nothing like that. It’s a generic all-drug regimen. I mean, don’t get me wrong, you might pay a thousand bucks for supplements and folic acid, but it’s nothing like what you’re gonna pay for some of these therapies, and you’ve actually got a durable answer. so I do think there is a role for these things, but I just don’t think it’s getting to the source of where these bacteria are hiding in the body.

Dr. Heather Sandison, ND (38:51.565)
Got it. For listeners who have either a diagnosis of mild cognitive impairment, or maybe they’re ApoE4 positive, they’ve got high risk, family history, maybe even somebody with Alzheimer’s disease and dementia, what practical lessons do you want them to take away from the paper you re recently published and also from your work and its implications for Alzheimer’s?

Richard Ira Horowitz (39:18.678)
So

The main the main points for me is when I when I did this dip dive into the medical literature, again discovering the 16-point model was applies to chronic Lyme, it applies to long COVID, applies to Alzheimer’s. When I did a one-year deep dive into this book, what I discovered is the same 16 MSIDS factors was applying to ADHD, autism, Alzheimer’s, allergies and asthma, the three B’s, C cancer, cardiovascular disease, chronic fatigue syndrome, myalgic encephalomyelitis

Fibromyalgia, hormonal dysregulation, immune disorders, autoimmune disorders, including rheumatoid arthritis, where the 16 factors were showing up in these patients. Same for MS, multiple sclerosis, all 16 factors show up, as well as mood disorders, depression, anxiety, OCD, psychosis, bipolar disorder. And these viruses. So it’s kind of like, hold on. We’re in the middle of a chronic disease epidemic where 60% of Americans have at least one chronic illness, 25%

Of Americans have two or more chronic illnesses. Just this morning, a paper just came out that we are like one of the worst countries in the world with our healthcare system. I don’t know if you you saw this, it was just came out this morning that you know we’re spending more money on healthcare than almost any country in the world, and we’re not having great results. So, what is it about this chronic disease epidemic that can explain it? And again, from the take-home message for me is inflammation is coming from multiple sources. For those people that have gotten viruses like COVID,

Which then caused long COVID. Yes, it may be spike proteins, but in our experience, the VGF, the vascular endothelial growth factor, which is a sign of endothelial inflammation, was also coming from Bartonella. and we found that when we treated Lyme and BART and affected the microbiome, they’ve shown in long COVID the wrong type of bacteria in the gut, bifidobacterium, you people will get better. So the take-home message for me is as we get older, I mean, I just turned 70 years old. Now I feel great for my age, and I’m doing a lot of things.

Richard Ira Horowitz (41:19.094)
To you know block inflammation and open up anti-inflammatory pathways, the take-home message for me is if you want to live a long, healthy life, you got to figure out where the inflammation’s coming from. It’s not enough to go to the doctor, check your blood pressure, check your cholesterol, get a mammoth, get a colonoscopy, check your product, all good. But for me, people over 55 years old, if the NIH now said, which is on their website last year, 42% of Americans over 55 are going to become demented.

It’s like, what?

Dr. Heather Sandison, ND (41:49.623)
Does not have to be

Richard Ira Horowitz (41:49.783)
And nobody, I mean, and nobody at the top of the healthcare chain is going, my God, four out of ten people listening to this podcast are scheduled to become demented. Like that is just not acceptable. So my take-home message is look at the 16 MCIDS factors. Again, they’re not all going to be appropriate for every person, but you want to make sure you’re treating infections. A lot of my patients didn’t know they had mold when they came to see me. 90% of my chronically ill patients now are testing positive for mold. Mold suppressed.

Your immune system. It can lead to cancer, right? With gliotoxins and aflatoxins and trichothicines. These are hidden factors. So my first message is that MCID’s model, I believe, to change, it’s a paradigm shift for how we look at chronic disease medicine. And the next step is: you know, if the NIH were to take randomized multi-centered trials, take this model and apply it to all these chronic illnesses, because we’re not doing all that well right now with chronic illness in the United States. And I think it’s a starting point to say, okay,

Okay, let’s do really great science and look at these 16 factors. Right. Bob Bobby Kennedy recently said, let’s get everybody off SSRIs and psych drugs. But

Why are people all depressed and anxious, right? I mean, it might be social what’s going on in the United States and around the world, but it’s also these infections and toxins. It’s all 16 MSIS factors causing mood disorders. So that I think for me is really the major factor. And then for me, over 55, I would be starting to check people for Alzheimer’s biomarkers and do like a Mocha test. You know, do a simple cognitive test in your office and start to check these biomarkers because now we may have options instead of just anti access.

amyloid drugs or improving the antiamyloid drugs by treating some of these factors.

Dr. Heather Sandison, ND (43:34.242)
Yeah, I couldn’t agree more. It’s a really exciting time and it’s a way to stay optimistic, right? In the face of these statistics around how much complex chronic disease there is and how many people are suffering, there are clear paths forward. And so for anyone who is feeling overwhelmed or discouraged, I want them to know about your book. Because this I think that that that is a way to describe this path. So will you please share? I know it’s not out yet, but I’m sure it’s available for pre-order. So where can people find it? What is it called?

and when did they come out?

Richard Ira Horowitz (44:04.29)
Yeah. So

The book will be out in October. It’s called Ending Chronic Illness, a Revolutionary New Program to Reverse Inflammation and Heal Persistent Disease. And and what I did in the book is I have sections on prevention and treatment, but it’s also natural treatments. It’s it’s using nutraceutical, it’s it’s using vitamins and minerals for prevention. It’s looking at diet like the Mediterranean diet and how to adjust the Mediterranean diet, right? Which is so beneficial with exercise and sleep for you know helping to stop cognitive issues later in life. So there’s a whole section on natural diet.

Natural methods, but also pharmaceuticals. Like if you have migraines, I have no problems using a Jovi and you know some of these drugs out there, but maybe you don’t need them. Maybe you know you have a mitochondrial dysfunction in the brain and you need CoQ10 and B vitamins and you need to be on a low histamine diet because that’s how my wife stopped her migraines, is just getting off histamine foods because she didn’t realize she had mast cell activation. So what I do in the book is I go through all these major chronic diseases and explain how you can use the best of both worlds, the best

Of pharmaceuticals and what modern medicine has to offer, but also how to sometimes get yourself off these drugs and use natural methods to stay well. Because in my case, my whole family died of cancers of different types. I have no one left in my family. I’m the last survivor. And it’s in part why, again, when I wrote the chapter on C is for cancer, cardiovascular disease, chronic fatigue, I wanted to make sure people know, because everybody knows someone getting cancer these days. It’s like, why is it happening?

Infections, toxins, microbiome, it’s the same issues, but if you go to your doctor, they’re not going to tell you to look at these things. So I it’s it’s basically the book will be out October 13th from Simon and Schuster. You can go to ending chronic illness.com to look at the book in pre-order. And really what I hope will happen is people will go to their doctors, give them even a copy of the book if if they have not gotten it, let them read it, because I believe it’s gonna be the paradigm shift. I’ve seen so much chronic illness in my lifetime that we have

Richard Ira Horowitz (46:03.864)
Have to do better than what we’re doing right now. And I didn’t expect, by the way, when Simon and Schuster gave me a contract to write it, I didn’t know that all these chronic diseases were going to have all 16 factors. This was a complete surprise to me, just like when I did the search on Alzheimer’s and discussed, you know, that all 16 MSIDS factors are associated there. So it should give people hope and it should give them like new avenues of healing. And every story in the book are personal patients who’ve come to see me over my 41 years, that I’ve gotten off Crohn’s and ultra selection.

or I’ve, you know, reversed their MS because it wasn’t true MS. It was Lyme-induced or Bartonella-induced neuroinflammation with demyelination, with mold. It describes in detail how to use the model. And I think it’s going to benefit a lot of people and give people hope.

Dr. Heather Sandison, ND (46:48.929)
I’m sure that it will. Dr. Horwitz, thank you for being here today, but more importantly, thank you for the decades that you have spent advocating for patients with complex chronic illness. And for, you know, not giving up, for continuing to ask the difficult questions that challenge conventional thinking so that we can find real solutions. And I I think, you know, whether or not people agree with our conclusions, your work, it just reminds me over and over and inspires me that like.

Curiosity, rigorous investigation, compassion, humanity, and this willingness to look deeper are where the breakthroughs start and and how people really again get those outcomes, get those solutions. So thank you, thank you for your work and thank you for your time today. It’s always a privilege to talk to you.

Richard Ira Horowitz (47:35.674)
it’s that’s my my pleasure. Thank you for having me on today. Really great pleasure for me too.

Dr. Heather Sandison, ND (47:40.949)
If you’ve learned anything from this podcast episode today with Dr. Horowitz, please share with others who might benefit. There is so much unnecessary suffering happening, whether it comes to Alzheimer’s or other complex chronic diseases. So please help us spread the word so that others can get the help that they deserve. Thank you so much. Until then. Until next time, be well.

Dr. Heather Sandison, ND (48:05.688)
Okay.