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In this episode, you will learn about groundbreaking work being done to move the needle in understanding the impact of Borreliosis.

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About My Guest

My guest for this episode is Dr. Alan MacDonald.  Alan B. MacDonald, MD is a hospital pathologist by trade, and his world is microscopic images.  He diagnoses disease daily based on the images from surgically removed tissues, blood smears, and microbiology specimens.  In his private research, which he does at night or on weekends, he interprets images from diseased tissues.  In hospital pathology, there are many texts which illustrate the image profiles of tumors and other medical diseases.  Some of the reference materials do not provide a “perfect” image match to an individual patient situation. New lessons, which come from patients which do not “match” the published image archive, are the subject of “case reports” which enrich and expand the knowledge contained in medical textbooks.  Many of the images of “spirochetes” in textbooks demonstrate only the “perfect corkscrew” profile which leads a reader to “doubt” the legitimacy of other Borrelial forms such as the cystic or granular forms.  Dr. MacDonald's website is an effort to educate about the “forgotten” spirochetal forms which are really Borrelia and which exist in diseased tissue.

Key Takeaways

  • Is acceptance growing in understanding the impact of Borrelia in many conditions?
  • Does autoimmunity exist in absence of infection?
  • What are the different forms of Borrelia?
  • Was Willy Burgdorfer part of the problem or part of the solution?
  • Does Borrelia impact liver detoxification?
  • How might Borrelia impact an unborn child?
  • Can Borrelia be sexually transmitted?
  • What are the challenges with testing for Borrelia?
  • What role might parasites play in Lyme disease or in MS?
  • What is the role of biofilms in chronic conditions?
  • How do Tick-Borne Relapsing Fever (TBRF) Borrelias potentially lead to more severe illness?
  • What role might Borrelia play in Alzheimer's, Lewy Body Dementia, or cancer?

Connect With My Guest

http://AlzheimerBorreliosis.net

Related Resources

Support Dr. MacDonald's Work

Interview Date

November 30, 2022

Transcript

Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast.  They are not a full replacement for the discussion.  Timestamps are provided to facilitate finding portions of the conversation.  Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed.  Please Contact Me with any corrections.  

[INTRODUCTION]

[00:00:01] ANNOUNCER: Welcome to BetterHealthGuy Blogcasts, empowering your better health. And now here’s Scott, your Better Health Guy.

The content of this show is for informational purposes only and is not intended to diagnose, treat or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health related decisions with your own personal medical authority.

[00:00:35] SCOTT: Hello, everyone, and welcome to episode number 176 of the BetterHealthGuy Blogcasts series. Today's guest is Dr. Alan MacDonald. And the topic of the show is Moving the Needle in Borreliosis. Dr. Alan B. MacDonald is a hospital pathologist by trade, and his world is microscopic images. He diagnoses disease daily based on the images from surgically removed tissues, blood smears, and microbiology specimens.

In his private research, which he does at night or on weekends, he interprets images from diseased tissues. In hospital pathology, there are many texts which illustrate the image profiles of tumors and other medical diseases. Some of the reference materials do not provide a perfect image match to an individual patient situation.

New lessons which come from patients who do not match the published image archive are the subject of case reports, which enrich and expand the knowledge contained in medical textbooks. Many of the images of spirochetes in textbooks demonstrate only the perfect corkscrew profile, which leads the reader to doubt the legitimacy of other Borrelia forms, such as the cystic or granular forms. Dr. MacDonald's website is an effort to educate about the forgotten spirochetal forms, which are really Borrelia, and which exist in diseased tissue.

And now, my interview with Dr. Alan MacDonald.

[INTERVIEW]

[00:02:03] SCOTT: I had the great honor to meet Dr. Alan MacDonald many years ago, probably the first time at an ILADS conference, and several times since. He was profiled in the Lyme documentary Under Our Skin. And he's dedicated his life to attempting to move the needle in the realm of Borreliosis, the causative agent of Lyme disease. And as we'll learn, potentially many other conditions as well.

Thanks so much for being here Dr. MacDonald.

[00:02:29] DR. MACDONALD: Thank you, Scott. Good to see you.

[00:02:32] SCOTT: Why did you become so passionate about your work on Borreliosis and really make that the major focus of decades of your life? Did you have a personal experience where Borrelia touched your own life?

[00:02:46] DR. MACDONALD: Well, my wife did suffer from chronic Lyme for many years and she was treated, and the treatment took about three years for her to go through a complete course and to get to a point where she was feeling better. And some of the medicines that were supposed to work didn't work. So, we were rolling out new ones as we went along.

She was able to get to a point where the infection was clinically inactive. I'm not sure whether it's ever under the microscope inactive, but clinically inactive. And she's in a balance right now and she's doing well. She has arthritis, and some of the joints that were impacted had to be replaced. The hips and the shoulders. And we hope we don't have to do knees. But the knees may be next.

[00:03:35] SCOTT: Fortunate that she has you in her court to help navigate these often challenging waters. As I mentioned, you have been attempting to move the needle in Borreliosis for decades, and yet your findings, many of which have major implications for medicine, have not always been so readily accepted, not been accepted with open arms oftentimes. Why do you think there's so much resistance to your work? And are you finding that acceptance is growing over time? Do you feel like there is a vindication for Dr. Alan MacDonald on the horizon?

[00:04:13] DR. MACDONALD: Well, thank you for that. But I think that, over time, the politics have shifted slightly to a more liberal view because more people are publishing eye-opening discoveries in Lyme disease other than me. And as more people publish eye-opening discoveries, then it becomes more acceptable in the conventional big picture to say, "Okay. Well, maybe what he was trying to do back then did have something to it."

My mythology unfortunately started with dead babies, and dead babies because of Lyme in utero. And then it moved from dead babies to Alzheimer's disease. And those are highly charged emotional concepts. And although there's a basis for comparison of what happens in the Lyme-infected patients with what happened in the very, very far past with Syphilis, everything that Lyme disease can do, Syphilis did. And so, it's a model, it's a bridge, because they're both spirochetes, they're both chronic, and they both can do terrible things. But not everybody gets everything. It's not like there's a syndrome. You have to be aware of nuances, and you have to be aware of exceptions to the rule, and new opportunities to make a diagnosis.

And what I've tried to do is to use DNA evidence rather than antibody evidence to prove the point. If I can find with a DNA probe that the troublemaker is in the disease tissue, then I think I'm well along to have a credible argument. Whether people want to accept that argument or not, it's up to them. But all I can do is bring the DNA evidence. And I've been using DNA probes since the 80s to find points where, under the microscope, you see the bug.

And that's the goal in all Lyme disease is to see the bug in the diseased tissue. People have leaned on antibodies. and blood. And antibodies and blood haven't really helped because there's a good furor about whether it's a manifestation of an active problem. Or whether it's just a scar in the blood showing up as an antibody for past exposure?

In order to make a really convincing Koch's postulate type argument, you need to fulfill four of his precepts, which is you regularly grow the bug and you find the bug in diseased tissue. Those are the first two. And then the last two are unethical, because what they say is that you have to use the bug that you grew to infect a new naive patient and then have that establish a disease all over again and then grow it from the disease patient. And so, those two postulates can't be done ethically because it's not right. But to get two of Koch's postulates, growing it in pure culture and finding it regularly under the microscope I think is good enough for the 20th century.

[00:07:11] SCOTT: It sounds to me like you were just a few decades ahead of your time and being on the very leading edge of this whole research exploration. I want to start the discussion early on by saying that there are some scary things that we're going to talk about. And many of the things that you've discovered aren't necessarily good news. Saying that, I think it's important to note that if you're treating Borrelia, that people can and do still lead healthy productive lives. They don't have to go down this path of what we're going to talk about in the next hour or so.

I'm just wondering before we get into the real details, can you share a few hopeful words that could really help to lift people up that might find some of this information rather discouraging?

[00:08:00] DR. MACDONALD: New antibiotic combinations and new therapies are being rolled out all the time. And if you look at a scorecard of people who treat patients every day – I don't treat patients. I just do research and try to assist in the diagnosis. But the people who actually treat say that, with a proper program of antibiotics over a proper period of time, and that will probably be more than a year if you have severe disease, that 80% of people will get better. Unfortunately, 20% will not. And that 20% figure is a very vexing figure because it's a challenge to deal with the 20% that aren't getting better.

And we're looking to see that if the disease has become entrenched and doesn't appear to be working, whether we can roll out new things to treat those patients rather than the simplest antibiotics which were used in the 80s. Some of the newer things are things that used to be cancer chemotherapy drugs, like daptomycin and things like that. At Hopkins, they found that that helps. And some people are using a non-antibiotic called Dapsone or Disulfiram and using that over chronic period of time.

There are always new ideas and there's always new opportunities to see how the patients respond. And then give those patients what the best you can do in hope that they can turn the corner.

[00:09:26] SCOTT: For many years, there's been this invalidating post-treatment Lyme disease syndrome label that has been given to people with chronic Lyme disease that there is no remaining infection. That some other process, maybe an autoimmune process, continues after the "eradication of Borrelia". And you alluded to this already I personally don't think that Borrelia can be fully eradicated from the body. But I also don't think that it has to be something that has to be eradicated in order for us to have a healthy, productive life. I'm wondering if you can just talk to us about where you stand on the potential for persistence of infection in chronic Lyme disease. And even if autoimmunity was a contributor to ongoing symptoms, couldn't persistent infection be the explanation or the trigger for that autoimmune process?

[00:10:21] DR. MACDONALD: The autoimmune connection has been formulated by people who want to make sure that they argue persuasively. And it doesn't persuade me. But they want to argue persuasively that the body has more or less turned on itself.

And my take is that the immune system is not stupid. And so, the immune system is not there to turn all of its furor against your normal cells that you were born with. I think that there's a – As a workaround. And that is if the bug infection enters and penetrates the cell that's having trouble, the cell line, the synovium or brain tissue, and lives on inside the cell as a parasite, but inside the cell, that the immune system will sense that there's something wrong and attack those cells. And in the process of doing it, you can misname the activity as autoimmune when it's really proven that there's bacteria inside the cells that are being taken out by the immune system. It's completely appropriate for the immune system to take those cells out. Those disease cells are infected and the immune system works to remove those and try to clear the field.

Calling it autoimmune is I think a miscarriage of medical thinking. And I don't think that all these things that are considered to be autoimmune are actually in fact anything other than the intracellular inside the cell lifestyle of the bug. It's notorious for penetrating cells living inside of cells, persisting inside of cells. And it does that in the joint. It does that in the bone marrow. It does that in, Dr. Sapi’s showing now it's inside the breast. It's certainly inside the brain and inside the liver. And it has a nice hiding place if it's living inside a healthy cell and not killing it.

I wouldn't say that autoimmune is appropriate. I had a case where a colleague of mine was diagnosed with an autoimmune liver condition called primary biliary cirrhosis. And it's a terrible disease and often can move to a point where you have to have a transplant because your liver is shut. And she was diagnosed as an autoimmune hepatitis and put on a liver transplant list. And I got a biopsy from her, and we did the proper DNA studies. And sure enough, the bug, the spirochetes, were living inside the liver and inside the liver cells. And she received appropriate antibiotic therapy and then she got off the transplant list. Because it wasn't autoimmune. It was infectious masquerading as an autoimmune situation. That happens over and over again in situations where the Lyme spirochete selectively targets an organ which you wouldn't think of as being a Lyme type problem. It can do the eye. It can do the brain. It can do the lymphoid system. It can do the thyroid. It can do the liver. It can do bone. All of these things are places where it can hide. And where it hides, it will cause trouble.

And so, you keep in some sort of a balance between its troublemaking capability and your availability to keep it in check, and you can do well. But you have to be able to think about the possibility that autoimmune doesn't make sense. Autoimmune is also sometimes treated with steroids. And if you give somebody who has a real infection steroids, the infection will just march right on, because that's just all it needs, is to shut down the immune system.

Some Lyme infections are so severe that they actually have a natural ability to suppress these post-immune response. And the T cells and the B cells are not working up to par because the infection, overwhelming infection, has suppressed that ability for that system to work. If you throw steroid medicine on it, with steroids kind of interfere with normal immune function, you're really increasing the skids for bad outcome, bad scenario.

[00:14:27] SCOTT: I 100% agree with everything you just said. I remember moderating a conference in Amsterdam several years ago. And on the stage were Joe Burrascano, Ann Corson, Dietrich Klinghardt, some amazing people. And the question that came from the audience was, "Does autoimmunity exist in absence of infection?" And they all kind of look to each other. And I think it was Dietrich Klinghardt that took the microphone and said, "Uh, no." That was the extent of the answer.

[00:14:55] DR. MACDONALD: Very concise.

[00:14:56] SCOTT: Your work has focused largely on Borrelia. Many practitioners suggest that Bartonella and Babesia can also be significant symptom producers in the broader context of Lyme. Can also be very challenging to treat. Have you done any work in the realm of co-infections? Or what are your thoughts on the role that those co-infections might play in a chronic Lyme scenario?

[00:15:20] DR. MACDONALD: I have done relatively a small amount of work. I published on Babesia and the co-infection in Lyme. But that was back in the 80s. I haven't done Bartonella at all. But Dr. Breitschwerdt can do that and run circles around me. So, there's no reason for me to expend energy and something that he could do better than I can.

It's interesting that both Babesia and Bartonella must live inside of living cells. The theme is coming back. We had really hiding inside of living cells masquerading as autoimmune. And now we have Babesia living inside red cells and causing a chronic problem and hiding inside the cell. And Bartonella, of course, must live inside of cells.

This intracellular theme is repeating itself. And all we need to do is make sure that we think about that before we just throw out autoimmune and not give it a good amount of careful thought.

[00:16:19] SCOTT: Over the years, we've heard about the spirochetal form of Borrelia, the L form, the cyst form, which I believe you actually put on the map many years ago. Now we hear about the persister form. You've talked about the granular form.

Talk to us a little about the different types or morphological forms of Borrelia. And can these granules shed from a Borrelia spirochete? Can they lead to new spirochetes in the body? Can killing spirochetes lead to more spirochetes? And then lastly, how is a "cyst form" different from what we now refer to as a persister form?

[00:16:58] DR. MACDONALD: Well, in the model of Syphilis, which comes to our aid and rescue again, all of the forms that you just described were well worked out in the last century. There's no mystery that Syphilis, spirochetes, though you’d like to see them exist as a corkscrew, can exist as a straight bacillary form and not have a coiled corkscrew appearance. It can break up into little granules. And that was found in the work of the people at the Institute Alfred Fournier in Paris where they found these granular forms and syphilitic chancres where it had busted open and there were all these little granules in the lesion. And the L form and cell wall deficient form, of course, with Lida Mattman, was very carefully studied. And then you left out the biofilm form. The biofilm form is a community of organisms, which includes all of the other specialized forms.

Inside the biofilm where the bug makes a protective layer of goo around this living microbes. And the biofilm matrix, which is a glue, protects the bugs against antibiotics and immuno action. All of that is part of the chronic Lyme terrain.

If I'm going to try to describe what the cystic form is, just imagine a mechanic's rule where you wear it on the belt, and the rulers all wound up inside the belt. And you can pull out. And it depends you know it depends on how far you go. But you can get an intact spirochete coming out of the cystic form, which is equivalent to the mechanics ruler in carpentry.

It's just another way for it to help itself escape from immune recognition. Because when it does that, it turns inside out. The outside is protected from the immune system. And the inside is on the surface when it turns itself inside out now.

Now, the spirochetes of Syphilis could regenerate from granular syphilitic forms. And that's well established in animal models. We've got some limited evidence that the same thing is happening in the granular form with Lyme disease, where the little dots actually over time start sprouting little tails. And the curlicue gets longer and longer. And eventually, there's no more form. And just the spiral forms come back.

The spiral form is actually a caricature of what the spirochete lifestyle can look like in the normal person. It's all permutations of the morphology, which is correct. But not intuitively obvious. And Dr. Scott Worthen, who did the Warthin–Starry stain, he developed it at University of Michigan, had a big matrix of line drawing showing that on the top line they're all spiral. And then in the second line they're somewhat spiral but they have blobs at the end. And then it gets down to a ring form. And then a cystic form. And then at the bottom, there are three lines of granules. It looks like the period at the end of this sentence. And all of those things were proper and legitimate forms in Syphilis. And all of those things are proper and legitimate forms in Lyme disease, too, as the infection matures in the post.

Now, the cyst form may require a special antibiotic approach because it doesn't work as well to try to kill the cystic form with usual antibiotics. And so, there are some other combinations which are used. And my wife received some one of the combinations when she was being treated with Joe Burruscano. And it worked like a charm and it enabled her to get over the hump and then get into a clinically stable platform.

You have a little modification of your style and choice of antimicrobials. But it needs to be constantly re-evaluated over the time of the treatment for the patient and has to be customized. It's now a one-size-fits-all.

[00:20:56] SCOTT: And would you differentiate the cyst form from a persister form? Or is that just new terminology for essentially the same thing?

[00:21:04] DR. MACDONALD: I think they're the synonyms. You could have various forms. A persister form implies that the bug is not actively dividing over a long, long period of time. If the bug is not actively dividing, the antibiotics which kill only in the moment of cell division can't kill a non-dividing form. It's resting. It's sitting there. Just thumbs its nose at the antibiotics because it only can – antibiotics can only kill if they get it during the cell wall active part of the lifestyle.

Biofilms also have an excess of granular forms inside of them. They have very few of the spiral forms. And when you see them, they're around the edge like this frosting of the cake. But in the center, it's all granular forms, or cystic forms, or L forms. And forms that normally would not be thought of as spirochetal. They are entirely spirochetal. And they have the DNA to prove it.

[00:21:59] SCOTT: You worked in the early days at a time when Willy Burgdorfer was really part of the present and not the past of Lyme disease. The man after which Borrelia burgdorferi was named. The same man that many consider a hero, like I did when I met him nearly 15 years ago and yet from Kris Newby's book, Bitten, we see a different side of Willy Burgdorfer as more of a contributor to the problem that we face today rather than part of the solution.

And you being one of the major influencers in Lyme disease and the history of Lyme disease, I'm wondering, how do you think Willy Burgdorfer should be remembered?

[00:22:40] DR. MACDONALD: Well, let's give Willy the credit for doing the pick and shovel work for discovering in the miasma of tick guts that he found the spirochete. And then he made the essential connection. The light bulb went off. And he said, "This may be the agent of Lyme disease as a spirochete."

However, he also dissected – in his dissections found a small worm, too. And that was a small nematode. And that was kind of put on the side. Now, there might be a role for double infection with the microscopic nematode and the spirochete to cross disease in some patients. Then you have all the co-infections, which he wasn't aware of. But eventually they came to light. Those are all the wonderful things that Willy was able to do with his skill, and his microscope, and his sweat equity to just go ahead and pile through and solve the puzzle.

Now, whether he did other things in other situations is also in Kris Newby's book, he was brought over from Switzerland and he was recruited to go to the Rocky Mountain Lab and had a scientific home there for his entire life. And while he was at the Rocky Mountain Lab, he was approached by the defense department, and he was recruited because of his expertise and ticks to help them with some experiments if they wanted to try as maybe uh useful in combat situation. He was asked to help find ways that they could use tick-borne diseases to neutralize a foreign adversary.

He worked with a number of organisms other than the Borrelia spirochete in that work. And he did that work relatively in the first few years of his association with the government. And he may have been compelled to do that work as a condition for him getting citizenship. I don't know. But he was able to help them with some of those studies. And some of the studies then became secret, because they're secret work. And so, we never really know all the studies.

But we do know that he was able to work at Fort Detrick for a period of time. Fort Detrick is in Maryland, I think. And Fort Detrick is where most of this biological warfare stuff has been historically based at the Fort Detrick Laboratory. So he did have a connection there.

Beyond that, I don't know how enthusiastic he was about doing the work or whether he was compelled to do the work with a gun to his head more or less, it's figurative gun, or not. He's not particularly verbal about those years. And some of those things that were found were found only after he passed away in his repository of documents.

And there was a lot of pressure by the government to keep it secret. I don't know how much of it actually is still secret or not. But he didn't work with viruses. He didn't work with uh spirochetes per se as an agent of biological warfare. He was working with other things like Rickettsia. And Rickettsia organism, like the Lyme organism, must live inside a living cell. And so Rocky Mountain Spotted Fever is Rickettsia is inside the living cell killing all the cells inside of the blood vessels. And then you can have a fatal outcome.

It's an intracellular agent of the cell. And there are other things that he may have worked on which are similar to those non-Lyme agents that could be utilized in a situation where insect vectors could be used in part of the proposed activity.

In World War I, there was a lot of Trench Fever. And people who died in World War I, not all were killed by bullets. They were killed by trench fever and other infections as they were living in these filthy trenches. And they couldn't get out of them. And they couldn't move. And sanitation was horrible. There were a lot of lost lives due to infection in World War I. And I think some people say more people died of infection than bullets in World War I. And that was before we even had an idea about germ warfare.

But I think people who were paying attention to the military then said, "Well, if it happened in World War I, and then maybe if we had some control over it, and maybe going forward, maybe we could use it as some sort of an advantage." But that's all speculation. I think it's fertile ground for thought. But there's no way to really go too far with it.

[00:27:34] SCOTT: Yeah, complex topic for sure. You alluded to the lady who had liver issues where you found Borrelia spirochetes. I want to talk a little more about the role of Borrelia on detoxification, on the function of the liver. Talk to us about your work in finding Borrelia in liver cells, even granulomas that are attempting to address these intracellular infections. And how much of an impact does Borrelia have on the liver? How might that increase the need for supporting the liver while we're treating chronic Lyme disease?

[00:28:09] DR. MACDONALD: Okay. Well, liver is a massive organ. I mean, it's the largest organ in the body, if you think about it. And the liver has been established over the many years that we've learned about Lyme disease to be part of the Lyme disease target tissue. Lyme disease can target the brain. It can target the peripheral nerves. It can target the heart. It can go inside the eye. But it also goes in the liver.

And so, Lyme hepatitis is a fertile area for discussion and consideration. I think that it is the most under-diagnosed category of chronic infection in people who have chronic infection with Lyme, because the tension is not focused on the liver. And it's also complicated by the fact that that's a first cousin of Borrelia Burgdorferi, which is Borrelia miyamotoi, which I've found in the liver. And that they tend to travel together. And other agents can also travel together and interfere with normal liver functions.

Liver as a function for nutrition, as a function for protection as its own immune system. It has a very important detoxification role. And it helps make a lot of things that we need to have a healthy life. They all come to the liver.

Lyme hepatitis is not well understood and not diagnosed nearly as often as it should be. And I think that's just because people have been stuck on the CDC categories, which doesn't include liver. They never mention liver. But it is real. And I found infection in babies that had died in utero and the infection that was easily diagnosed was on a cultured liver. And the spirochetes grew out of the liver of the aborted or miscarried babies.

But also, in adult life, with chronic Lyme disease, there's a liver component in many. And some of the things that may be misinterpreted – if the enzymes are up and you get on antibiotics they might say, "Well, you know I think maybe you got to get rid of those antibiotics because it's an antibiotic result, a bad effect of the antibiotics." And they don't think about the fact that it might be doing its proper job by killing the bugs in the liver. And part of that is a side effect. And that the enzymes go up because the bugs are getting killed and it's actually working properly.

I mean, that's sort of a controversial term. But I think that Lyme disease in the liver are as that are neglected and need more attention. I've got a case that I just finished where a person had chronic liver enzyme elevation. And all the tests for Lyme infection were negative. And then the mother contacted me and asked me to look at her biopsy. I did. And I found that she had a double infection in her liver biopsy. She had one with Borrelia Burgdorferi and she had one with Borrelia miyamotoi. And they were living inside the sinusoids of the liver, which are a little narrow capillary-like channels that go across.

And so, on one side, you'll have a liver cell. And then you have, where my pen is here, you'll have the – in between, you'll have the sinusoids where the blood goes through. And inside the area where the pen is, all the spirochetes were present. And in my knuckles, there weren't any spirochetes in those cells. It's a selective target. But it's a very important target because that's where the working – that's where the rubber meets the road, in the sinusoidal and the cellular interaction.

And of course, all the other things that the liver does, detoxification and making sure that things stay healthy, are way beyond our ability to cover right now. But it's a very important organ. It's not being studied. It's not being biopsied. And if you don't biopsy it, there's no way to prove or disprove that the infection is or is not in the liver. And so, that's one thing that we need to think about, is if the enzymes are whacked and you are one wondering about the possibility of Lyme infection through a biopsy. And the biopsy will tell you, if it's there, it's there. If you don't do a biopsy, you won't diagnose it. And then it will go unopposed. And the disease will progress to worsening. Biopsy early. Think about it. Look for it. And then you've got better patient care going.

[00:32:27] SCOTT: Whether or not Borrelia and co-infections can be congenitally transferred or acquired during pregnancy seems to me to be pretty clear at this state of the evolution of our understanding of Borrelia. And you've talked a little bit about this. But what has your work shown in terms of the potential for these infections to impact a healthy pregnancy potentially lead to miscarriage and for the potential to be transmitted to the fetus during the pregnancy?

[00:32:54] DR. MACDONALD: Well, Syphilis comes to our rescue here, because Syphilis was the Great Plague. And during the time when Syphilis was a great plague, the number of stillborn was huge, and miscarriage, huge. And as a result of that – and I remember this because it impacted me when I got on my marriage license. I needed a blood test. What was the blood test for? Syphilis. And it was a Syphilis blood test that had to be negative before you get a marriage license, right?

And the reason for that is that if you have a husband and wife and one of them had uh Syphilis, then they could go to the unborn baby and kill the unborn baby like that. Bang! You had to have a negative blood test in order to get a marriage license. Now, that kind of dropped off the face of the earth after about 1974-75.

But Syphilis, when it was in his heyday, had major, major impact on stillbirth, miscarriage, and malformations in the children. That's spirochete, remember, Syphilis, Lyme disease, each can do whatever the other one can do without any hesitation. If it existed in Syphilis, it does exist in Lyme disease, too. And therefore, they are models for each other. And they resonate. And there's no exceptions. Syphilis could get the eye. Syphilis could get the hearing of the ear. Syphilis could get any organ in the body until you got to the eyelashes and fingernails. I don't think there's any Syphilis of the fingernails. Everything else is fair game for Syphilis. And it's true that not everybody gets everything.

But if you were aware of it and somebody came and came in with a problem and it didn't seem to fit in the other characters of – other diagnostic categories, you would always think of Syphilis as a necessity to do a complete thought, complete examination, complete testing to make sure it wasn't some form of Syphilis. Same thing with Lyme.

And people resist the fact that the CDC website only has meningitis, and heart block, and skin erythema migrants, and joints, right? Four we're stuck like a broken record. If you read the CDC website, there's only four things that they talk about, right? And all the other things that we are talking about now are off the radar for the CDC. And people make their judgments about what's real and what's not based on what's on the CDC website. It is stuck in a rut from the 1980s and it hasn't opened up.

Only recently has the CDC permitted with noblesse oblige to say that if you find under the microscope the Borrelia in tissue, that's a legitimate way of diagnosing. You know how long it took to get that onto the website? 30 years. They had their back up. And they never ever accepted microscopic positive, or autopsy positive, or biopsy positive as proof of Lyme disease. You had to get the blood test, which is totally, totally just bad medicine.

But they don't practice medicine at the CDC. They count beans. They're bean counters. And we don't have any real internal medicine or any other specialty thought leaders on the payroll of the CDC. We have a void at the CDC. And you know what else? It's a military organization where they're actually given a uniform and a rank, and they get a military pay grade, and they become military officers, EIS officers with a uniform, right? And so, that's military intelligence. What do you think of military intelligence? Is that an oxymoron? Some people say yes. It's like Postal Service. Oxymoron, right? Military intelligence, oxymoron. CDC and good medicine, oxymoron, right?

I mean, you can't bring something to the table if you've never ever read about it or permitted it to be a possibility in your brain. You have like a conceptual blockade the Maginot Line in World War I, World War II. A huge fortification that was supposed to keep Germany out of France. Maginot Line. If a Maginot Line in the CDC in relationship proper diagnosis and complete diagnosis of Lyme disease, it's a disgrace.

[00:37:23] SCOTT: I think I know what you will say to this next question, but I think it's an important one that people will be interested in your thoughts. The debate continues on sexual transmission of Borrelia. Even some of the best Lyme doctors have said that sexual transmission of Borrelia is likely a rare occurrence. And that when it occurs, the course of illness is generally milder than when it's transmitted from a tick. What are your thoughts on the possibility of sexual transmission? And how common do you think that is?

[00:37:54] DR. MACDONALD: Well, Lyme disease infection can be transmitted sexually if you look carefully. And there are a few uh research studies that have looked carefully at conjugal pairs of a husband and wife, partner, partner, who have the infection at the same time, right? And so, they go and they test them.

And they can do very fancy DNA studies. And then if you find the infection in one and you do a very detailed DNA fingerprint of the first partner and then do the same DNA footprint of the second partner, they both have the same DNA subtype of the infection. The odds of that happening, by chance alone, are infinitesimally small.

DNA evidence comes to the rescue. And DNA evidence says that in a conjugal unit, where they are monogamous, that the subtype, DNA subtype, of the Lyme infection when they're both infected is identical gives you the answer to whether it can be sexually transmitted, right?

I mean, that's the simple question. Nobody's looking for it. It's very difficult to get semen and a vaginal specimen matched and then studied with the expensive molecular techniques to see if there's an infection in either one, if there's an infection in only one and not the other. And then if the infection in both is available, whether it's the same genetic subtype.

But if you go and jump through all the hoops, when you find the infection is genetically matched with all the subtypes to make it like a forensic, forensic type investigation, the answer is yes, it is sexually transmitted in some situations. And Syphilis, why did I need a Syphilis blood test in order to get a marriage license in the 1970s? Because it was sexually transmitted Syphilis. Anything Syphilis can do, Lyme disease can do. End of sentence. Full stop.

[00:40:13] SCOTT: Let's talk a little bit about testing. Testing for Borrelia and co-infections has certainly improved over the years. But it's still far from perfect. Far from black and white. How might Borrelia's ability to bind to antibodies lead to false negative test results? How might these immune complexes lead to false negative results? Can treating first and then doing some of these tests maybe improve the chances of finding it? Talk to us a little about the limitations that you see today. And where would you like to see things go with Lyme disease testing in the future?

[00:40:49] DR. MACDONALD: Okay. At present, we are dealing with laboratory machines looking at blood analysis and deciding based on the machine reading of a color how much bright color is produced in the process of doing the test. Whether the antibody level is first present or absent. If it is present, is it in high enough level to jump over the hoop or jump through the hoop to say, "Oh, it's high enough that I don't have any hesitation in calling it positive." And it doesn't cover all of the possible in the real-world protein types of different forms of Lyme disease. It has some intrinsic limitations.

Those intrinsic limitations have been used by the CDC to develop their two-tier system, the Dearborn system. It has produced a party line that if you're machine reading, your ELISA test, is insufficient to be high enough to call it positive, then they will do a second round of testing with the Western blot. And the Western blot has a certain number of required positive results on like the bands on the – rungs of a ladder. You have to have a certain number of those to say that, "Okay. The infection is confirmed."

Pound for pound, when you look at all of the ELISA tests that have ever been done, the number of CDC approved high enough level to be real CDC definition positive is somewhere around 50% or less. And as you get out into the chronic territory, it goes down to 20%.

One of the worst things that's ever been done is to rely on the shortcomings of a blood test for confirmation of whether you have Lyme disease or whether you had it, or whatever. Blood tests are the enemy rather than the friend.

And so, if you have a real disease and your blood test doesn't make it through the CDC gauntlet, you will be denied therapy by people who depend on, like a crutch, the CDC rules. If you are in the care of somebody who doesn't think that the CDC rules are fair and medically sound, then they will offer patient's therapy even though their ELISA blood test is negative, right? There are many opportunities to have a negative.

And one of the things that we learned in laboratory of medicine is that immune thinking, only positive results count, and they have to be good positive results, in immunopathology. Negative results are never ever to be trusted because there's lots of reasons to get a false negative. And so, if you have a biological positive by physician judgment, that should trump the results of a lab test saying that there's a negative result.

Now, I recently have done some research to look at a new way of looking at blood in people who have chronic Lyme disease by clinical judgment by the physician taking care of them and whose ELISA tests are negative. And I wanted to see if I could find evidence under the microscope that spirochetes are still in the blood. And I got 30 specimens from my consultation practice. I have material from around the world. People send me blood slides to look at. And so, I had an international uh sampling of people who are clinically positive, ELISA blood test negative. And I deployed my blood test, and I found that in those 30 patients, 30 of 30 of them, 100% percent, had spirochetes that I could see in the blood. And those spirochetes were coated with antibody produced by the patient to the infection.

The spirochetes in the blood, and then the patient makes an antibody to the spirochete, which is great, right? And it latches on through the spirochete and continues. The spirochete doesn't kill it. It just continues to circulate through the blood. And I could detect antibody coated spirochetes in 30 of 30 ELISA negative patients with chronic Lyme disease.

Now, what does that mean to me? It might mean nothing to anybody else. But to me, it tells me that one of the reasons why the blood test might be negative perennially when you actually have a chronic infection and live spirochetes in your blood, is that these spirochetes doing their thing allow the antibody to be bound to them. And when it's bound to them, it's taken out of solution. It's on a solid spirochete now. It's not in the solution anymore.

The only antibodies that the machine can see are the ones that are dissolved in blood. If all of it's taken out on the spirochete and coated on the spirochete. And this happens a million times in high infection rate. It's conceivable that all the antibodies which are really there are missed because they're not in solution anymore. And that's called an immune complex disease. And there's other ways of finding immune complex disease.

But immune complex is a phenomenon which is a part of laboratory medicine, we must deal with it, where the antibody grabs onto its protein. And then because it grabs onto the protein, it can't react in the ELISA test anymore. And so, you get a false negative when it's really there big time, on the surface of the spirochetes piece or on the surface of the biofilm.

That's one of the things that I developed, is an antibody coated spirochete test to determine that you have not only the antibody, which was missed by the machine, because it wasn't in solution. It was not a solid platform. But it works equally well for burgdorferi and miyamotoi. And right now, there's not a lot of tests for miyamotoi. I can pick up miyamotoi infections in addition to burgdorferi infections because they both can coat the spirochetes.

And I've got beautiful pictures of some patients who have a mixture of Miyamoto and burgdorferi and use different color probes to show that these spirochetes are all over the place. And some of them are coated red. And some of them are coated green. And they have a different genetic backup, makeup. And that takes my breath away. That is like, "Boy, if I were persona non-grata, that should really make me super persona non-grata’d to the CDC." And I wear that banner proudly. Thank you.

[00:47:49] SCOTT: I think another thing that you pointed out in your work previously as well is that the biofilms are actually pulled out of the sample before testing. If you have these organisms in biofilm, that's another potential reason that you get these false negatives. You mentioned steroids. That you have to have a healthy immune system. Not be an immune suppressed. So many things that can lead to these false negatives.

Several years ago, there was a Borrelia culture test that you worked on with Eva Sapi and Joe Burrascano. It seemed like that was the gold standard. It didn't rely on the immune system. You were looking for the actual antigen or the actual bug. And the CDC and FDA, as I understood it later, warned against the use of the test. It was taken off the market. My question is do you think we will see another culture test emerge in the future?

[00:48:40] DR. MACDONALD: Yes. I think that that was a political move by the CDC. And the science behind their politics wasn't really very robust. It was more or less you are guilty by accusation. It's like a Kafkaesque thing, where if you've read the trial, you know you're guilty because you're accused of being guilty, but you're not proven to be guilty.

Interestingly, the floods that came out of the culture vials were put on smears and then they were stained with a DNA stain. And then they were confirmed by microscopic visualization of the bug in the blood in blood culture.

One of the predominant forms in the blood culture in that early work was the rounded cyst form. Not the squiggly, corkscrew spirochete form. And so, cystic forms prevailed in early studies of the blood culture test. And because it wasn't squiggly, it wasn't trustworthy from the CDC, because they have a trustworthy limit. And if it's not spiral, it's not real. And if it's not real, then we're not going to allow people to use it only because we're going to speak out and say that it's a bad test. Well, it's a pretty good test.

And spirochetes do grow in artificial culture medium. And sometimes they start out as cystic and then they sprout their tails and they become a spiral later on. Syphilis could never be grown in a laboratory culture. If you wanted to try to culture Syphilis, you were out of luck. Even today, you can't grow Syphilis in an artificial laboratory culture medium. You can put it into a rabbit testicle, and the rabbit doesn't like that. But the spirochetes will grow inside the rabbit testicle very well.

And so, if you want a culture method, you have to take a syringe and then get a rabbit and then bang into the testicle. And then the rabbit's unhappy. But let the spirochetes grow very well inside the testicle. Another reason for sexual transmission, isn't it? Right? It loves to grow in the testicle. And for people who says sexual transmission is not real. Just look at the rabbit testicle model for Syphilis and let's talk again after you've read the paper.

[00:51:10] SCOTT: Another area where I think you've made significant contributions is in the realm of parasites. And so, many practitioners don't treat parasites, because testing for parasites is notoriously difficult. Lots of false negatives. There's a commonly held belief that parasites are not an issue in the U.S.

For those that do treat parasites, the general order of operations has been to treat the parasites, particularly the larger worm parasites, treating those first, because they may then house or contain other smaller organisms that are essentially taking up residence inside the parasite. And that if you wait until later to address the parasites, you could potentially then re-expose the person to the organisms that are within the parasite. Talk to us about what you found relative to parasites being hosts for other smaller organisms.

[00:52:05] DR. MACDONALD: Well, that's a very large topic. But I think, to cut to the chase, there's a condition called River Blindness. And Jimmy Carter had a foundation, or has a foundation, and its goal is to eliminate this parasite related disease, this River Blindness disease. And he's been very, very successful.

Liver blindness takes place because the worm gets into the body, but it's carrying a bacterium called Wolbachia. And the Wolbachia then is the one that causes the problem with the blindness. The parasite carrying the worms is like a chauffeur. And the worms will eat bacteria as a food source. It's not unheard of for that to happen.

I've used the Wolbachia River Blindness model to do some work and to look at the worm that I told you about that was found in the tick dissection with Dr. Burgdorfer. And I have found in some safe situations of specimens provided to me that there's a worm. And inside the worm are the Borrelia spirochetes. Not the wall Wolbachia spirochetes. They're kind of riding as a kind of a chauffeur-driven mode of transportation. And then the worm can work its way through the body and then deposit these things willy-nilly as it goes along.

That's a model that is interesting because it's understudied. But I think that it will need more attention. Parasitology as a scientific discipline is sort of in danger of extinction. We don't have – we're not turning out world-class parasitologists anymore because people have other interests. But it's a very important discipline. And without a parasitology as a source that you can go to, you're not going to be able to make sense out of things that are intrinsically parasitic or a combination of parasite-carrying bacteria like the River Blindness model of the Jimmy Carter Foundation.

[00:54:17] SCOTT: We know then that ticks can host parasites. Do we know if the ticks can potentially then transmit those parasites to humans along with Borrelia and other vector-borne infections? And if that is the case, do you believe that treating Lyme disease should incorporate anti-parasitic therapies as well?

[00:54:39] DR. MACDONALD: I think that there's a lot of politics in that equation. One of the basic stumbling blocks is that what's living in the tick gut is a gemish, a mixture of bacteria of various types and parasites of various types. The current dogma is that in order to have the Lyme disease infection transmitted from the tick bite to the human, it must go through the salivary gland. And then the saliva of the tick is what transmits the infection after it establishes a bite site and starts to take a blood meal from the patient.

However, there's another type of – another possibility, and that is that regurgitant transmission is also, for me, on the website, on this radar screen. And with regurgitant transmission, as a process of feeding and gorging yourself on blood, sometimes as a regurgitation from the gut backwards into the host again. Maybe the earliest transmission would be salivary gland, fine. But as the tick becomes engorged and large like a grape, there's also the possibility of regurgitate transmission.

And one of the other ways that it can transmit is that it goes through the digestive system in some situations, and then the insect vector leaves its fecal material on the skin, and then you scratch it and then that has gone through the GI tract of the parasite. Nothing to do with the salivary glands anymore. It's already down deep into the poop of the parasite vector. And that way, you can get a transmission of infection.

I think that the rigidity of believing that it must be salivary transmission only is a false flag. And parasites can be transmitted by other methods, including regurgitant transmission. And you just throw up and all the stuff in your gut goes “guhhhh” into the bloodstream.

[00:56:45] SCOTT: I love your analogies. I seem to remember you presenting probably at ILADS talking about Borrelia forums with a big tray of Play-Doh.

[00:56:54] DR. MACDONALD: Yes. That was one of my teaching props. I wasn't running for office, but I was hopefully that would –

[00:57:02] SCOTT: You say that Multiple Sclerosis is a parasitic disease. What connection have you discovered between parasites and MS? What type of parasite might be involved in MS? How do we think that parasite is acquired? And is it then directly impacting the myelin sheath that surrounds the nerves? And have you seen cases where antiparasitics led to improvement or resolution of Multiple Sclerosis?

[00:57:29] DR. MACDONALD: Well, MS is supposedly an autoimmune disease, right? It's a disease where the body attacks its own myelin and destroys it. And it's supposed to be an autoimmune disease. If you really are steadfast in belief of that as an autoimmune disease, then I have nothing I can tell you to change your mind.

But if you're willing to open your mind up to the idea that might be a collection of diseases that sort of all focuses on myelin loss but it's not necessarily intrinsically autoimmune, it just happens that the innocent bystander phenomenon happens.

Now, you know with drones and war, there are rockets that are deployed. And the bad guys are taken out with the rockets. And then the innocent bystanders are also sometimes killed. Children have been killed with drone-type strikes. There's an innocent bystander possibility, which I think is going on in Multiple Sclerosis where there was an agent that is moving through the nervous system in the brain and leaving a trail of injury behind it. And I think that, in some situations, it may be that it's an unspeciated, a worm without species. And I've gotten a collection of Multiple Sclerosis cerebral spinal fluids from the Rocky Mountain Multiple Sclerosis laboratory and done some work and found that whole worms, little mini tapeworms, not big ones, but mini type, mini scale, microscopic scale tapeworms, were present in two of the Multiple Sclerosis spinal fluids. The whole worm.

Now, the odds of that happening by sheer chance alone are zero. As I used to say with spirochetes, they're not sitting there waiting for a bus. They're there to do trouble. And worms end up in the central nervous system are there to do trouble.

And there's something called visceral larva migrants, where the larva gets into the body and it migrates from place to place and doesn't really find its home but leaves a trail of destruction behind it as it goes through the body. And Multiple Sclerosis would fit that model very well, because there would be a flare up in one area and then it will calm down. And then there'll be a period of quiescence, and there'll be another flare up in the area. And it's almost like it's moving around from place to place and not all the areas stay equally hot. Some of them cool off. Some of them heal. And then a new fire, if you will, erupts.

And so, finding and photographing under the microscope these novel worms has intrigued me because if worms are taken in and the species the worm has never been actually agreed upon or even seen, or thought, or imagined, that unwashed fresh fruit and unwashed vegetables which could carry parasites could transmit the eggs of the worm and then the worm gets in. And then starts causing trouble.

I think that there are opportunities to look at this further and use some of the parasitology skills to focus Multiple Sclerosis studies on could it be a product of worm moving through the brain, and use some of those skills to answer the question. I have enough to convince me that if I can see a whole microscopic worm in a Multiple Sclerosis spinal fluid, that it's not sitting there waiting for a bus. It's there to do hard.

[01:01:12] SCOTT: Wow!

[01:01:13] DR. MACDONALD: And that's that's where I am with it. I think that antiparasitics are not poison. Now you can give them safely. I think that you have to have a good judgment and how you dose it, whether you give it pulsed or rest, and pulsed and rest, that kind of thing. But I think it's an avenue for possible new therapy and Multiple Sclerosis that it could be – I think it's generally agreed upon that Multiple Sclerosis is due to an environmental process. There's a Multiple Sclerosis band across the globe, and it's in like the area between the U.S. and Canada. It's in the 59th parallel and it goes around the world. Multiple Sclerosis hot spots follow that that northern climb.

And you look and see the world map, you'll see that that's where they do turn up. Multiple Sclerosis is big in Scandinavia. It's big in Russia along the 54. It's a high number along our border with Canada. I think that there's an opportunity to find an environmental agent, maybe a worm, on unwashed fruits and vegetables that would be a pathway to get that into the body. You wouldn't need an insect. You'd take it in through your food. And then the hatching of the eggs happens after it gets into you. But then it goes to the brain. And then trouble starts. But that, in my beady little brain, is a possibility.

[01:02:38] SCOTT: Let's talk a little bit more about biofilm. You say that the term chronic and biofilm is equivalent. That to have chronic infection, biofilms must be present. That you can't have chronic without biofilm. And in these conditions, I also tend to think of an overlap between hypercoagulation and biofilms. That biofilms which are providing a hiding place for these microbes can be found in the blood can also be a contributor to hyper viscosity and impact normal blood flow. Where in the body has your research shown the highest concentration of or presence of biofilm?

[01:03:18] DR. MACDONALD: Biofilms were the brainchild of Dr. Eva Sapi. Let's give full credit to Eva Sapi for finding that Borrelia could exist in a biofilm form. And so, I was working with her, and we were looking at first in test tube models. And then we proved that, in test tube models, actually we call in vitro models, that the spirochetes over a period of time would grow and then form biofilm. And then you could see the biofilm and identify it and all the structural things that you need to say, "Yes, that's a biofilm."

It's a community of bugs that is surrounded by a self-generated goo or matrix, protects it. And the specialization of the microbes inside the biofilm so they look different from the microbes outside the biofilament. And they hang around. And they can actually break off in little pieces and spread around and metastasize like cancer cells. Break off and set up new housekeeping around the body.

All that work was done and published in 2012. And then in 2012, they said, "Well, all right. Then maybe we'll begrudgingly say it could happen in the test tube, but it could never happen in the body." Oh, no.

And so, in 2016, we published a case where evidence of the battery of tests and skin where it did pop up in one of the chronic Borrelia lesions that are called Borrelia lymphocytoma, skin lesion.

And since then, we found that chronic Borrelia infections in the blood, in the tissue, in the brain, in the liver all have a biofilm component of Borrelia. It's there. And it's there where the disease is chronic. And it stares part of the survival mechanism for the bug to elude destruction by the immune system and by the antibiotics.

Antibiotics don't get into biofilms very well. In order to get into the biofilm to kill the bugs, you have to have some kind of biofilm buster open protocol. And once it's open again and not protected by its goo and slime, then you have a better chance of getting a complete cure. But as long as the biofilms are around, you're going to have some chronic persistence of the bug.

Now, what's the best biofilm buster? Well, I really don't know. People are working on it all the time. And there are some things coming out of Johns Hopkins, well, Dr. Zhang, before he went back to China, was working on biofilms. And he came up with a triple drug recommendation for three different drugs. One of them was Daptomycin. To see whether that could help other antibiotics to get into the biofilm and then kill it.

Others, which are very dramatic, are like bacteriophage type therapy. Where bacteriophage is a virus that prey on bacterial cells. Not on human cells. Bacteriophages are viruses that attach to the outside of the cell and then they kill the bug, kill the cell, and then spread out and keep spreading.

If you could harness the bacteriophages to kill biofilms, that would be another possible way with probably not too much toxicity. A very exciting way to get some progress on that.

[01:06:24] SCOTT: I think that some speculate that biofilms can be a contributor to stroke. And I'm wondering, do you think we can have similar vascular events elsewhere in the body where these biofilms are present?

[01:06:39] DR. MACDONALD: Yes, that's a very good question. There's a condition where the heart valve gets inflamed and gets infected. And it can cause a lot of trouble. Because the heart valve, they move, "Lub-dub, lub-dub, lub-dub." And on the surface of it, if you have a little kind of an attached extra thing on the edge of the valve, and the yellow thing is one of those, it's like a biofilm, that it could break off. And the heart valve infection is called bacterial endocarditis. And it's been around for a long, long time. And if it's not caught and dealt with properly, you can lose the function of the valve and then have to have the valve replaced.

All of the collections of bacteria on the infected valve, which is only the one with the yellow, are biofilms. No exceptions. And that's for strep. And that's for pneumococcal.  All the other things that can cause endocarditis act as biofilm type infections. No excuses. No exceptions to that.

Lyme disease can be a free-type, free-floating biofilm. It can be attached to a tissue site. It can be deep in the tissue. It's an adaptation for chronic infection. And so, I think that because of the biofilm model for other types of bacteria, the biofilm of Borrelia model is very robust. And I found that the Alzheimer plaques in Alzheimer's disease are biofilms. No exception. Alzheimer's plaques are biofilms. And they're coated with amyloid. And the amyloid is there because there's an antimicrobial action.

Now, the world's most powerful people in Alzheimer's research would say, "Well, yeah, amyloid is not that good guy. It's a bad guy. And it's toxic." The toxic theory of amyloid is kind of waning and going away because all the things they decide to try to develop new drugs to stop amyloid in Alzheimer's, they have all failed. Billions of dollars in research on amyloid, anti-amyloid therapy in Alzheimer's disease have all failed.

In my view, all Alzheimer's plaques are biofilms coated with amyloid. And of all the Alzheimer's brains that I looked at with DNA probes, the biofilms are DNA positive for Borrelia. They all have Borrelia biofilms coated with amyloid. No exceptions. That makes Alzheimer's an infectious disease, Scott. That will get me escorted out of the country club. And 100% of my attempts to have a dinner in the country club, that will get me thrown out of every country club you can see. Because it's politically not correct. But scientifically, I think it's extremely correct.

[01:09:41] SCOTT: And fortunately, I think there are now people like Dale Bredesen that are at least starting to look at the infection connection in dementia, in Alzheimer's. There are a few of you out there that are starting to open people's minds.

I want to touch a little more on Tick-Borne Relapsing Fevers, the Borrelia miyamotois and others that now really seem like in some areas that Tick-Borne Relapsing Fever is even more prevalent than Borrelia burgdorferi. What does that mean in terms of testing for Lyme disease in terms of the contribution that mixed Borrelias may play in Alzheimer's or even cancers that we'll talk more about later?

[01:10:24] DR. MACDONALD: Well, Relapsing Fever was at one point in our history of probably 20 years ago considered an orphan disease and it was on its way out. And the reason for that was that people who were trained and studying that were retiring and going away. And younger people coming up with those skills of research and diagnosis were not coming up to replace them. We were losing our residue of experts in Relapsing Fever, and that all turned around, thank God. And Dr. Tom Schwan is a world-renowned expert on Relapsing Fever and also Borrelia.

Biology is that, like Lyme disease, the fever with Relapsing Fever, Borrelia, it comes in clusters and spikes. And then there's a symptomatic febrile period where the bacteria are in high number in the blood and then they disappear, and the fever goes down. And then another bunch comes back, and they start to get a high number. And then they have a fever and then it goes down.

Relapsing Fever is that waves and waves of Borrelia Relapsing Fever type here in the blood. And then they are suppressed and then they appear again. And there may be four or five relapses in Relapsing Fever. In the worst case, Relapsing Fever can kill you. And that happens in Africa. In African Relapsing Fever. And there have been fatal outcomes here too.

The problem with Relapsing Fever up until, let's say, 1990 I guess, was that it required a tick. They're called a soft tick to transmit or a body louse. And of course, we have good hygiene, so we don't have a lot of people walking around with lice. And we don't have a lot of places where the soft tick, which is a big, large tick can live a long lifespan.

They tend to live in areas in the Northwest in mountainous areas. They'll be in caves. They'll be in sometimes cabins. And they'll set up housekeeping there. And then when people camp out near that, they can come and bite the person and transmit their Relapsing Fever Borrelia to the person. And the infection is then, depending on your geography, either possible or not possible.

We don't have Relapsing Fever, soft ticks in general, in areas where Lyme disease is highly, highly represented. We don't have it in New England. We don't have it in the west coast. We don't have it in Minnesota of the type that they have in the west coast, in California, and in Nevada, and the Rocky Mountains.

That changed when we discovered miyamotoi. Because miyamotoi is a bacteria that kind of is exceptions to the rule. It's not transmitted by the big, fat, soft tick. It's transmitted by the same tick that transmits Lyme disease. And so, it has an environment where it lives happily and it overlaps. Every area where you have Lyme disease, you can have the miyamotoi Relapsing Fever.

It doesn't produce the high counts of Borrelia spirochetes and the fever spikes that the ordinary Relapsing Fever does. It's more like a Lyme sneaky beak kind of thing. And originally, it was called to attention because it was seen in people who are immunosuppressed or who had lymphomas and were on chemotherapy. And they found that these little spirochetes, which were not Lyme spirochetes, but the miyamotoi Relapsing Fever, they were present in the spinal fluid.

And so, people were immunosuppressed by chemotherapy would get that infection. And that led toward awareness. And then led to better testing. And now we're seeing it's a worldwide problem. And everywhere where you have Lyme disease, you can have a reservoir of Relapsing Fever in the ticks that transmit. So, they could transmit both infections with one tick bite. You get both Borrelia burgdorferi and Relapsing Fever in tick bite. Or you can get sequential, where you get Lyme disease in one tick bite and Relapsing Fever miyamotoi with a second tick bite.

That's how miyamotoi has come into public awareness. It's still relatively under the radar and kind of out of range for people to think about it because they haven't actually personally experienced a patient with it. They had some outbreaks in Russia and in Japan. But as we look further, miyamotoi Relapsing Fever is part of the fabric of chronic Lyme disease. It's treated exactly the same antibiotic lines. The problem is, if you don't have a blood test to pick it up, and there is no blood test right now to pick up miyamotoi, then you have to have a higher index and suspicion and then go to DNA testing to prove it. Once you've proven it, then you give, and people can have the same chance that recovery is with chronic Lyme disease.

Tthey may make the disease more severe and may mean that, instead of managing somebody at home, you have to put them in the hospital if you have a double miyamotoi and Borrelia infections, double-headed, you might have to have them in the hospital. They may have a more stormy course. That's all I can tell you about that.

[01:15:55] SCOTT: Yeah. And my understanding is that IGeneX does have a Tick-Borne Relapsing Fever ImmunoBlot. But I think a lot of times people don't realize that it's different from the Borrelia burgdorferi or Lyme ImmunoBlot. And if you don't run both of those, you may miss the presence of some of these Tick-Borne Relapsing Fevers.

[01:16:14] DR. MACDONALD: Yeah, I think IGeneX has gone even further than that. And they are encouraging people to think about other members of the Relapsing Fever group of organisms. It's a long list. Miyamoto is only one of them. There are other ones, hermsii, and other things like that that they're making an argument that those infections, contrary to what the textbooks say, could also possibly be transmitted by the small, hard tick that transmits Lyme disease.

Now that's a big gulp. And I'm not sure that that has been backed up by field studies which show that that's true. But they are making an awareness of the marker for Relapsing Fever. It's called glpQ. The glpQ gene. And that's only present in Relapsing Fever Borrelia. It's not present in the Burgdorferi. If you have a glpQ marker, and that's what they have in their blood test, it's a glpQ marker, then that means that you're not dealing with Lyme disease, but it's a first cousin of miyamotoi. So, we'll see how that works out. I'm not sure that we will have a rapid answer to whether really a Borrelia hermsii or whether traditional Relapsing Fever could really be transmitted by a hard tick or not. That's a big gulp. But I think awareness is good and treatment is good. And hopefully we'll get a better result.

[01:17:42] SCOTT: I want to talk a little bit about Lewy body dementia. A form of dementia that I understand is different from Alzheimer's. Even though Lewy bodies can be found in maybe a third of those with Alzheimer's. We have this Lewy body dementia. It's the same type of dementia that Robin Williams had. I know you've looked at tissue from four people with Lewy body dementia. What did you find that connects Lewy body dementia and Borrelia? And kind of piggybacking on your earlier conversation about amyloid in Alzheimer's being protective, could alpha-synuclein, similar to the amyloid in Alzheimer's, also be a protective response to the DNA of Borrelia potentially?

[01:18:29] DR. MACDONALD: Yeah, Lewy body, in its pure form, could be reduced to patients who have a Parkinson's-like illness. Because all Parkinson's has Lewy body in the Parkinson lesion. That's a condition where you have the shakes and you have Michael J. Fox type contortions. And it's a motor illness. And some patients, there's also a dementia that's associated with the Parkinson's shaking, too. So, you can have both.

The pure Lewy body disease is a disease where the lesions are on the top of the brain in the cortex, just like the distribution of the lesions for Alzheimer's disease. My interest was to check Lewy body cases which were diagnosed elsewhere and see if I could find any uh evidence of Borrelia spirochetes in association with those brains. And I did. And I found them. Four or four of them had Borrelia DNA in association with Lewy body dementia.

And the Lewy body itself is actually a collection of protein. And it's a modified alpha-synuclein protein. We all have healthy alpha-synuclein in our body, and that helps us to keep in good balance. And the Lewy body and in Parkinson's disease is thought to be relatively connected with a toxic form where the healthy form gets degraded and it becomes toxic. And then that collects in these globular things. And then it sets up housekeeping inside the nerve. And then eventually it overwhelms the nerve and then the nerve dies and then the Lewy body is kicked out into the free space of the brain and leaves a kind of a residue of past infection.

I did some studies and, I first of all, looked for possibility of Borrelia burgdorferi and two patients with Lewy body disease. And I found that, and I reported that in a poster in 2016 or so. And I I was able to make a case study. There was an infectious type of Lewy body, and that infection would be a Borrelia infection.

Later on, I got a few more cases. It's hard to get a real pure case of Lewy body dementia. You can wait and wait and wait. And so, it took about four years for me to get a couple more. But I did that, and I did the same studies, and I found that they also had evidence of Borrelia infection. But there was miyamotoi in there too in addition to burgdorferi.

So that miyamotoi and the burgdorferi are unholy two. When they happen in the same situation, you're going to have a more worrisome situation. Those patients had the symptoms of dementia, but they also have very scary hallucinations where they see uh flying insects, or monsters, or they have visual hallucinations which are very, very scary. And that's part of the definition, the clinical definition of a Lewy body disease, Lewy body dementia.

Now, it's interesting to go back in the in history where, Parkinson's disease, after – clusters of Parkinson's disease after the world epidemic of influenza would be described. And they called it post encephalitic Parkinson's, after the flu. The virus did something to the brain. And then those people had Parkinson's disease.

And among those, there was a subgroup that had not only Parkinson's movement disorder, but they had dementia, Parkinson's dementia. It's like a spectrum of movement disorder, and then movement disorder plus mental confusion, and then overt dementia. There's an infection connection between some cases of Parkinson's disease and some cases of Lewy body of any type.

The mixed Alzheimer's Lewy body you've talked about, that's 30%. It invokes two separate pathways. One pathway involves only alpha-synuclein and never anything else. And the other pathway involves something like amyloid, amyloid plaques. And that's the Alzheimer with the Lewy body as a side order, I haven't been able to get more specimens other than the four that I published. But it was interesting that the four did have evidence of spirochetes inside nerves that were labeled for death because they had Lewy bodies in the cytoplasm. And those spirochetes with Borrelia spirochetes.

[01:23:20] SCOTT: You've mentioned the connection between Borrelia and Lewy bodies. What gives us the thought that that would be that the Borrelia would be causative rather than a correlation? Could it be that the Borrelia is an innocent bystander and something else maybe is the deeper cause of dementia? Or if you did the same type of evaluation in a brain and someone that didn't have Lewy bodies, would we not expect to see Borrelia there?

[01:23:53] DR. MACDONALD: The answer to that is that the DNA is going to come to the rescue again. Borrelia DNA belongs in living spirochetes. And so, as long as the spirochete is alive, the DNA of the Borrelia is going to be inside the living organism and that's where the infection comes in.

The Lewy body itself is not thought of as being connected to a cellular product. It's sort of like a glob of goo. And that glob of goo is very rich in about 90 different proteins. One of them is a toxic alpha-synuclein protein. If you get the Lewy body under the microscope and you see that it is inside the neuron, number one, they are on label for death. And number two, it's the right size, and the right shape, and sometimes it has a little targetoid pattern and it stains properly, then you know that that's a Lewy body. And then it might be an opportunity to use my DNA probes to answer the rest of the question. The rest of the question is, is there cell-free, outside of the living body of the spirochete, cell-free incontinent DNA of Borrelia inside the Lewy body? We know there's 90 different proteins in Lewy body. Is there a possibility you have any kind of DNA in the Lewy body? And the answer is yes. That Borrelia DNA, cell-free DNA exists in the body, Lewy bodies of four patients in Lewy Body dementia.

Now it's not waiting for the bus. It's there inside the toxic agents, inside the toxic signature, inside the cell, it's label for death. And that's about as powerful an argument as I can say to say that infection connections exist between Borrelia infections and some patients who have Lewy body, pure cortical Lewy body disease.

I haven't gotten my hands-on Parkinson's to test it and see how that would carry forth with Parkinson's. But I'm working on that. Logically, it would be expected now that I would be able to find cell-free Borrelia DNA inside the Lewy bodies and Parkinson's disease. But I haven't gotten the hands on to look at the brain tissue to see if that's true or not. If it is, that would open up a big opportunity for the research. And it was set to Michael J. Fox foundation on its head, or on its ear, or just flatten it out.

[01:26:26] SCOTT: We are understanding that Borrelia can play a role in these neurological conditions, Alzheimer's, Lewy body dementia, potentially Parkinson's. That's still to be studied.

Might there be a connection between Borrelia and cancer? I know you've done some research with chronic lymphocytic leukemia or CLL. What has your research elucidated relative to the potential contribution of Lyme and Tick-Borne Relapsing Fever Borrelias in some types of cancer?

[01:27:01] DR. MACDONALD: All right. I started my research on Borrelia and cancer connection with giooblastoma multiforme tumor, the one that killed the president's son, Beau Biden, and it killed John McCain, and it killed Teddy Kennedy. And it's a killer. It's a bad, bad brain tumor. It's very lethal.

I researched cases that were diagnosed from Long Island area. I got five of them. And I found with my DNA probes that they all had an overwhelming positive signal for Borrelia inside the area of the tumor. 5 of 5. I only used a Borrelia burgdorferi eye DNA probes because I didn't have the other ones that I would advise later on manufactured. But Borrelia burgdorferi DNA was loaded inside the tumor cells of glioblastoma multiforme.

Recently, I've come back to those and looked at Borrelia miyamotoi separate, a Relapsing Fever thing. But it's first cousin of burgdorferi. And that DNA probe study shows that the tumor cells are also loaded with Borrelia miyamotoi, too. It's a double infection. And glioblastoma. That is um in the process of getting reviewed for publication.

I'm glad that I kind of waited, because had I just stopped with the burgdorferi back in 2016, I would never have thought to put the miyamotoi probes on glioblastoma tumor tissue and see if they lined up. But I'm glad I waited.

The key is that the healthy glial cells, when you mix healthy glial cells in tissue culture in a test tube with live Borrelia, the Borrelia will penetrate and live inside the healthy glial cells. Instead of housekeeping, hide from the immune system. And for a period of time, they will do not not too much. But they're inside. They're protected inside the healthy glial cells.

When you get glioblastoma tumor cells from a brain bank and then put them in culture, the Borrelia will penetrate those cells, too. And so, in real life, if you have somebody who had a brain tumor, had died, and the tumor is in wax. And we go back a couple years after they've passed and use the DNA probes see if they have any Borrelia content at all, they all light up like a Christmas tree both for burgdorferi and for miyamotoi. Now we have double infection again, right? We have two of them, right?

And I'm extending those studies to look now at other types of cancer. We have recently a breast cancer patient who knew about my work and said, "Well, if you found that in Lewy body and glioblastoma cancer, maybe it could be in my cancer, too." They had the neurosurgeon biopsy an area in her brain, which is metastasis of the cancer from the breast to the brain. And she sent me four slides. And on that side were individual single separate tumor cells that had taken apart from each other and we're in the fluid. And they all lit up for Borrelia burgdorferi DNA. I said, "Well, maybe if it did that, maybe I'll look and see if miyamotoi also lit up."

Here's another double header, right? These are disturbing, because when we think of infections that can cause cancer, we usually think of viruses. There's a whole bunch of tumor viruses that can cause cancer because the virus gets inside the cell and pollutes the nucleus. And then the cells become cancerous. And that's it, you know?

But we haven't thought about bacterial related infections inside cells to cause cancer. Now I think we're going to be forced to think about it. And the Borrelia DNA is interesting because it has a structure that's close to the structure of human DNA. Unlike any other bacteria that's known, the DNA molecules have covalently linked ends. And those are only seen in human DNA. Not in other types of bacterial DNA.

If you mix the Borrelia DNA inside the nucleus with the human DNA, it could possibly get in there and mess things up for the human side and cause uncontrolled growth, which becomes cancer. That's a little threat of a possible link, which will need to be proven with more elegant studies. But the model is there now. We have bacterial infection-induced, or facilitated, or promoted, transformation from benign, to human, to cancer. And we have a model for glioblastoma. We have a model for breast cancer. And we have a model for one of the leukemias. And they all have double infection.

[01:32:17] SCOTT: With glioblastoma, we know now from your work that Borrelia can play a role. Oftentimes, people harbor Borrelia for decades. What is your thought on what might then trigger the rapid spread and eventual fatality that occurs in most glioblastomas? It seems like it's maybe smoldering for years or decades and then really kind of accelerates? What do we think might be that accelerant?

[01:32:44] DR. MACDONALD: I don't think we've done a study over a period of time. That's called a longitudinal study. We don't have a longitudinal study. First of all, it wouldn't be ethical to watch the patient go from something that can cure with antibiotics. It's something that you can't cure with anything, even radiation. It would be unethical to do that.

But I think that a percentage of glioblastoma tumors just explode out of nowhere and go from you know zero to 100 miles an hour in speed and divide so fast that it kills the patient. That's a primary glioblastoma.

There's another type of glioblastoma, which develops from lower grade brain tumors that don't divide as fast, but they're still glial cells, but they haven't gone berserk like glioblastoma cells. Those are secondary glioblastoma. You start out with a four-grade system. Grade one is close enough to call it cancer, but not far enough that you can tell where it came from. And then grade two, it's a little closer to being explosive cancer, but it's still kind of sort of under the microscope like a benign glial cell. And then grade three and grade four is like the explosive fast-growing type.

It's possible that if in some people they start out with a low-grade cancer, and we find in the low-grade cancer, there's evidence Borrelia DNA in that, then you can say, "Well, yes. All right. It starts with a little bit of a deviation from normal." But it's technically a low-grade cancer. And then it goes to higher grade cancer and higher-grade cancer. And then pretty soon it's glioblastoma grade 4.

I have no access to information or material to test that hypothesis. But we do know that it goes from zero to 100 miles an hour in glioblastoma of the usual type. And about 80% of glioblastomas are in that explosive type. Not the slowly to develop type where it goes through the stages.

In any event, Borrelia DNA inside your cell is not a healthy situation. You don't want to have it. And if you can get to the infection before it gets to the DNA machinery, then you're going to have a better chance of survival. Not everybody who gets an infection in the brain with chronic Lyme disease will ever have a glioblastoma tumor. There's a lot of people out there who have brain fog and neuro Lyme. But there's not a lot of people that have a double infection with Miyamoto and burgdorferi at the same time.

I'm banking on the idea that the double infection is the risk factor. And that either one all by themselves might not be capable of becoming a high-grade cancer. That's a hypothesis. That's not proven. But I'm trying to you know keep it so that people will listen and say, "Well, I've got chronic Lyme. I don't want to die of glioblastoma." And I'm saying to you, well, it may be that your chronic Lyme will never ever get to glioblastoma unless you get another infection with a separate miyamotoi and then you get a double infection, and then you're going to be at higher risk.

That's hopefully a word of reassurance to people listening. I don't want people to say, "Oh, my God, I've got Lyme brain. And therefore, I'm going to get a glioblastoma." No. I say I think you have to have a double infection. And miyamotoi infections now are still relatively rare. And combined infections proven in humans are very, very rare. And so, I think you need like a – they used to have a hypothesis that cancer has a two-hit hypothesis. You get first hit and the DNA is damaged. And the second hit, the damaged DNA becomes more damaged and then you're on to cancer. Two-hit hypothesis. So, the one-hit wouldn't do it. But the two-hit would.

[01:36:37] SCOTT: And again, just to be somewhat hopeful for people listening. If someone does have Borrelia burgdorferi and Borrelia miyamotoi, you've already mentioned that the treatment is very similar. My hypothesis then would be that people that have been or are being treated for their Borrelia would have less of a chance of a development of one of these more significant presentations that we've talked about.

[01:37:04] DR. MACDONALD: Yeah, I think that's a very fair formulation, because we don't have any evidence to the contrary that in spite of antibiotic therapy, somebody went through chronic on antibiotic therapy and then died of glioblastoma. We don't have any untreated antibiotic cases in our list of cases so far. We don't have it. And maybe that's good news. I hope it is. And just get going with the therapy. That's all I'm saying.

[01:37:38] SCOTT: The work that you've done over the past decades is so ground-breaking that I'm wondering why there aren't more people that are replicating, validating and moving this work forward. Do you have collaborators at this point in some of the medical schools, and university research, and those types of things? I mean, it just seems like there's such a missed opportunity here.

[01:38:02] DR. MACDONALD: Well, I have a number of colleagues who are interested but are not at the point where they want to devote precious, or grant money, or resources to continue in the path that I've established myself, which really didn't come from a lot of money. I mean, I got some nice donations from people early on. And every once in a while, I get some more donations. But I've always gotten small follower donations. I think the largest one I've ever gotten is like under $20,000. I mean, that's what helped me to get to this point.

But if you have a government grant and you have – or a foundation grant, they might not permit somebody to deviate from mainstream type ideas into some of my ideas. They might say, "Well, we'd rather put the money on something which is mainstream. And so, don't waste your time."

I just saw an article on Lyme disease and pregnancy. They did a nice study. And it was published in Frontiers of Medicine. And the large number of patients who took questionnaires and answered the questions and had categories of Lyme, which they said you know definite, or probable, or possible, or not, not Lyme.

And at the end of the article, they made a comment that the type of work that I did, which is under the microscope pathology of microscopic sections, if somebody – Only three percent of all the people in their program had any kind of microscopic work at all. That's almost 40 years after I put all of this out on the map and gave everybody a road map for free. And a cookbook and a recipe book on how to do it. 40 years. And only three percent of the people. And none of them did an autopsy. Zero. They might study the placenta. They might study a little bit of the blood. But nobody got into the nitty-gritty and said, "Well, what is under the microscope autopsy tissue telling us?" That's what we need. That's how I got to all of these discoveries with dead babies, and Alzheimer's disease, and my leukemia studies. Every bit of it was under the microscope pick and shovel work.

And either the people don't want to get involved with that don't have the interest in cultivating the skills that I have. I'm here ready to treat and to teach people all my bags of tricks, but nobody's interested. You can't make sense out of it because maybe some of it has to do with the fact that CDC only this year. But microscopic proof under the microscope as being legitimate for CDC to embrace it. So, you know, that's okay now.

And for 40 years, in spite of all the work that I did, and Dr. Duray did, and other people have done, none of that microscopic work had any sway with the most powerful organization and the best funded organization in the world in Atlanta, zero. And that isn't how we made progress in medicine. We made progress in medicine by looking under the microscope and seeing how we can do better. What did we miss? What can we learn from the next case? How can we apply all of the microscopic knowledge from autopsies to better medical care?

And if you ask about – I live in Naples, and we have two hospitals. And they're big. None of them do autopsies. Zero. Because autopsies have become non-essential. You used to have to do a certain number of autopsy to get the Joint Commission to approve your hospital is a good place. And then that autopsy requirement was dropped. And as soon as that requirement was dropped, then all autopsy seats accepted medical examiner, forensic cases. And they don't have the time to do the kind of research I'm doing because they're up to their neck with Covid-19, and knife club, and gun club, motor vehicle accidents, and plane crashes. I mean, it's like medical examiners are the last bastion for autopsies. God bless them. But they're not going to do the kind of work that I did.

[01:42:46] SCOTT: Your research continues. Tell us how people can support your work and continue moving the needle in Borreliosis?

[01:42:53] DR. MACDONALD: Well, I think there are two avenues. I think that I would like to scale up on donations of tissue blood or whatever in situations where people think that they might have an unusual form of Lyme disease but they are not getting an answer from the serology. So, they have some biopsies that were done and that was wasn't helpful. And well, they had some blood studies were done and the blood studies were not helpful. I'd like to get some donations from those people. And then that's how I've made a bunch of my discoveries, is that people donated blood and tissue to me. And based on those studies, I came up with things that I could not have imagined before I started my study of their tissue.

So, like donation of, but I would prefer to have it from people who have chronic Lyme disease in one form or another, physician diagnosed, antibody negative chronic Lyme disease, or antibody positive, too. Anybody who has a patient friend or relative Lewy body disease, or Parkinson's disease, or Alzheimer's disease. I'd like to get my hands on some more of that.

The tissue part of it would be nice if I could get more people to – and I can't handle them all at once. I'd have to schedule it. Make appointments. But I would like to have more people participate in giving me the access to their tissue. And the other thing is that if people want to write a check for $25, or $50, or something and they can put it in my GoFundMe account. I have a GoFundMe account. That helps me buy the cost of the chemicals and the reagents to do my work. I never charge anybody for doing any studying. My research, that's always been free, and it always will be free. But I do need uh some help with reagents and stuff like that.

If you have a beautiful paper and it's ready to go and you want to put it in a journal that costs $3,000 to publish the article, you're kind of stuck. I don't have $3,000 beyond what I'm doing here with my work. Anything that could be done in that regard too would be also terrific. Those are the two things I think would help.

[01:45:07] SCOTT: I will put the link to the GoFundMe in the show notes for people listening to our conversation as well. My last question is the same for every guest, and that is – and I think I've known you now for, I'm going to guess, close to 15 years. And your brain obviously is working as good as ever. What are some of the key things that you do on a daily basis in support of your own health?

[01:45:32] DR. MACDONALD: Stay away from red meat. I exercise a little bit. I walk my dog. I get out. I try to take a nap when I get a little fatigued. And some meditation, things like that, to kind of – because sometimes when the ideas are coming in it's fast and furious, your brain gets sort of – I don't know. It's a point where you have to rest it. You have to shut it down a little bit because sometimes it's so – so many things are coming through that are positive or good results, you just have to rest your brain and then calibrate and recalibrate and have a balance between – I try to limit my work to about five hours a day. Now, in the past, I would work 12 hours a day. But that got me too fatigued. But I also have a life with my wonderful wife. And I don't want her to be a research widow. So, I have to break away from the microscope and kind of have some kind of a balance and see a movie, or get out and walk, or – we haven't traveled because of COVID. But we would be traveling too for a safer environment. But those things are balanced for me. That helps me to have some balance.

[01:46:46] SCOTT: You are a hero. You are a legend. I have so much respect for your work. And just the difference that you make in people's lives, the difference that you make in this world for so many people that have dealt with these conditions. It's just such an honor for me to have this conversation with you. And just want to respect and honor you so deeply for all the amazing contributions that you've already made and for those that I'm sure are to follow. So, thank you so much, Dr. MacDonald.

[01:47:20] DR. MACDONALD: Oh, so kind of you, Scott. Thank you for having me as a guest. And all good wishes. And we'll keep on forging ahead.

[OUTRO]

[01:47:27] SCOTT: To learn more about today's guest, visit AlzheimerBorreliosis.net. That's AlzheimerBorreliosis.net. AlzheimerBorreliosis.net.

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