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In this episode, you will learn about the role of microbes in chronic disease.

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About My Guest

My guest for this episode is Dr. Stephen E Fry.  Stephen E. Fry, BS, MS, MD has a BS in Microbiology and an MS in Molecular Biology and a Medical Degree all earned at the University of Arizona. He completed his Post graduate training at Banner Health and St Joseph’s Medical Center in the Phoenix metropolitan area.  He has been in General Practice in the Scottsdale, Arizona since 1992 and has had a special clinical interest in CFS, autoimmune, and vascular disease.  He has lectured nationally and has numerous publications, abstracts, and patents.  His science interests are in the microbial causation of chronic disease, biofilms, and their treatment.  Because of these interests Dr. Fry has worked on new methods for disease detection which have culminated in the development of a Next-Gen Sequencing system for microbial identification.  Dr. Fry is the founder of Fry Laboratories LLC, a CLIA clinical diagnostic laboratory that participates in CAP (College of American Pathologists) and API (American Proficiency Institute) validation systems. He founded the Southwest Center for Chronic Disease to help fund basic medical research.  His laboratory, Fry Laboratories, specializes in vector-borne diseases, molecular methods of detection of prokaryotes, archaea, protozoans, fungi, and viruses. Dr. Fry enjoys family time and has a private pilot’s license, is an avid skier, sailor, and bicyclist.

Key Takeaways

  • Where do things stand today with Protomyxzoa and Funneliformis?
  • What is the role of biofilms in chronic infections?
  • Are fungi or viruses likely more health-impacting?
  • Is kombucha a healthy drink?
  • Why is Next-Gen Sequencing the leading edge technology for exploring the presence of microbes?
  • What microbes play a role in ME/CFS, ALS, MS, Parkinson's, RA, and Cystic Fibrosis?
  • How has the landscape changed in chronic illness patients since COVID came on the scene?

Connect With My Guest


Interview Date

December 20, 2022


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.  


[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 177 of the BetterHealthGuy Blogcasts series. Today's guest is Dr. Stephen Fry, and the topic of the show is Microbes in Chronic Disease.

Dr. Stephen E. Fry has a BS in Microbiology, an MS in Molecular Biology, and a Medical; Degree all earned at the University of Arizona. He completed his postgraduate training at Banner Health and St Joseph's Medical Center in Phoenix. He's been in general practice in Scottsdale, Arizona since 1992 and has had a special clinical interest in Chronic Fatigue Syndrome, autoimmunity, and vascular disease.

He has lectured nationally and has numerous publications, abstracts, and patents. His science interests are in the microbial causation of chronic disease, biofilms, and their treatment. Because of these interests, Dr. Fry has worked on new methods for disease detection, which have culminated in the development of a Next-Gen Sequencing system for microbial identification.

He is the founder of Fry Laboratories, a CLIA, clinical diagnostic laboratory, that participates in CAP, the College of American Pathologists; and API, the American Proficiency Institute validation systems. He founded the Southwest Center for Chronic Disease to help fund basic medical research. His laboratory, Fry Laboratories, specializes in vector-borne diseases, molecular methods of detection of prokaryotes, archaea, protozoans, fungi, and viruses.

Dr. Fry enjoys family time and has a private pilot's license, is an avid skier, sailor, and bicyclist.

And now my interview with Dr. Stephen Fry.


[00:02:19] SCOTT: I've had the honor to talk with Dr. Fry at several conferences over the years. I'm very excited today to have him on the podcast to share his work and his thoughts on the contribution of microbes in chronic diseases. Thanks so much for being here, Dr. Fry.

[00:02:33] DR. FRY: Sure thing. Thanks for inviting me, Scott.

[00:02:36] SCOTT: What was your personal story or journey that led you to the passion you have today for exploring microbes and their contribution to chronic diseases? Did you have your own health journey that was the catalyst for the work that you're doing now?

[00:02:52] DR. FRY: Well, good question. A lot of factors. I think, number one, I've always been interested in the sciences. And my dad was a chemical engineer. My mother was a librarian. And my uncle was a nuclear engineer. And so, that's sort of the background. I always had chemistry sets. And my dad, from his different jobs with Kaiser Aluminum and working as a radiochemist in Los Alamos, there was just a lot of chemistry stuff down in the basement. And I grew up mostly in Northern Virginia.

And good school system in Northern Virginia. If you had any interest, I think the school system sponsored a lot. And I think probably in junior high school, early high school, I really sort of an interest in chemistry probably because of my dad. But then I read Microbe Hunters by, I think, it's Paul de Kruif. And that book has been around a long time. That was inspiring and sort of opened up that area. And then biology was like easy for me, simple. That was not a tough class, biology and history. I can just read the stuff and breeze through it. Easy to get As.

Then, really, I think the shift, I started out as a chemistry major at University of Arizona. My freshman year and my college roommate's friend or relative came in and say, "Hey, I'm a microbiology. It's really cool. There are lots of jobs in microbiology." And I said, "Oh, okay, I'll take a class." And, "Boom!" I mean, I'm just talking to my friend here. And same thing for her. Her senior year in college, she took a microbiology class, and that transformed her career direction.

I did that and off to the races. And then I did a masters. I got a degree in microbiology with a minor in chemistry. And of all things, anthropology. And then I went to graduate school in the medical microbiology department at the University of Arizona. Then it was a newer medical school. And my professor, I was thinking microbiology, but he was really more of a molecular biologist. I ended up getting a molecular biology degree in a microbiology department. Okay?

And then we were right next to the Cancer Center. My first job out the door was working for Dr. Syd Salmon, who founded the Cancer Center. And we were doing the human tumor stem cell assay and we were growing tumors. We would get a thyroid in, or an adenocarcinoma colon in, or a prostate, or something in and we slice and dice and then break it up into fine little particles and try to grow it in a Petri dish.

And interestingly, a lot of that stuff used to grow up fungal. And we, at that time, thought it was contaminated. And we finally figured out that we had to throw in tons of this generalized stuff off the shelf called Fungizone, which I think I have to look up what is in Fungizone. But it really took care of the problem then.

And then on to medical school later on. And I think – Then into practice. And then what I saw in my practice was that I had a lot of these tough indolent patients that I just couldn't get better. Mainstream medicine was really putting Band-Aids on these people and our audience in alternative medicine. That's well-appreciated. I got into this mystery of microbiology. What's going on? And what's the bug?

And because of my background, I would say I am very biased as to causality. And I never bought, and we'll get to this discussion later on, this concept of autoimmune disease and when my retired former colleague, who we were in the same department together, he was more into immunology. He became an allergist immunologist here in town.

And when my friend described autoimmune disease, I said, "Hey, you know what? That makes really no sense to me. Why would the body attack itself?" Okay? And I've kind of come over to the other side a little bit over the years especially with the recent publication.

Anyway, I started in the autoimmune arena, microscopy in the late 90s. Set up a lab in my own office. And I was very busy then. At one time I had 32 employees. It was an industrial clinic. And doing those 70, 80-hour weeks and fitting this in in between.

Then PCR came along. And I brought in PCR in '09. Oh, let me short shortcut this. In '03, I started developing more assays. Started going in the meetings. Lyme disease meetings, A4M, alternative meetings, mainstream meetings also. Other doctors found out what I was doing and asked if I would run assays for them.

I incorporated in '07 and started taking business from other physicians; mostly some of the microscopy work that an assay that we had developed and then the serology. Used the tick-borne disease serology, some autoimmune testing. Like, the gold standard ANAs.

Then we – my wife likes to point out and take credit for this, that she was reading an article in Forbes Magazine about these new DNA sequencers. And I saw it and I said, "Whoa! I hadn't kept up." And I said, "Well, of course." Okay? And my colleague at the time said, "Yep. Okay. Let's get into it." His friend had been working with the same device. And this turned out to be the Ion Torrent, which is now owned by Thermo Fisher. It was the company Ion Torrent with their PGM machine.

We bought one in 2012. And we were up and running and had that assay developed and ready for use and started offering it clinically for bacterial sequencing in 2013. And I still think we take the credit for contiguous same entity Next-Gen Sequencing for infectious diseases commercially with CAP, or College American Pathology, American Proficiency Institute EI for validation. In other words, validation is important. Other people are out there, they don't want to do validation for some reason. We think it's important.

Every quarter, they send us samples, whether it's a pulmonary sample or a blood sample and say, "Okay. Tell us what's in the sample." Okay? Including Lyme disease, everything else. And we tell them what's in the sample. And I'm pretty sure we've been batting a thousand since we've started. Okay?

Anyway, we started offering that. And then in 2015, 2016, era we started offering 18S. Those are larger, more complex organisms. You're 18S, it has to do with your RNA, mitochondria, etc. We started doing fungi, protozoans, algae in 2015, 2016, which actually led, if you look at our papers that are published, some innovations and discoveries in cardiovascular disease.

We discovered looking at bacteria, and fungal, and protozoal populations in diseases like ALS, MS, Chronic Fatigue Syndrome. And interestingly, you could take our plots and distribution plots. And if you gave us a raw sample, we could tell you from the population of organisms in those patients and identify them without having any clinical information whether they were normal or "normal". Actually, we had hard time finding normal controls. But you could say, "Hey, this patient has CFS. This patient has ALS. And this patient has Multiple Sclerosis or something like that based off of that distribution."

Interestingly, a prostate cancer article came out about a month after ours last month showing that there are unique fungal populations in patients that are normal controls in patients with prostate cancer. And they use the same sort of population analysis that we did. And this is sequencing where we take all the blinders off. You report everything. And that's one of the things you need to do is just find everything and even minute amounts.

That's sort of that progression of this microbiology interest. And one thing just led to another. And again, I'm biased. And it's interesting that in cardiovascular disease, prostate cancer, our own work, and published work shows, "Hey, we need to think about these diseases differently." And it's microbes. That's what Louis Pasteur said in one of his quotes, "Microbes are at the heart of everything."

I mean, there's aging, and then there's the number one cause of death right now. 17% of the people die of heart disease. And is it just cholesterol? Or is there an infectious process behind it? And we are the second laboratory to show that plaque is indeed most likely a fungal infection. And I'm glad we weren't the first. Okay? It's kind of bad being the first in a way. We're the second lab to show that. And that's created some interest.

[00:12:11] SCOTT: Just a brief follow-up before we move on. The cancer work that you were doing early on where you had to introduce some antifungals because you thought that was contamination, do you now have a different perspective where maybe that was actually a fungal contributor to the cancer?

[00:12:28] DR. FRY: That's exactly right. In our paper that was published, I think it's October 1st, adenocarcinoma, carcinoma in the colon. We looked at 12 samples from one of my neurology colleagues. And we wanted fresh. I had one of my staff there in the operating room, Dr. Mitchell Kaye, who was our colleague on that project. He was right there and said, "Okay. We've already have a diagnosis of adenocarcinoma. Punch biopsy. Let's go ahead and give you what he thought was the best part of the tumor directly." And he said, "This may get in because there was another paper published on flora of prostate."

And he used the Da Vinci technique, which is a much cleaner, less invasive technique for the prostatectomy. And we got some bacteria and some samples. Not very much. But we got overwhelming fungal reads. And then we confirm that with fungal stains, the Calcofluor-white stain, which is one of the stains we use in our lab to confirm fungal presence.

Then we – I remembered one of those infectious disease specialists who did a big study in Chronic Fatigue Syndrome, and he found in the urines a lot of these Chronic Fatigue Syndrome patients had lots of ochratoxin A in their urine, like huge amounts. And I said, "Oh, there may be something there."

And I remembered in my practice that I had a lot of fellas who they went somewhere, went to the tropics, or went to Minnesota, or something and picked up something and they developed fatigue syndrome. And within a year or two, in their 40s, they developed prostate cancer. A light went off and I said, "There's got to be some association here." And so, we looked for levels of ochratoxin A using immunofluorescence. And they all lit up like a Christmas tree. Okay?

And then in the review process, one of the knowledgeable – I'm sure it was a mycologist got on the board, got involved, and said, "Hey, how can you tell this is not dietary?" And we really can't. Okay?

And so, in that paper I outlined a number of experiments to prove it, which is basically, "Hey, you got to figure out some way to grow this stuff." And again, we have a hard time drawing a fungi. It's difficult to grow fungi. Everybody knows that. I mean, I was talking to my colleague who's a podiatrist and he said, "Hey, I send this Onychomycosis nail clippings, and I never get any results back." We know that's what it is. At least half the time, some of it's bacterial. But we just can't seem to grow anything.

And so, you have to try to grow it and then you have to show that it's producing in the test tube a toxin. Okay? And then the real Koch's postulate to prove it would be, "Okay, let's take this fungi and put it into some sort of animal. Hey, inject it into the prostate, if you want to, of that animal and see if that animal develops prostate cancer in a couple of years." The problem is a couple of years.

The hypothesis there, let's take the whole loop now they're into it, is I suspect there's some viral hit to break the integrity of the tissue. And we already know now that there are circulating levels, low-levels of fungi in everybody and normal controls. And some particular fungi attaches to where there's been some kind of damage. Maybe it doesn't need damage. Maybe these fungi just like that environment. We know certain bugs like certain parts of the body. And that starts to grow.

And originally, I was in a mutagenesis lab. So, ochratoxin, we know, is very toxic, very carcinogenic. Has been related to urogenital tumors in Eastern Europe. And those papers are out there. That's a known fact. And so, it produces the mutations or the toxin that causes the DNA damage, mutagenesis, producing your tumor cell, okay?

Now, normally, most people don't know, our bodies clear three or four thousand tumor cells or aberrant cells every day. Okay? But the other aspect of ochratoxin is it's very immunosuppressive. My thought is that the toxin is bathing the surrounding tissue in an immunosuppressive chemical so the body's normal T cell, B cell, humoral immune system, cell-mediated immunity just doesn't work in the region. So, these tumors get a chance to grow.

And then I just had one of my colleagues got diagnosed with prostate cancer. We did the test. I think we used prostatic massage material, full of fungus. He went on itraconazole. He didn't take it long enough. So, he just had a relapse. And his ochratoxin levels right now, your ochratoxin toxin levels are through the roof. Okay?

And I'm not saying that everybody with prostate cancer would be producing urinary mycotoxin or ochratoxin. And I'm just using ochratoxin an example. It may be producing other toxins that we know about or even a toxin that we don't know about. But I'll go for ochratoxin all day long because we know that's a bad player. Okay? And so, that's the loop.

Theoretically – not theoretically. In the use of itraconazole is already in the adenocarcinoma of the prostate literature. And I quoted that on our paper. I had a couple of my patients try itraconazole. It lowered PSAs, okay? And to the point where they didn't have evidence of the disease. If you kill the fungus, you kill the immunosuppressant. And I would assume the body's normal housekeeping functions are taking place.

And this sort of goes along with a lot of the new these dramatic cures now on anorectal carcinoma, leukemias, where now we're potentiating the immune system to fight these cancers, okay?

I think, normally, our immune systems probably, in most individuals, competent individuals, take care of it. But again, you've got this toxin playing a role in immunosuppression. And who knows if we don't have generalized immunosuppression with this? Anyway, you got me on a roll.

[00:18:43] SCOTT: Looking back on some of my earlier notes on my blog, it looks like I first met you and got introduced to your work around 2011 back in the time when we were talking about FL1953, which was later renamed to Protomyxzoa rheumatica, that at the time was classified as a protozoan. It was later, as technology evolved, reclassified as a fungal organism, Funneliformis mosseae. You once referred to it as the premier pathogen. I'm wondering if you can take us on that journey. Are Protomyxzoa and Funneliformis, are they the same? How common are they in chronic conditions versus the healthy population? How do we acquire it? And is it a primary player in chronic illness? Or is it one of many?

[00:19:28] DR. FRY: Right. This gets into a larger discussion. Let's start with Valley, Coccidioides immitis. You're in Colorado now, and a little further south from you, we start the Valley fever belt. And by the way, Valley fever I think is in about 12 states now. Because of a global warming, they predict we'll probably have 18 to 20 states with endemic Valley Fever probably in the next decade. Okay?

Here in Arizona – So, it started with San Joaquin Valley Fever, San Joaquin Valley in California. And this is a fungi that was originally thought to be protozoan. Okay? Here's the flip. They thought it was protozoan at first. And with more work over the years, they realized it was fungal.

And, so I've had Valley Fever. My wife was really sick with Valley Fever. I got Valley Fever when I was in college. And then when I did my medical school, microbiology course, everybody got skin test for Valley Fever. And I was the only one in the class that had a huge reaction. I've had Valley Fever in the past. And that's just a fact of life living in the southwest.

Now, the majority of people that get Valley Fever may have a cough, chills, some respiratory symptoms for a few weeks, and that's it. But we have some people who have indolent Valley Fever. I think in Arizona we had about an average of 3,000 people every year that have chronic Valley Fever. And it can certainly kill you. It kills a lot of dogs. The vets are well aware of Valley Fever.

Normally, it goes to the lungs. But you can get it anywhere. And when we see systemic Valley Fever elsewhere, skin lesions, that sort of thing, then those people buy into a year of Diflucan, or one of the other antifungals to keep it at bay. Anyway, that's that discussion.

And so, we start out. We had a patient with lupus, and we had an isolate. And we sent that at the time that was I think 2009 or 2010 before we had sequencing. And we paid $50,000 to have that organism sequenced by a subsidiary I think probably of Illumina right now in 2010. And we got the reads on it, or the sequence of that. And it turned out, by comparing that to the database, and I have to talk about the database. At that time, the database had about 300,000 entries. Okay? This is the infancy of sequencing information on life. Okay? Life forms.

And if you have less than a 5% match – So, we match up the DNA, what we get from the sequencer, the sequence, to what's in the library. Okay? The database. And there was no match, but it seemed to look protozoal. And so, we put it there. And very pridefully, we decided to name it. I'm never doing that again. We're just going to put serial numbers on, okay? And we find a lot of organisms that really are related to organisms now with serial numbers.

Let me just talk about the NCBI, National Center for Biological Information. CBI. That then was 300,000 entries. Now they're over, get this, 100 million entries. Okay? Which has caused complications for us. Because in our sequencing, we sequence what is ever in the sample. And we don't have this heavily curated database where, "Okay. Let's just say we've got 20,000 or 30,000 entries. We're going to pair what we find to those 20,000 or 30,000 entries in the database." They curate the 100 million down to 30,000 and then try to make a match.

For us, it's become more of a chore on database analysis. We have to buy a new computer right now because it's too slow. So, we still take the information we get from the sequencer and match to this ever-growing, ever-enlargening database of microbes. But we get better results. So, if something new has been in any of the database, we'll be able to match it up or get a close match. That's the value of that. And I think we're the only ones doing that clinically anywhere. And so, the playing field keeps moving, but you end up with better, more accurate results.

To get back to Funneliformis mosseae and Protomyxzoa rheumatica, we still think Protomyxzoa rheumatica, whatever that was in that patient, is probably still protozoal. But we started finding much more of what we were calling Funneliformis mosseae. And that was, at that time, the best match. This was in 2015 forward. With a well-known common soil fungi. Okay?

And this was our overriding finding and these prostate cancer patients. And a lot of patients who had chronic illness. And we were finding lots of fungi in those patients. And then we have this stain. We have three stains. We have sort of like a modified May Grunwald Stain, which is sort of a hyped-up Giemsa Strain to look for blood parasites, Babesia, malaria, stuff like that. And it's a very good stain. But also, we tweaked it to allow us to see more biofilm communities. And then our second stain, because of what we're finding is basically a Hoechst stain. So, we adopted a stain from cell biology. And that stain picks up DNA.

When you look at those pictures, you see a background of black orbs. Those are red blood cells. They don't have any DNA. That's like the internal standard for that stain. And then we have another stain that's a combination of that along with an FDA-approved, the Calcofluor- White stain that picks up chitin. Okay? All fungi produced chitin. That's sort of a standard. We'll see these biofilm communities and we found a lot of these globs or biofilm communities that we find in people, more so in people who are chronically ill, had chitin them and they were secreting DNA. Okay? That's actually still been our most popular assay out of the lab is our stains, you know? And then it's like, "Okay. Let's do sequencing to find out really what we're seeing here." Okay?

And the Funneliformis mosseae story has changed as this database has dramatically expanded to a few thousand, to 100,000, to 300, 000, to 10 million, to 15 million, to over 100 million now. Okay? And what we find now when we try to match things up is that a lot of fungi have their serial numbers. Okay? Which makes things difficult and retrospectively for mainstream medicine that doctors do not like to treat a fungi with a serial number. Okay? It's just the medical legal environment. And that's the environment we're in. And we just have to play that game. Okay?

We used to report on a classified fungi, which we saw very frequently in chronically-ill patients, especially in pulmonary cases, Cystic Fibrosis, wounds, that sort of thing. And now we've narrowed that down. We've heavily curated our fungal database. They're really of 600 known pathogenic fungi. Okay? That's been really an evolution of the system.

And let's backtrack a little bit. How big is this arena that we're working on? It's really interesting to see that there really only about 30,000 or 35 000 bacteria. That's genus species. That database is kept pretty conserved. And I think it's just the fact that they're bacteria and have a certain thing that makes them what they are is that there's not a lot of variation or genomic variation to make it a bacteria.

Also, 16,000 archaea. We pick up archaea. We don't know of any – it's a whole new class. We don't know of any archaea that produce disease yet so far. You see a lot of archaea in these thermal vents in the ocean. Okay? I think that's where they were first discovered.

And then when we get on to protozoans, there are hundreds of thousands of protozoans. When we get the fungi, the estimates, there are four or five million genus species of fungi out there. And as sequencing proceeds, most of them have serial numbers. Okay?

And then when you get to viruses, and we had been working on a project with Los Alamos National Research Laboratories. They have this huge supercomputer. All the viruses that we've ever discovered on the planet are loaded in that. We're working with them. We're about halfway through the project. And we're developing an assay to pick up all vertebrate viruses. And then Covid hits. And now it's back to – we're up there in October talking to the group. We have to get funding again to finish that project. One day, we'll have sequencing for all viruses. No one has true – There are shotgun sequencing which we don't feel a lot of our competitors do shotgun. It's inherently error-prone. We do what's called targeted sequencing. Let's liken that to –

In shotgun sequencing, you're looking for a needle in the haystack. And in targeted sequencing, we're looking for a unique needle and a stack of needles. Okay? That's a precision of target sequencing.

And in our discussions with the FDA years ago, the FDA feels that as things go forward with NGS for Infectious Diseases, we really should be doing targeted with more precise sequencing. Okay? As far as we know, we're the only ones who do targeted sequencing. And we have a number of patents on that and so forth. So, anyway.

[00:29:19] SCOTT: So, coming back then to the Funneliformis mosseae, that fungal piece, at one time, we thought was the premier pathogen. Are we saying now that there really isn't as much of a focus on that one specific organism? But that over-time, it's become a number many different serial identified fungal organisms? And that we clinically, at this point, are not necessarily focused on treating or attempting to reduce or eradicate that specific organism? Or is that still clinically relevant?

[00:29:50] DR. FRY: Yeah, I think that it's expanded. We don't see so much of that anymore. A lot of it's shifted over on cloud. For instance, in our prostate project. The reviewer said, "Okay. If it's really that. Prove it." Okay?

The interesting thing is go out and try to find a standard sample pure culture of Funneliformis mosseae. And this is an extremely widely known fungi in agriculture. It helps plants grow. They actually sell Funneliformis mosseae packets to help things grow.

Interestingly, we bought some of these packets and tried to map it, and there's nothing in there. It's paste. Okay? There's a little deception going on in the nursery and agricultural industry. We found that also in some probiotic products also just as an aside. Okay? They're paste.

What we found is that we were challenged and said, "Okay. We couldn't find a standard. But let's just go ahead and pull something off the literature-based PCR probe." And we queried what we were calling Funneliformis mosseae and we could not firm it, though we could confirm it from dirt and soil from outside the lab. Okay? So, it was there.

And we have to consider though PCR and PCR probes. The probe is only as good as your sample set. And we know that PCR probes miss stuff. We actually did a challenge. This is interesting We assume that PCR is very precise and picks up the genus and species of what we're looking for. You make a map of a portion of it and it should be the same and everything in that genus species. And that's not true.

In our work, we looked at 48 samples that were negatives from a PCR multiplex panel for urines, urinary tract infections. And all but three matched. We found something actionable. But we had a good percentage of those, which were bugs the PCR probe was supposed to pick up and didn't.

And there was a recent lecture that I participated in out of China. And it was out of the Pulmonary Department in Shanghai, one of their big hospitals. And culture and PCR missed 50% of strep pneumonia. You would think strep pneumonia would be a no-brainer for culture and PCR. But here, we have the infectious disease specialist, and they're pretty hip on sequencing. Thank God. And they knew the vernacular. They knew about sequence counts and reads. And they missed half of strep pneumonia. These are these inland pulmonary patients, or septic patients who are dying of strep pneumonia and the older technologies weren't picking it up. Yeah, I hope that didn't confuse you or the audience.

[00:32:44] SCOTT: Well, it sounds like it's just an evolving, growing more precise overtime scenario, right?

[00:32:50] DR. FRY: What we found when we did a re-analysis of the data and said, "Okay, let's eliminate that as a possibility." And it still could be Funneliformis mosseae, is that we found matches with what looks like, and we've said this on paper, a new phylum of fungi. Undiscovered. It's sort of related to two different groups of fungi, but not exactly. And our conclusion was from the – we spent weeks and weeks just pouring over the data and re-blasting it. And that's what we found, is it's something new.

And we know it's fungal because it's got chitin in it. And we know tumors can produce chitin, but no one really knows why. But also, there was ochratoxin production. Naturally, we're pretty convinced there's fungi there. It's like, "Okay. Exactly, what is it?" This is really the Southwest Center for Chronic Disease who are non-profit is trying to raise a bunch of money right now to go back to that. Also, breast cancer and carcinoma in the colon. I think it's all sort of the same thing. Is that, "Okay. What's the fungi? Can we grow on a test tube?" And I think I know how to grow it based off of my stem cell biology stuff, I hate to say, of 40 years ago. We could go back to some of those technologies and not put Fungizone in. And maybe we'll have some success there. Okay? Basically, you have to isolate it, grow it, prove that it's producing toxin. And again, put in an animal and show that it's doing it.

[00:34:24] SCOTT: Let's talk a little bit about biofilms. Where they're found in the body? Whether we think they're primarily fungal-driven biofilms, bacterial-driven biofilms. I know in the past you've talked about even doxycycline potentially having fungal antibiofilm properties. Does a biofilm strategy need to be part of a more comprehensive chronic illness treatment approach when we're talking about these microbial overgrowths that contribute to chronic illness?

[00:34:55] DR. FRY: Right. Biofilms interesting topic. Very interesting. Very relevant. My introduction to biofilms is I was doing a project. Actually, I was talking to the provost at a meeting, biotech meeting in Phoenix. And I ran into the provost of Northern Arizona University. He introduced me to Dr. Jeff Lee, who was a biofilm expert, microbiology expert at Northern Arizona University. We did some experiments together looking at biofilm, pseudomonas biofilm, pseudomonas and notorious biofilm former.

And incidentally, just a little annotation here, you can have microbes that are resistant to a drug genetically through either plasmid or main genome resistance. But if you get rid of their biofilms, they respond to the antibiotics anyway. Okay? That's an importance there.

And then Dr. Lee got me to go to the American Society for Microbiology sponsored subsection meetings, the International Biofilm meetings. My first was in Victoria, Canada. And I met Dr. Bill Costerton, who's the Dean of Biofilms. Great guy. I think he died of pancreatic cancer five or six years ago. Great guy. Very busy. He was like the god of biofilms. He knew a lot.

And he got started and it initially looking – the oil industry came to him, the pipeline industry came to him, because the pipelines, you would think with a petroleum product, they would be clean. But it turned out that was a huge problem with these metal casings were rotting and leaking. Okay? And it turned out it was a biofilm problem. And I don't know what the intervention was on that. But that guy, Bill, started on it. He was a microbiologist. I think he was formerly a Jesuit priest or something. But he got into that. And really intelligent guy and encompassing person. Trained and taught a lot of people. That was my introduction to biofilm.

Back to that, is that what we found in people, we would see these biofilm communities and multiple publications, we analyzed. Probably the best is our cardiovascular paper published in 2017 with Dr. Rich Heuser. Rich had a project going in. He was doing another project cleaning out Greenfield filters, removing filters, doing thrombectomies, cleaning the vessels out of debris. And then we did a side project looking at coronary plaque.

And we found when we analyzed these obvious biofilm communities, they were mixed populations of bacteria, some protozoans. But predominantly, fungi. Okay? And that's what we found that plaque was composed of, mostly fungal. Okay?

And so, fungal organisms, bacterial organisms, I think we see mixed communities that make sense in nature. And they develop these biofilms to protect that entity from all the elements. And they all share DNA. They share RNA. And when they've looked at the soup of biofilms, that's a problem.

Knowing this information and going to the meetings and the alternative community is really big on magnesium. And if you're a biofilm person and understand the magnesium story, it's like, "Holy cow!" Actually, I discovered this accidentally. I built a supplement and developed a supplement with magnesium in it. And my patients are doing okay. I tried this on through my – I just gave it to them. And they crashed and I could not figure out why. Okay? Could have also been some of the B vitamins, probably folic acid that was in it also.

I discovered this theoretically and clinically, is that magnesium really is required to stabilize DNA. And if you rip magnesium out of a DNA setting, nascent DNA collapses. Most people don't know the rebar, the actual structural integrity of a biofilm is a DNA lattice. Okay? This is extracellular DNA that's used as a structural component to help maintain biofilm structure. And they've done bench experiments. You pull the magnesium ion out of that and it collapses. And you put magnesium in and it stabilizes that. And clinically, patients who are taking lots of magnesium supplements for whatever reason had a hard time getting them better, okay?

I mean, that brings in the folic acid discussion. I found the same thing with high-dose folic acid, which if you remember Carol Ann Ryser, Carol Ann Ryser was in the era where we had a lot of birth defects in the United States and then discovered it was mostly amongst indigent women. And the nation, the United States, decided to put folic. And the problem is folic acid. We put folic acid in our bread supply. And a lot of other countries followed suit. And just like a flick of the switch, this birth defect problem just disappeared. It was really amazing. Okay? I think that was '86.

Folic acid was required for growth. But then a lot of patients taking folic acid supplements, and they would crash, too. Now it turns out that for Covid and other RNA viruses, folic acid is an essential nutrient that these viruses need for replication.

If you know any rheumatology, we use lots of methotrexate in rheumatology. They think it works as an immunosuppressant. But there's some good bench experiments showing for these viruses that if you put folic acid in, the viruses grow like crazy. And you put methotrexate in, it stops growing. Methotrexate is really a folic acid analog. And you put folic acid in even with methotrexate, these viruses start growing again. And now we know that patients, rheumatology patients, incidentally who are on Plaquenil, or chloroquine, or methotrexate have fewer deaths and less severity of disease. It's not just magnesium at that. It's a little off the biofilm subject, but it's another sort of clinical finding that I've made backed up by the science. Just any practitioner or patient out there, I just say just be careful. If you're taking something, see if you have any side effects or downgrading of your overall health.

[00:41:34] SCOTT: Folic acid is synthetic. In the methylation arena, practitioners are using things like folate, folinic acid, 5-methylfolate, those types of things. Would we anticipate that those other forms of folate also could have the same result? And if so, could that be why some people feel worse when they start trying to support methylation?

[00:41:59] DR. FRY: I don't know the answer to that. I just don't know. And that's a – We get into the complexity of the chemistry. I don't know. One way to find out would be do the same experience again with all the different folic acid analogs. See what happens. I would throw methotrexate into that mix. And that's really just a tissue culture experiment. Take your favorite virus that does respond. There are some other ones. And just do those experiments. This leads into – you're probably going to need a discussion of what I think is going with everybody. But we'll leave that for your later questions.

[00:42:32] SCOTT: You have a stain assay that looks at biofilms. Have you been able to come to any conclusions from repeat testing from practitioners seeing improvements potentially correlating that to what they did? Or do you have any thoughts on some of the more helpful interventions in addressing systemic biofilms?

[00:42:54] DR. FRY: Right. I think it's interesting. What we found, and we discovered this early on when we developed these "biofilm stains", is that in the winter, in general, people would have more. I think in the winter, we're eating fewer fresh fruits and vegetables. There's less sunlight. And sunlight isn't just about vitamin D. Our body, when sunlight hits our skin, makes many other peptides that are functional. And it's cooler. Okay?

And so, winter is a tougher season for health in general, I think. And I always have patients who weren't doing well. They would go in the middle of the winter to southern Mexico, or a Caribbean cruse, or stay in the islands for a month or two and always come back feeling better. Okay?

I think that's one thing that we found. Just an observation. And then patients were feeling really well or very healthy had virtually none. And patients that were worse had more. And the interventions, whatever the – and we never knew what they were taking, because we just didn't get around to it. Clinically, I saw that with interventions. When patients were feeling better with whatever the intervention was, there were fewer "biofilm communities".

And I think these biofilm communities are reflecting sort of an immune status in patients. And it may not be the problem unless it consolidates into a clot, or stroke, or plaque, or something like that in the vascular system, or blood flow. And I think it's an issue when you get into capillary flow. It could explain why people just don't have – their metabolism sort of slows down and they put weight on. And I think it has to do with some of this sludging that may be going on in the vascular system.

Well, I know a lot of us practitioners, you try to do a blood draw on a patient and you pull the blood out and it gets clogged up. Okay? We've actually taken this stuff. And you think it's just a vibrant clot. But it's usually not. And these sicker patients, you have more of a problem with that. I think it's back to some sort of compromise in their system and it leads into this viral load concept that I have.

[00:45:21] SCOTT: I remember talking with you at ILADS many years ago and you were suggesting at the time that fungi were likely the most disease-producing or health-threatening class of organisms. I think I had a slightly different perspective. I felt like chronic viruses were significant in many people. I'm wondering if you still feel that the fungi are really the biggest – in terms of organisms, the biggest threats to our health.

[00:45:47] DR. FRY: I've turned around in your viewpoint. Yeah. Covid has been horrible, but educational. Okay? I started – I closed my clinical practice in 2017. And then I think it was late 2019, early 2020, I just missed the busyness. I like to be occupied, busy. I wanted to stay in contact. So, I open up online consults Tuesday and Wednesday afternoons. And then I started testing patients. And now we've been working on a viral project. And I was trying to be more open-minded. I started testing.

And what also helped is that I was really into the tick-borne disease arena for many years. And that was our bread and butter for a long period of time. And then I realized that, in Arizona, we really don't have any Lyme disease. And the ticks that we find here, we don't have a lot of ticks here. And most people don't know, but when we go out and collect ticks and look for Lyme disease, the lime belt starts around mid-Texas.

Really, if you look at the Sonoran Desert, in the desert climates, it's just too hot. Okay? And we start to see Lyme Disease North of the Grand Canyon. And then we also see it when they've done the collections. And I can't quote you. And it's a long time ago since I looked at this. And then when you get in the mountains, you cross the California desert and then you get to the mountains, we start to see it again.

And so, where are my patients – and I never had any – I only had one patient with true Lyme disease. And he was a veterinarian that got bit by a dog, okay? And there's a surgeon, a veterinary surgeon.

And so, plenty of mosquito bites. I mean, we have plenty of mosquitoes here in Phoenix Metro. We have irrigation. We have pools that go stagnant, to all this stuff. So, we have – Actually, I think Arizona still has the most number of confirmed cases of West Nile in the country almost every year. Okay? Got a real big problem with it this summer.

And so, I started testing for the tests that are available, the arboviruses. And I can't tell you how many hits I got of patience. The screen's available for the arbor viruses. There's an Eastern, Western Encephalitis, St. Louis Encephalitis, La Crosse, a West Nile Chikungunya, Dengue. And then I think there's some other one, Zika. Okay?

Those are the commonly available tests we have. And after reading one article about this, it's a recent article, we have over 35 arboviruses that are alpha viruses in the northern hemisphere. But we don't have tests for them. There's no commercial test for them. Okay?

And then for the tick viruses, I've heard – We know about Powassan.  Then we know about Colorado Tick Fever. Those are viral. And then there's only one or two labs in the country you can get tested for serologies there. But we know there are 35 to 200 viruses that ticks carry. Mosquitoes, same story. We have potential disease out there with no test whatsoever for it, which has been my interest in developing it. And viral assay to pick up everything.

But then we get into this story. Here's the Chikungunya model, which we know a lot about now. Chikungunya is an alpha virus and a Togaviridae family introduced in San Martin by someone from Southeast Asia in Christmas of 2013. That person was acutely ill. Bit by a mosquito there. And then we thought the vector was just the tiger mosquito. Now we know that the Anopheles Aegyptus mosquito can carry it also.

And it's spread like wildfire through the Caribbean, Latin America, South America. I think the year before last, Mexico reported an endemic 80,000 cases a year. And most of my patients with Chikungunya – And, again, let's back up. These diseases, all these diseases, symptoms our fatigue, myalgia, arthralgia, central nervous system issues. And that's the litany. They probably would all meet the Fukuda criteria for fatigue syndrome. A lot of them start to develop autoimmune symptoms, lupus, that sort of thing. I've seen cases where mosquito bite, all of a sudden they have type 1 diabetes. They're insulin dependent.

And so, Scott, I think you're on to it. And I was bullheaded. And I should have been listening to you before and pushed into this. But there's so many. I would say probably 20% to 30% of my patients I the screen had a one hit for at least one of those. Okay?

And then I have a lot of stories where patients – I was just talking to a doctor in California last week. And one of these tough fatigue patients, a young fellow – I consider a young fellow in their mid-30s now, right? He was unresponsive. And I think there's a – This doctor, I guess Dr. Patterson out of Stanford. And I guess he went out and started his own clinic. And he was giving this old HIV cocktail. The guy is great for a couple of weeks and then crashes again.

This is sort of proof that these antivirals – And then now for Covid, now that we have Paxlovid, which is really two drugs. We have patients who have fatigue syndrome. And they get Covid, they go on Paxlovid, and all their symptoms disappear for a few days. Okay?

And I started using more Ribavirin a couple years ago with a response. That's sort of a tough drug. That got its fame in treating it what? Hepatitis C and B? I've sort of moved into – Again, when I was talking about prostate, I said I think there's some viral hint that compromises the tissue. And Covid, again, it's very instructional, it just bakes the hell out of your vasculature.

For me, when I got Covid, exposed to Covid the second time. I'm vegan. My blood pressure runs. I used to have high blood pressure. Changed my diet. My blood pressure usually runs 105 over 60. And my blood pressure post-Covid was hitting 160 over 110 and no change in my diet. Obviously, just produced, I'm sure, profound inflammation in my vasculature. It took about six months for that to settle down. I think these viral hits is sort of the initial damage.

And then we also know that we have chronicity of disease. I've suspected in the last two or three years, we get a viral infection and it's still in your tissue. We don't get over it; it remains dormant in your tissue. Just like herpes, it remains dormant in your nerve tissue. You're getting under stress, you get another viral infection that comes out the harness. And then you get a cold sore. And so, we don't get rid of this.

And so, good evidence. We have – I think it's Dave Walt out of Mass General or Harvard. He's a pathologist. And he did this really – It's now published. A really elegant study in long-term Covid.

We know the spike protein has a short half-life when someone is competent. The spike protein doesn't hang along very well. They took patients that had died long Covid. They had died. They went down to tissue analysis, and whether it's in their muscle tissue, brain, they still have Covid on analysis, okay? They still have the virus there.

And then they found they've all – As a company. He developed this instrumentation platform to pick up biomarkers, proteins, peptides, whatever. Really small quantities. They did the study. We're finding 15 to 20 picograms per CC, which is infinitesimally small. But they're present in long Covid patients versus normal controls. And so, they still have infection. They're still sick. Okay?

Again, these long Covid patients – I had my colleague who's a rheumatologist, and he knew that I was treating – I was the go-to person in Phoenix other than one other fellow for CFS patients. And he said, "Hey, these are just like CFS patients, are they?" I said, "Hey, I'm sure most of them meet the Fukuda criteria." It was sort of another. And again, Covid is horrible, but it's been instructional. We have all these analogies.

And then we get to – let me get back to the cycle of a viral infection, is – Chikungunya is a great example. We know a lot about it now back to that subject. People who get Chikungunya – by the way, half of those patients we know now go on and develop rheumatoid arthritis. And a lot of them develop certain negative rheumatoid arthritis. It's becoming a real problem.

Now that they know – In Latin America, they know a lot about it. There's a rheumatology group in Sao Paulo that's done a lot of work on this. And by the way, right now, the best treatment for Chikungunya is methotrexate interestingly, a rheumatology drug. And they did the experiments showing you deprive Chikungunya-infected cells of folic acid and they stop growing, and methotrexate to stop growing. Give it folic acid, it starts growing again.

We get a PCR-positive person after infection for weeks or months after infection. The PCR, it goes away. That means it's probably embedded in the cell. Then we get serologies. If you have a serology test for it, you get IgM, IgG; it can persist for months to even years. But even in Chikungunya, that fades away after a couple years. So, we don't have any tests for this internal disease that's going on. There's no test.

Now, there's another …  a few years ago. He did a study looking – and there was a way to look at your T-cell epitopes to see what viruses you've ever been exposed to in the past. Very sophisticated. They never could get the assay launched. It was way too expensive. It was thousands and thousands a patient. But it turned out that people in the northern hemisphere in temperate zones probably were exposed to 14 to 16 viruses in their lifetime. But people in the tropics, mosquitoes to me, sometimes 70 to 80 different viruses. And this leads into my hypothesis on aging.

Aging, there's a lot that's encoded in aging and our genomics certainly. But my theory is that aging is caused by viral load. It's immunosuppressive. And our immune systems don't work very well. And that's what does us in. And to support that, the life expectancy in tropics is significantly lower than the life expectancy in the temperate zones.

Then we have this chronic problem. And then we go back to what have I been doing clinically for patients and my colleagues, is we're using antibiotics. We're using nutraceuticals. We're using thermal therapy, sauna, hot tub, hyperthermia treatments, oxidizing, things like high-dose vitamin C.

Here's a little anecdote. One of my professors who was Stare. I forgot his first name who wrote a monologue on a nutrition. He was Chief of the Harvard Nutrition Program. And his colleague was – One of them Geoffrey Bourne, Linus Pauling, etc. Linus Pauling made this observation – No. No. No. Actually, it was Geoffrey Bourne who was a primatologist who made this observation. Told his colleague Linus Pauling about it.

He was studying macaques in Africa. And just like the chimpanzees, great apes, huge amounts of green leafies every day. But they figured out the vitamin C content, they're bringing in 40 grams of vitamin C a day. And he told this to Linus Pauling. And he says that's where he got the idea about vitamin C being healthful. There's that will anecdote there. And then we have these other alternative therapies. I think they all do something.

And if you look up curcumin, and berberine, and there's – Everywhere, somewhere, whether in India or China. Those countries are big into nutraceuticals. The bench studies show, Pica virus, they have activity. Okay? And some of them better. Some of the antivirals they use is controls.

For me, I was a little more simple. And this really more than justifies naturopathic therapy in my opinion. And it has value it. And they're really familiar with all the possibilities there. And it makes sense. But I started with Doxycycline way back 30 years ago with Thomas McPherson Brown, tetracyclines. They work. They have antiviral, antibacterial, antiprotozoal, antifungal activity. Patient stat, plus a dietary change works. And then azithromycin, Didier Raoult showed that in that big study in Covid that he felt that azithromycin was doing more of the heavy lifting in these acute Covid hospitalized patients than maybe in chloroquine.

And then I had looked into it and heard about Ivermectin for treating CFS back about – I think it was about 13 years ago. Probably – and more like 10 years ago. And when I first tried it on patients, they would hurt so bad I was never going to go there again.

And then, actually, it was the same patient who wanted to try it again. And I tried it around like a fraction of that little three milligram tablet. And lo and behold, that got her back in school and working again. That became sort of my third trial drug in patience, I think after azithromycin. And I had miracles with Ivermectin on cases that were really tough, tough cases.

To bring some memory, I had a patient who he was border patrol. Came out of Rio Grande Valley with 30 ticks on him. Got really sick after that. Went on all the meds. He was Lyme positive. Meeting criteria. And he just didn't get any better. And what really turned around was a combination of doxycycline and Ivermectin.

And then I found that Ivermectin, because it's long half-life, did not needed to be dosed daily. I think in Covid, acute Covid, sure, every day. But twice a week was enough. Okay? Because it's half-life. And that helped a lot of patients. And I think hyperbaric saunas play a role. For instance, bats. Bats have lots of viruses. They harbor lots of viruses. Why aren't they dead? When the bats sleep at night, or during the day, sorry, they raise their core body temperature to 104 degrees. That's the hyperthermia thing.

Again, Scott, back on to you. What happens is I intimated in prostate cancer, I think we get an initial viral hit. That's the initial damage. And these commensals, the stuff that's floating around, get a foothold after that. And that probably is what does. In a heart attack, your coronaries, they fill up with, I think, fungi. Okay? And that's what does us in eventually. Okay?

For instance, in Multiple Sclerosis. A great paper came out in science this year. Big study of military recruits. And they found retrospectively in thousands of cases. And they had serums for 20 years on recruits and the military that they were able to see zero conversions to EBV positive in these patients. And then also a neuropeptide formation. And that demarcated their advanced to Multiple Sclerosis.

And if they showed that serum change, there was 40 times the instance of Multiple Sclerosis in that population versus the other population. It's back to – I remember there was a paper published in the 90s about high-dose – I think it was acyclovir or valacyclovir showing an efficacy in one-third of the patients. Maybe that's it.

But then we have – again, we have this finding from – Oh, what's his name? In Madrid, there's a Carrasco’s work looking at fresh brain sections in MS, ALS, and Alzheimer's patients. They're just full of fungus, by PCR and by stains. I think you get this opportunistic circumstance.

Again, I'm a gardener. So, a gardener, you're looking at everything. And it's just the gestalt. I guess, you need fertilizer, you need the right soil. There are microbes there. So, we're a terrarium, and you get a hit, and it allows opportunistic organisms to come in. And they probably do the coup de gras. But I think it's this viral environment that is the initial hit or compromise. Does that make sense?

[01:03:17] SCOTT: It does. I want to come back to the fungal conversation just for a minute, and that is also a conversation we had in the past around kombucha. Many people promoting it as a health drink. I think for people that have Mast Cell Activation Syndrome, histamine intolerance, we know maybe that's an issue. But I know you also suggested it could be a bad choice due to the Saccharomyces cerevisiae that it contains that can also be a contributor to osteoarthritis. I'm wondering if you still feel that way. And what about the use of Saccharomyces boulardii as a healthy fungus in those with fungal colonization?

[01:03:52] DR. FRY: Right. If you remember, this conversation, it all came about through an article I read or a presentation in American Society for Microbiology. And in Germany, 35 people died and they were septic with Saccharomyces cerevisiae. Okay? After that, I said, "We need to be careful about doing this." Okay?

But to be honest, I have kombucha every day and I survived on that stuff. I don't get my kombucha for lunch. It has caffeine in it. And I've never been more regular in my life. Okay? But when we think about these fermented beverages, if you understand the fermentation process and if you've ever done in the lab, you take your biscuit sugar, whether it's a kiwi fruit or whatever. You have sugar, a few other things, something, ginger, whatever you put into it to give it flavor. And you get the yeast. You throw the yeast in there and it grows. And then what happens is it gets to its maximum and you get this alcohol content.

In beer production or wine production, you get around 5%, 6% and they all die off, okay? And so, the live viable is probably less. And maybe the same thing goes on in Kombucha. I don't know. Because, also, kombucha is a fermented tea. They put tea in there. Okay? Leaf. I think it's leaves or powder. And then that's what I like is that midday kick to keep me going. And again, regularity. And I sort of like the Synergy ginger flavor the best. They have so many flavors.

But I've sort of backed off on that. And I think, in Germany, what happened, they probably got a really high-dose of some probiotic. And remember, people that are sick, a lot of people have leaky gut. Just to tell you how leaky. We have a quick great case in the value of sequencing. A colleague of my wife. She's a retired County judge, a County prosecutor. He was in the hospital. He was in the ICU in February. He'd gone to Mexico in December. Picked up something. And we traced it back probably to something that he was eating. So, we have leaky gut. And he had a variety of – he had necrotizing pancreatitis that was going to kill him. He was on IV antibiotics for a bacteria. And we came up with a Candida, something related to viswanathii a known offendant in India. One-third of cases of pancreatitis have that bug. And he had another bug, another yeast, or fungi that was related to a rotting tropical fruit. That's the Smoking Gun.

And so, obviously that leaked into his gut, got in and ended up in his pancreas. And two days of Diflucan, he's out of the unit in seven days. He's discharged from the hospital. Okay? I think we have to be careful.

These are non-offensive. It's just that I wonder how much the dose is. And really, what happened in Germany? In general, I think these things can be helpful overall for your health in moderation.

[01:07:02] SCOTT: Given that many of our listeners are dealing with chronic Lyme disease, we know historically testing can be very difficult. I'm wondering what you would recommend or what you offer through Fry Labs now in the realm of Borrelia, Bartonella and Babesia? Are we finding that tests are now more sensitive? And then lastly, in your opinion, are those the significant players in someone with "Lyme disease"? Or are there other more significant threats to their health?

[01:07:31] DR. FRY: That's a loaded question. And there are a lot of labs out there. Again, I try to be as ethical and reasonable as possible. And I'm a Dharma bum, a seeker of truth. Okay?

And I think a chronic Lyme disease patient, when you rule out everything else, most likely probably has a viral infection. But you have to rule out everything else. In terms of serologies, we used to offer the whole gamut of all the vector-borne diseases. And we would see lots of Rickettsia titers. And occasionally, we find someone that met the criteria for acute or chronic Lyme disease based off of their IgG titers or IgM via our Western blot that we still do we do. We've got a nice FDA-approved Western blot that we found. It's a Lyme blot actually that we found to be; has the highest sensitivity and specificity.

But also, we get Lyme standards every four, or three or four months. And it's a validated test. And we validate. And we don't see a lot of that. We see titers that are suggestive. Also, the other big one we'd see is Toxoplasmosis. But then the default is sequencing. Okay? Is it really floating around in the blood? Okay?

And so, there are a lot of people paying for a multiplex PCR for close to what we charge for sequencing. But, hey, we look at everything. Okay? We think we're assaying and looking for the presence of over 30,000 types of bacteria. Not just four or five. Okay? I mean, it's like one page we got a sample, if we're thinking of chronic Lyme, a lady out of Virginia. And it turned out she truly had Bartonella. But she had Bartonella bacilliformis, which is unheard of out of the Peruvian Andes. But it turns out reporting for Bartonella bacilliformis now in sand flies in Virginia. Holy cow! It's out there. And that's a very lethal bug. Daniel Arroyo died from it studying it, a Peruvian medical student.

And so, our thing is really do serologies and do sequencing. And sequencing is like we're very proud of what we do. And again, use it as screening. But sometimes we find stuff that's very actionable.

What we found really for mainstream, the real application is chronic UTIs. Interstitial cystitis, chronic wounds, pulmonary disease, chronic GI disturbances. That's the real value. And what we see for the chronically ill in the blood is mostly these unclassified fungi that I think are the secondary opportunistic player in this milieu of possible underlying viral disease.

And I think you've got it is that there's these 35 to 200 viruses that ticks carry. They may certainly have had Lyme disease. In my experience, doxycycline works great for 99% of these patients that have confirmed validated Lyme disease. Why are they still sick after a tick bite? It's the other stuff. Okay?

And if you look at the gamut of diseases of these vector-borne diseases that the ticks carry, most of them respond to doxycycline. That's really a catch-all drug. And I normally would put patients if they were a positive for Lyme disease, I wouldn't put them on for two weeks. I'd do at least a month of doxycycline. And there's some other stuff.

[01:11:15] SCOTT: With the Next-Gen Sequencing, I know you have a Pan-bacterial assay, a Ppan-eukaryotic molecular sequence panel as well. How does the practitioner know which one to order? And then when you get the results back, are people generally having dozens of different microbes that are showing up? How does the practitioner decide what is the actionable microbe or microbes in looking so broadly?

[01:11:41] DR. FRY: Good question. Number one, it turns out we need a broader scope. Anybody else doing sequencing now and offering it a service, mostly shotgun, they don't give you a choice anymore. No one gets a choice anymore. You do 16, 18S. It's better for workflow anyway in the lab. And you should be looking for all of it. Now, you can only order 16, 18S. Okay?

True, though, because of blowback for mainstream, we have curated the fungal database to the 600 known pathogenic fungi because doctors just don't like to treat something that doesn't have a name because of liability. Okay? And then, also, we know that there are nascent GI oral bacteria in the body at low levels. The sequence counts or reads are probably low teens, seven, or eight, or five. And we would always get the practitioner to call us up. We'd have to stop everything we're doing. Go back and spend a day. Going in and redoing and looking at the data to pull up, "Okay. What is it?" And it was almost invariably a normal flora. Okay?

Now with our software, we've set cutoffs for normal flora that are these lower reads. We don't get that anymore. And the new soon to be revised report tells you the bug. It tells you its relative percentage in the finding if it's there. And that it also tells you whether it's pathogenic or unknown clinical significance. And then our new drug resistance assay – And that's not ready yet. We can only do three samples at a time. We have to go through to at least 20 or 30 to make it worthwhile.

It's funny, Medicare doesn't pay very much for drug resistance sequencing. And so, it'll provide you with the bug. Traditionally, what drug to use, and then what the drug resistance genes are. Okay? But anyway, you no longer get a choice. And we've eliminated the little stuff. And then, also, it'll tell you whether the organism is pathogenic or not.

[01:13:47] SCOTT: I want to talk about some of these patterns or fingerprints of the more challenging chronic illnesses that you're seeing from your testing. Let's start with ME/CFS. You've looked at organisms like Pseudomonas and a shellfish parasite, Perkinsus. The algae Spumela as well as the Funneliformis that we talked about as well, or the fungal, the array of different fungal organisms. Talk to us about how you view ME/CFS today as a condition and the microbial contributors that you think are most relevant.

[01:14:21] DR. FRY: Right. You probably read those papers more recently than I have. That was a little while ago. But anyway. Anyway. So, we found distinct populations of bacteria, mostly bacteria, some eukaryotes. But there was a shift, let's put it this way, in the type of bacteria that we found. And this is taking all the blinders off. We're reporting the three or four reads. Okay? Stuff that really there's not much there.

And so, what we found were distinct population groupings of microbes. But the most interesting was that in the ALS population, we found a lot of algae. And that's in the literature. There's a Philippine study that indicates that. There's sort of this aquatic connection, okay? And that's really fascinating. Because when you talk – For instance, there's a certain lake. I believe it's in Maine. And if you live within 10 miles of this lake, your incidence of ALS skyrockets. Okay?

There's another similar body of water location study out of Australia. And then, personally, we had some friends up in Flathead Lake in Montana. That's I think the largest freshwater lake west of the Great Lakes. And I was getting patients from Polson, Montana, up in that area. And I would talk to them and in their church groups, this high incidence of Multiple Sclerosis and ALS in that area. There's an association with that.

And then our colleague, our German colleague, Klinghardt, Dietrich, he was talking about how there was a big group of MS patients along the Rhine Valley. And they drain the swamps and the incidence decrease.

I believe, again, it's the mosquitoes and the viruses. Okay? Is the underlying challenging factor. And water equals mosquitoes, right? Mosquitoes have to have water to breed in. I think the populations, again, in ALS that's the mystery. And then maybe something came in along with that to do something. I have to tell you, if we're going to talk on ALS, I have a case of the patient confirmed ALS. We change his diet to whole food plant-based diet and doxycycline. And this was my daughter's friend's father. As far as I know, 12 years out now, he's still fine. But he was McDonald's every day and smoking every day. We cleaned up his lifestyle. And he's much better now. Okay?

Also, we know this is getting into the CCSVI phenomena. And that's –

[01:17:19] SCOTT: Chronic cerebral spinal venous insufficiency, for people listening. Yeah.

[01:17:22] DR. FRY: Right. This is really Paulo Zamboni's idea in Italy. He was a cardiovascular surgeon. And I think one of his family members, wife or someone, got MS. He started doing ultrasounds and found that the veins are all blocked up in these patients. And it's true. Okay?

Prepping for this, because I thought it might come up today. I actually looked. Zamboni has retracted what he has said about this. But then I was looking at the study that he did, and he did the 12-month follow-up. Okay?

And so, when you talk to the practitioners and they show that their veins are clogged up and have cerebral spinal venous insufficiency, in Alzheimer's disease, in ALS, in Multiple Sclerosis and in Chronic Fatigue Syndrome, these patients have obstructed return flow through the venous system.

Imagine this. So, if our model is right – and Dr. Heuser, who's one of the top cardiologists. He's on board with this. He sees this gunk in the blood vessels all the time. You see a lot more of this in the veins than you do the arteries. We think about strokes and vascular disease in the brain and elsewhere, it's all about arterial. No one thinks about the venous supply because we have this corrective flow. But it does flow things – slow things down overall. So, it's clogged up.

What's it clogged up with? Our cardiovascular paper tells us what it's clogged up with. We have this CCSVI phenomena. And so, they would go in and do balloon catheters. And I had some of my patients do it. And it was a miracle. They were walking and talking again. But over the weeks, it went away.

The contribution of Zamboni to this is that he was right. Okay? It's the blood flow obstruction. And again, I think it's a viral insult and this other stuff starts to grow. And then when it starts to grow, you get toxins produced by these organisms. And who knows if we don't have this immunosuppressive effect of a virus in the first place challenging the system all the time? Just like in long Covid, we have the spike protein production, which is the body has to deal with and react to all the time. It just takes us down a notch again and again and again and when we get another hit. And it's Herpes virus, Epstein-Barr virus, Coronavirus right now. And we just build this accumulation of viral load that takes our immune system down and you don't get rid of it. But you have to survey it and keep it in check all the time. And you get to a certain point, you've exhausted your immune system and then we start to get disease.

[01:20:00] SCOTT: I want to just um close the loop on the ALS and the algae connection, the Hydurus, the Ochrophyta. Are we thinking now that those maybe are commensal or correlation, but not necessarily likely causes or triggers?

[01:20:15] DR. FRY: Yeah, that's what I think.

[01:20:19] SCOTT: And is anything done in those scenarios to treat those algal overgrowths? Or not necessary?

[01:20:25] DR. FRY: Well, we know – When I was looking into it, there was one recognized algal infection. I forgot what it was. And the infectious disease community treats it. I think it was with clindamycin or something really powerful like that. But I kind of like haven't been hooked up into that particular disease category for a while.

[01:20:50] SCOTT: In Multiple Sclerosis, you've mentioned the connection to Epstein-Barr virus. I know in one of the earlier studies that you published on, there was not a difference between patients and controls. Wondering what that might suggest? Might it suggest that microbes are not a significant contributor in Multiple Sclerosis or –

[01:21:11] DR. FRY: Well, I actually think they are. And so, again, it's a viral insult. And I'm not convinced it's totally just Epstein-Barr. And who knows? It's hard for me to believe. In Africa, if you understand Epstein and how he figured all this stuff out in Africa, I think it was Burkitt's lymphoma. I mean, you're seeing this huge incidence of Burkitt's lymphoma in Africa where it was really we found out. I think the average age of contraction of EBV was age three. Where in the United States, if we believe all this, it's actually really in high school and college. And if you look at this military study and you believe that it's just EBV, it can even be later on with … results later on. Who knows? So, it's not EBV.

For instance, we all know that when patients, they've had mono in the past that's EBV. Mono can actually be other diseases, by the way. We get mono. And then they get whatever causes them to be sick later on, whether it's a tick, or a mosquito bite, or something and then get fatigue syndrome, they get another challenge is what I'm thinking. And we know that these serologies just go through the roof for EBV again. And I think it's this immune suppression that causes EBV to just pop out again. And it may not be causality, but it could be a marker of something else happening. Another viral insult. Okay?

But again, we need better tools. So, back to tools for the practitioner. I would use the interleukins, the CD counts, CD4-CD8 ratios, CD57. SED rates are not that helpful. But ANAs, rheumatoid factors, too, that are – And those are simple monitors. And that brings in a whole another discussion in a minute of autoimmune disease and that contribution to the whole scenario.

But I think we need to use all the markers that we can and the serologies to give us a picture. I think that's worthwhile and it's not that expensive. And then there's the whole thing of – And now I believe because of the nature paper this spring that, yeah, there's truly a genetic component to autoimmune disease where our TLR7 genes are switched on one single point mutation. You've got Lupus. And they're switched on caused by viral RNA insult. That's the trigger. Do we really get rid of that particular virus or not? But it turns the system on. And then we get true autoimmunity. And so, I always screen my patients, do they have a little bit of whatever that genetic factor is going on to contribute to their disease?

[01:24:02] SCOTT: I want to do a few rapid fire conditions before we start wrapping things up. I want to talk a little bit about Parkinson's disease. I think many people are now suggesting that there's a significant gut microbiome component that can contribute to Parkinson's. Wondering what your thoughts are about the potential triggers for Parkinson's? And by the time someone develops a manifestation of the actual condition, is it too late to make significant reversal?

[01:24:29] DR. FRY: Yeah. Parkinson – this is Zamboni's group, CCSVI. I think 95% Parkinson's patient had left internal carotid obstruction. Complete obstruction. Okay? Number one. It's this gunk stuff going on again.

And the gut association – An article just came out in the last three weeks about how we find this large Bacteroides population. Okay? Everybody's saying, "Oh, gee! It's the Bacteroides population that's causing a problem."

Now, we've done hundreds of gut flora studies and we map out Bacteroides, ruminants, everything in our gut study. And the thing is, commercially, that really didn't take off for us because we actually have to pay our bills. And anybody else doing gut flora is subsidized by either they sell your data and don't tell you. Or they're subsidized and that's attached to a vitamin product or something like that. We don't do that. It's just like, "Hey, you have to pay for service." And there's no way we could offer a product for 200 bucks. It's like impossible to stay in business.

But the bottom line is that if you change what you eat, you can dramatically affect it. Bacteroides population is affected with high meat eating. Okay? Let's go back to MS, another neurologic disorder and Roy Swank's work from 1990. Roy got into looking at dietary differences in Europe and how people and their incidents of MS and found out that people who were more veggie did better. He did almost recommendations in a lot of his patients. He was either chief of the department or full professor at University of Oregon neurology. This is a long study, a 30-year study, published in 1990. And patients who are more whole food plant-based did not die of Multiple Sclerosis. Okay? They died of some other cause.

I think it's the type of diet. The finding is Bacteroides, it's diet. That's why the Bacteroides. If you've got a whole food plant-based diet, the Bacteroides disappears. And we already know whole food plant-based diet, patients live on the average 17% percent longer when they change their diets. Why does that work in this model?

It turns out that the high fat, high protein fuel disease. Dr. Campbell did a study way back when he wrote the China studies. One of the deans of a whole food plant-based diet. Retired. Emeritus professor at Cornell for nutrition. He actually did the China study with the assistant director of medicine for China.

He did these studies long ago. What causes coronary disease in pigs? It's the protein. It's not necessarily the fat. It's the protein. High protein diets and high fat diets fuel disease. And they're low in, of course, bioflavonoids. When you switch to whole food plant-based diet, you're getting all these bioflavonoids and lectins. And I'm the opposite of Dr. Gundry. I think we need these plant lectins. Because the reason why people flare up with wheat and all these lectin-containing products, they have underlying disease. And the lectins are fighting. You're having a Herxheimer reaction eating this plant leptins, I believe. Okay?

And so, for instance, one new cure for Covid is banana plant lectin. And I read an article about that a couple weeks ago. Am I telling you to prevent Covid by eating two bananas a day? Well, it can't hurt. Can it? I hope that answers or gets to some of those questions you were talking about.

[01:28:07] SCOTT: Let's touch briefly on rheumatoid arthritis. You've talked about the role of toxoplasma, fungal pathogens. How significant of a contributor might these be in people with rheumatoid arthritis? And what are a few of your general thoughts on toxoplasmosis as a contributor to chronic diseases? My observation over the years has been that those people that have Toxoplasma seem to be more severely symptomatic in their chronic condition.

[01:28:33] DR. FRY: Yep. RA, favorite topic. McPherson Brown got started on that in '92. And he thought it was Mycoplasma pneumonia. We never find Mycoplasma on any synovial tissue we looked at. Though, it seems like a lot of people have positive serologies to Mycoplasma pneumonia. Mycoplasma pneumonia is ubiquitous. Okay? It's all over.

And what we've done on sequencing of joint fluid from RA patients. Mostly fungal. We have found Toxo in these patients. But there are a number of labs now looking at viral etiology. I would love to get our pan viral assay going. There's like thousands of frozen and joint fluids ready to go by a group in England. If someone's ready to assay them.

But it's interesting in the Sao Paulo study by the rheumatology department there, it wasn't even in the fluid. It was in the synovial cells. Okay? It was in the cells. Not the fluid. This is a tough problem. I'm beginning to think now that RA is mostly viral. Okay? Chikungunya is a model. But other viruses. Now, parvo has been implicated in it. And again, if it's an RNA virus – We've known traditionally RNA viruses are very difficult to extract. And then you have to map them. You have to extract them and extract them so that the RNA is still intact and mappable. Okay? So, that's one challenge.

And, gain, I think there are 12 viruses implicated in RA now. And then there's also this autoimmune component that probably plays a role. And is it really an autoimmune component? Is it really that those particular individuals have a problem dealing with RNA viruses? It may not just be the switch. They just simply have a problem dealing with some of these RNA viruses.

Toxo? You're right. If someone really has Toxo, it's hard to get rid of. Some Toxo – there's a Toxoplasmosis. I forgot what subtype it is, in Guiana, that's lethal. Causes pneumonia. But the last study I read, it's an older study, 25% of the population is seropositive for Toxoplasmosis. And then French women how they're into eating steak tartar, that's the fashion. And French women have a really high serial positivity for Toxoplasmosis. We know that Toxoplasmosis is related to lots of schizophrenia and mental illness.

And if I remember correctly, the last time I looked up, if you have Toxo, chronic Toxo, the treatment is very, very difficult. And we don't know if we really get rid of it. And of course, we screen. That's the TORCH assay we do in women that are pregnant to make sure they don't have Toxoplasmosis. So, get rid of that kitty litter.

[01:31:25] SCOTT: Well, Klinghardt used to say get rid of the cat, too.

[01:31:29] DR. FRY: Yeah, yeah, yeah.

[01:31:31] SCOTT: One of the invisible illnesses is Morgellons believed to be associated with Lyme, believed to be associated with Bartonella, believed to potentially be associated with H. pylori. What have you observed in testing people with Morgellons?

[01:31:48] DR. FRY: I've probably treated probably eight or nine patients. They seem to respond to antibiotic therapy a little bit. Nothing great. And you have to see it to believe it. Mainstream thinks these people are nuts. And a lot of them come in. They're all a little off. But to see people pulling filaments out of their skin is incredible. Okay? It's really amazing. All right? So, what is it?

Initially, we thought it was fungal. And we thought that it was really chitin that was being secreted. But it looks like it probably truly is keratin. I've evolved into this concept that it probably is of viral infection that's actually transforming the cells in the body. And I've had people who were genetically unrelated come down with Morgellons at the same time.

I had a couple genetically unrelated who were down in Louisiana and both contracted Morgellons. Two healthy individuals contract at the same time. And so, the dermatologic diagnosis is a keratinocytosis or something like that. And, so I think now, back to you, I think it's a viral infection now. And they actually have transformed and mutated those cells to produce – I mean, skin cells produce keratin. So, they made them hyperkeratin producers. That's what I think now.

So, then I would look at – going forward, I would look at potentially antivirals. But I suspect the damage has been done. And then you would have to look at it as almost like a cancer and look at chemotherapeutics to treat those cells. But how are those cells different from the cells surrounding them? And that's always a challenge in oncology.

[01:33:44] SCOTT: Wow! I love this conversation, because clearly your thoughts and the information that's led to your thoughts evolving over time has been impacted by technological advances and the work you've done over many years. And I love your transparency and kind of letting us see a little bit into the fun place that must be to live in your brain.

[01:34:09] DR. FRY: Yeah, I'm just trying to figure out what's going on.

[01:34:11] SCOTT: Yeah. No. I love it.

[01:34:12] DR. FRY: What's been the goal is to figure out why is this person sick? Why is this person not feeling well? And I believe that science is the way to figure this out. Yeah.

[01:34:22] SCOTT: Do you think it could be more difficult for someone to clear fungal overgrowths or colonization if they have ongoing environmental exposures to water-damaged buildings? How important is improving their external environment from a fungal exposure perspective in order to optimize treatment outcomes with these fungal overgrowths?

[01:34:47] DR. FRY: I think environment is everything. Okay? It's what your grandma said. Go out and play and get some fresh air, right? And sunlight, fresh air, all this stuff, tipping the scale. We do know that in regular foods there are carcinogens, pesticides in it. Eat organic. It's not as expensive as it used to be by any means in words. A little bit more than organic. And they've been multiple studies. Just looking at cancer rates in people that eat organic and don't. Okay?

I believe these organic phosphates, these pesticides all play a role. Plastics that are on environment all play a role in our immune systems. And I think that the last environmental medicine meeting I went to just pushed to how important this stuff was. For instance – Oh, who's the Roundup expert that does all the – the French guy. I can't remember his name. But he says it's not necessarily the chemical that we think is Roundup. It's all the other petrochemicals in the process of making roundup that are more of a problem and they're all very carcinogenic. Okay?

We have this environment around us. I think back to – it's back to Rachel Carson, Silent Spring. There are more chemicals – this is another argument for whole food plant-based. There are far more chemicals in meat and dairy just because of the food chain than there are in the plants themselves. That's another reason.

And in terms of moldy buildings, that certainly can play a role. I think I was looking at one study where the outgassing of black mold in buildings was toxic. Okay? It's not necessarily the fungi itself or the spores, but it's the outgassing of toxic chemicals. I think if you've got a water problem, you just need to clean it up. Okay? I mean, I don't think it's the cause, but it certainly has potential for suppressing our immune response.

[01:36:55] SCOTT: I mean, do you see any – when you do your Next-Gen Sequencing, do you see commonly Aspergillus, Chaetomium, Stachy, or any of those actually found in the body?

[01:37:07] DR. FRY: No. No.

[01:37:08] SCOTT: Okay. Cool. Interesting.

[01:37:11] DR. FRY: I think if we did nasal or lung, that may change. But I don't think so. And again, I'm in Arizona. It's pretty dry here. I mean, I'm from Virginia. I used to live in Florida. I mean, who doesn't have mold somewhere in the building or in the house somewhere in those environments? But here, our relative humidity most of the time is 10% to 15%. I think we've had four inches of rain this year so far. And the year is almost done. Versus my daughter's in Maryland now. And I'm from Virginia. And she says, "Oh, it rains a lot here." Environment plays a role.

And we know a lot of people in the old days used to move to Arizona mostly because of Tuberculosis. And actually, we had a lot of people who had TB moved out here and stayed out here. Sunlight is the cure for a lot of people for TB.

[01:38:01] SCOTT: You've had a lot of interesting cases that you've worked with. One of them that I wanted to get your thoughts on is what are the potential contributors to Cystic Fibrosis?

[01:38:13] DR. FRY: When you read the literature and they've looked at flora in the lung, they admit, there are fungi and bacteria in the lung. Traditionally, this is – I forgot the name of the gene. But these Cystic Fibrosis patients have a gene defect that essentially makes their mucus thicker. Okay? But then when I talked – I've got a colleague of mine who was from an area, Nebraska – Not Nebraska. Oklahoma, Texas border, agriculture community. There's dust everywhere. High incidence of Cystic Fibrosis. That's just because they're all settled via the same dramatic family that it rolled in in the 1800s. I don't know. But there's a high incidence in these rural communities. A lot of dust. And again, a lot of pesticides. That may play a role.

But the couple of cases of patients with Cystic Fibrosis, we find a lot. We have the luxury of being able to say how much is there with our sequence counts or reads. We can say, "Wow! There's a lot of fungus here in the sample versus everything else." That's most likely the problem. It's just like this pancreatitis case we're talking about, the bacterial reads were in the teens, maybe 40. But the fungal reads was a thousand.

We just had this prostate case turned out to be cryptococcus. His reads were 6,000. Just huge. That's the problem. Okay? We have – Actually, we had one case. It was my daughter's distant cousin's niece, or nephew, or something with Cystic Fibrosis. 12-year-old. Not doing well. Just crashing. And we found lots of the unclassified fungi in the sputum that we could get. And the primary care physician, the pediatrician, was so advanced looking for any answer. Posaconazole, 30 days later, doing great. Okay?

And, oh, we have another case. This is published. We had a guy with atelectasis and lung issues. On inhalers. This is unclassified story again. And the primary – Or the pulmonologists did not want to continue because he was treating an antifungal – using antifungal on a patient with pulmonary disease with lots of unclassified fungi. And that's a case of what we published. And he responded on 30 days of terbinafine and doxycycline. Then he failed. The pulmonologist was unwilling to continue therapy because I don't know the name of the fungus that I'm treating. And finally, he found another practitioner willing to continue.  Said he's going to need at least three months therapy. He did. And he was fine after that. It was terbinafine and doxycycline that I think probably works synergistically in that scenario and aquatic pulmonary disease.

[01:41:09] SCOTT: If we come back to the Covid conversation, you've already suggested that, in some cases of long Covid, there could be the potential for persistence of Covet itself. I know other practitioners have also found higher incidents of reactivation of EBV, or higher numbers of positive bartonella tests, or higher mycoplasma results I'm wondering if you yet are able to tell from your next-gen sequencing how the patterns – You talked about the counts of these different organisms that you're able to kind of prioritize and assess the potential impact on health. Are you seeing any changes in what organisms are rising to the top in those people that have had the immune dysregulation of the Covid experience? Does that make sense?

[01:42:05] DR. FRY: Good question. I can't say that by diagnostic code that that's what they have when the sample comes in. I don't know the full answer to that. But knowing what I know, I think having Covid, that virus is very immunosuppressive. I think this accounts for – I mean, you hear these stories. I mean, when I had Covid, when I was exposed, the first time I had Coid I didn't get sick. But everybody else did for certain reasons. Okay? The second time I got it, I got real sick. And my feet literally turned purple. Okay. I went on some blood thinners.

And I think it's these commensals, these opportunistic bugs when the systems immunosuppressed that go crazy. Okay? And very immunosuppressive virus. And then if you have chronicity of a disease and it's there, again, your immune system is challenged.

I don't know if you know, but we have – this first came out, and actually it was in the Wall Street Journal recently. The industry came out at the end of 2021 saying that we had an increase in all cause death this is not Covid as being the diagnosis of 40% percent. That's huge.

And then three doctors at Walter Reed were noticing there were a lot of new deaths in military personnel. Again, 40% in all-cause death. Okay? And who knows why? But what's different is we have had an epidemic recently that's still ongoing. Okay? And spike protein, whatever, is very immunosuppressive. And I think it's opportunistic. And what are they dying of? Increasing cancer, stroke, heart attacks are the main ones.

[01:43:58] SCOTT: Lots of the vascular related.

[01:43:59] DR. FRY: Vascular disease and cancer, of course. But lots of vascular. Lots of strokes. Okay? A very pertinent question. And I think this will unfold as we get into it. And then, of course, Covid is by no means so over. As I said flippantly to one small group last week or week before, they said most of the susceptible population has died rather quickly around the first couple of rounds. And I think as we get more iterations of it – I mean, the mainstream public doesn't seem to care anymore. I mean, I just had a friend who got coveted coming back from Denver and she got sick. And no one's wearing a mask anymore. Now we have full bore transmission. Just so is influenza and RSV now. We're seeing a huge spike in influenza right now. And it's earlier season, full season right now. Lots of Covid. But again, we don't see the hospitals filled with the deaths anymore.

I think, again, the Paxlovid is probably working. No one seems – For a while, prescribing Ivermectin would get your license tagged for a little while, at least in my state. Now they don't seem to care anymore. And NIH is actually saying, yes, it could be an option. And again, the FDA isn't going to say anything because it's an off-label use. Right? Anyway.

[01:45:25] SCOTT: You always have some amazing new research, some brainchild that you're working on. I'm speculating you have something significant that I haven't asked you about. What do you think is the next big thing? The next big realization that will positively impact those people currently dealing with a chronic condition?

[01:45:48] DR. FRY: I think is you have this conclusion for a long time, and I've grudgingly moved around to it, is that it's mostly viral. And we need better tests. Okay? And now, I got into this years ago. We only had a handful of antivirals available. Okay? And then we probably didn't know that a lot of the herbs, nutraceuticals, curcumin, moringa, all this stuff had antiviral activity. Berberine, all this stuff. And they do.

And this is the other thing I want to make comment on, is that I developed – I would try one thing on a patient and then another thing and another thing and sometimes it would take me two or three years. The patients believed in me. Stuck with me. And we finally come on the right combination that would work for them. Okay? And that argues for a multifactorial pathogen, I think. And these viruses have huge variety. And that may be what we've been dealing with.

And so, if we can nail down and say, "Okay. You have this, this, or this," that's really valuable. And this is our push with our partners in Los Alamos to complete that project. Okay? Then we're still going to have deficits though and non-invasive testing where it's just a blood test or something.

Say you've got someone with viral disease, but their PCR, their molecular tests are negative for it. We need other possible assays to determine that. Okay? And I have some ideas around that. But I think the most important thing now is to finish that particular assay.

And our short-term stuff for our lab, we have DNA sequencing. Serology is just down doing a Western blot because most of the serology is going to be done commercially now. And our prices went up for our assays. And we're still doing the stain. So, we still have big demand for that. But the sequencing, we offer all at once. Medicare covers it.

And if we're on the state Medicaid plan or access plan, they cover it. Insurance. The patient's met the deductible. Almost all now. We used to have a problem with one insurance company and they're paying all of it now. It's expensive, but it costs a lot to do it. It's not Multiplex PCR. It's really days of work to knock it out. We're trying to get into automate, increase the throughput. A lot of players have dropped out of the marketplace for Covid. We're still in the game. Because, obviously, all that worked dried up. And so, those are some of the challenges.

[01:48:31] SCOTT: And and is it true that in order to do the testing through Fry Labs, do they all require a physician to sign off on the requisition or any of them available through direct –

[01:48:40] DR. FRY: That has been in discussion for two years now allowing direct access testing. And after a conversation with our FDA consultants, we now, as of Monday, offer direct access testing for sequencing. And patients can order it for themselves. Again, insurance may or not pay for it. It just depends on your insurance carrier or if you have a medical savings account. It's not cheap.

But I would say for bacteria, it's the definitive assay. We like it. Just to let you know that the feds have picked up and analyzed our – we made our 16S sequencing assay into a kit. That kit is available now. The feds have been looking at it for a couple of years. We have a couple of – One paper out and another coming out. And now that's in field trials in Nairobi for disease surveillance. They like it. They love it.

You can take an unadvanced lab that can do sequencing, give them our kit. And it makes it very simple for them to do. It's cloud-based bioinformatics. And they love it. They say it works great. We're very prideful of that assay. Works great. And now it's available.

The main application for that to your readers would be if you've got a chronic urinary tract infection, interstitial cystitis, pelvic disease, GI issues, chronic lung problems. Again, it's only as good as the sample. Okay? A blood test is useful. But, again, I think a lot of people that have chronic autoimmune or fatigue issues, it's probably mostly viral. But then when we get a directed disease area like a chronic wound, again, I think we'll find something actionable there. Okay?

Let me make one comment about stool real quick. Stool, we don't see pathogens very much. We see a shift in the population. I was talking about Bacteroides, fermented bacteria before. For me, these are a nightmare to interpret even though I've got software to help me with that. But a lot of times, a dietary change in health. The main one thing we see is candida, candida overgrowth. And that's Diflucan. Changing diet to really sugar.

[01:50:56] SCOTT: My last question is the same for every guest, and that is what are some of the key things that you do on a daily basis to support your own health?

[01:51:04] DR. FRY: Number one, exercise. I swim – Or I bicycle every day five miles. I swim three days a week half a mile. I do stretching, weights every day. I'm whole food plant-based.

I have to relate that story. My wife had a cardiac event in '09. I was actually giving a lecture for Carol Ann Ryser. I got a call, "Hey, your wife's being cathed right now." And so, I took the first flight back. And then one of her good friends knew about John McDougall's program. And so, she went to the 10-day immersion program. And so, my wife and I have been plant-based since then.

And I was borderline hypertension. My cholesterol was high. My father died of a heart attack. And his father died of pneumonia and heart attack. And now, my cholesterol, non-fasting, runs around 150, 160. My blood pressure runs – As I said before, I usually run to 105, 110 over 60. I'm older than 60, by the way. So, usually most people my age have high blood pressure.

My wife, after changing her diet, was skiing 11,000 feet in Colorado, 6 months after her event on a whole food plant-based diet. And it's the only thing shown to reverse cardiovascular disease, whole food plant-based diet. We do that.

And then supplements. And I believe in curcumin. The kombucha is a mainstay in my diet right now. And again, we'd like to do – we've noticed a difference between pasteurized orange juice. And I grow a lot of citrus. And fresh citrus. There's something in the pasteurization process. It's knocked out. I don't know what it is. But fresh citrus.

And I think what happens, you get more of the rind when you make your own juice. That seems to be a factor. And then what else do we take? And sunlight. Okay? I swim. I try to swim midday. Get some sun. And I really notice a difference if I don't get sunlight. Sunlight's key.

And then if we go back to – who's the guy who discovered the D3 isomer? Mike Holick out of Boston, who's also a dermatologist. He says, "Hey, Dermatology is always a factor in skin disease. But he says 10 to 15 minutes without sunblock, okay, in the middle of the day is what we should be doing. Here in Arizona, maybe you don't need 10 minutes in the summer. Right now, this time of year, I don't think anybody's getting any vitamin D due to the shortest of the day right now. But that's a big deal. That's it.

I've gotten rid of all the bad habits. I don't smoke. Probably did in college. And I don't drink anymore. I don't tolerate it anymore. But alcohol, may be a drink or two a day may be good for you. But certainly, more than that is bad for you. And smoking, of course, is like – If you're smoking, you just don't care about your health. You don't care.

[01:54:06] SCOTT: This is such a, fun great conversation. We've had some good conversations over the years at different conferences. And I was really looking forward to our conversation today to see what new things you've learned from your advanced leading-edge diagnostics and lab assays. And you certainly didn't disappoint. You gave me lots of new things to think about. And so, I just want to thank you for not only spending a couple hours with us today sharing a lot of your knowledge, but for being transparent, for making a difference in the world and just for doing all of the amazing things that you do. Thank you, Dr. Fry.

[01:54:41] DR. FRY: Thanks a lot. Thanks for having me, Scott.


[01:54:43] SCOTT: To learn more about today's guest, visit stephenefrymd.com. That's StephenEFryMD.com. StephenEFryMD.com. Or visit FryLabs.com. That's FryLabs.com. FryLabs.com.

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