Episode #158: Chronic UTIs and Interstitial Cystitis with Ruth Kriz, MSN, APRN

Welcome to Better Health Guy 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 or his information to facilitate self treatment. As always, please discuss any potential health related decisions with your own personal medical authority.

Hello everyone and welcome to episode number 158 of the Better Health Guy Blogcast series. Today's guest is Ruth Kriz and the topic of the show is chronic UTIs and interstitial cystitis. Utilizing her functional medicine background as well as experience in microbiology and teaching pharmacology, Ruth Kriz has spent the majority of her professional career as a nurse practitioner working with chronic UTI and interstitial cystitis patients. Her practice expanded to patients from almost all the states in the US as well as from 35 countries who came to her seeking answers.

Beyond symptom management.

Through molecular testing, an understanding of the genetics common to these patients, and an understanding of how this contributes to chronic infection and biofilms, she's been able to successfully treat this population. These factors have broad implications for other chronic infections such as sinus, prostate, ear infections, wounds and others, as well as fibromyalgia, cardiovascular disease and other conditions in which biofilms are an important contributor. She has closed her medical practice, but she has reinvented herself as a consultant to help practitioners nursing learn how to utilize her approach for curing these patients.

And now my interview with Ruth Kriz. I had the privilege of meeting Ruth Kriss several years ago as part of the Forum for Integrative Medicine where she was a speaker. I followed her work since that time interested in interstitial cystitis, which actually took me quite a while to even be able to pronounce. And so looking forward to doing this conversation, this podcast for quite a while and just want to thank Ruth for being here today. So thanks for joining us Ruth.

Oh it's a pleasure to be here Scott. My next question was now that you can pronounce it, can you spell it?

I can because I have it in my notes in front of me, but I actually think I could. So what was the personal experience that drew you to making the focus of your life's work? Working with people with complex chronic health conditions? What was the driver for the passion that you've had for your career and still have? Very well.

Life has interesting twists and turns. There's an old saying, if life gives you a lemon, you make lemonade. And it turns out that I myself was diagnosed with interstitial cystitis in my early 30s. And having gone through many frustrating experiences within the typical urological community and being told that what I had was chronic degenerative and incurable and to go learn to live with it, I decided that that was not a good enough answer. That started me on my quest to find some answers that I wasn't getting from the medical community.

I started the conversation today mentioning interstitial cystitis. That was originally what I had intended the focus of our convers conversation to be. But then in our preparation conversation, you really enlightened me and so love for.

You to talk a little bit about.

The symptoms that might characterize chronic UTIs and how that evolves potentially into an interstitial cystitis diagnosis over time. And then why do you say that IC or interstitial cystitis is a, quote, trash can diagnosis?

Certainly that's an excellent question and the source of a lot of confusion both with patients and the medical community. Just a little bit of history here. IC was first identified, characterized in the mid-1800s. The amount of damage to the bladder wall was seen even back then by doctors looking into the bladder with the naked eye and seeing that it was damaged because the cultures were negative, they said it wasn't an infection. And that myth has been perpetrated for over a century. Everybody has looked in other places except for infection as the cause. As I started being able to utilize more advanced culturing techniques, first of all, soy broth cultures with Dr. Paul Fujuzato, a PhD microbiologist who had an interest in chronic UTIs and interstitial cystitis. And he was finding bacteria that traditional standard urine cultures weren't finding. Then later on, once molecular testing with PCR and next generation sequencing became available, I discovered that I was finding infection in 100% of the interstitial cystitis population. Then when I started listening to patients talk about their history, it fell into a very common pattern. Well, I started getting UTIs at this point in time, and then they got more frequent and I would take the antibiotics and I would get better. And then they started becoming more and more frequent. And then I started getting negative cultures back. And then I got an IC diagnosis. I theorized this was on a continuum, that people may start with UTIs just like everybody else. But then for some unknown reason, which I think I figured some of the pieces out. Later on, we'll talk about it the cultures became negative, their symptoms became more chronic, and when a urologist looked at the bladder wall, they could see the damage, and they won the IC diagnosis. I think that this is a process all on a continuum in which you may start out with UTIs just like everybody else, but there's something special about this group of people in which the chronic UTIs continued to the point where the bladder wall damage could be seen by the naked eye. Therefore, they got this other designation, new diagnostic code, if you were of ic. And that made practitioners conclude, oh, if you have ic, then you can't have an infection. And so oftentimes these patients, if they tell a practitioner they have an IC diagnosis, they won't even get a standard urine culture to check for infection, because they all know that it's not based on negative cultures in the past and the damage that can be seen in the bladder wall.

So it sounds then like the goal is to appropriately treat and address the factors involved in chronic UTI so that we don't then progress to an IC diagnosis that can then be much more debilitating, much more complex to treat that we want to have that early intervention. One of my mentors, Dr. Dale Bredesen, he talks about the 36 holes in the roof when we talk about dementia and cogn decline and Alzheimer's disease. And so I'm wondering, just at a high level, if you could start us off by talking about what you perceive to be some of the holes in the roof in chronic UTIs and IC that we need to think about to explore potentially to treat. What are the holes that we need to plug in the roof, so to speak.

Oh, I love that analogy. I think there's not quite 36 that Dr. Breslin has. I think there's probably closer to eight or 10. I started trying to figure out what was common about this population that made them different. And the breakthrough came about eight years ago for me, when a lot of people were getting the 23andMe genetic test back when they actually gave you more data than they are giving you now. I had 156 patients that sent me their results. I started looking at them after a while. I noticed that there were a lot of things in common. For instance, 100% of them had a vitamin D receptor mutation. I thought, well, that's interesting. What does that have to do with urinary tract infections? Lo and behold, it turns out that the bladder wall needs vitamin D to produce a peptide called cathelicidin, and that peptide prevents urinary tract infections. So if you have a vitamin D receptor mutation, you make vitamin D every bit as well as everybody else who goes out in the sunlight, preferably without sunscreen, because that will block vitamin D production. SPF 15 blocks by 87%. So you do need sun exposure without sunscreen, at least on other parts of your body, maybe not your face, but other parts, in order to make vitamin D. And they make the vitamin D, but their body can't hold onto it because of this receptor problem. Sure enough, all my patients, when I check the vitamin D levels, they were quite low. Now, I want to define low. Labs in the United States use a reference range of 30 to 100. You get a reference range by take your thousand people off the street, measure their vitamin D, find the mean, and then go out to standard deviations. Well, the problem with this with vitamin D is that it's a seasonal number. So we store up vitamin D because it's fat soluble during the summer, and we store it, and that's what we live off of during the winter months. And then we start building the level back up again in the spring when the sun is high enough on the horizon. And a lot of this depends upon what latitude you live at. But the problem with the reference range is I don't know where these people lived who were tested. Did they live in Florida? Did they live in Maine? We know that people with darker skin tones need more sun exposure to generate the same amount of vitamin D. Were these people white or black? Were they checked at the end of summer or the end of winter? But I do know they didn't get thrown out of this quote, unquote normal reference range. If they had a vitamin D receptor mutation. I believe that that reference range was falsely skewed to the low end. If you only go out one standard deviation from the mean instead of two, I think the optimum level is between 50 and 80. And lo and behold, all of my patients had numbers in the low 30s or lower if they weren't supplementing. My goal was to get their vitamin D level above 50 so they can make enough cathelicidin so their body's own immune system can help fight urinary tract infections. The next one I found was something that unless you've had biochemistry you may have never heard of before, called cbs cysteine beta synthase. And in the methylation pathway, if anyone has access wants to look up the big busy diagram on that. I think Scott's going to be providing some of the slides separately, but CBS is in the methionine or that last portion of the diagram, it helps break down homocysteine to cystathione, which goes into cysteine that the body uses to make glutathione for detoxing. However, if you have a CBS mutation, which 100% of these 156 people did, instead of making a lot or an appropriate amount of cysteine, you make a lot of ammonia. And once again, we had to ask the question, so this population makes a lot of ammonia. How does it impact bladder health? I poked around the Internet for a very long time, and just like a lot of things medically, the veterinary literature is ahead of the people studies. And I found in the veterinary literature some excellent research that talked about ammonia damaging the gag layer of the bladder wall in animals. And I have to believe it has the same effect in people. That's the definition of an interstitial cystitis patient. Somebody that when you look through a cystoscope with the naked eye, you can actually see the damage to the bladder wall. When they hydro distend the bladder, And I do have a picture of that on the slides. The bladder wall cracks, it bleeds. Those are called glomerulations, another hard word to pronounce, and that is diagnostic of interstitial cystitis. That gag layer has been damaged. We do know that chronic infection will damage that layer because the bacteria can become attached. If you have a high ammonia level in your urine and that layer becomes damaged, that also is a portal of entry for infection. Knowing that there's high ammonia, higher than other people in this population, is part of the explanation or one of the holes for why this group of people can't get over urinary tract infections as well as others. And those infections can become chronic.

Wow. So that's great information at a high level in terms of a couple of these holes in the roof. We're going to talk about more of them. In our conversation. I wanted to get into, and I'm gonna throw out a number of questions and then just kind of let you go again.

But if we look at the lab.

Side of things, you hinted at the fact that a very high percentage of patients have documented infection when you use the proper tools.

Wanted to look at.

If we think about things like chronic infections like Lyme or CO infections or parasites, we know those can also be difficult to find with conventionally available tools. It's certainly gotten better over the years, but it's not possible. Perfect. So why is it difficult to find evidence of infection in these conditions? How do you prefer to test? Are we looking always at urine? Are there other things that we're testing? And then what are some of the advantages of the molecular testing over some of the standard culturing techniques? Are there specific labs that you find most helpful in identifying the pathogens that may be contributors to these conditions?

Let's talk about standard urine culture and technique, because that has been considered the gold standard, the best that we've had for over 150 years. But it's now the 21st century and we do have better techniques. Standard urine cultures rely upon a specimen that gets collected, and at some point it gets picked up by a courier, taken to a lab, and at some point, some of the urine is put on a culture plate. The culture plate gets incubated, a lab technician looks at the colonies that grew and decides which ones are important, identifies those organisms and does sensitivity testing. There's lots of ways for error to happen here. First of all, I don't think anyone's urine should be checked if they have symptoms with a random urine. We don't know if they walk into your practice at 2 in the afternoon, if they just finished lunch and had 16 ounces of liquid to drink, and the urine is over diluted. Of course you're not going to have a significant colony count. So it needs to be a concentrated specimen. I have my patients empty their bladders, wait two hours without drinking, and then do the collection. Unless they're doing a first morning specimen that's concentrated. That's where you're going to get the best idea of what's really growing. Secondly, standard urine cultures not only can be handled improperly, I worry about someone walking in, giving a random specimen at 8 or 9 in the morning. It goes out in the collection box in all kinds of weather at five o' clock, when everyone leaves the office. The courier comes at 8 or 9 at night. It gets delivered to the lab by midnight. It may not be plated until 4 or 5 in the morning, and who knows what bacteria is dead or alive by that point. Also, we know that standard urine cultures will only grow bacteria that is still alive. So we may have lost some significant pathogen identification right there. Next, we know that if more than two pathogens grow on the plate, it is generally thrown out and reported as contaminated. And that shows a lack of understanding of biofilms, which are like apartment buildings with lots of different residents. We also know that if anything fungal will grow on the culture plate. Oh, must be contaminated, throw it out and report it as contaminated. Whereas in biofilms, there can frequently be a fungal component which can make people every bit as symptomatic as bacteria. By the way, the standard urine cultures favor fast growing bacteria and we know that that's not the case. I think Galaxy Lab trying to grow Bartonella takes two months. So we know not all bacteria are rapid growing. E. Coli frequently comes up because it's very fast growing and if you don't grow 100,000 colonies within 24 hours, it's not considered significant. Well, I don't quite know who came up with that theory, but that's what they operate under, that if you don't have 100,000 colonies in 24 hours, it couldn't possibly be causing you any problems, really. So there's a lot of issues with standard urine cultures that make them unreliable. Some estimates have said that you miss 30% of what's really there with the standard urine culture. Let's talk about the 21st century PCR or polymer chain reaction I think was started in about late 70s, early 80s, but it didn't reach commercial value until more recently. And you take primers that are specific for each pathogen and usually most Labs can run 24 cells at once. And that means they're limited to being only able to check for 24 pathogens at a time. One of the labs that I've utilized, pathnostics, can run 48. They're doing two groups of the cells of 24 and you're actually looking at pieces of DNA that have been duplicated and you get enough of the sequence that you can match it to the DNA of the pathogen, the bacteria. It's highly accurate. You can get pretty fast turnaround. However, the problem I'm finding with most of the labs that do molecular testing and utilize PCR is, is that the organisms that they have chosen to test for are the ones that you commonly find on a culture plate. So if you're dealing with a biofilm, you're dealing with someone with chronic infections. Those aren't necessarily the ones that you're going to find in their biofilms. You will oftentimes find other pathogens that are not commonly identified, either because they're slow growing or, or because they're not the ones that the general population with occasional acute UTIs are going to be having on the culture plate. That's the first technology that's utilized is pcr. It's excellent, it's very specific, has high specificity, high sensitivity, it's very reliable. Now actually, before PCR came along a few years earlier, someone came up with the technology of next Generation sequencing ngs. NGS is higher in the technology required to produce it. The equipment's far more expensive, and it takes much longer to get those results. With the next generation sequencing, you can actually take these strands of DNA that are recovered from this specimen and match them to an international database. That's what MicroGen DX is doing. They are taking a specimen, in this case urine, recovering all the DNA that's not human. They run a quick PCR test for level one results that look at 22 different pathogens, but only these are all bacteria except for one, which is fungal, Candida albicans. But then they take all of the DNA, they run it through next generation sequencing, they compare IT to over 50,000 sequenced pathogens and report that on a level 2 report, 5, 7 days later. Using that, we are finding 100% of these patients who were diagnosed with IC, often based on negative urine cultures, have a truckload of pathogens that are actually there, but the culture wasn't finding them. The same with chronic urinary tract infection patients. These people are not really getting repeated acute new UTIs. They have infections walled off in biofilms which reproduce, although more slowly because they're in the biofilm, and periodically shed off into the urine and cause acute symptoms. The patient gets diagnosed with another acute UTI and are treated as if it were an acute uti, which may beat the infection back for a little while, but not really eradicate it. And therefore it just surfaces over and over and over again.

So in these chronic UTIs, what are some of the common microbial issues or overgrowths that you see in your patients when you're using the pcr, when you're using this next generation sequencing, are we generally seeing bacteria or virus or fungal organisms or parasites, or is it a combination of all of those things?

Well, there was a lab that has since closed that was testing urine for bacteria, fungi, parasites and viruses. It was very expensive, and I didn't have more than maybe 20 specimens that were ever sent by patients. They were finding predominantly bacteria, occasionally fungi. We never found any parasites, and we did find in a few patients some viruses in the burkholder family. Some of those viruses are still being checked for by pathognostics, but nobody else is routinely checking for viruses or parasites in the urine itself.

You mentioned earlier that most commonly people think of chronic UTIs as being associated with E. Coli. Is that true? You've already really kind of answered that. And then what is the most common bacteria that you see in these chronic UTIs in IC and then extending on that, how is that bacteria acquired?

Oh, well, that's the right question. Let's go back to the CVS mutation and the person producing more ammonia than other people. If you have more ammonia that's in the bladder mixed in with the urine, you're going to have a higher urinary ph than most other people. I recently found a fascinating study that talked about urine PH correlated with which bacteria were found, it turns out in the more acidic, and we're talking a very narrow range here, I think 6.4 to 6.7 in the more acidic urine. It favors the growth of E. Coli. E Coli is what they say 90% of people with UTIs have. Now how much is that is because of the urine ph. How much of that is because of it being rapid growing on a culture plate? That's debatable. But with the higher ph, the pathogen that's favored is enterococcus and that's what I'm finding closer to 90% of the time in my chronic UTI IC population is the enterococcus. Now yes, occasionally E. Coli is in the mix. Sometimes we have to treat that and then on the repeat test we find the enterococcus and that's the one that tends to be the persister longer term. I think that is because of the.

Ph issues when we think about complex chronic illnesses. Certainly the chronic Lyme conversation often comes into the stage. These vector borne infections are things like Borrelia and Bartonella babesia, maybe other protozoans. Do they play a role in these conditions? And then a listener asked about urea plasma or mycoplasma as a contributor as well.

I will tell you first of all that next generation sequencing will identify mycoplasma and ureoplasma and maybe they come back about 5% of the time and absolutely can give people urinary symptoms. I don't think those are the predominant players. Those aren't the ones that were commonly coming out of the biofilm once we start disrupting them. The tick borne infections are an interesting problem. The piece of my background that I didn't give you was that I had never had a urinary tract infection in my life. So my history is a little bit different than 99% of my patients. Mine started after a tick bite and that was the first symptom that I had was the, besides the fever, the funny black dot on my abdomen with a big round red circle around it. And this was in the 1970s, before the word Lyme disease that ever even been coined. An area I did not want to be a pioneer in anyway. So Lyme can absolutely be a player and a trigger for interstitial cystitis. And my urine cultures came back negative from day one. I had three patients who had a positive Lyme diagnosis who also had interstitial cystitis, which is why they contacted me. They were getting bladder biopsies done by the urologist. And that's the way they used to diagnose ic, was with a bladder biopsy and not just the visual inspection or a series of negative cultures. And I was able to talk with the urologist and have them agree to send some of the biopsy specimens off to two different labs that did DNA testing. All three patients, both labs, Lyme was identified by PCR testing as being in the bladder wall. One of them had protozoa, one of them had Babesia, none of them had Bartonella. Two of them had already been treated for Bartonella. And one of the practitioners that I'm working with recently had a microgen test come back with Bartonella henseli come back in the urine. But that's the only one I've seen. And I think that's mostly because the Bartonella is hemabartinella and it attaches to the red blood cells and isn't necessarily shedding off into the urine. So, yes, the tick borne infections absolutely can be a player. And I will tell you that a number of my patients, once we clear up the infections that we can find with the molecular testing, if they're still symptomatic, it's because they either have Babesia that didn't come back on a positive test because Babesia is very hard to get reliable diagnostics for, or they have mold mycotoxins there. The Babesia symptoms are a real sleeper. Most of my patients will not report that they're having any Babesia symptoms until after we get the Lyme off the playing field and then they tell me they're having night sweats or they've been diagnosed with exercise induced asthma or air hunger symptoms. I think that the Babesia, it gets competitively inhibited until later down the treatment process. But treating with an herbal for the Babesia 100% of the time has eliminated the last remaining vestige of bladder symptoms in this population.

Let's outline why these infections become chronic. What are some of the key considerations when one has chronic UTIs that eventually really need to be explored to prevent that development into ic? And what are some of the mechanisms behind why the infections become chronic in certain people?

Certainly part of this we did cover. You know, they become chronic because their immune system isn't working well because of lack of vitamin D. They become chronic because they have a CVS mutation or variation in which they're making a lot of ammonia. The gag layer gets destroyed, and that's a happy breeding ground for bacteria. One thing that I did bring up earlier about a negative culture that I don't want to forget is, is that because these people have had repeated courses of antibiotics, certain classes of antibiotics, particularly the beta lactams, have the capacity to drive the bacteria into a cell wall deficient form. Well, we know this, that Lyme does, that the Borrelia doxycycline can drive the spirochete into a cyst form. We also know it exists as an L form or cell wall deficient form. Well, guess what? Other bacteria have that capacity as well. And with long term courses of these classes of antibiotics in particular, it will drive it into a cell wall deficient form. And cell wall deficient bacteria cannot grow on a standard urine culture plate. Let's talk a little bit of physiology. Anytime you have an infection or inflammation, the body's normal, healthy response is to produce more fibrin to try to wall the infection off. Everybody does that. This production of fibrin, which is like that spider web stuff that things attach to that make a blood clot, is very closely regulated by the body. It's like having an accelerator and a brake on a car. You want to move it at a steady speed. You don't want to go too fast, you don't want to go too slow. The same thing happens with this regulatory system within the body. You have the coagulation pathway, you have the fibrinolytic pathway. Fibrinolytic, meaning you're going to break down fibrin and this balancing act takes place so you don't make a huge clot and die, and you don't break down too much too fast and have a bleeding problem. Most practitioners learn the coagulation pathway. Very few were ever exposed to the idea that there existed a fibrinolytic pathway. But there are certain genetic reasons why some people don't do as good a job as others in breaking down the fibrin. The connection here with these infections is that fibrin is one of the major components of biofilm. You get the connection here. You have an infection, you produce fibrin. The fibrin goes into biofilms, it walls off the infection and the end result is a chronic infection. That's the pathway that has to be realized that not all infections are acute, that many people walk around with chronic infections and don't even know it. Maybe the body has done its job in walling it off sufficiently that it's not going to be a problem for them. But this bacteria within the biofilm can still reproduce, slowly spill out and give people bladder issues.

Is there an aspect of these chronic infections that can be persistent due to re exposure from intimate partners? And are there times when a spouse or partner needs to be treated as well?

Yes. Glad you brought me back to that point. It turns out that one of the sources of ongoing infection can be simply a woman's vagina. Women who have had lots of courses of antibiotics maybe have wiped out the healthy Lactobacillus population that competitively inhibits bad bacteria or pathogenic bacteria. They have fostered the growth of certain strains of fungal infections. Candida glabrata tends to be a very common problem because they've been given lots of courses of fluconazole. And Candida albicans may not be there, but this Glabrata species that's azol resistant has now taken over. Women who are postmenopausal don't have healthy vaginal environment with a thick enough vaginal tissue that's moist enough to sustain the growth of the Lactobacillus. And they become colonized with pathogens and those continue to seed into the urinary tract. Well, sexual partners also can have a low grade chronic prostatitis. And when they have sexual relations with their partner, those vaginal tracts become infected and then that can seed into the bladder as well. And many of my patients say that their symptoms flare after intercourse. That's an index of suspicion that their sexual partner should have their semen, not their urine. The semen checked. And as long as we're talking about men here, let me just do a little parentheses. Men with urinary tract infections should always have their semen checked as well. About 10% of men have retrograde ejaculation. And every time they ejaculate, this bacteria goes into their bladder as well. If you're only treating the men for the short course of antibiotics for urinary tract infection, when the source is actually the prostate requiring a longer course of treatment, you will never clear the urinary tract infection. It too will keep coming back for the male. So Microgen does a women's complete kit, which includes testing the urine and vagina. It's just a swab. The woman can do herself. And the men's complete Kit has tests the urine and the semen. And so it's a good idea when you're first starting to do molecular testing in this population, whether male or female. Now let's check beyond just the urine and the bladder to see where this infection could be coming from.

I mean, you kind of have to wonder with males as they get older, often developing prostate cancers. The contribution of low grade infection over years and decades. The damage that you mentioned to the bladder wall, for example, potentially similar things happening in, in this context. How many cases of prostate cancer could potentially be avoided? If we were thinking along these lines.

I've had the same concern. We know women who have certain chronic infections of the cervix develop cervical cancer. It would make a lot of sense to me if you had a low grade chronic infection in the prostate that that could likewise turn into abnormal cells and malignancies.

I wanted to touch a little bit on genetics and epigenetics. We've already touched on CBS mutations. You mentioned some of the coagulation genetics. I don't think we've touched yet on detoxification mutations in the realm of glutathione, for example. But what are some of the key genetic contributors that you see in your patients that we haven't already touched on?

Well, I don't think we went into enough depth on the genetics with the biofilms for my satisfaction.

Sure, yeah, great, go back to that.

I think that this has been. This was actually the major game changer for me. There's a gentleman named David Berg, B E R G and David started a lab in Phoenix called Hemex Lab. Hemex Lab was bought by Esoterics when David retired and Hemex became the hematology division of LabCorp. That only happened about five and a half years ago. And why this is important is that the hematology handbook for practitioners put out by LabCorp was about a quarter inch thick. Then they acquired David's material through esoterics. And within a month, their hematology lab for Handbook for practitioners became over an inch thick. The reason is that David started looking at not just the genetics behind bleeding disorders, but the genetics behind coagulation disorders. The coagulation disorders or variations or genetic mutations. To loop back to my previous comment, deal with people who make fibrin and don't break it down. Well, and so this extra fibrin goes into biofilms, but it also goes into atherosclerotic plaque. And these are people who end up with cardiovascular disease. I became really interested in fibrin because of the biofilm connection. And it turns out that 20% of the general population genetically have one of three different hypercoagulation mutations or variations. In my chronic UTI NIC population, it's closer to 70%. At this point I was getting about 60%, but I'm not sure I was necessarily checking everybody, particularly the patients. I had done before meeting David Berg and noticing the connection. One of the the centers that is using this testing in their chronic population now is telling me that they're finding 70% of their chronic UTI IC population has one of these three variations. Let's talk about them and why it works to make spectacular biofilms here. Biofilms can be made by pathogens, by the way. I'm not saying the microbiologists are off base on that particular particularly. Klebsiella and pseudomonas are notorious for making their own biofilms. But people also make BioFilms now. Leiden Factor 5 L E I D E N Factor 5 Most practitioners have heard of and they know that these people have a high incidence of heart attacks and strokes. Well, it turns out that when you make extra fibrin coagulation pathway, your body has two main players in the fibrinolytic system. The first one is TPA tissue plasminogen activator. TPA is the clot buster. If you go to the ER with a heart attack or stroke, you might be given to break down the clot before it can do more damage. The second big player in this fibrinolytic system is called tat, T, A T or thrombin antithrombin complexes. If you have Leiden factor five, when your body makes extra fibrin, your body's supposed to kick in with making a lot of TAT complexes to break down the extra. And if you have Leiden factor five, you cannot make enough TAT complexes to do the job. Maybe it'll go up a teeny tiny bit, but not sufficient to really break down all the extra fibrin. So the biofilms become larger, more dense, stronger, better able to wall off infection. There's another genetic problem that most people haven't heard of called a pi1 p a I hyphen one plasminogen activator inhibitor. And pi1 is considered so rare that even the hematologists in my experience haven't been checking for it. I had a number of patients who had had a history of heart attacks, strokes, deep vein thrombosis, pulmonary emboli. They had all been worked up by hematologists who told Them, they had no genetic predisposing factors. It was just kind of a fluke that that's happened to them. And when I checked them, all six of them had a PI1 mutation. So I know that at least their hematologists were not checking for it. And I guess condition is rare because if you never check for it, you never find it. I've had over 150 patients with the PI1 mutation, so maybe it isn't that rare after all. In any event, PI1 likewise prevents the upregulation of Tat complexes and and the biofilms become quite large. The third genetic piece is a little bit different in that it's just simply a straight number. Either it's high or it's not. And that's lipoprotein A. Lipoprotein A is a form of bad LDL cholesterol. And if it's elevated, and I think there's about 10 genes that are related to this, so you don't need to do this genetic test. You just look. If it's elevated, they have a problem. If it's not elevated, you don't anyway. The lipoprotein A binds to tpa. It has a little bit different mechanism of action in the inability to not effectively break down the extra fibrin. But the end result is the the same. Whether you have a Leiden factor 5 PI1 or elevated lipoprotein A. You are going to make biofilms that are more extensive than other people who don't have the rest of the 80% of the population. So for the vast majority of these chronic UTI IC patients, you need to break down the biofilms based on their genetics if you expect any antibiotic to effectively get to where the infection is walled off. Bill Costerton, the father of biofilms, published a brilliant article in 2011 that actually demonstrated that antibiotics do not do a good job penetrating biofilms. And so what you end up having is a lot of drug resistant strains developing. It's like vaccinating the bacteria so they've gotten just enough exposure to develop resistance, but not enough to actually kill it.

My opinion is that in conditions like chronic Lyme disease, that this whole coagulation or hypercoagulation issue is probably the most overlooked area. If you talk to people that have been treating for years and ask about their coagulation status, testing and so on, most of the time they are unfamiliar with it. And so I had the great fortune to have learned some of this from David Berg and then also from Dr. Ann Corson and I do think that it's critical and the connection that you're making as well to kind of a spectrum here also that you have these coagulation issues that then also become biofilms, making these infections really chronic. So I think it's a really critical area for people to talk with their practitioner about, to do the testing to make sure. For me personally, it was a very significant area to explore. And part of what held me back, every time Babesia would flare up, the whole coagulation thing would go off the rails again, and we kind of need to dial that back in. So I urge people to really listen to the prior podcast with Dr. Ann Corson, talk with your practitioner about this. It is also applicable in the chronic Lyme arena as much as in this conversation that we're having here today.

Other areas that I'd like to put on the radar as well. I think the biggest one is fibromyalgia. Now, contrary to the Lyrica commercials that say that it's believed to be due to overactive nerves, I have a different theory. I've had about a dozen patients with fibromyalgia diagnosis, and 100% of them have had one of these three coagulation problems. And I think the connection here is that the fibrin starts clogging up the microvasculature. All of these people will report cold hands, cold feet. You shake their hand, at least we used to pre Covid, you could tell their hands were cold as the microvasculature starts clogging up. And then some of the little bit larger vessels start clogging up with fibrin, you don't get as much oxygen to the musculature. And so what happens is these muscles have to revert to anaerobic metabolism. They start making a truckload of lactic acid. And anybody who's been a weekend warrior knows how you feel on Monday morning after revisiting the gym that you haven't been to for two months or deciding you're going to mulch your yard or whatever. That's how fibromyalgia people feel. You know, their muscles are killing them, and it's because of this lack of adequate oxygenation, because the microvasculature is not able to transport the oxygen to the muscle tissue. So with all of these patients, when I put them on, my favorite fibrinolytic for people with these genetic problems is lumbrokinase. It's marketed under the name of Belooki from Research Nutritionals. But when you get them on A fibrinolytic that can start breaking down this fibrin. Lo and behold, after a few months, their hands and feet start getting warm again. And after six months or a year, what, fibromyalgia. Now, this can take longer if people are older and this process has been going on their whole lifetime. But basically, I have successfully reversed 100% of fibromyalgia in every one of these patients. It's all related to these coagulation issues.

Yeah, Buluc is definitely my friend. It is still something that I use very low dose for maintenance of my own health. The oxygen delivery piece, the nutrient delivery as well. And then I also think that if you have these coagulopathies, that you probably also are less able to remove toxicants from various areas in the body as well. And so we have less oxygen, less nutrition, and less ability to take out the garbage, so to speak. And that that kind of becomes this vicious cycle. Another area that I know is one that you love and is one that I'm aware of, but quite honestly need to learn a lot more. I'm very excited to hear your thoughts. And that is NRF2 and the role of NRF2 in chronic UTIs. And I see. What is it? And how does activation of this NRF2 pathway help people dealing with these conditions?

Okay, rather than get into a long technical discussion of what NRF is, I read about it on Wikipedia, and it's this biochemical thing in your body. Let's just say it's a supplement with magic properties. I first got the connection and introduction to NRF2 by a speaker who was promoting that product as a way of shunting more of the homocysteine and cystathione into cysteine and less into ammonia. Well, that got lots of points in my mind, because, yes, if you have too much ammonia, let's make more of it. Produce cysteine so you can make more glutathione so you can detox better. That gets several important points. Then I learned that NRF2 has the amazing ability to down regulate NF Kappa B. And I'm not an expert on NF Kappa B, but I have learned that mold toxins, particularly some of the aflatoxins and ochratoxin A, will upregulate NF kappa B. And that's why those particular mold toxins cause kidney damage. And nrf2 or nrf2 will down regulate nf kappa b. So it helps protect the kidneys from mycotoxin damage. So I think anybody with chronic UTIs and mycotoxins would benefit from NRF2 being added to what they're doing. Then the end of October this year, there was an article that appeared that I want to say it was in Science Direct, but I could be wrong on the reference that talked about NRF2 and its ability to prevent bacteria from becoming embedded in the bladder. The studies were only done with E. Coli, so we don't know for sure its effect with other pathogens. But I think that's very encouraging, that NRF2 does have some positive effect on preventing infections from becoming embedded in the bladder wall, hence becoming chronic. They did not explain the mechanism, but it sounds like a winner on all three fronts to me for the ability to reduce ammonia production, protect the kidneys from damage from mycotoxins, and potentially to reduce infections from becoming embedded.

And that ammonia is also, as I'm understanding, part of what destroys that gag layer that you mentioned that leads to more damage and eventual movement into that interstitial cystitis arena. And so in people that have chronic UTIs, dealing with this ammonia component potentially is another way to keep them from progressing down this spectrum, correct?

Exactly. And let me just mention one thing about this pathway here. When I first started thinking about this, I wanted to see, to validate my observations about the ammonia production in this population, and I started trying to measure it. Well, lo and behold, a blood level of ammonia is very unreliable and even a urine level isn't far behind because it depends upon how much protein you ate at the last meal and how many hours prior. And it's like trying to nail down a moving target. So there aren't any studies that will document high ammonia levels in this population for that reason. The other supplement, however, that is helpful is ornithine. If you look at the urea cycle on the methylation pathway map, that's the very first one on the far left. You see that ornithine, which is made by the body, will help clear the ammonia out in this metabolic pathway. Ornithine is a supplement over the counter, cheap, comes as 500, 700, and I think I saw 750 the other day, milligram dose. So it's well established that ornithine will reduce ammonia levels in people with liver failure. So we know it works to reduce ammonia. I've been recommending it that this population should take some ornithine in order to reduce and clear the ammonia that does make it to their bladder. I don't think it's going to cure anybody, but it may slow down and reduce the damage done to the bladder wall. If someone consistently takes this. Bedtime is when the ammonia will be at its highest concentration. So that's a good time to take the ornithine. It can be taken three times a day. And because high ammonia can also give people brain fog. I have had some patients who complained of brain fog. I've suggested to them that they take the ornithine more than once a day.

And.

And a couple of them did report back to me that their brain fog was gone.

On the mycotoxin conversation, you mentioned that the mycotoxins can increase NF kappa beta, this inflammatory cytokine, potentially leading to kidney damage. That NRF2 support can be helpful here. Is it helpful in the removal of mycotoxins or is it more mitigating the damage that the mycotoxins toxins may be inflicting on the kidney, for example?

I think it does both. I think it certainly mitigates the damage by downregulating the NF kappa B. But I think because it shunts more of the cystathione into cysteine, you're going to get better glutathione production by the body because it has more building blocks. Now, is there a better way of doing this is the question. Many people, including myself, have significant mutations with the GST genes. So I'm not sure, no matter how much cysteine I pour into my body, how much glutathione am I really going to be able to make? And I know a number of my patients have GST mutations as well and they don't detox well, probably because they can't make glutathione well. So yes, making more cysteine would help with the detoxing of the mycotoxins. I'm a big fan of the transdermal glutathione patches or a topical glutathione product. I know people like liposomal glutathione orally. I'm not wild about the taste, but there are alternatives and I know with the topical you don't have to worry about it being broken down by the GI tract.

I wanted to come back briefly to the biofilm conversation and ask if treating biofilms, does that potentially help to liberate organisms that then make it easier to detect in some of these PCR and next generation sequencing tests that you talked about? Or is that not necessary with these technologies?

Oh, I am really glad you brought that up because I failed to mention it earlier. If you can only find free floating or planktonic bacteria in the urine. You're not going to find the vast majority of what's walled off in a biofilm. You may be only seeing the tip of the iceberg, as it were. So taking a biofilm disruptor initially for five or seven days before collecting the urine is going to give you a much more reliable test result. The other thing that's helpful is, or almost I should say essential, is to stop anything that's mucilaginous. Elmeron, the pharmaceutical, puts a mucilaginous coating on the bladder wall, prevents the acidic urine from further irritating the bladder and people feel better. Unfortunately, it's also been linked to cases of blindness, so I don't recommend symptom management with Elmeron. There are over the counter supplements like marshmallow root and aloe vera, which also have the same mucilaginous properties that give symptom relief. Those all should be stopped a week before you do a urine collection if you want to have a better chance of finding what's really there. Now, as far as starting on biofilm disruptors, there is one that I prefer. Kirkman Biofilm Defense is a good generic biofilm disruptor that is safe. I don't like the ones that have EDTAN being used long term because it depletes minerals. But the Kirkman Biofilm Defense, the Kirkman Biofilm Defense can be taken long term without any, you know, untoward effects. Is a good one to start with until you know the genetics. If you have pseudomonas or Klebsiella that has shown up on cultures or prior molecular testing, their priority one puts out a product called Biofilm Phase 2 Advanced that has bismuth in it, which has some excellent studies showing that it helps prevent those particular pathogens from making their own biofilms. I think it probably also works on H. Pylori biofilms because it's part of the multidrug protocol used for H. Pylori is giving a bismuth product. If somebody has any of the genetic mutations we talked about earlier with pi1 Leiden factor 5 or lipoprotein A. I think that the belucchi, the lumbrokinase, which is 12 times more potent than nattokinase and many times more potent than the other fibrinolytics, would be the direction to go in. I particularly want to point out to people who have concerns about fibrinolytics that it's not an anticoagulant. Anticoagulants stop the coagulation process further upstream. The fibrinolytics break down the fibrin after it's already been formed. It will never cause spontaneous bleeding like an anticoagulant can. Yes, if you get a cut, you might bleed a little bit longer. Women with their menstrual cycles, if their bleeding becomes a little heavier, can stop the fibrinolytic for those couple days because it has a much shorter half life, and then resume it when their period is lighter or at the end. But a fibrinolytic is very, very safe.

Extending on the vitamin D conversation, how is vitamin D connected to cortisol and then to progesterone? And is it common to see estrogen dominance in this population, or even pcos, for example, or endometriosis? Is estrogen dominance always an excess of estrogen or can it be the result of low progesterone?

Oh, you asked such brilliant questions. Vitamin D has a lot of uses in the body. It's involved in over 10,000 biochemical processes, the neurotransmitters converting T4 to T3. Vitamin D is really, really important. One of its jobs is that it's the precursor of 17 hydroxyprogesterone. 17 hydroxyprogesterone is the precise precursor of cortisol. So if you're looking at a population who is up multiple times at night to urinate because of these chronic infections and inflammation of the bladder, you're looking at somebody who has chronic pain because of the bladder issues. You're looking at somebody who simply has stress. In life, there's going to be a lot of extra demand for cortisol production. And so the 17 hydroxyprogesterone is going to shunt into the cortisol production. And I believe that the body does have sort of an order of operations. It may take this to support the adrenals before it thinks about shunting some of this to the thyroid or to the bladder wall or the 17 hydroxyprogesterone also is needed to make progesterone. And so if your body is focusing on keeping your adrenals upright and functional, or you're not making enough 17 hydroxy progesterone because you have a deficiency of vitamin D, then you're not going to make as much progesterone. Now, I'm going to circle back to these 156 people who did the 23andMe. I didn't mention earlier that one thing that 100% of these people also had a variation or mutation on was Cytochrome P451B1, 100% of them had a genetic variation mutation at that. Actually, there's three of the genes that 23andMe checked for. For 1B1. Everybody had at least one of them that had a problem. Now, some of the cytochrome p450 genes, these enzymes in phase one liver detox are upregulating and some are down regulating. If they're down regulating genes, they just don't work as fast. And therefore trying to metabolize a drug that would use that gene would stay in someone's system longer and they could have more side effects. But if they have an upregulating one that has a mutation in it, it's like trying to type too fast. You're going to make mistakes. And that's what happens with the estrogen estradiol that's predominantly produced by the body. Instead of being metabolized and cleared. If you have a 1v1 mutation, you will make it into estrone. Estrone is the form of estrogen that has been associated with estrogen dominance and breast cancer. These women who have the chronic bladder issues have a high incidence of endometriosis. They have a higher than the general population incidence of polycystic ovarian syndrome, or pcos, because they aren't making enough progesterone to balance the estrogens. And the estrogens that they do have are often higher levels proportionally than it should be in the estrone form. With my women, I'm checking their hormones. I don't do a total estrogen. I will look at the estradiol and the estrone and the progesterone levels and see how well they're balanced or not.

Let's talk about the potential connection between chronic UTIs IC and Mast cell activation syndrome. Is there a role for stabilizing mast cells for reducing histamine to improve patient symptoms? And can things like mast cell stabilizers or ketotifen, for example, can those be helpful in this population?

I got a backup to ancient history. I mentioned early on about my association with Dr. Paul Fugazzato, the PhD microbiologist who was using the soy broth culturing technique to find pathogens in this population that had negative cultures. Dr. Fukuzato visited me in the D.C. area back in the late 1980s. And one of the things that we did, we had a number of labs that we were visiting. He had a lab there who was willing to learn his culturing technique, who took over for him for many years before we had molecular testing. But One of the other places we went was Columbia Hospital for Women, and they were in D.C. there was a urologist there who had a lot of IC patients, and he and I spoke frequently, and I had a good relationship with him. And he invited Dr. Fugazato to come down and share with him what he had learned. And we were invited into the basement of the building where the pathology lab was, and we met the pathologists, who on his shelves had boxes and boxes and boxes of slides of bladder biopsy specimens. It turns out that one of the characteristics of a bladder biopsy specimen to look for and diagnose interstitial cystitis was the predominance of mass cells. You could see under the microscope when you were looking at this biopsy specimen. And so the interstitial spaces is the area bathed with lymphatic fluid behind between the cells of the bladder wall. That's where we get the name interstitial cystitis, because these spaces would be swollen, congested with lymphatic fluid full of mast cells. You could see the swelling, inflammation, all the inflammatory markers were going on. Now, I want to give you one other side thing before I talk about the mast cells. Dr. Fukasato, as a microbiologist, said, where's your immersion oil? The pathologist got a puzzled look on his face and said, oh, I never use the oil immersion lens on my microscope. That's a higher resolution than I use for pathology to look at structures. I went down the hall to the micro lab, grabbed the bottle of immersion oil, came back, we dropped it on the slide, we put that lens on the microscope, and lo and behold, we could see bacteria in the bladder wall. That was another piece that the puzzle for me to continue pursuing my quest for treating interstitial cystitis as an infection, because I saw that bacteria in the bladder wall of the biopsy specimens, and the pathologist never looked at that resolution on the microscope, so had to put that in there. Okay, back to mast cells. Why are mast cells present? Well, mast cells go to areas of infection, for starters, and inflammation, and they pump out histamine. That's their job. And the histamine causes redness and swelling and an exacerbation of symptoms, so you get more blood flow so the phagocytes can go and destroy the bacteria so they have a functional purpose within a person's body. And you're calling on my knowledge base from long ago, but that's my understanding. It's what I remember. So how do antihistamines play a role in this Population? Well, for years, many, many patients were put on amitriptyline to help manage their symptoms. And it did work fairly well, because if you given antihistamine and you reduce the mast cells or you reduce the histamine put out by the mast cells, you aren't going to get as much inflammation and symptoms. So mast cell management with some of the higher techier antihistamines helps with symptom relief. Is it going to address the root cause? No. Is it going to cause a cure? No. Some people respond well to leukotriene inhibitors like the singulair, the monoleukase cast, however you pronounce that anyway, because the leukotriene inhibitors, that's another pathway of inflammation besides the histamines. So, yes, people will respond positively to managing some of these inflammatory cytokines. But is that really going to cure them? They're still going to be triggering it as long as there's infection.

Is there a Correlation between chronic UTIs and IC and hypermobility syndromes or Ehlers Danlos syndrome?

If it weren't for the fact that I didn't have about five or six patients who had EDS diagnosis, I would say no. But I'm suspicious there is. Do I know what the connection is? Not really. The one thing I can think of is, and correct me if I'm wrong here, don't EDS people pretty universally have significant MTHFR mutations?

I would think so, yeah.

And if you have the significant MTHFR mutations, particularly the C67, you may be making more homocysteine, which in combination with the CBS would, would make more ammonia. And you've, you've fed into that pathway. So I don't know enough about EDS to know what genetic pieces there might overlap, but I'm suspicious there are some that do. I just don't know what they are.

One of the common issues that people with these conditions deal with is significant pain and discomfort. We know that oxalates can, because of their sharpness, that they actually can shred tissue, kind of like little pieces of glass, can lead to significant pain and discomfort as well. We know they can come from food, but they can also come from fungal overgrowth internally. Some people now refer to oxalates as secondary mycotoxins. Wondering if you've seen a connection between oxal oxalates and chronic UTIs and interstitial cystitis. Is that an aspect that you consider.

As part of treatment back in the 1990s? You're getting the advantage of someone who's been here Way too long.

I love it.

Back in the 1990s when people were on fishing trips for other causative reasons besides infection, because everybody knew it wasn't an infection. Most people still think that the case. But anyway, the oxalates became a huge player on the radar in the IC population as a whole, and many, many people started getting tested for and treating for oxalates. And it did help a significant small percentage of this population. In my experience, because I'm treating bacteria, because I'm treating fungal infections, I have seen not that much oxalate factoring into all of this picture. Certainly if someone has had a history of kidney stones, I want to know what their oxalates are like on microscopic urine. You should be able to see the crystals. Certainly the organic acid test from Great Plains is going to tell me about the oxalates. I will say that the oxalate crystals can scratch and damage the bladder lining and be a portal of entry for infection. And so it does need to be considered in one of the holes. Is it one of the bigger holes? Not in my experience, but that doesn't mean it can't be a contributing factor for some people.

I want to take another little diversion with you because you have so much great information. I know this was very interesting also, and that is the diversion into Lyme and mold and CD57. And we know CD57 was used decade or more ago as a marker in the Lyme arena. It's somewhat fallen out of favor because it's not incredibly specific, but you've kind of made some correlations between low CD57 and different immunoglobulin subclass deficiencies. Wondering if you can tell us a little about that. And then what percentage of your chronic UTI and IC patients do you think are also dealing with either Lyme disease or mold illness?

CD57 is a natural killer cell, and natural killer cells can be very, very specific. And I know that Raphael Stricker tried to associate it with Lyme disease and I think that they almost got it right. My Observation is the CD57 level does not correlate with how sick a person is. It correlates more closely with how long it has been since the original infection. I used to play a little game with my patients in which if I would see a low CD57 I could usually nail down within a decade when they got their tick bite. And the longer had been, the lower the level. I like to see it around 200. I will caveat is that with children I often with lyme kids with Lyme. I'd also often see them in the 3, 4, 5, hundreds. They have a paroxysmal response with that piece of the immune system to the Lyme. In any event, if somebody's number and when you get older, it goes down, maybe it's 150 or so, but if it's under 100, I can almost 100% of the time either find Lyme or mycotoxins. And so then it kind of became, I don't want to say a game, but it became a puzzle for me to look at. How could I figure out which one was worth pursuing? Because the testing that I use is not covered by insurance generally and I don't want to waste the patient's money. So let's look at how we can figure this one out. Certainly the questions on the history if they had a known tick bite, had they lived in a place that had a roof leak, pipe leak, water damage, a flood, that would be kind of obvious what directions to pursue first. But I started noticing that if I looked at their immunoglobulin G, that usually the lower the CD57, the lower the IGG. Then I started looking at subclasses one through four and there's nothing in the literature on this. This is simply an observation from looking at a lot of these labs and a lot of patients for a lot of years. And it wasn't 100% foolproof. It was just an association that if there was a mold issue, IGG subclass 2 tended to be on the low end. If there was a Lyme component, IGG subclass 3 tended to be on the low end. And if they were both low, I better check both of them. It was a useful association. I would never use that to be diagnostic in and of itself, but I thought that was an interesting correlation, that the CD57 does reflect the IgG levels and which subclasses can take a hit.

Then using this approach as well as all the other evaluative tools that you have in your population of UTI and IC patients, what would you speculate in terms of the number of them that are, or the percentage of them that are dealing with chronic Lyme disease or with mold illness as a contributor to their overall condition.

I don't have hard statistics on that, but I would say off the top of my head, the tick borne infections, probably about 15 to 20%. The mycotoxins did not really get on my radar until much later in the game. I was speaking at the Forum for integrative medicine with Dr. Neil Nathan. And that's what put the mold toxins on my radar hearing his talk. Then when Great Plains came out with its mycotoxin urine test, I started doing that testing and discovering that my sickest patients and the ones that still had persisting symptoms even after we cleared out the infections found on the urine testing. Pretty universally those last guys standing had a mold issue. I should differentiate the difference between finding fungi in a urine test versus finding the toxins from the mold on a Great Plains urine test. Those are two different things. Just because you don't find fungi DNA in the urine from microgen DX does not mean that that person doesn't have a mold problem. Most people with mycotoxin or mold illness, they have inhaled the toxins from the mold spores in the environment. That does not necessarily mean that the mold itself is in their body. Now I have had a few people that when we do a microgen nasal test have found the same mold spores in their sinuses. And I get a compounded anti fungal nasal spray to address that. I've had a couple of people with chronic cough that the sputum was filled with the same mold that was in their house. I had some children after Hurricane Harvey in Houston who had chronic respiratory issues. Lo and behold, we weren't able to get sputum on the children. We did the nasal and we found the same fungi that was being found by army testing of the children's bedrooms. We ended up doing a nebulized glutathione as a biofilm disruptor and then a nebulized amphibious pitresin B to treat the mold in the lungs and the sinuses with the mask in the children very successfully.

As we move into our last several minutes together, I want to touch on some of the treatment interventions that you found helpful. We talked about microbes such as Enterococcus, Borrelia, Bartonella, Babesia protozoans. Do you tend to address these chronic infections more with traditional pharmaceutical antibiotics or anti parasitics or are natural interventions helpful? What are some of your favorite tools to mitigate the chronic infection aspect of these conditions?

Let me just as a caveat say, I had far better success with herbals for the tick borne infections than I ever did with the pharmaceuticals. With the exception of a few that I pulsed in for the pharmaceuticals and not for everybody. The urinary tract infections are different. Ballgame. I would love to believe that everybody was created equal and that their immune systems were as robust as everybody else's and that if I simply produce the correct environment in their body, their own body could get rid of these infections. That's not been my experience. As much as I would love to do things naturally and not have to resort to antibiotics, I have had not good success with that approach at all in this population. I think it's because their genetics are different. They are not created the same as people who can do a good job breaking down the fibrin in the biofilms. Their bodies make far too much ammonia, causing the bladder wall damage. They can't hold on to the vitamin D as well. So there are genetic differences that make them more difficult to treat, which means that I can't treat them like an acute infection. And I do have to pull out the bigger guns in order to be successful. If somebody figures out another way to do it, hey, I'd be happy never to have to resort to the antibiotics. But the reality is I haven't been successful trying these other, other methodologies. That being said, we can mitigate some of the long term effects of that. First of all, I would never give somebody a suppressive dose of an antibiotic. Giving a sub therapeutic dose is a bad idea that at the end of the day will only result in drug resistant strains. It might suppress the infection temporarily for a couple of months, but it's always going to come back with drug resistance. We haven't fixed anything. We put a band aid on it. Secondly, I don't like the use of long term antibiotic use in which someone, and I know there's some practitioners doing this. You look at one microgen report and you give the patient the antibiotic that they're going to take for the next year. Once again, I think that that's going to drive the bacteria into cell wall deficient forms and it may suppress the infection for a while. But when they come off the antibiotic, their gut may be a mess, will probably be a mess and they will have other pathogens that have surfaced out of the biofilm that was never sensitive to that antibiotic to begin with. Are you going to give another year of antibiotics for that new pathogen that surfaced? I think it can be handled a little better. I prefer testing, doing a two week course of treatment with the appropriate biofilm disruptor based on someone's genetics and the pathogens found, and then five to seven days later retesting and seeing who the big players are next that have come out of the biofilm. So we're chipping away at the biofilm consistently and systematically and we go after the big players that come out. We don't Worry about the scrappy little 2, 3, 5% guys. We're looking for the big players. We address those and we go through this process repeatedly until we win. We get the bacteria on the run. I don't want my patients waiting until they become symptomatic again. If we've knocked the infectious load back to a low load, I don't want them waiting until they become symptomatic because the bacteria have now sat around and reproduced and we're back at square one. We just consistently chip away at it with the right biofilm disruptor and the two week courses of antibiotics. Now, there are a few of these that I don't use for two weeks. Those are more esoteric prescribing issues. But when we get a negative back, they test once a month. So we have three negatives in a row. And then I know the bladder wall has healed because that's the sensitive time. It takes about 3, 4 months for a bladder wall to repair. After you've gotten rid of the infection, it's just like a cut on your arm. The tissue isn't going to heal until you get rid of the infection. It's the same thing with the bladder wall. But during that window, when the bladder wall still hasn't completely healed, it is still going to be more susceptible to being reinfected in order to avoid some of the repeated oral antibiotics. I've worked with Randy Breton, pharmacist at Infuserve America in St. Petersburg, Florida for the past nine years, and he and I have been utilizing bladder installations with the correct antibiotic. Now, many of my patients say, oh, my urologist gave me bladder installations. Well, number one, they were doing something to manage symptoms. Heparin and soda bicarb used to be used. Before that it was DMSO as an anti inflammatory or they were using gentamicin installations, assuming that it was E. Coli. Gentamicin is only going to work on gram negative bacteria, not on enterococcus, which is gram positive. And these installations were once a week. I mean, isn't that just going to create more drug resistance? Anyway, they were doing bladder installations, but not twice a day for two weeks with the correct antibiotic based on molecular testing. We do put some EDTA in as a biofilm disruptor to punch holes in the biofilms with most of the antibiotics, but not all. And we got some really fabulous results much quicker than an oral antibiotic ever would because we're putting the antibiotic right where the infection is. So many patients have elected to do the bladder Installations, they are more expensive. Insurance generally is not going to cover them, but they get better results and faster results because we can target the site of infection.

So a couple follow up questions then. The determination around which antibiotic to use. Am I understanding correctly that the testing that you do provides a sensitivity assay as well relative to the specific bacteria, that specific patient, which things they might be most sensitive to? Correct?

That's the right question. Microgen DX will look for a number of drug resistance genes. The two that they are not looking at that I would really like them to do. One is phosphomycin, which I generally don't have to worry about because that hasn't been in the US as long as it's been used in Europe. Monerol is the brand name and so most bugs haven't seen it enough to get resistant to it. The other one is nitrofurantoin. Generally most people have been given many courses of Macrobid which is in that family and there is a lot of drug resistance out there to it as a result. That's often used even as a low dose suppressive dose for months on end. So I don't have that data for those drug resistance genes, but they do check for beta lactam resistance, esbl, methicillin, aminoglycosides, most of the other categories of drugs. So you know, and they will give you a chart based on the literature as to which antibiotics should work. That being said, I often cross check those results with the Sanford guide to see which ones are more effective. I'll take a green box over a yellow box any day now. Pathnostics is another Lab that does PCR testing, but only of 48 organisms. They do actual sensitivity testing and they will check for sensitivity to nitrofurantoin and phosphomycin. So it's a little bit of a catch 22. I start with Microgen because I want to know everything that's there. When we get down to only a few survivors remaining and the vast majority of those it's going to be Enterococcus and Klebsiella is number two. And we have, if we've been doing a lot of courses, antibiotics and we have developed some multidru resistance and I want true sensitivities. The urine specimen needs to go to Pathognostics instead of Microgen. I use microgen 90% of the time and it tells me what I need to know. But if you really want a true sensitivity test that isn't going to be thrown off by cell wall deficient forms Pathnostics will give you that piece of information more than just what's in the literature.

You mentioned these antimicrobial installations that may also contain some anti biofilm agents. Is there a place for ozone insufflation or installations of ozonated saline, for example, in these conditions?

I think there is. I just think they haven't worked out the details as well as I would like. I've had a number of patients who have tried it and it has sent them off the planet and sometimes it has taken them months to get back to where they were. I think that it's a good tool. I just think that the dosages or potencies that have been utilized in people with acute UTIs is way too much for people with the chronic bladder damage. And I'm not quite sure how to solve the problem of how much is too much for any individual patient.

In some conditions people think that the germ is the problem. I think more commonly now we also think about the host response as being part of the problem, the inflammation, the mast cell activation, all of these things. And so I'm wondering if you found tools for creating immune tolerance or integration with our microbiome. Helpful things like low dose immunotherapy or ldi, for example.

I have not had people successfully using ldi. To be honest, I haven't had that many who've tried it. I would say that phage therapy is the up and coming hot button on many of the interstitial cystitis blog sites. It used to be you could only get phage therapy in the country, not the state of Georgia. I had a number of patients who would fly there, get their urine tested, have the therapy produced based on their bacteria found, which pretty universally was in our caucus and did have good success for the next six, nine months. But then they'd have to go back. I think activating the pieces of your immune system that are going to attack the infection get a lot of points. However, if you understand that a biofilm is involved in which you have an apartment building worth of bacteria just growing the one that likes to grow out and targeting that one isn't going to fix the whole problem. We're back to if you only plug one hole in the roof of your house, your house is still going to leak. If you only address one bacteria and you've got a party going on, the rest are still going to party, even if you take out one of them.

I want to touch a little bit on detoxification. You mentioned the importance of glutathione for supporting detoxification that it can also help with reducing ammonia. You mentioned the liposomal glutathione. You mentioned the transdermal patches from Patch md, which I'm actually wearing one today because I've learned about that from our last conversation and just decided I needed to explore it as well. Anything else in the detoxification realm that you find critical for your patients? Do you use binders? Do you use sauna? Do you use biomat? What are some of the other tools to round out the detoxification component?

I am a big, big fan of infrared sauna, particularly for adults. I will not put a child in a sauna after puberty and their sweat glands are developed. That's a different issue. But I would never advise anyone to put a child in a sauna and I prefer them using biomats. I've used both infrared sauna and biomats very successfully. I have some concerns if you're only using a binder, particularly for mold toxins, that you're really only going to be binding up the portion that the person's own body has been successfully able to process. I think using a biomat or sauna to mobilize the toxins means you're going to need to give more glutathione for the liver to process it. Because you want the liver processing the toxins, you don't want them going through the kidney. That's why they do urine tests for mycotoxins, is because the vast majority of them that your body processes, it's going to use the kidney. And we don't want to damage the kidney from the toxins. We want the liver to do the work. And that means you have to use a binder in the GI tract within 8, 16 hours of mobilizing the toxins in order to have those not get reabsorbed and then cleared by the kidney ultimately. So, yes, you need to be very thoughtful about it. I don't like people using binders every day because they also inhibit the uptake of the fat soluble vitamins which are A, D, E and K. And so I don't think it's healthy for someone to be taking a binder every single day for years on end, particularly children or women with osteoporosis or anyone with a vitamin D receptor mutation. Although I guess you could use the transdermal patches for the vitamin D. So I think you have to be careful. It's a marathon, it's not a sprint. I generally only have my patients detoxing three days a week and doing their fat soluble vitamins on the alternate days. I've actually had very good success with that protocol. Generally, within six, nine months, the mycotoxin testing is negative.

Dr. Ann Corson has said that mycotoxins in the gut are much like throwing sparks on a silk scarf. And so I'm just kind of in my mind thinking about the damage to the gut, leaky gut and so on, and correlating that a bit to what you've talked about with damage to the bladder, the gag layer, or these glycosaminoglycans that have been damaged or destroyed from exposure to ammonia to these microbes and so on. What are some of the main tools we might think about while we're addressing the microbes, addressing the biofilms to help repair that lining and really heal that, that area?

I don't think I've done as good a job with that as I, in retrospect, would have, could have, should have. I certainly want all my patients to stay on probiotics. I think that Saccharomyces boulardii is a fabulous one if there's any fungal component there because it will competitively inhibit other fungi in the gut. I know that there are many products that are out there that help with gut repair. If patients come back when I do their immune IgG, IgM, IgE and IgA, if they come back with low IgA either on that or on one of the gut health tests that you have, like a comprehensive stool that's done by Genova or doctor's data. If the IGA levels are low, I worry leaky gut and food allergies. And so that's a direction that's worthy to pursue. I know that there's a number of products that are out there from different companies. Restore and Designs for Health puts out a GI repair product. And I know that Zymogen has a bunch. So there's lots of different directions that go. And everybody has sort of their PET protocol for GI repair. I can't say that I ever got strongly married to any of them in particular, but I think anything that you can do to reduce the inflammation by eliminating the food allergens and doing something that will help repair the gut lining itself and keep it healthy and colonized with healthy gut flora gets points. Now, this is a juggling act. If you're giving somebody oral antibiotics, you know you're always going to be disrupting the gut flora. And that's another reason why the installations get a few extra, extra points. But also treating intermittently gives people A drug, an antibiotic holiday and time for that gut flora to recover from the last round of antibiotics. So it is a juggling act.

So you mentioned then several things that can be helpful for the gut. Are those similar things that can be helpful for repairing then the lining of the bladder or are those different types of tools?

Oh, no. Okay, history lesson again. There has been in use in Europe for a number of years a product that gets instilled into the bladder that has hyaluronic acid in it and it's been used in the IC population without even knowing about the infections with some limited but noticeable effect to heal the bladder wall. And it was marketed under the name of. And I don't know how to pronounce it. Yeah, little I, capital A U R I L, which was a combination of sodium hyaluronate, chondroitin sulfate and calcium chloride. And it was applying for use in the US and the FDA turned it down. And when the FDA turned it down, then Infuserve America could no longer compound it. But I did have a number of patients when we got to the end stages, did those installations very successfully. So we don't have anything right now that's going to do the same thing. The tissue in the bladder is different than the tissue in the gut and so it's not going to repair the same way with the same products.

So just reviewing then a couple of the things we talked about since we're trying to kind of bring this treatment conversation together. For NRF2 support, I know you like the pure encapsulations. NRF2 detox, I believe is the name of the product. And then for biofilms, you mentioned the Kirkman biofilm defense, possibly lumbrokinase or baluc. And then if pseudomonas or klebsiella were present, the priority one phase two biofilm advance, which has the bismuth that you talked about as well. So some fantastic tools for people to think about here to talk with their practitioner. I'm interested in once someone gets to the place where they have symptomatic improvement, what is the longer term picture or prognosis? Do they generally need to stay on maintenance antimicrobials indefinitely? Do they need to be on certain things to keep their environment more acidic and minimize regrowth of bacteria? What's the longer term picture look like?

If they have one of the three genetic problems, they need to stay on the lumbrokinase the rest of their lives, not just for optimum bladder health, but to reduce their long term risk of cardiovascular disease, because remember, the fibrin is going to deposit not just in biofilms, but as atherosclerotic plaque. Most of these people have a family history of cardiovascular disease. You know, they'll tell you they've had, you know, parents and grandparents with heart attacks and strokes and hypertension. So they don't want to go down that pathway either. I think that if they're. They're always going to need to stay on vitamin D because they need to keep their vitamin D level up if they want their bladder wall and their immune system that utilizes vitamin D to be able to help fight any future invaders. I think that staying on the ornithine isn't going to do any harm, and I think it might be a beneficial effect to keep the ammonia levels cleared out and maybe the NRF2 as well, I think preventing them going down this path again. They have a big investment in chronic UTIs and interstitial cystitis have ruined people's lives. It's made them miserable. They have lost spouses, they've lost jobs, they've lost being able to go places and do things. And when they are able to get rid of these infections, they don't want to go back down that path again. I don't want to go down that path again. I have been well now for 32 years and I have no need to let any of these pathogens find a happy home in me again. So, like you, I will always stay on the baluki. I will always take my vitamin D and periodically get it tested to make sure it's above 50. I take Ornithine at bedtime. I'm doing what I can to stay healthy. And I think most people want to do the same thing once they know what the tools are.

I'd love for you to tell our listeners about some of the resources that you're putting together for people to learn more about these. These conditions. I believe you're working on a practitioner course. I know you have a phemologist site. I know there's some other resources where people can access support and information. So tell us a little about those tools.

When I decided that I needed to work my way out of my medical practice and transition into teaching practitioners, my products that I kept stocked in my office got spun off to another company called them ologist.com you can go on the website. They have the products that Scott and I have just been talking about. And these products are certainly available other places. It's up to you where you want to order them from. I felt a need to to have these various products from various companies so people could source them all at one place and know which ones I had found worked well for my patients. Now that I've started Cris Consulting, there is a website available there and there is a link that practitioners can use to schedule time with me if they would like me to work with them individually and doing the appropriate testing. I have lab numbers, lab names, and I'm working with people helping them learn how to interpret the microgen and the pathognostic results and the hypercoagulation results and know what their patient will need. There's also a contact form there for patients and if you would like to be linked up with a practitioner that I have spoken with, you can fill that out and I will send you someone who hopefully is geographically in your area. But if I don't have anyone, I do have several practitioners who utilize telemedicine who will be able to order the appropriate testing for you and get you on the right path with the right supplements and the right antibiotics if needed to eradicate the infections that your body has been walling off in biofilms. I will say that my practitioner training modules are still a work in progress. I'm having finally tied up most all the loose ends from my medical practice. I'm now able to refocus on the training modules and those will be available to practitioners. Those training modules will go into much greater depth than I certainly could have Ms. Scott here on the podcast, but it will also give you access to a lot of my patient handouts, my protocols for treating different associated conditions, as well as lab interpretation guides and dosing guides for some of the supplements. Based on the lab work, there's going to be extra resources that will be available to practitioners once the modules are complete. In the meantime, I am here to support you with your patient load and as I get more requests from patients, maybe sending more patients patients your way if that's something you would appreciate.

Beautiful. So many good resources. I know another one you mentioned as well in our prior conversation for people that need support and information was liveutifree.com so that can help people get to some community based information that can be helpful as well. My last question is the same for every guest and that is what are some of the key things that you do Ruth Kriz on a daily basis in support of your own health?

Oh well, I think I mentioned the supplements just a few minutes ago. I try to eat clean, organic, from scratch. I don't eat the processed foods I work out. I'm 73. As long as we're telling the public here, I am a powerlifter. I've done a fair amount of running in my day, four or five hundred miles a year, until I discovered that these short, stubby legs were much better for powerlifting than running. I try to stay active. I feel great. I've got lots of years left. But I know that when I was in my 30s and I had chronic pain, I never imagined that I could have a life as full as I have now, where I can go where I want, do what I want, pretty much do anything that I enjoy and have three beautiful kids and grandkids that I can enjoy now. Whereas previously I wasn't sure my quality of life was worth going on with because I was too sick, I was told by my urologist, who was chief of urology at one of the leading universities in dc, that I was the sickest IC patient he had ever seen. So I want people to have hope and not think that this is chronic, degenerative and uncurable.

You have definitely taken your pain and turned it into your passion, taken your mess and turned it into your mission. You are making such a big difference for people in the world. This is an area that I think there is not a lot of knowledge about. And so what you're doing is, is so critical to help to minimize the suffering and the struggle of people that are dealing with these conditions. This, I think, is probably one of the longest podcasts that I've done. There was so much amazing information, connections, puzzle pieces that you put together. I just want to thank you for being so generous with your time today and sharing all of this information and for doing the critical and important work that you do. So thank you so much for being here today.

Oh, it has been a pleasure to have somebody who appreciates what I've spent 40 years of my life doing. This has been a lifelong mission to figure out the pieces of the puzzle that nobody else had the time or interest in pursuing and being given a skill set that enabled me to do that, as well as wonderful contacts, Dr. Fukuzado, Dr. Berg. Just lots of people who contributed to my knowledge base.

To learn more about Today's guest, visit RuthKriz.com that's RuthKriz K-R I Z.com RuthKriz.com thanks for listening to today's episode. If you're enjoying the show, please leave a positive rating or review as doing so will help the show reach a broader audience. To follow me on Facebook, Instagram Twitter or MeWe. You can find me there as Better Health Guy. To support the show, please visit betterhealthguy.com donate to be added to my newsletter, please visit betterhealthguy.Com newsletters this and other shows can be found on YouTube, Apple Podcasts, Google Podcasts, Stitcher, and Spotify.

Thanks for listening to this Better Health Guy blogcast with Scott, your Better Health Guy. To check out additional shows and learn more about Scott's personal journey to better health, please visit betterhealthguy.com.