Watch the Video- Better Health Guy channel
Watch the full video wtih Scott, The Better Health Guy, for an overview of how
these hypercoagulation genetics predispose 20% of the general population
to chronic infections due to biofilms.
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Continue the discussion on the Provider only Wellness Tribe Community.
CONTINUE THE DISCUSSIONKey Takeaways
What are the symptoms and conditions associated with hypercoagulation?
Why is the “fibrinolytic pathway” a better term than “hypercoagulation”?
What genetic predispositions are involved in coagulation disorders?
Can hypercoagulation be treated naturally or are pharmaceutical interventions required?
What is the role of vitamin K in coagulation?
How might long-term antibiotics for chronic Lyme disease contribute to coagulation issues?
What is the difference between fibrin and a biofilm?
What are some of they key labs to explore in order to assess for the potential of hypercoagulation?
Are statin drugs contraindicated in those with high Lp(a)?
What role do platelets play in the coagulation discussion?
What is the connection between long COVID and biofilms?
How does lumbrokinase compare to nattokinase?
Why are D-Dimer and PT/PTT not ideal tests for exploring hypercoagulation?
Video Transcript
Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast. They are not a full replacement for the discussion. Timestamps are provided to facilitate finding portions of the conversation. Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed. Please Contact Me with any corrections.
[INTRODUCTION]
[0:00:01] ANNOUNCER: Welcome to BetterHealthGuy Blogcasts, empowering your better health. And now, here’s Scott, your BetterHealthGuy.
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.
[0:00:35] SCOTT: Hello, everyone. And welcome to episode 207 of the BetterGealthGuy Blogcasts series. Today’s guest is Ruth Kriz. And the topic of the show is Hypercoagulation.
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, as well as those dealing with hypercoagulation.
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 genetics contribute to chronic infection, hypercoagulation, and biofilms, she has been able to very successfully treat this population. These factors have broad implications for other chronic infections, sinus, prostate, ear infections, wounds, and more; as well as fibromyalgia, cardiovascular disease, and other conditions in which hypercoagulation and biofilms are an important contributor.
She has closed her medical practice, but she reinvented as a consultant to help practitioners learn how to utilize her approach for curing these patients and currently is working with MicroGenDX.
And now my interview with Ruth Kriz.
[INTERVIEW]
[0:02:10] SCOTT: I first learned about hypercoagulation over a decade ago originally from David Berg. And then later continued to learn more from my mentor, Dr. Ann Corson. And now, I’m learning more from Ruth Kriz. It’s my belief that hypercoagulation is one of the most commonly overlooked contributors to chronic illness. And today we’re going to get into the thick of it, no pun intended, with Ruth Kriz. Thanks for being here, Ruth.
[0:02:37] RUTH: Thank you so much for having me. It’s just a real privilege to be able to share again with your audience. This subject is a major interest of mine having experienced four DVTs in my 20s, four miscarriages in my late 30s and early 40s. And my family history is also one of numerous heart attacks and strokes on both sides. Since I believe that medical issues have causes, learning about how a person’s genetics for hypercoagulation, that those can be identified and normalized, has really been life-changing and life-saving for me personally.
[0:03:13] SCOTT: Wow. Absolutely. You’ve had a focus in your work on chronic UTIs and interstitial cystitis, which I will say originally took me a while to pronounce correctly. We talked about that back in episode 158. People can refer back to that conversation, which was amazing.
Is hypercoagulation a common factor in that population as well? How did you initially begin to understand the significance of hypercoagulation as a factor or contributor to the issues that your patients were dealing with? And what are some of the symptoms or conditions that you might associate with coagulation issues?
[0:03:55] RUTH: Well, a lot of credit has to go to David Berg. A name of a person that we both love dearly for having been groundbreaking in his research. It turns out that about 20% of the general population carries one of four different genetic variations that contribute to the buildup of fibrin. And that results in clotting events, chronic infections embedded in biofilms. Or the deposition of atherosclerotic plaque since all of those depend upon fibrin production.
In my chronic UTI, IC population, I found one of those four genetic problems 70% of the time. And the result is that patients who have one of these have chronic infections. It could be chronic UTI, prostatitis, sinus infections, or even long COVID. Because it turns out that viruses can also be harbored in the biofilms.
You can also have things that would trigger this fibrin production. Because I worried for a long time about, “Well, what about the other 30% that doesn’t have these genetics?” If you have high homocysteine, you have mycotoxins, tick-borne infections, autoimmunity, or anything that produces chronic inflammation, that can trigger fibrin production through the so-called coagulation pathway.
You also ask about symptoms. And they really aren’t specific. It has to do with whichever pathogens are being harbored in those biofilms. People who are still harboring COVID, a virus, in a biofilm still experience some of those symptoms. And, therefore, they say I have long COVID.
Kids who get strep infections, if that strep is being embedded in fibrin biofilms, they can develop PANDAS. Someone with urinary tract infection pathogens, when those get embedded in biofilms, they will experience UTI symptoms. But they still may not be spilling enough of the infection out for it to be identified particularly with standard urine cultures.
I’m not sure that someone’s own experience is a bit major clue to, “Oh, I must have a biofilm.” This is hard to tease out. But, fortunately, we do have more information. We do have tests that can help people identify how that pathway is running for them and therefore make the connection between their chronic condition and a biofilm problem.
[0:06:49] SCOTT: Yeah. It’s definitely interesting how everyone’s symptoms, as you point out, are so varied. I know for me, inner thigh pain is a sign for me to kind of go and retest and make sure that I’m not becoming more hyperviscous. Sometimes tooth pain is another one that I experienced as well, which we probably don’t think about so much related to hypercoagulation. That’s really interesting that it depends a lot on which infections or which toxicants maybe are stored in the biofilms. That’s an interesting perspective. Thank you.
You said anything that produces chronic inflammation will trigger fibrin production through the “so-called” coagulation pathway. Why do you say “so-called”? And can you review with us how this critical pathway works?
[0:07:39] RUTH: Okay. Everyone, hold on to your seats. This can get complicated. There is a diagram that I do believe is going to be available if that would help for you to look at it. The coagulation pathway is a series of clotting factors that get triggered. When we think of acute injury, we think of the pathway that’s triggered through the extrinsic trigger or injury part.
What I want to focus on is the intrinsic pathway, which is what is going on continuously in your body to manufacture a substance called fibrin. This fibrin can be used to make a clot, but it’s also the key component for many types of biofilms in the body particularly those that are triggered by infection. And when a person produces too much fibrin because of their genetics or because they have some of those inflammatory or infectious triggers, we end up with extra fibrin production. And then the body is supposed to compensate by upregulating the production of plasmin to break down that extra fibrin. And that’s called the fibrinolytic pathway.
And so, this is always in balance. Otherwise, someone would have a bleeding problem or have hemophilia if they were breaking down the fibrin too quickly. Or they would have a clotting problem or hypercoagulation if they have too much fibrin that isn’t getting broken down quick enough. However, there’s this intermediate stage in which you’re always making just a little bit more fibrin than your own body is capable of breaking down. And that extra fibrin has to go somewhere. And so, it usually ends up either in a biofilm or it slowly builds up in a person’s arteries contributing to atherosclerotic plaque.
[0:09:59] SCOTT: Hypercoagulation has been a major factor in my own health journey. You were a part of uncovering fairly recently some of the pieces that we had missed and really helping me to better understand why my recovery from chronic illness was so difficult.
We’re going to focus today’s discussion on the more chronic aspect of hypercoagulation. Not so much from an injury like you talked about.
We’re going to talk more about the fibrin side of the coagulation discussion. If we have too much fibrinolysis, as you mentioned, we bleed excessively. And most of the people probably listening here with chronic Lyme, and mold, and those types of conditions were probably talking about the opposite, which is more sticky, hyperviscous, hypercoagulated blood that results from that fibrin build up that you talked about. What happens next?
[0:10:55] RUTH: I meant to tell you my funny little story. I remember when I was in my pre- nursing courses, and we were assigned the coagulation pathway to learn. And I’m trying to memorize this the night before the exam. And it was getting very late. And I’m a morning person. I was tired. Nothing was sticking in the brain. And I finally said to myself, “Well, I’ll never need to know this. I can always look it up.” And after all, how many questions are really going to be on the test about it? And so, somehow, I passed the test. There must not have been too many questions. I think it’s kind of funny that now this is what I talk about day-in and day-out with practitioners. Because this is such an important pathway for the explanation for why some people get an infection. They take a couple of days of antibiotics or their body’s own immune system takes care of it. And then there’s this other subset of people who do exactly the same thing. And months, and sometimes years later, they’re still struggling with those same infections. Yes. Yeah, we all have our stories.
In an attempt to try to simplify this thing that I refuse to learn as a student, these factors are numbered I through XIII. And when the pathway gets triggered, the intrinsic pathway, it actually starts with number XII and it keeps triggering successive factors on down to Factor I, which is fibrinogen. And then for reasons that I haven’t quite figured out other than maybe they discovered this one late, Factor XIII is a fibrin stabilizing factor.
Once you make the fibrin all the way by triggering Factor X through Factor I, fibrinogen converts to fibrin, and Factor XIII stabilizes it. It makes it rigid. It is not slime. It is not fragile. It is actually a fairly rigid three-dimensional structure. And that’s what’s crosslinking and making up biofilms. And crosslinking and creating atherosclerotic plaque in combination with cholesterol. And it crosslinks and it traps red blood cells if you’re looking at a clotting event.
You asked earlier about why do I call it the fibrin pathway. And I don’t think I answered that quite as well as I wanted to. The end result of this pathway is fibrin production. The end result is not usually even a clot or coagulation. The end product is fibrin. It really should be the fibrin pathway. Not the coagulation pathway. Although, that can be one of the possible outcomes. The vast majority of the time, that really isn’t. It’s simply the production of fibrin.
The key factors in this pathway fall into two genetic issues. These are the ones that cause people to always make too much fibrin whether they have an external trigger or not. Those are Factor II and Factor V, which is also called Leiden Factor V, which most people have heard of. Factor II actually wasn’t even discovered until 1996. This is a prothrombin gene. And so, you always make too much prothrombin, which means that reaction is always going to be pushed to making too much thrombin. When you convert prothrombin to thrombin, you spinoff prothrombin fragments 1+2.
And the beauty of this is that you can measure, at Labcorp, Quest, any commercial lab – you can measure someone’s prothrombin fragments 1+2. And when you get that number, you can tell how much fibrin that person is generating in real time. This is huge to actually know does this person make too much fibrin. And if they are making too much fibrin and it’s not because of a genetic mutation with Factor II or Factor V, it’s because they have one of these other triggers. They have mast cell activation. They have high homocysteine. They have tick-borne infections. They have autoimmunity. Anything that’s causing chronic infection, chronic inflammation will push that production more and more fibrin whether or not you have one of those genetic problems or not.
Now, if you have one of those genetic problems and you get Lyme, or mold, toxin exposure, and mast cell activation, you’ve got double trouble. And you’re going to make a lot of fibrin very quickly on a consistent basis. And then those people are of course going to be more susceptible to a clotting event. Most often, they’re not going to have a clotting event. They’re simply going to have a lot of infection walled off in biofilms that are going to be very difficult to treat and take a whole lot longer than for other people. Factor V pushes Factor X, which activates and converts prothrombin to thrombin with the same result of high fragments and excess fibrin production.
And I have to clarify one thing here. A lot of people check – on the lab test, they’ll check fibrinogen activity. That’s almost a misnomer. Actually, it is a misnomer. Because it’s more a reflection of a buildup of old fibrin than how much fibrin someone is generating in real time. Just because somebody doesn’t have a high buildup of old fibrin doesn’t exclude them from generating a lot currently. You can’t confuse the two markers. I hope that clarifies. We look at fibrinogen activity to look at a buildup of old fibrin. We look at prothrombin fragments 1+2. We look at fibrin generation in real time.
[0:17:41] SCOTT: Now that’s very, very helpful. Prothrombin fragment 1+2 is one of the tests that I use to monitor my own coagulation. Or better said, maybe fibrin buildup status over time. And for me personally, and we’ll talk a little more about why that’s the case with my own health journey, but I feel like that’s a more important thing for me to know a couple of times a year than knowing my cholesterol, for example.
[0:18:10] RUTH: Sure.
[0:18:11] SCOTT: The other one that I find helpful we’ll talk about later, which is the T/ATs. With what you shared, it sounds like people that have these Factor II and Factor V Leiden mutations will always be prone to the creation of too much fibrin. But even without those genetic predispositions, we can still, as a result of many different triggers, move in that overproduction of fibrin direction.
If we’re talking about Factor II and Factor V, how common are those two mutations? And does that also explain why the population has a lot of cardiovascular disease, chronic infections you already alluded to? And then knowing what you talked about what can we do about that?
[0:18:57] RUTH: The Factor II people are really only 1 to 3% of the population. There aren’t many of us out there. I happen to have two copies. I am in 0.03% of the population, which makes me special.
[0:19:10] SCOTT: I knew you were special, Ruth.
[0:19:15] RUTH: But it also explains my clotting events in my 20s. It also explains my miscarriages. It also explains why people on both sides of my family die of heart attacks and strokes because they all carry – I get the Factor II from both sides.
You also ask about the incidence of Leiden Factor V. According to the literature, that is found in 15 to 20% of the general population that carries at least one of the Leiden Factor V genetic mutations. And these are people who have been known to have more clotting events, more miscarriages, more heart cardiovascular disease. And so, instead of waiting for those people to have their clotting event, if you know that their fragments are always too high that are being produced, wisdom would say, “Why don’t we slow that down with a little bit of an anti-coagulant so that these people are now making fibrin just at the same rate as people who don’t have these mutations and prevent these coagulation incidences and miscarriages for them?”
People who are making too many prothrombin fragments, particularly because of their genetics, the goal here is to stop making so much fibrin. How do we do that? Well, if you remember Factor X pushes that reaction of prothrombin to thrombin. And, nowadays, we have a lot of newer anti-coagulation medications like Eliquis and Xarelto that actually block Factor X activation which slows that conversion of prothrombin to thrombin down.
And what I’ve observed in myself and others with these mutations, that it only takes just a low-dose, baby dose, 2.5 milligrams of Eliquis twice a day to normalize the prothrombin fragment 1+2 values on a lab test. And this indicates that fibrin production is now normal. Even though I take a low-dose Eliquis, the reality is I’m not anti-coagulated. I don’t wear an anti-coagulation bracelet. I’m just normalized with my anti-coagulant.
And I know that sounds counterintuitive, but that’s what’s happening. If I slow down the activation of Factor X, I don’t make as much fibrin, and now I bleed at the same rate as everybody else does who doesn’t have that problem. I also think it’s important to do something about breaking down that extra fibrin that I’ve been making and accumulating my whole life. And we will talk about the process of fibrinolysis and how that piece works.
Yes, I can stop the generation of a lot of new extra fibrin by blocking Factor X. But I still have the problem of dealing with all the fibrin that’s building up in my body my whole entire life until now. We’ll talk about that under fibrinolysis.
[0:22:49] SCOTT: Plus, you have to wonder if doctors that were treating patients having miscarriages would run your Labcorp panel that we’re going to talk more about. What a difference that potentially would make? I have to think that, many times, people aren’t even looking at fibrin, prothrombin 1+2, those prothrombin fragments, the thrombin-antithrombin complexes. I would guess it’s probably not super common.
[0:23:16] RUTH: It isn’t. I’ve been working with a number of practitioners. I have a large infertility clinic of about 20 practitioners in the UK. And we have just gotten a lab over there to run the majority of these panels looking for these factors in the population who has had multiple miscarriages and infertility issues.
[0:23:40] SCOTT: Wow. You mentioned Eliquis. You mentioned Xarelto. How often do you find that your patients need some pharmaceutical intervention versus more natural interventions, enzymes? Things that we’ll also talk about later. Can we do it without pharmaceuticals? Or do we commonly need to incorporate some of those as well?
[0:24:03] RUTH: Well, I would be happy if I could find anything out there besides a pharmaceutical that would slow down the production of fibrin. So far, I don’t know of anything that does that. Anybody out there has any information, I’m open to hearing about it. But in my experience, pretty much everybody with Factor II mutations and Leiden Factor V mutations, yes, you can ramp up the amount of fibrinolysis that you’re doing with supplements. But at some point, for most people, it just isn’t going to be enough. They can’t break it down fast enough. And therefore, the intervention to slow down the production is the safest route to go before there is an event.
[0:24:51] SCOTT: Is it a fair statement to say that the pharmaceuticals are more necessary in those that have these to genetic predispositions? But in those without a genetic predisposition that are triggered by an infection, a toxin, something along those lines, that those people may be less necessary to use a pharmaceutical intervention?
[0:25:11] RUTH: Absolutely. But we know who those people are because we can measure their prothrombin fragments 1+2. And I have had some people who have both mold, and tick-borne infections, and had autoimmunity before all this started, and high homocysteine. I mean, the cards have really been stacked against them. And we did, for a period of months, use a low-dose of an anti-coagulant just to slow down the fibrin production while we addressed and got rid of those other triggers.
[0:25:47] SCOTT: Is there anything else that you think is important to check for on the fibrin production side of this pathway?
[0:25:57] RUTH: Yes. We’re going to go into the weeds here with the whole issue of Leiden Factor V. The insurance companies in the United States, probably because of cost, want people or the labs to do the screening test for this genetic problem first. If the screening test shows there a problem, then they will pay for the genetic Leiden Factor V test.
The screening test for this is called activated protein C resistance. APCR. And the job of APCR is to put the brakes on Factor V so it can’t keep pushing Factor X as hard. This is a resistance issue. If the resistance comes back low, it reflexes on the panel that I’ve set up with Labcorp to doing the genetic test. If you use another lab and the APCR is low, the patient will have to go back for a redraw for the genetic test. But it should be covered by insurance now because the APCR was too low.
Now, protein C has a co-factor, protein S. And on my panel, I check not only for APCR with the reflex, but I also separately check for protein S activity. And this one is important because both protein C and protein S are vitamin K dependent. Where does vitamin K come from? The vast majority of a person’s vitamin K is synthesized by the lactobacilli colonizing the GI tract.
And if you have a population that’s been put on long-term antibiotics or multiple courses of antibiotics, it is highly likely that their colonization of their gut with lactobacilli has been compromised significantly. As a result, they don’t synthesize enough vitamin K to keep protein S and protein C happy.
And so, if I look at protein S activity, I can tell the status of someone’s healthy gut flora. That’s a great test to know about even independently of whether you’re doing the whole panel or not. But the reason why I care about this in regard to fibrin production is that if you have low protein S activity, and that’s a co-factor with protein C, those people, even if they do not have a genetic Leiden Factor V mutation, will behave as if they do and make too much fibrin. This is a big deal.
[0:29:15] SCOTT: Let’s then take a little vitamin K diversion. Tell us about the role of vitamin K. And part of the reason that your comments are interesting is I commonly hear people say that vitamin K produces clotting factors that can increase the potential for blood clotting. Can vitamin K potentially make things worse in someone who already has hyperviscous or thick blood?
[0:29:39] RUTH: I’m not a hematologist. And I know that vitamin K is used in several different pathways in this whole process. And I don’t know how they speak to each other and balance each other out. But I do know that a lot of the misunderstanding with vitamin K comes from the fact that, for many years, the only anti-coagulant we had was Coumadin. And the way Coumadin worked was by suppressing, depleting vitamin K, which was its antagonist. It kept it from working. And so, people on Coumadin are told don’t eat leafy green vegetables and lots of other things to limit their vitamin K.
In my experience, looking at hundreds of these lab results, even supplementing someone with low protein activity with vitamin K has not resulted in increases in prothrombin fragments 1+2. I have not seen that supplementing vitamin K has caused a problem. If some of you have more information on this, I’m happy to look at it. Maybe it does have some minor effects. But, functionally, at the end of the day, it’s not causing a problem.
[0:31:08] SCOTT: Yeah. And I think there’s so many good things that vitamin K does as well. One that we don’t think about a lot, but there’s a correlation between vitamin K levels and mitochondrial function as well. And we know that lots of people with chronic illness have low energy production, right?
[0:31:23] RUTH: Interesting. Yeah. And you need it to tell the calcium to go stick on the bones for osteoporosis. I think there’s a lot of things that we don’t quite understand about the fat soluble vitamins and how they balance each other. But I don’t think depleting someone in vitamin K is a good idea. I mean, I have an experience with my nursing background with people only having access to Coumadin and lots of health issues resulting from withdrawing that vitamin K.
[0:31:56] SCOTT: Yeah. I mean, I personally recently did a micronutrient panel. And one of the things that I was low in was vitamin K. Definitely makes sense that we wouldn’t want to restrict it when we don’t even know if it presents a potential problem. Many listeners, myself included, that have dealt with chronic Lyme disease and other chronic infections have been on long-term antibiotics. For me, it was every day for almost four years. That was a very different time. That’s not something I personally would do again. But that’s the tools we had in 2005 when I was diagnosed with Lyme. Does that mean that people who have been treated for Lyme and other infections with long-term antibiotics were more likely than to have issues with the synthesis of vitamin K because of our microbiome? And as a result, be more prone to low activated protein C resistance and protein S activity. And, thus, be more prone to fibrin production as a result of those long-term antibiotics.
[0:33:03] RUTH: You just connected all those dots beautifully. And that is my concern with using antibiotics long term. Whether we’re talking about urinary tract infections, or tick-borne infections, or kids with PANDAS. I think the end result can be that because we’ve depleted the lactobacilli, we aren’t producing as much vitamin K, there is more fibrin produced. And the end result, instead of getting rid of the infections, is you’ve actually walled them off to even a greater extent in the biofilms.
[0:33:40] SCOTT: What is the difference then between the term you used, which was fibrin biofilm, and what we generally think of as a biofilm? Is there any difference? Are some biofilms unrelated to fibrin? Or do they commonly overlap?
[0:33:58] RUTH: Oh, this is one of my favorite topics. Once upon a time, the oil industry discovered petroleum-degrading bacteria in slime in their oil pipes. And they took a couple billion dollars out of their back pocket. Built the Biofilm Research Center in Montana. Hired some very bright microbiologists like Bill Costerton. And, hence, the term biofilm was birthed.
Everybody visualizes the slime that they’ve talked about and tried to educate people about. Although, there’s still a lot of people out there that the word biofilm is a foreign language. But it’s another discussion for another day. It turns out that that’s not what’s in people. People have several different types of biofilms. Quickly, in your gut, you have a polysaccharide biofilm which is more slime-like, but it is nobody’s friend.
You find extensive polysaccharide biofilms with ulcerative colitis, Crohn’s disease, colorectal cancer. That gets broken down by digestive enzymes, and the enzymes in pineapple, and NAC, N-acetyl cysteine. That’s not what we’re finding in bladders. In bladders, we primarily are finding two types. We’re finding fibrin, which we just talked about. How that gets generated? And we still have some more genetic work to do on that one. And extracellular DNA. Extracellular DNA biofilms are actually manufactured by the pathogen itself. Some pathogens can do this. Many do not.
And so, if you have an infection that makes its own biofilm, it really doesn’t matter your genetics or not. You’re still going to have a biofilm problem. We think of some of the nastier infections that make biofilms. Pseudomonas, very hard to get rid of. Klebsiella, Enterobacters. The one people are probably most familiar with is H. pylori. That makes its own biofilm.
If you’ve ever wondered why, when H. pylori gets treated, they give the person a bunch of antibiotics plus bismuth subnitrate. Well, bismuth doesn’t have any great shakes antimicrobial properties. But it does a great job breaking down extracellular DNA biofilms. And now, the antibiotics can get to the H. pylori and kill it off.
[0:36:48] SCOTT: A lot of things there. A few comments that I want to make. And then feel free to disagree with any of them. But I think one of the things that we often think is all biofilms are bad. And that’s not necessarily true. There are some biofilms in the body that are not necessarily pathogenic. You talked about NAC, which does degrade biofilms. And if we had some healthy biofilms in the gut, that’s another thing. That when the pandemic came along, I was taking NAC for a long period of time because research was showing it was helpful if someone got COVID. But could there be some potential downsides of long-term use of NAC in terms of breaking down beneficial biofilm? Interesting question.
The bismuth conversation, I believe that’s one of the ingredients in Dr. Paul Anderson’s supplement for addressing biofilms. And then I believe that project you mentioned that was more in industry and looking at biofilms in pipes, that ultimately resulted in one product that’s fairly popular called AquaLaurin as well that can be a significant biofilm degrader. At the same time, it can also be very, very powerful. And my personal experience was I did too much too fast. And it wasn’t a fun ride.
[0:38:13] RUTH: Yeah. There’s a lot we just don’t know yet about beneficial, non-beneficial. Where you want it? Where you don’t want it? I don’t think that people’s normal gut flora gets compromised by NAC. I mean, the body makes cystine. I mean, it’s something that’s there. I just didn’t see it compromising the gut flora. I probably should do some research or have somebody who does research let me know what the healthy lactobacilli in the gut. How they are sustained in their life cycle and what their happy home looks like? It is not the same polysaccharide biofilm. Because, otherwise, we tell people not to do digestive enzymes or eat pineapple. I think we have to think through this logically.
The one thing I should also say on the types of biofilms is the COVID biofilm. Because that’s a big deal right now. In the early days of COVID with the far more virulent strains that were circulating, 20% of those people who got COVID got long COVID. I don’t think it’s a coincidence that 20% of the general population has one of these genetic problems. We’re busy discussing. I think there’s a huge overlap between people who have the genetics for making biofilms either because they generate too much fiber or they don’t break it down efficiently. And the people who end up with chronic infections, including long COVID.
Now, the COVID biofilm is a little bit different. It’s not a polysaccharide. To my knowledge, it’s not an extracellular DNA type. But it is a combination of fibrin plus amyloid. Amyloid is another type of biofilm. We associate it with Alzheimer’s. But a lot of the literature that’s out there nowadays, maybe it’s guilt by association. Maybe it’s not causative. But those amyloid fibers that get generated combine with the fibrin. And that’s what makes up a COVID biofilm. And that’s why the limited articles that are out there about COVID biofilms do have suggestions for a fibrinolytic for the fibrin part. And then they’re using EGCG and liposomal curcumin to break down the amyloid portion of the COVID biofilm.
[0:41:01] SCOTT: I mean, it’s a very interesting point. It comes back to decades of Alzheimer’s research and the idea that if we could just get rid of amyloid, that things would be better. And I think what many, Dr. Dale Bredesen and others, have concluded is that the amyloid is actually protective, is actually antimicrobial. And if we take away the water from the fire hose before we put out the fire, we may actually make things worse.
[0:41:28] RUTH: Yep. No. I think that we’re so ready to jump to conclusions because we see something associated with something else that we point the finger and blame it when maybe that’s the body’s compensatory mechanism.
[0:41:46] SCOTT: Correlation is not always causation. Right?
[0:41:49] RUTH: Yes. Yes. Yes. Yes.
[0:41:51] SCOTT: Okay. Now we had a nice little relaxing portion of the conversation. Let’s dive back in. How does the body address or respond to this extra fibrin production either because of the person’s genetics or the numerous external triggers that can also lead to extra fibrin production?
[0:42:14] RUTH: Sure. I mentioned that there were two genetics associated with the production of fibrin. There are also two other genetic problems that are connected to fibrinolysis or the ability of the body to break down that fibrin. The first way that it kind of puts the brakes on the whole system is thrombin-antithrombin complexes. And that’s one of the body’s breaking mechanisms to slow down the excess fibrin production. People with Factor II, Factor V or one of the other ones don’t do a good job upregulating their T/AT complexes. But those T/AT complexes do get measured on the Labcorp panel that has been put together for me.
But the one we really have to focus on is the most important way the body breaks down fibrin, and that’s by producing a substance called plasmin. And the body takes plasminogen. And please don’t confuse this with Dr. Goodenowe’s plasmalogen. But plasminogen gets manufactured by the liver and then the body has to activate that plasminogen to produce plasmin. And the vast majority of these extra fibrin, hypercoagulation issues are really genetic problems that relate to plasminogen activation.
[0:44:00] SCOTT: Thrombin-antithrombin complexes, which many refer to as T/ATs, that’s the other test that I do along with the prothrombin fragment 1 + 2. Of course, I did your full panel at the beginning because there’s lots of useful information. But then looking at what could I do over time, those were the two that were most consistently not normal. That’s what I tend to use every six months or so to try to get a sense for, “Are the enzymes I’m taking dealing with whatever fibrin production or hypercoagulation I might be exhibiting at that point in time?”
And interestingly, interpretation is important too. And we’ll talk a little more about how practitioners can reach out to you. But I know if the T/ATs are elevated, that’s actually a good response of the body to deal with the issue.
[0:44:56] RUTH: Yes.
[0:44:57] SCOTT: But my interpretation is, even if the T/ATs are elevated and there’s no other obvious indication of hypercoagulation, that the body is having to upregulate its beneficial response in response to something. When the T/ATs are elevated, I don’t just personally feel like, “Okay, everything’s good.” I feel like, “Well, that’s interesting. Why is my body doing that?”
[0:45:20] RUTH: Yeah. No. I think that’s exactly right. These results are not just a matter of, “Oh, the lab flagged this is in range or out of range.” Because this is a dynamic system that keeps compensating and trying to balance each other. And so, if you end up doing these panels, I am available to go over them with people on Zoom calls. Because we need to know, “Oh, if this is up, then did this compensate? Did that compensate? If this isn’t going up, is it because of this problem? Or is it because of that problem?” There are a couple things that have to be looked at more carefully than just absolute numbers in or out of range.
[0:46:07] SCOTT: All right. Continuing on. You mentioned plasminogen. Not to be confused with plasmalogen. Let’s get into the genetics of PAI-1 or plasminogen activator inhibitor. What are those genetic contributors? And how are those diagnosed?
[0:46:25] RUTH: PAI-1, plasminogen activator inhibitor, PAI, actually has four types. One of them works on platelets. And because of this, instead of measuring the level of inhibitor, the panel measures PAI-1 activity. Because this is telling us how much plasminogen is being activated and how much plasmin the body has produced to be able to work on the extra fibrin.
Once again, here’s where we come into a little bit of history-making here. David Berg at Hemex Lab in Phoenix, when he retired, his lab was sold to Esoterix in Denver. You should go visit them sometime. And Esoterix was purchased by Labcorp as their hematology division. Prior to Labcorp buying Esoterix, it was a hematology lab, but it specialized in bleeding disorders. And so, they were already running the test for PAI-1 activity. And their reference range was greater than 31. If it was greater than 31, it was flagged. Because that meant there was too much PAI-1 activity. You were making too much plasmin. And you had a PAI-1 deficiency and a bleeding disorder.
Now that we are setting the limit at less than 4.4 for not enough PAI-1 activity, because we’re looking for the coagulation or the fibrin problem, they have not put that on the reference range on the lab in spite many attempts on Ruth’s part. Just warning all you practitioners out there. Just because it doesn’t get flagged doesn’t mean there isn’t a problem. If there is low PAI-1 activity, that person is not converting plasminogen to plasmin. And they have a problem with extra fibrin that didn’t get broken down.
So, on my panel, if there is low PAI-1 activity, it will reflex to the PAI-1 genetic test. Now, normal is 5G/5G. There is a problem genetically with something called a 4G deletion. This is not a variation. This is not a mutation. This is not a 30% compromise. This is an out-and-out deletion. You only got four of those G’s instead of five from each parent.
And of all of my patients that had a genetic problem, 80% of the time what popped up was they had at least one 4G copy. This is huge. This one is considered so rare the hematologists don’t check for it. I guess if you never check for it, it will always be rare.
[0:50:02] SCOTT: It’s interesting with PAI-1. You talked about the reflex aspect of your panel, which is only available through Labcorp. Coming from a software background, I think of that as if-then. If I’m out of range on this value, then we’re going to go look at the genetics. That’s really more of a cost issue. I personally feel like I wish I had looked at that years ago and probably missed it because I did have that PAI-1 4G/4G deletion. And when we talked about that result, you pointed out that that is probably a very significant contributor to my years of chronic infections, years of biofilms, years of chronic illness. And I only just learned that from you in maybe the past year. To me, that seems like a very significant thing to know. And to your point, unfortunately, probably most people have never even had that test done.
[0:51:01] RUTH: It’s not commonly done even by the hematologists. It is more recently being considered in the high-risk pregnancy community. It turns out that women with a 4G deletion, even one copy, do have a higher incidence of miscarriages. Because just like the Factor II and Factor V people, the placenta gets clotted off in that first 6 to 12 weeks of pregnancy. And so, the obstetric community is starting to realize this. And these patients are put on Lovenox throughout the pregnancy to prevent a clotting event in the mother, as well as to prevent a miscarriage.
I have mentioned a couple times about the difference between people who got one copy versus two copies. And, functionally, the activity is still so low it’s not even measurable by the lab. The Leiden Factor V people who have low activated protein C resistance, so far, all but one patient that I’ve seen with low APCR has had a Leiden Factor V mutation.
In those who have low PAI-1 activity, 95% of them do come back with at least one copy of the PAI-1 4G deletion. Those are pretty strict parameters. The question from some of my other practitioners has been, “Well, why don’t we make the cut off 5.0 instead of less than 4.4?” And if we do that, we would end up with more false negatives. But I do have one practitioner who, even if they come back with a PAI-1 activity of 6.0 or lower, will run the genetic test. And she has found some. We probably are missing some people with a PAI-1 4G deletion with that cut off being as low as it is.
When you look at some of the results coming back if you’re doing MicroGen testing and they have multi-drug resistance, and they have multiple pathogens, and it’s really obvious they have a biofilm issue, then maybe your index of suspicion would be higher and it would be worth running the PAI-1 genetic test on some of those people if they were right at the border and didn’t get it reflexed.
[0:53:32] SCOTT: When we have this PAI-1 4G deletion, we don’t make enough plasmin to break down the fibrin. And then that’s leading to fibrin buildup. Correct?
[0:53:43] RUTH: Exactly. Exactly. We do have one more genetic one to go. Hang in there, everybody.
[0:53:51] SCOTT: Yeah. Let’s talk about that then. The next genetic factor that your panel looks at and that we want to consider is lipoprotein(a) or Lp(a). How does that fit into the fibrin buildup conversation?
[0:54:05] RUTH: Lipoprotein little a is a form of bad LDL cholesterol. It’s unique in that whereas you can bring down other forms of LDL with diet, or exercise, or statin drugs. The lipoprotein(a) does not respond to any of those interventions whatsoever. And what’s really kind of scary to me is a lot of people are being put on statin drugs based on an elevated LDL total without checking first to see if the reason why the LDL total is high is because they have high lipoprotein(a).
And some really interesting studies have been coming out over the past year or two showing that a statin drug will actually increase lipoprotein(a) by 19 to 23%. And this creates an even higher cardiovascular disease risk. It creates even more biofilm issues. Because the function of lipoprotein(a) in the body is to bind up TPA. Now, TPA stands for tissue plasminogen activator.
And although most practitioners are familiar with TPA. It’s the clot-buster that’s used in the ER when you come in with a heart attack or a stroke. And, really, have been interested to learn that most people don’t know what TPA stands for. But it’s tissue plasminogen activator. And this is produced by the intima or the lining of the arteries, which I think may explain why these people have more issues with hypertension. Because those arteries themselves become more rigid and less elastic with the fibrin building up in that location.
This ties into the pregnancy issue as well. Elevated lipoprotein(a) are more prone to preeclampsia. And so, even in your 20s or 30s, if you’ve had high lipoprotein(a) your entire life, and when you’re pregnant, there’s a 45% increase in blood volume. And if those arteries can’t be flexible to accommodate that, that end result is going to be high blood pressure or preeclampsia. This is a big deal to sort out even for your younger patients that you don’t think have a cardiovascular disease risk. If they have high LDL, be very suspicious that they’ve got a lipoprotein(a) problem.
And I think the prime example of this is – maybe my age is showing. But Bob Harper, who used to be the personal trainer on Biggest Loser, had a massive myocardial infarction at age 52. Here he was a pristine diet; hours of working out in the gym. And, yet, nobody ever suspected that he was an undiagnosed lipoprotein(a) person. And the end result was, all this time, all of this atherosclerotic plaque was building up in his coronary arteries. And he was in the gym. And if it hadn’t been for some doctors that were there at the same time, he probably wouldn’t have survived.
And so, this particular test, even though we say it’s a genetic problem, is not a genetic test. There are about 10 different genes that regulate lipoprotein(a). And it’s just a measurement. Either the number is high or the number is normal. And so, we don’t know which combination of genes are at play in each person. Because we all got dealt different genetic hands. But I think this explains why some of them respond to treatment for elevated lipoprotein(a) better than others.
[0:58:37] SCOTT: Yeah. It’s so unfortunate with the atherosclerotic plaques that we don’t do more. I mean, we do the coronary artery calcium scan. But now there’s the Cleerly AI testing, which I’ve had some education around. And is really interesting that you can see calcifications. You can see soft plaques. But what you’re saying is if we looked at some of these things, does the person have elevated lipoprotein(a), we can potentially avoid a lot of that buildup in the first place.
[0:59:10] RUTH: We can. If you think about it, if it’s a genetic underlying trigger, even children are building up this in their arteries. I don’t think the kids are going to be getting in trouble with events yet. But if there’s a family history of this, of course, once the kids get to be older, puberty, they should be checked.
I particularly worry about some of these genetics in young ladies being put on estrogen birth control carrying a PAI-1 4G deletion. That’s a real recipe for a problem. Or a Factor II or a Factor V. And that also says that we should be thinking about this preventatively. We don’t want to just bring down lipoprotein(a). We want to clear out the fibrin that’s been accumulating their whole life. How do we do this? We use a fibrinolytic that does the work of a person’s own plasmin.
[1:00:18] SCOTT: We’ll come back and talk more about some of the treatment interventions shortly. But I want to clarify one point that you made around statin drugs increasing lipoprotein(a). Potentially worsening our fibrin buildup. Would you say that statins are a contraindication in people with these Lp(a) issues from more of a hypercoagulation or fibrin buildup potential? Would it be better for us to use other tools in someone that has high cholesterol that’s also dealing with high lipoprotein(a) and resulting fibrin buildup?
[1:00:56] RUTH: Absolutely. I don’t think anyone with elevated lipoprotein(a) should ever take a statin drug. I think that that is absolutely contraindicated. Will produce more lipoprotein(a). Will bind up more plasmin. Will deposit more fibrin. And it will hasten cardiovascular disease.
When I see someone with a lipoprotein(a), actually with any of these genetic issues, particularly postmenopausal women, people with a strong family history of cardiovascular disease, doing the scans of the carotids, the coronary arteries I think is really, really important. And I personally have had a great experience with using lumbrokinase. And I use the Boluoke brand. That has the documentation for it. But anyway, my arteries were 23% blocked. My coronary arteries. And after three years of being really good about taking the Boluoke, I came back with a CAC score of zero at age 74.
And my joke is I thought the cardiologist was going to fall off his little rolling stool in the exam room. He said, I’ve never seen a 74-year-old woman with your genetics in your family history come back with a score of zero.
[1:02:29] SCOTT: I haven’t ever had that test done to date. But I have had two Boluoke already this morning. And I’ll have another one later in the day. That’s hopeful information for those of us that are concerned about cardiovascular health.
Coming back to your panel, what I believe you’ve said is that once you measure Lp(a), if it is normal, that we don’t really need to look at it again in the future. Is that still correct?
[1:02:57] RUTH: Yes. That’s correct. Because if you don’t have the genetics that would cause you to have elevated lipoprotein(a) and it’s not elevated, it isn’t going to suddenly become elevated later in life. It doesn’t have to be rechecked if it’s normal. However, if it is elevated, this is something that it is really important to monitor it and make sure that the things you are doing to lowering it are actually working.
Traditionally, the medical profession has used high doses of niacin. Sometimes up as high as one or two grams a day. But the problem is these are often associated not only with a flushing response, but elevated liver enzymes. And there’s also some recent concern that the niacin can contribute to more cardiovascular disease through the inflammation of the arteries. It’s a little uncertain as to what’s the best approach for most people. The newly approved drug, Repatha, certainly avoids some of those issues. But we don’t really have any long-term data on its use in this population.
That being said, we know there’s definite cardiovascular risks walking around with an elevated lipoprotein(a) because you’re binding up your TPA. We have to sort of look at the benefit risk ratio here. And this is something for patients and practitioners to discuss.
For my lipoprotein(a) patients, which was about 12% of my chronic UTI, IC population, I was able to use a low-dose sustained release niacin at about 500 milligrams a day with dinner. And by the way, there was a really good study that showed taking it with a big meal works better than taking it at bedtime. And then they also took Boluoke, which will reduce lipoprotein(a) an additional 20% to 30%. That can clean out the fibrin that’s been deposited in their arteries their entire lives.
And I think they need both approaches. You have to both lower lipoprotein(a) and clean out the fibrin that’s been deposited their whole life. And I recently have seen a couple of articles that question whether it’s worthwhile lowering lipoprotein(a) because, “Well, we do this. But we don’t really see any long-term benefit in reducing cardiovascular disease.” I think that’s because they haven’t thought about what it does in the body with it binding up TPA. And they’ve done nothing to clear out all of that fibrin that’s accumulated in the arteries before they discovered that that person had a lipoprotein(a) problem. I think you need to do both things if you really want to see a reduction in cardiovascular disease risk.
[1:06:03] SCOTT: One of the other markers on your panel is homocysteine, which I quickly jump to thinking as an indication of methylation status. Help us tie homocysteine to fibrin buildup.
[1:06:17] RUTH: It’s very pro-inflammatory. They’ve known the association between high homocysteine and cardiovascular disease for decades. This is no big surprise. And because any long-term inflammation is going to trigger cytokines that push that fibrin pathway into making more fibrin, that’s going to automatically be a factor with biofilms and with the coagulation fibrin production.
I want to kind of interject something here. When you look on the Labcorp panel for homocysteine, there’s a little note that says that after the age of 60, it will go up one to two. I think it’s nanomoles per liter. It could be a different measurement unit. And that bothers me because that doesn’t mean it’s healthy and okay for older people to walk around with a high homocysteine.
I think what’s going on is that you need B12 to process, break down the homocysteine to run your methionine cycle. If you get older, you don’t make as much gastric intrinsic factor. You won’t do as good a job absorbing B12. And so, you are more likely to have your homocysteine go up. But that’s not healthy for anybody to walk with a high homocysteine no matter what your age. I don’t tell people coming back who are over 60, “It’s okay if your homocysteine is high.” I think it’s still pro-inflammatory no matter what age you are.
[1:08:07] SCOTT: Before we jump into our next topic, I think some people think of platelets in a hypercoagulation discussion. And we know that some coagulation abnormalities can involve platelets. But is that an aspect of the discussion that we’re having around fibrin buildup? Around the approach that you work within your patients to improve these issues? Where do platelets come into the conversation?
[1:08:34] RUTH: Very little, to be honest. We know that platelets get sticky and can contribute to clotting issues. We know that viruses can attach to platelets and make them stickier. But when we’re looking at these genetics, these people don’t have a platelet problem. They have a fibrin problem. And so, doing anything that works on platelets isn’t going to fix a fibrin problem.
[1:09:06] SCOTT: Decreasing the activation of platelets is often done in more conventional medicine with aspirin, maybe with pharmaceutical medications. Do you think that’s a reasonable approach? Where do you stand on the long debate around whether or not aspirin is good or bad as people age to minimize their risk of heart attack and stroke?
[1:09:27] RUTH: Well, there are some natural products that can reduce platelet stickiness like curcumin. But once again, that really isn’t the problem. These products are not going to break down the extra fibrin that’s accumulated in biofilms or arteries. I recently had to do some research for a practitioner. The person, we discovered some genetic problems with breaking down fibrin. They went off to a hematologist and the hematologist said, “Oh, take a baby aspirin.” And so the practitioner came back to me and said, “What do you think about that?” Well, it turns out that there was a study published in 2023 that there was – I’m quoting here, “There is no benefit of aspirin reducing cardiovascular disease. And that the risk of GI bleeds made those recommendations inadvisable. They qualified it by–” this was the US Preventative Task Force, USPSTF if you like acronyms, “concluded with moderate certainty that initiating aspirin use for the primary prevention of cardiovascular disease events an adult 60 years or older has, and this is bold letters, NO NET BENEFIT.”
These are recommendations kind of hot off the press. I know that hundreds of thousands, if not millions of Americans take their baby aspirin every day because they were told it was going to help prevent heart disease. And, yet, here, within the past year, they have said that their study showed that it did not benefit, but that there is an increased risk of GI bleeds. And, therefore, those recommendations are inadvisable.
[1:11:31] SCOTT: There are some long COVID approaches that are incorporating aspirin. Let’s talk a little bit about long COVID, some of those treatment options. In my opinion, this whole conversation around hypercoagulation or excess fibrin has been maybe the top overlooked issue in chronic illness for many years. And that was before the pandemic that I had that perspective. Now I think it’s exponentially more true now that we know that spike protein can be a trigger for hypercoagulation, for endothelial inflammation or endotheliitis. How does long COVID fit into the discussion on coagulation?
[1:12:13] RUTH: Sure. It’s a biofilm issue. You know how you study something and after a while you’re convinced everything is caused by that? Well, I have pictures of COVID biofilms and there are articles that have been published on COVID biofilms. This is not just Ruth has spent too much long talking about biofilms. We end up with this combination of amyloid and fibrin biofilms that we talked about earlier. And because the COVID is still encased in this biofilm, it’s still triggering symptoms.
Now, it is one of the ways the body is trying to protect it from an out-and-out full-blown COVID crisis event. But enough of it is still there that’s pushing people to have more fatigue. Maybe ongoing respiratory issues. It looks kind of different in different people. But there’s definitely a whole cluster of COVID symptoms that are persisting in this population after they have finished with their COVID. And, therefore, they have long COVID.
I mentioned earlier about the 20% number of the genetics. People who have mutations with Factor II or Factor V and make too much fibrin. And the people with PAI-1 deletions or elevated lipoprotein(a) who can’t break down fibrin well. And I believe that the vast majority of those people are the people who are in the long COVID population.
Besides just my suspicion, it turns out that there’s another marker on my panel that I’ve been tracking for years before COVID ever appeared called alpha 2-antiplasmin. Sometimes abbreviated α2AP. And this is the body’s braking system for the production of plasmin. When people are pushing their bodies to make more and more and more and more plasmin because they have a lot of fibrin being produced rapidly, this could be because of the cytokines storm with COVID, the body can only do that for so long. And then it kind of says, “Wait a minute. Time for the emergency break.” And they upregulate alpha 2-antiplamin. I didn’t frequently see it elevated pre-COVID. But if I did, I knew that that person’s body had been pushing long and hard for many months.
There was a study that came out year ago, July, in which they had 65 long COVID patients. A year after having had COVID, 100% of them still had elevated alpha 2-antiplasmin. This tells me that these are people who weren’t doing a good job making plasmin to begin with. When they got pushed with COVID, it made big COVID biofilms. One of the reasons why they still have long COVID is because they still cannot make enough plasmin to break down the fibrin in their COVID biofilms. I think that we need to think about this as to what is the best cytokines for these people.
Everybody kind of confuses nattokinase and lumbrokinase. Lumbrokinase is 12 times more potent than nattokinase. And so, that is the one – if I had long COVID, I would be taking to break down the fibrin part in addition to the ECGC and the liposomal curcumin according to the articles published on how to break down a COVID biofilm.
[1:16:28] SCOTT: Long COVID, it’s an interesting conversation. People like Dietrich Klinghardt, Dr. Marie Matheson and others talk about persistence of replication-competent SARS-CoV-2 somewhere in the body. Maybe it’s in the gut. Maybe it’s in other locations. I believe that there’s been some autopsies that have been done that showed SARS-CoV-2. But there’s other very smart people that suggest that long COVID is not persistence of replication-competent virus. But it’s more this S1 subunit of spike protein that gets stuck in the monocytes and creates downstream effects. With what you said with COVID being in biofilms, does that suggest that your perspective is that some people with long COVID still have SARS-CoV-2 that is active and replication-competent in their bodies?
[1:17:27] RUTH: I’m leaning that way. Once again, I’m not a virologist. But because I know that that’s what happens with kids with PANDAS, that they have strep walled off in biofilms and that’s why their strep titers remain high because the strep is still producing the toxins. It just makes sense to me that that’s the way COVID would work as well.
[1:17:50] SCOTT: I lean in the same direction. It’s interesting that now it’s been almost 5 years and that we still don’t seem to have consensus on whether or not long COVID is persistent COVID or chronic COVID. It’s almost like the chronic or persistent Lyme as compared to post-treatment Lyme disease syndrome, whatever that is.
[1:18:16] RUTH: Titles are cheap. Titles are cheap here.
[1:18:19] SCOTT: Okay. Let’s talk then a little bit more about nattokinase and lumbrokinase. Or Boluoke lumbrokinase is the same. Boluoke is the name brand. Is there ever a place where you might use nattokinase with or instead of lumbrokinase or Boluoke. I know you say Boluoke. Tomato, tomato. Do we believe that lumbrokinase breaks down or binds spike protein in a similar manner to what is suggested with nattokinase? And I have reached out to Canada RNA with this question in the past. Why is it that nattokinase is so popular if it’s 8%, I guess, as effective as lumbrokinase based on your 12 times more effective figure? Does it have some other benefit outside of its fibrinolytic properties? Or is it more of a cost issue?
[1:19:12] RUTH: You’re asking all the right questions. And I’m not convinced I have the right answers. I would like to think that, just with other pathogens, if you break down the biofilm, that the body’s immune system can handle it. And so, I’ve not seen the literature you’re talking about with nattokinase and the spikes and the subunits having an effect on that. That would surprise me just because nattokinase is a fibrinolytic. And I’m not aware of these other properties that sounds like an interesting theory. I just haven’t seen any literature to substantiate it. I think if people are finding it effective in Long COVID, it’s because of the biofilm-disrupting properties that are making it effective. Not necessarily because it does anything with the COVID itself. But like I said, I’m not a virologist. I do bladders.
You did ask about would I use nattokinase instead in any circumstances. The one situation in which I think nattokinase might be more beneficial is if someone has compromised kidney function. Nattokinase does break down to urokinase. And urokinase, according to some studies, people with kidney disease, urokinase has been found to be helpful to not only slow down progression but also to show some improvements in some cases. But they didn’t tell me how much they were dosing or how often.
[1:20:55] SCOTT: Building then a little bit on the COVID conversation. Some doctors are using a triple anti-coagulation therapy to deal with coagulation issues related to COVID. Is that approach required from your perspective in some people? Or do we think we can generally support the resulting coagulation, hypercoagulation issues with more natural fibrinolytics? And, of course, we have to think back to the earlier part of the conversation. If there was a genetic component, then there may be more of a place for some of those things. But what are your thoughts on this triple anti-coagulation therapy that’s being used in the long COVID arena?
[1:21:35] RUTH: I’m not a big fan of one-size-fits-all to be perfectly honest. We know people had cytokine storms when they had active COVID that triggered coagulation problems when they were hospitalized. In long COVID, we’re not having in events in the long COVID population because we aren’t having these cytokine cascades or cytokine storms. I’m not sure that anti-coagulants are appropriate unless they have high fibrin production as evidenced by prothrombin fragments 1+2.
I like to know the person’s genetics. Because if they have lipoprotein(a) and need niacin, that’s going to be very different approach than if the person has PAI-1 4G deletions. We have the tools. We can think about what is that person’s body doing? How much fibrin are they producing? What are their genetics? Is their problem on the production side or on the breakdown of fibrin side? And then address it appropriately.
[1:22:49] SCOTT: That makes a lot of sense. If there are microclots in Long COVID, which some suggest, exploring more as to why those are present. And then making more decisions about which direction to go. We didn’t, I don’t think, touch on how treatment may be different in those people with a PAI-1 4G/4G deletion. Is that primarily with fibrinolytics? Or is there something different that would be done in that population?
[1:23:19] RUTH: More fibrinolytics. Enough to break down the fiber that’s being normally produced. And maybe more fibrinolytics if they’ve got a complication of tick-borne infections, or mold toxins, or something else. Pushing more fiber in production. But you can get that number. And then there’s actually a chart from David Berg that shows how much Boluoke or lumbrokinase is needed based on their alpha 2-antiplasmin numbers. There are some good information out there that it’s not a guessing game of how much does that person need or not need.
[1:24:03] SCOTT: Most conventional medicine practitioners, if you talk about coagulation issues, they’re running D-Dimers, they’re running PT/ PTT. They’re not running TATs. They’re not running prothrombin fragments 1+2. I would venture to guess. I mean, maybe there’s a small number. But I feel pretty comfortable with that statement. Why is D-Dimer, and PT/ PTT not adequate? And why do you not even incorporate them into your panel?
[1:24:34] RUTH: I’ve been asked that many a time. It turns out PT, prothrombin time, and PTT, partial thromboplastin time are actually being used to measure how long it takes for your blood to clot. And this is really helpful for someone having an acute clotting event. Or maybe they’re being monitored for heparin dosing. But this doesn’t look at the slower fibrin production which takes place with biofilms or a person trying to break down their biofilms. And that’s what that prothrombin fragments 1+2 and PAI-1 activity is going to tell us.
It’s going to tell us what is the fibrin production. It’s going to tell us how well that person is able to break down that fibrin. Those tests are fine for those situations when someone has an acute clot. But it’s still not going to tell us for the purposes of biofilms and cardiovascular disease what’s contributing to those processes that are slower and take much longer.
Now, D-Dimer is another one that gets misunderstood. Because it’s on a clotting panel, we as practitioners associate that with, “Oh, if I want to know if this person is having a clot, I got to check PT/PTT, and D-Dimer.” But D-Dimer is a degradation product of fibrin when it gets broken down.
If you think about it, if someone’s body is acutely making a clot, then of course they’re going to upregulate fibrinolysis. Their body’s going to try to make a heck of a lot more plasmin. They’re going to break down more fibrin. And the D-Dimer will go up normally.
[1:26:35] SCOTT: Yeah, in a healthy person.
[1:26:37] RUTH: This will not apply to the person who has a PAI-1 4G deletion or elevated lipoprotein(a). Maybe it’ll scrunch up a little bit, but not nearly enough. And there still will be too much fibrin that gets accumulated. And so, what I like – I don’t put it on my panel. But once you put somebody on a fibrinolytic, like lumbrokinase, Boluoke, if you’re doing follow-up labs to check some of those values, if you put a D-Dimer on it, you’ll see it go up because the lumbrokinase is working. And that’s a good thing. And I have gotten a few panicky communications from practitioners, “Oh, no. I put them on lumbrokinase and now they’re making a clot.” And I’ve had to reassure them, “No. It just means that the lumbrokinase is doing its job and they’re breaking down all that extra fibrin that their own bodies have not been doing a good job breaking down.”
[1:27:43] SCOTT: D-Dimer seems like a test that a clinician could interpret incorrectly and move in the wrong direction.
[1:27:53] RUTH: Yes. Yes.
[1:27:56] SCOTT: Let’s talk more then about dissolving these excess soluble fibrin, these fibrin biofilms. Looking at the enzymes. Talk to us about proteolytic, which maybe doesn’t matter so much as I’m understanding, and fibrinolytic enzymes. And how and when they might be used in a treatment protocol? Are there specific brands besides Boluoke, the lumbrokinase that we talked about that you find most clinically effective?
[1:28:26] RUTH: Sure. This is a hot topic now that a lot of lumbrokinase distributors are throwing their hat into the ring. For years, I’ve used Boluoke as the major fibrinolytic. It’s the brand that doesn’t have any other enzymes or other substances added to it. And it’s the one that’s been studied most extensively. Those of you who are practitioners and have access to Researched Nutritionals, there are dozens of pages there of the studies they have done showing its bioavailability, its efficacy. And comparing it to nattokinase, which is where I got the 1/12th as potent numbers from.
Many of the newer brands are less expensive. But when I look at the ingredients in order to get it patented, I presume, they’ve had to put other things with it to make their product unique and special. And so, when you start adding things to Boluoke, which needs to be taken on an empty stomach, I question, “Have you compromised its bioavailability?”
And I haven’t seen any literature from any of the other companies yet. Maybe they’re doing their studies now. But I haven’t seen those studies that show me does it have the same bioavailability if you add nattokinase to it? Or does it have the same efficacy if you make a combination product?
And so, until I see some sort of documentation, if you really want to break down your fibrin, if you have one of these genetic problems in which you don’t break down fibrin as well as the rest of the population, 80% of the population, where you make too much, that’s not a risk I personally wanted to take would be to spend even a little bit less money to get something that may not do as good a job. And that was my decision.
Serrapeptase is the other one I think is kind of in this group. It is actually made from the secretions produced by earthworms just like lumbrokinase. It is less potent. And this was what I chose for children or for very sensitive individuals to start with. It does have proteolytic properties. But we use it for the fibrinolytic properties. Proteases break down proteins. Once again, this isn’t the problem. The fibrin is the problem. We need a fibrinolytic. Just like all biofilms are not created equal, all biofilm disruptors are not created the same.
[1:31:24] SCOTT: I’m almost afraid to ask, but knowing where lumbrokinase and serrapeptase come from, are these reasonable interventions for vegetarians and vegans?
[1:31:39] RUTH: I don’t see a problem. You’re not eating the earthworm. You’re eating the secretions made by the earthworms. I don’t see a problem. But I’m not a vegetarian.
[1:31:50] SCOTT: Nor am I.
[1:31:52] RUTH: I’m a powerlifter. I do my protein. I guess it’s a matter of conscience. I think that nattokinase, which is made from soy, would be the strict vegetarian-approved one. But I think it would be very hard to take enough of it in order to get adequate fibrinolysis on a daily basis.
[1:32:18] SCOTT: Do we even know – I’ve never seen it on the bottle. But is it safe to say “no worm was harmed in the creation of this product”?
Okay. We’re talking about lumbrokinase, nattokinase, serrapeptase. We know lumbrokinase really is significantly more effective. Talk to us about how we might dose these products. I know you mentioned earlier, it can be based on lab values based on David Berg’s work. Is that primarily what you do? Do you use symptoms? Do you start low and work up? Do you start low and retest and work up? How do you approach dosing?
[1:32:57] RUTH: Well, once again, I don’t believe in one size fitting all. A lot of this has to be determined by how medically fragile the patient is. Some people don’t have many symptoms. We can start out a little more aggressively. Some people, even the tiniest amount, can pull the rug out from under them.
And so, there’s another brand product, since we’re mentioning brands here, called Kirkman Biofilm Defense. And that’s the usual one that I start out. Two capsules together once a day for a week before people even do any testing of their urine to break down the biofilms so we can see what’s been harbored in that bladder. Or men do it for a week before we check if they have a prostatitis. That’s a good starting point for most everybody.
The reality is that, at some point, I like everybody to transition over to the Boluoke. They may start with one a day. They may start with one every couple days. They might start with the serrapeptase, which I give children. And gradually build up to where they can tolerate two capsules together once a day. This is an empty stomach. Nothing else with it. And nothing but water for half an hour.
First time in the morning is great time to get that down. Because if you’re a grazer like I am, you may not find many other opportunities to get another dose in. This is also helpful because if a patient needs to take something for the extracellular DNA biofilm at a different time a day, those cannot be combined. They do not play well with each other. They have to be taken at separate times a day. They may take the Boluoke in the morning and they may take the one with the bismuth subnitrate for extracellular DNA half hour before dinner or at bedtime.
It really has to be individualized. But the reality is if you genetically don’t break down fibrin as well as the other, let’s say –
[1:35:14] SCOTT: 80%.
[1:35:16] RUTH: 80%. Well, it’s 80% for all four. But I’m just thinking, if I subtract the Factor II and Factor V people, maybe we’re talking about 65% breaking it down. But if you genetically have trouble breaking down fibrin, you have to help your body the rest of your life. Boluoke is your new best friend for the rest of your life if you want to break down the extra fibrin and your body will make just normally. Whether you even have any other triggers or not, like Lyme or mold. I think we have to just look at what does your body need?
[1:36:00] SCOTT: When we’re dosing Boluoke, is there ever a scenario where you would dose more than once a day? I’ve seen some practitioners do two capsules three times a day. Maybe even higher in some cases. Or am I hearing correctly that doing the full number of capsules one time per day in the morning will have enough of an effect to carry us over to the next morning?
[1:36:25] RUTH: Excellent question. I don’t ever dose more than two at one time. But there is a schedule. And I probably should send that to you. I don’t know if people listening could access that. That was written up by David Berg. Talking about dosing it based on the alpha 2-antiplasmin numbers. And there is a protocol that if it’s less than 125, the dose is two capsules together once a day. If it’s between 125 and 150, it’s two capsules twice a day. And then if it’s over 150, there is a protocol where you go up to a higher dose of six a day for a week and then work your way back down. And this works beautifully to bring the alpha 2-antiplasmin numbers back down. And then the maintenance becomes the two once a day.
[1:37:20] SCOTT: Yeah. I take three a day. Two in the morning and 1 in the evening. I do really good keeping the morning away from food. But to your point, by the time you’re later in the day, it’s a lot harder. Okay. When we start thinking about incorporating tools like lumbrokinase, to me it seems like they are also having an effect on biofilms. That we could potentially then be re-exposing the immune system, re-exposing the mast cells to chronic infections, to heavy metals, to other things that are coming out of Pandora’s box or coming out of biofilms. Is that another reason why some people might feel worse when they’re starting these because they’re having an upregulation of their immune and inflammatory response as a result of what’s coming out of the biofilm?
[1:38:18] RUTH: Absolutely. Absolutely. And that’s why I don’t want people to herx a lot. Because that increased inflammation does what? It triggers more fibrin production. It is sort of a balancing act. And sometimes with some of these things, it can take months to get to the bottom of it, or to eradicate it, or clear it from your body.
I think that people need to regulate that themselves. They get in situations where, “Well, the doctor said I should take so many of these and so many of these a day. And here we are two weeks later and I can’t get out of bed.” Well, I like patients to be able to say this is the goal. You regulate it. You build up to what you’re tolerating. And if it’s pushing you too hard and too fast, back off.
If I have somebody wanting to take a week of, let’s say, Kirkman Biofilm Defense before they collect their urine specimen because I want to see what pathogens are going to come out of the biofilms, if they get wickedly symptomatic on day three, I’ve accomplished the goal. Collect the urine. Back off. Wait until we get the results. And then we’ll re-figure out what you need to be doing. It’s common sense.
[1:39:47] SCOTT: I think it, to me, makes sense before we jump into with the exception of what you just said which is to provoke a test to minimize false negative results and get a more sensitive test result. I like the idea, if someone has fibrin issues, of using something like Boluoke, which is probably going to be a little better tolerated than bringing in the biofilm sledgehammers and unleashing all of these things into the system and triggering mast cells and triggering more inflammation.
In those people where their biofilms are primarily fibrin, it sounds like we can potentially manage them well with Boluoke. And then if they have other issues besides fibrin that are also a component of their biofilm burden, then we could use some of those things later in someone who’s had many different chronic infections, chronic illness, those types of things.
[1:40:45] RUTH: Absolutely. Absolutely. And some of these alternative products do have a place. They are good anti-inflammatories. They do work on the mast cell activation. They have many ways in which they are helpful as adjunct therapy. But they don’t necessarily break down the fibrin. That’s not what we’re going to use them for.
[1:41:12] SCOTT: If we’re thinking about maybe natural things that have fibrinolytic properties, we’re thinking maybe ginger, don quay, garlic, turmeric, maybe vitamin E, ginkgo, bacopa, maybe quercetin, do those have a place in supporting optimal coagulation?
[1:41:31] RUTH: If you have a genetic problem, those are probably not going to be good enough. If you have some that have been triggered because of other things going on, exposures to mold or tick-borne things but you don’t have genetic problems, I think they have more of a place. But you still might need more potent fibrinolytics while you’re still actively addressing those things.
The one you brought up about quercetin, I particularly want to focus on. Because quercetin reduces COMT protection, catechol methyltransferase. And I found a high percentage of my patients had COMT mutations for those I had that data on. And that concerns me. COMT has a couple of job descriptions. It helps to break down epinephrine or adrenaline. These people oftentimes have trouble falling asleep, particularly if they watched a scary movie, had a fight with their spouse, or got anxious about something before bed. They had sleep issues to begin with.
And the second thing it does is that COMT breaks down glutamates which amplify pain signals at the nerve synapses. And so, if you have chronic population with chronic pain because of Lyme or urinary tract infections, you don’t want to be amplifying that pain even to a greater extent because of a lack of COMT breaking down the glutamates.
And then the third thing that COMT does, it’s sort of like the wheelbarrow that takes ADP, adenosine diphosphate, off to the mitochondria to make ATP. And so, these people already have a lot of fatigue issues. I would not want to give quercetin to anybody with a COMT mutation for those reasons. We’ve got a chronic disease population. They’re battling enough back battles. We do not need to be adding to their sleep deprivation, their pain perception, or their fatigue by further lowering their available COMT.
[1:44:03] SCOTT: And that probably is a very good explanation of why not everyone tolerates quercetin. Yeah. Thank you for those insights.
You mentioned earlier, PANS, and PANDAS, and the potential for having some of these infections in biofilm. Do we treat hypercoagulation in children? And what considerations, if any, need to be given to the pediatric population from a fibrin buildup or hypercoagulation perspective?
[1:44:33] RUTH: I kind of got into this through the back door. I had a number of women who had bladder issues, with chronic UTIs or IC. And in conversing with them occasionally, something would come up about their child who had PANS, or PANDAS, or Lyme disease. I had this sneaking suspicion that maybe they had inherited some of their mother’s genetic reasons for why they had those chronic conditions.
And so, when that came up, I would treat the children by first checking their genetics. Because even if I knew the mother’s genetics, I didn’t necessarily know their father’s genetics. And universally, these children all had one of these or more. Things where they were making too much fibrin. Or they weren’t breaking it down efficiently.
And so, when I normalized their fibrin production and breakdown and then I went after the underlying infections, whether it was viral, and I used the Beyond Balance herbal drops for the children, or PANDAS, in which it was a strep infection that had been still embedded in the biofilms. And I knew that because the strep titers were still high. And I would give them something for the strep in addition to breaking down the biofilms. And the Lyme disease, once again, I used only herbals with knowing how to break down that child’s biofilms. And I had excellent success great. The PANS went away. The PANDAS went away. I could prove it with the strep titers going down. Although, that lagged a couple months behind. And the kids got better from Lyme.
Once again, that convinced me that the biofilms were the problem. And knowing that COVID is a virus and PANS is caused by viruses that are embedded in the biofilms, there’s no reason why children should have to live for years and years and years on antibiotics for their PANDAS or their Lyme disease.
[1:46:58] SCOTT: If we think about the potential for complications in either adults or children, over-thinning, shifting from hyperviscous to more of a bleeding scenario, how likely is that that there could be any significant side effects when we’re bringing in fibrinolytic enzymes like those we’ve talked about?
[1:47:21] RUTH: I don’t think there’s any risk at all. Because, remember, we’re normalizing. We are not anti-coagulating. And we have the ability to check their prothrombin fragments and know if we’ve pushed them too far or not. Not only do we know this from a clinical standpoint of how this works. But, also, we have lab values to confirm that we’re being safe in this population. And to be honest with you, I never had any issues when they were being dosed according to the person’s α2AP level and then monitored.
[1:47:59] SCOTT: As we come into our last couple of questions, I wanted to ask you to talk a little bit about the panel. I’m not sure that we’ve mentioned the specific code. It’s incredible to be able to take this one code, go to Labcorp, get this full panel. It used to be much more complicated. I will tell you, sometimes Labcorp is a little confused. They can’t always readily find it in their system. You have to tell them to look it up manually. I’ve gone through that process. But it absolutely worked. Other than I knew something was a little wrong when they gave me a 24-hour urine collection container for my coagulation study. I asked them. I’m like, “I don’t think this is quite what I’m looking for.” And so, they figured that out.
But tell us a little more about the Labcorp panel. Tell us a little more about your consultation work. Do you consult directly with patients? Is your focus with practitioners? Can patients be part of that conversation? What are some resources that you want to refer people to in order to learn more about your work?
[1:49:06] RUTH: The panel that was put together for me by Labcorp is a specialty panel. Its number is 505443. It is a working panel. But because it is a panel put together for me as a practitioner, it will never appear on the website. However, practitioners can put that number in their EMR. They can order it through the Labcorp link system. And worst-case scenario, they can take a paper lab order form and write that number in.
The ICD10 codes that work, I do have a complete handout. But I can provide a list of ICD10 codes that insurance, Medicare, TRICARE, accept for running the panel. And this is a great gift. Because, previously, we had to order each test separately. And there was no reflex. And I was sending about 70% of my patients back for retests, which got a little bit cumbersome. Having that reflex ability has been amazing and wonderful.
Now, if you don’t want to run it through Labcorp, you can order the tests individually through Quest or another lab system. But be aware, it will not reflex. If the APCR comes back low or if the PAI-1 activity comes back less than 4.4, you will need to write the lab order for the genetic Leiden Factor V test, or the PAI-1 4G/5G genetic test and send that patient back for a redraw.
There’s another way in which this can be done. It turns out that the Professional Co-op in Florida negotiates prices with Labcorp, if a person doesn’t want to go through insurance or doesn’t have insurance, this panel that costs – I think it’s billed insurance around $2,000. It can be done through the co-op cash pay for 399. And then if there is an add-on PAI-1 genetic or Leiden Factor V genetic, there is an additional charge. I think the PAI-1 is 139. And the Leiden Factor V is 99. That’s a very cost-effective way. It’s still cheaper than the Labcorp cash price, which is $1,000.
I do have a website. It’s very simple. RuthKriz.com. On that site, there is the scheduling link if you want to schedule time with me as a practitioner to go over patient results. That would include MicroGen results or the hypercoagulation results. Like I say, I do bladders. I’m not going through every lab you’ve ever run on every patient here.
The other resources on the website, we are just now putting in a resource for patients in which they can go to the website and put in where they live. We’re starting with the states. We are going to get to the countries. Because I have about 350 practitioners in the United States and 70 practitioners I’ve talked with in other countries. The ones that have followed through and become more proficient in how to interpret these results are going to be listed on my website by state. If you’re from another country, you may just have to go through the referral process that’s listed on the website for me to email you individually until we get the other countries put on that format. Exciting things are happening. I’m getting more speaking opportunities. And I’m just really excited that Scott’s given me this one.
[1:53:20] SCOTT: Well, I’m excited too. And I also want to let practitioners know that you are in the final stages of launching your practitioner training modules. They can also find that very soon on your website at RuthKriz.com. That will be exciting as well.
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 in support of your own health?
[1:53:45] RUTH: Oh. Well, I resisted answering this question. Scotty’s saying, “Yes. You did. I had to ask you more than once.” But I realize that it is probably helpful for you to understand a little bit about what I’m all about as a person. I’m a firm believer that the quality of life matters. Not just longevity for the sake of racking up lots of years. Although, I wouldn’t complain if I live longer than my relatives given the genetics I inherited.
As a Factor II homozygous person, I know that I am always one blood clot away from potentially leaving this Earth. And so, I will always need a low-dose of Eliquis to keep my fibrin generation down to a normal amount on a daily basis. I also need to take Boluoke as a safety net to break down any extra fibrin before it deposits in biofilms or atherosclerotic plaque.
Exercise is a big part of my life not only as a stress reliever, but because it increases PAI-1 activity. This is huge. All of you practitioners out there who know the value of exercise, have another compelling argument for people with these genetics with too much fibrin is exercise will help your own body do a better job of breaking it down.
Several years ago, I started exercising with weights. And I graduated to a barbell. And I now can do squats, and bench presses, and deadlifts. As a result, my osteoporosis has reversed and if I’m given a platform here. I’ve been setting national records for my age group and weight class. Now, granted there isn’t a whole lot of competition in my age group, but knowing that longevity is related to strength. I’m really hopeful that I can continue adding life to my years and be here to support all of you who are looking for answers for yourselves and for patients.
[1:56:06] SCOTT: I love that and the graphic for the episode art for this conversation actually has a picture of you, as a lady who lifts. And I definitely could not do what you do. I think that’s incredible. This was such an incredible conversation. I think you guided us through the thickness of the weeds to really thin things out and bring us more clarity. Sorry for the puns there. But we are talking about thick and thin blood. I think you are just so incredible. You’ve been generous with your time. But I really think that you make a huge difference in so many lives. Bringing awareness around this conversation, around chronic UTIs, around interstitial cystitis, around some of the latest testing that’s available with MicroGenDX. I know that you are kind of the ripple in the pond affecting so many other practitioners that then can really exponentially impact their patience. I hope you are and I expect you will be here much, much longer. But I would say that you have lived a life very, very well-lived. Thank you, Ruth. I just so appreciate and honor you.
[1:57:24] RUTH: Oh. Well, thank you so much. I love what I do. And that’s why, at 76, I’m still doing it.
[OUTRO]
[1:57:31] SCOTT: To learn more about today’s guest, visit ruthkriz.com. That’s RuthKriz.com. RuthKriz.com. Thanks so much for listening to today’s episode. If you’re enjoying the podcast, please leave a positive rating or review, as doing so will help the show reach a broader audience. To support the show, visit BetterHealthGuy.com/donate. To get my newsletters, visit BetterHealthGuy.com/newsletters. To follow me on Facebook, Instagram, X, or TikTok, you can find me there as BetterHealthGuy. This and other episodes can be found on Apple Podcasts, Spotify, Amazon Music, YouTube, and Odysee.
[1:58:16] ANNOUNCER: Thanks for listening to this BetterHealthGuy Blogcast with Scott, your BetterHealthGuy. To check out additional shows and learn more about Scott’s personal journey to better health, please visit BetterHealthGuy.com.
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