Episode #123: Hypercoagulation with Dr. Ann Corson, MD

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

Hello everyone and welcome to episode number 123 of the Better Health Guy Blogcast series. Today's guest is Dr. Anne Corson and the topic of the show is hypercoagulation. Dr. Ann Courson grew up in Southeastern Pennsylvania and obtained her MD Degree from the University of Pennsylvania State University School of Medicine in Philadelphia in 1982. Dr. Courson has residency training in internal medicine, neurology and family medicine. She's been board certified in the practice of family medicine since 1993. In 2005 she began studying and practicing integrative medicine and was Board certified in Integrative holistic medicine in 2011. Dr. Courson became a member of the International Lyme and Associated diseases Society, or ILADS, in 2003 and studied with Dr. Joe Burscano and Dr. Charles Ray Jones. Her practice in Chester County, Pennsylvania is devoted full time to the treatment of patients suffering from chronic vector borne diseases and environmental illnesses. She has a wealth of knowledge and experience in treating these kinds of conditions and is passionate about finding solutions for her patients. And now my interview with Dr. Anne Marie Corson. You and I have talked about hypercoagulation over the years and the information that you shared with me has been tremendously helpful in my own health recovery journey. You presented hypercoagulation to over 300 practitioners at the Forum for Integrative Medicine in March of this year and I knew then that we had to share this on the podcast and my hope in this conversation today and for those people listening is that they'll really ask their doctor about the potential role of hypercoagulation in their chronic condition and that this conversation will also lead to more practitioners really deepening their understanding of this important topic. So once again, it's an honor to have you on the show. Thank you so much for being here, Dr. Corson.

Thank you, Scott. It really is a lot of fun to be able to be here with you today and to share what I have learned about this very important clinical issue in our chronic renal patients. So I just wanted to give you a little bit of history about it. You know, I first learned about hypercoagulability in 2005 from lectures that were being given by Dr. Gary Klepper during educational conferences that were sponsored by Mike Sheehan of the Bioresource Incorporated company out in California. And it was actually a conference in Denver that I went to in 2005. You know, Gary and his wife Raine, are really incredibly brilliant practitioners who were teaching the principles of German biological medicine, traditional Chinese medicine, and naturopathic methods using the different types of spaghetti, homeopathics, neuromodulating medicines, and nutraceuticals, among other things that Mike Sheehan bringing into the United States. And Gary had learned about the evaluation, diagnosis and treatment of hyperfitability from actually Dr. David Berg himself, who was the one that really brought this into the awareness of clinicians. And he learned in 2003 from Dr. Berg. And then Gary very rapidly incorporated this into his treatments and shared this information in his lectures. So I, when I learned about it in 2005, immediately began applying his treatment recommendations to my patient population as I recognized that many of my patients demonstrated, both on laboratory and physical evaluation, varying degrees of hypercoagulation stress. And then later, I was able to learn even more about hyper coagulability directly from Dr. Berg's lectures. He gave four lectures in 2011, and then again he gave other lectures in 2012 and at two different conferences that were sponsored by Dennis Schoen of Research Nutritionals. And Research Nutritionals does still sell links to the DVDs of both of those conferences on their website. So again, as soon as I learned about hyperpragability in 2005, it became very clear to me that nearly all my patients had some degree of hyperpritability and could benefit from treatment for it. As we worked on the underlying infections and toxins that were stimulating hypercoagability in the first place. And then over the years, I found that addressing it in my patients made their the treatment of their underlying infections and toxins, their detoxification, easier, and it shortened the time for them to regain health. So I really think that all practitioners should at least think about this incredibly common pathological state in all of their patients and investigate for it in those with suggested clinical findings. Because a great deal of the suffering that our patients endure can be reduced and the healing processes of their bodies augmented significantly. If all practitioners understood this issue.

I do feel, based on my own personal journey, that hypercoagulation is really one of the most overlooked issues in treating conditions like Lyme disease, like mold illness. So let's jump in with what Is hypercoagulation. And what happens in the body when the molecules that are encouraging blood clotting and blood thinning are imbalanced in health.

The body maintains this wonderful balance between making fibrin and breaking down fibrin. And when the scale is tipped in either direction and the body can't recover homeostasis as a result of some stressful event, say a genetic weakness, a physical trauma, an infection toxin, then the patient may experience either excessive bleeding, as in hemophiliacs, or more commonly, varying degrees of hypercoagulability or stickiness and the tendency to clot and to make excessive soluble fiber. So again, the body maintains this incredibly delicate balance of proteins to either encourage or discourage blood clotting. And it's a very, very complex and redundant system. A lot of checks and balances. So you think about it, after we cut ourselves and have an injury, we must be immediately able to stop that bleeding by plugging the holes. And then we also have to be very ready and able to thin the blood and contain that clot formation just around that small hole in order to avoid losing our blood and pouring it out of our body through the rent in the vessel. So there's always this balance. So a hypercoagulable state results when there is too many factors, an abundance of molecules that are encouraging the formation of soluble fibrin and clotting over blood thinning. So it's called the coagulation cascade of the proteins that do this. And there are a whole series of enzymatic reactions where the end product is the production of soluble fibrin molecules. Okay, so soluble fibrin can be a monomer, a polymer, a pro fibril, but it's only with a burst of thrombin that you get when a blood vessel has opened somehow, then those fibrin will link together to form cross linked insoluble fibrin or blood clot. So generally, in the absence of a tear in a blood vessel wall, there's not enough of a burst of thrombin to actually create a clot. So in the majority of hyperchrivable patients, they only make soluble fibrin, which is kind of making a sludge, which makes your blood more like molasses than water. So if the production of soluble fibrin outpaces the breaking down of it, or fibrinolysis lysis is breaking down, the fibrin will accumulate on the endothelial linings as sort of a sludge like layer, which then traps toxins, traps infections, and can trap things like thrombin, which is a biologically active molecule.

So this sludge layer that you just referenced leads to trapping of infections and toxins. How is it similar to the concept of biofilm? Is the sludge and hypercoagulation different from a biofilm, or is there some overlap between these two concepts?

Well, you could think of that sludge as it is laying up against the endothelial lining or the cell lining as a biofilm. There are also biofilms out in tissues which are niduses of toxins and infections that are growing out in tissue. And they can have fibrin incorporated into that biofilm, or there are also free floating biofilms in the bloodstream. And a lot of their matrix that they have are polysaccharide matrixes, all kinds of proteolytic glycans, all kinds of. You do have fibrin with those. And so you think of a biofilm as having also infectious agents in it, sort of like a shopping mall, and have a few dominant stores, a few dominant organisms, and a whole lot of little other ones too. But this, when you talk about this, the sludge of hypercoagability, it is fibrin, but it's a lot of other things in it. So there is an overlap. But I wouldn't say call the biofilm floating around the bloodstream just sludge, because that's really a more organized biofilm community like the ones that you see on a fry lab smear.

So in the context then of hypercoagulation, what happens in terms of oxygen delivery, nutrient delivery, when we're hypercoagulated? Does hypercoagulation lead to some cellular starvation of sorts? And do treatment protocols work better when hypercoagulation is addressed? Meaning if we're taking herbs, we're taking nutrients and things like that in our protocol, do they work better when they're more able to freely move throughout the body?

Most certainly. So there are a lot of consequences of being hyper coagulable and having excessive soluble fibrin laid down in the body that you're not breaking down. And if you think about the sludge layer of fibrin, if you just get 1 micron, which is 10 to the negative, 6 meters of soluble fibrin along the lining of endothelial cell in the inside of the blood vessel or capillary, it reduces the ability of oxygen to get through that sludge layer into the cell of the endothelium by 500%. So 1 micron, decreasing oxygen in diffusion by 500% is a lot, but it is Your tissues get very hypoxic. They have a lack of oxygen. You need oxygen, of course, for oxidative phosphorylation in the mitochondria in order to, to generate ATP. You need the oxygen at the end, except the hydrogen, to make water. So the congestion that develops as a result of this inability to get oxygen out, then you also have the inability to get all kinds of nutrients out, all kinds of transfer factors, hormones. And then you're not able to get waste back into the vasculature. So you get intravascular congestion, you get extravascular congestion in the extracellular matrix space. And this results in organ and tissue compromise. So nutrients, hormones, and tissue factors can't exit blood vessels, and metabolic wastes and toxins can't go from the tissues back into the lymphatics and in the vessels in order to be excreted. And then again, another problem that you have, we have too much soluble fibrin among the blood vessel walls that you lose the rapidity with which you can either vasodilate or vasoconstrict. So this sludge kind of makes a rigid blood vessel wall, and so it's hard for you to adapt to external temperature changes. A lot of these people are really heat intolerant because they can't dilate their blood vessels very well to release heat. Right. Or they can't develop a sweat very well, or they can't constrict their blood vessels when they stand up very well in order to keep them from dropping their blood pressure and they get lightheaded and dizz. A lot of things happen with the ability of the autonomic nervous system to control blood vessel dilatation and constriction. If there's too much soluble fiber, it really affects the body in a lot of ways, including just blood pressure control. So, yes, the treatment protocols work a whole lot better when hyperpritability is being addressed dramatically better. Herxdheimer's are a lot less, Herxheimer's are ameliorated. And people can tolerate higher treatments, either higher intensity antimicrobial treatment, more rapidly, sooner in their treatment. And so all of the herbs and nutrients that we use to do this and the enzymes we use really, really work a lot better when you've got free flow of fluid and you're not all jammed up with glue.

So you mentioned a number of things that can happen when we're hypercoagulated. But let's dig a little bit more into some of the key symptoms. And when you're working with a patient. What kind of clinical clues you in to begin exploring hypercoagulation as a priority? You mentioned that it's essentially an issue for all of your patients. But at what point do you say, now's the time, we really need to explore this? And then it sounds like essentially almost 100% of your patients that this has proven to be an issue for them. So talk to us about the key symptoms, what clues you in, and a little bit about your clinical observations.

Well, these are the people that complain of a lot of diffuse just body pain. They can also have trouble sitting still. They're fidgety. They complain that their limbs fall asleep easily when they cross their legs or they put their arm down on a table. They fall asleep a lot sooner than it used to. They're achy. They have sharp, stabbing shooting pains that come and go. They have neuropathies in the hands and feet. Sometimes they're very brain foggy. They get very irritable. They get sensory hypersensitivity. They get anxiety. They can't sleep. They're stiff when they wake up in the morning, they're stiff after being sedentary. They have nausea, especially in the morning. Sometimes they have painful teeth. And I sort of relate that to when people are hyperpluggable from babesia, the painful teeth. I don't know if that's true, but that's an association, I find. They can't exercise at all. Exercise crashes them. They have mottled skin on examination, cold and clammy extremities. When you look at their tongue, sometimes the edges are a little bit scallopy. When you go to examine their abdomen, it's kind of doughy and diffusely tender, especially in the periumbilical region. They look like they just have sort of tissue congestion. They look like they would have edema, but they don't. You know, the tissues are just puffy. You don't see a nice delineation between the bones. And the skin on the back of the hand tissues are just sort of puffyish. And they have often horrible capillary refill. Sometimes the capillary refill can be so bad in the feet that feet look purple when they're dependent. And another thing that I look at is sort of that generalized modeling sort of the skin. You know, when you see that sort of. They almost look like a model, like what a young baby looks like when they first are born and their bodies are constricting because of the cold outside the womb. Is that kind of a modeling that you see superficially. And then often you'll see an exaggeration of dermographia, sort of mast cell activation type things in these people. And sometimes when you examine their abdomen, I always put the stethoscope down the abdomen. When you lift it up, you see that it takes a while for that capillary refill to come back. And sometimes after the capillaries refill, you get sort of a red flare. You see a little red ring on the abdomen where you've lifted off your stethoscope, as long as it's accentuated a second or third time when you listen to all four quadrants of the abdomen on the skin. And that can give you a hint that you've really got dysfunction in the small capillaries. And you may have some mast cell activation. If you do an office pulse ox on people, the pulse ox just doesn't work in the people that are really hypercoagul because you just can't get blood flow down in there, so you can't measure a pulse oxygen very well.

Very interesting. Tell us then a little bit about the priority of hypercoagulation in evaluating and treating your patients. Is this something that you do in everyone right at the beginning, or are there certain things that lead you to say, okay, now it's time for us to go down the hypercoagulation path?

Well, just about everybody I see gets put on some kind of an enzyme. So I'm thinking about it. You know, there's sort of a bell curve of severity of it, and it's really only in the really severe ones that I will immediately, the first time I see them, do my whole blood workup, my whole blood panel workup. If I can just treat clinically based upon symptoms and they improve and it doesn't take a whole lot of enzymes, then I don't always do the whole workup. Now, if there's a family history of blood clots, if there's a history of antiphospholipid syndrome, if there's a history of any kind of Raynaud's, if there's a history of frequent miscarriages, you know, blood clots, those kind of things, then I'll definitely do that right away on patients. If there's a positive family history of something having to do with clotting abnormalities, and then if they're really sick, often, I'll do it. You know, the people that come in that are, you know, have untreated tick borne diseases, they are living in a moldy house, they have a high emf environment, they're eating regular food, so they're up to their eyeballs and toxins, they've got metal, mercury, magnesium in their mouth. Those people are all going to need an evaluation with the lab testing.

Is there any truth to the idea that when you're having blood drawn that if it's difficult to get the blood drawn or if it looks black, almost like motor oil rather than kind of bright red, is there any possibility that that can be an indication of hypercoagulation or hyperviscosity?

Yeah, I asked my nurse about this. He does most of the blood drawing. I do it when it's a difficult case. What will happen is we use a 23 gauge butterfly with a tube on it. So that's a very good test for us because they're really hyper plagiable. The blood will clot and you won't be able to get it out. Sometimes the blood will clot too rapidly in the tube. When you draw blood, you invert it a couple of times, then you let it sit for 10 or 15 minutes and then you spin it in centrifuge. If you're going to be separating it or if you're just keeping it in a blood tube, you just turn it upside down, it shouldn't clot. Right. Because you've got heparin in the tube to keep it from clotting on a purple top or a green top. So if the blood clots too much, then yes, that's a good sign. Now, I don't see too much the really dark blood. What I see is when people have a babesia flare, they're bright red. They're like arterial red from venous blood. Venous blood should have sort of a purpley hue to it, shouldn't be red red like arterial blood. But that's what we see with, you know, when you draw blood that they, they clot in the tube, you know, they got real problems.

You mentioned the familial potential that that may give you some clues that a patient may have hypercoagulation based on symptoms of others in their family? So talk to us a little about the genetic factors in hypercoagulation. What are some of the potential predispositions? And can someone without any predisposition genetically still become hypercoagulated when they have a chronic illness like Lyme disease or mold illness, for example?

Example. David Berg always taught us that about one in five people have some genetic SNP that tends to make them a little bit stickier than average under physiological stress. So they may be chugging along just fine in life and not have much of a problem until they get a significant stress. And that stress can be a chronic illness, a toxin, a surgery, an emotional trauma, physical trauma. So it doesn't have to be just an infection or toxicity. So that's 20% of the population. Right. But people who are chronically ill tend to also have hyperprigability. So think about it this way. If we have about 1 in 4 people have biotoxin illness from mold, about 1 in 5 have a genetic SNP that tend to make them too skin when they're stressed. You know, look at all the chronic people we have. You know, almost all of our chronic people are going to be hyperquagable to some extent. Like 95% of chronic patients. The patients that don't get chronic, you know, what is it? Only about 25% of the people who get Lyme disease get really sick from it and stay chronic. Well, you know, the chronic people that we see or that I see are going to be the ones that have these problems. So that's why so many of our chronic population have hyperclasmic. Now, if you are a practitioner that you see relatively healthy walkie talkie people, then it may not be as big of a problem for you, but your patients will still really benefit from you learning how to use enzymes properly. The kind of people I see, almost all of them are hyperpragable because of these physiological stresses.

And someone could be hypercoagulated in absence of that 20% that have the genetic predisposition. Right.

If you line up all of the, you know, the hits against you, you know, even if you have normal, you know, genetics and you're not, you know, you don't have a genetic weakness of protein S or protein C, or you don't have elevated lipoprotein A or alpha 2a plasmin, genetically right, you could be completely fine. But if you've got a whole bunch of things like a mouthful of metal amalgams and you're living in a smart home and, and you have tick bites and you have mold in the basement, you've got too many things that breaks the camel's back and then that's too much stress. And even a person who doesn't have a genetic SNP can still have significant hyper coagulant stress. Yes.

So let's then talk a little bit about those triggers or precipitating events that can lead to hypercoagulation. Are there some in your mind that are more significant than others? You've mentioned babesia for example, or maybe how heavy metals or mold. You alluded to the fact that EMFs could potentially be a trigger as well. So what are some of the key triggers that you see and which ones are more predominant in your patient population?

Well, to get right to the punchline, I think it's sort of neck and neck between babesia and mold. I think some of the toughest people I see are the ones that have real chronic babesia, delicate, and then have other factors. The other thing, which is a really real strong precipitating event is, say, if you're trying to detox heavy metals like lead and mercury too fast, that can trigger an incredible hypercoagulation crisis. But becoming a little hypercoagulable is normal for a lot of things. It happens during the natural aging process. It happens during pregnancy. Pregnancy is a hyperfiber state. So when you've got a chronically ill pregnant patient, you've got to really take care of that during pregnancy in order to avoid the consequences such as preeclampsia or all kinds of placental abnormalities or intrauterine growth retardation, et cetera, et cetera, et cetera. So, and of the infectious agents, you know, babesia is right up there. I think bartonella is very important, too, especially in the small vasculature. And that really manifests in the hands and feet, and it manifests a lot in the small blood vessels to the skin. And then, of course, cancer is a hyperpigment state. Cancer. I don't see a lot of cancer in my patients, though, So I don't have a lot of experience with cancer patients, to be quite frank with you, at least in my Lyme practice. Again, the heavy metals are horrible. Vaccinations can sometimes create a lot of inflammation, enough that precipitates somebody into a hyperpigmentation state. So often, if you're trying to buffer mandatory vaccinations, don't forget the enzymes when you're treating them with whatever it is, the phospholipids and the vitamin A and, you know, so you use that. And then I find some people get really, really sticky with the electromagnetic radiation pollution, and then the trichothecines of the sacchivotry and malamia trichoderma mold really create a lot of hypercritability. Some people, when they get a mole hit, they just have to be just sucking down bellucinatokinase at the same time for hours in order to get back to equilibrium from a bad mold hit. Trichophysios are worse than the ochratoxins or the aflatoxins or the gliotoxins, I think, in my opinion. But those are the things that tend to be the key precipitating factors and events that lead to hypercarbonal state.

So we have these triggers, but then we also can have other factors that either increase it or exacerbate. Exacerbate pre existing hypercoagulation. So what are the things that potentially make an existing coagulopathy worse?

Any type of infection, like if you had an acute infection on top, like your chronic Lyme patient, and you get the flu, you know you're gonna have your hypercoagulability exacerbated. Any febrile illness, if you have trauma, physical trauma, you get in a car accident, any kind of worsening of your gut dysbiosis, any kind of problems with dental infection, any new toxic load from the vaccination. If you have a Herxheimer reaction, you're in treatment for your chronic Lyme disease, you have a Hirschheimer reaction. That cytokine flare will exacerbate hyperprivability. Getting a mold hit from a horribly moldy store that you go into or movie theater or friend's house will also exacerbate it. And as you are detoxifying from things like molds and heavy metals, when you are pulling those out of people's bodies, that can also exacerbate isopercoagmability. So whenever my patients are having a Hirschheimer reaction, one of the first things I do is I usually double their enzymes because you will get from the cytokine flare, you will have activation of the coagulation cascade and that will increase the production of soluble fibrin, which will exacerbate your hypertension. And then another big one, I think is the glyphosate induced sulfate deficiency because of the deficiency of the heparin sulfates on the endothelial membrane.

So if sulfate deficiency related to glyphosate, for example, is playing a role in hypercoagulation, then do we focus on detoxifying the glyphosate? Do we figure out ways to increase sulfate? How do you approach that piece of hypercoagulation? And is there a way to increase the available sulfate in the body?

Yeah, it's very important that people take control of their diet and stop putting glyphosate into their body as much as they can. It's very difficult because it's in our air, our soil, our water. It's everywhere. But it really, this is a lot of the work Dr. Stephanie Seneth has done, and then there's even work before that I'll talk about in a second. So glyphosate impairs the sulfite oxidase enzyme, which leads to sulfate deficiency. And then you need sulfated proteins in the gut to maintain your gut impermeability. So you get leaky gut when you have a deficiency of sulfated proteins. Also, the glyphosate impairs the gut bacterial sulfite reductase enzymes, which leads to a production of toxic hydrogen sulfide. I think we've all had patients that get really sick from any sulfate. You know, they can't take an Epsom salt bath because it makes them sick. Well, these are the people who have such horrible gut dysbiosis that they have an overgrowth of bacteria, or the bacteria don't have the sulfite reductase enzyme functioning because of glyphosate poisoning. So what the gut bacteria, the dysbiotic bacteria do is they make toxic hydrogen sulfide gas, and that's really toxic to the body. So one of the things when you're trying, you think you're giving sulfate to people, and they say they don't tolerate it. You've got to fix your gut. Disabled, occurred. So how does sulfate deficiency lead to other chronic diseases? Well, it's really important because all of our cholesterol is carried around and really utilized as cholesterol sulfate. You wouldn't be able to, you know, take that molecule all over the blood unless it's sulfated. Okay, so there was a really neat article that I can give you these three articles I'm going to talk about in PDFs. I have them, and you can share them with the listeners. One from the Journal of Lipid Research in 2003 that really showed there was a review about cholesterol sulfate and why it was important in human physiology. And it's a regulatory molecule for membrane stabilization, especially along the endothelial border. It helps to regulate protein clotting factors, platelet adhesion, fibrinolysis, as well as carinitocyte differentiation. So in 2015, Seneff wrote an article where she had a theory that sulfate cholesterol sulfate deficiency syndrome is really an etiological factor for atherosclerotic disease. And she was explaining atherosclerotic disease as a cholesterol sulfate deficiency. And that was in the Theoretical Biological Medical Modeling Journal. Then she also wrote one of the. She has, like, six series she did with other writers about the effects of Glyphosate on our whole metabolism. And she was postulating that glyphosate's disruption of our gut microbiome induces sulfate deficiency. And that can explain for things like the epidemic of gout we have and other associated chronic diseases in the industrialized world. So you can see that it's very, very important, the sulfate. So how do we get. Also, vitamin D is transported around the body, is vitamin B sulfate. Sulfate is required for proper functioning of immune system cells. And again, by creating a deficiency in the heparin sulfates on the endothelial cells, as well as the cholesterol sulfate in the membrane systems, it contributes to hyperprint ability. So how do you fix that? Well, you can take Epsom salt baths, you can have some msm, also eating cruciferous vegetables, fresh ginger, garlic, coriander, turmeric. All the nutrients that have sulfate in them that you can absorb in an organic, biological way.

Yeah. So for people that are interested in more on this sulfate topic, one of my recent books that I really enjoyed is called called the Devil in the Garlic by Dr. Greg Nye. And he goes into all the detail on this whole sulfate and sulfur topic, including some of Stephanie Seneff's work. So I highly recommend that book. Let's talk a little bit now about the detoxification. You mentioned that necessary attempts to detoxify the body can trigger the coagulation cascade. So given that we really need to detoxify to recover health, but that doing it too aggressively can be counterproductive and further trigger hypercoagulation, how do we detoxify the body but minimize the potential for this increase in hypercoagulation? Do we need to go slower? Do we need to focus more on the enzymes? How do we balance that?

Well, that's really the art of practicing medicine, because what you're doing is you are making sure that all of the exit pathways are open. You make sure that people are moving their bowels every day. They have sufficient binders on board to bind toxins that are dumped into their gut from their bile. You make sure that their kidneys are working. You've got good kidney regulation and drainage medicines. Your phase one and phase two liver detoxification pathways, you're chugging on all cylinders. You've got whatever type of drainage and regulation medicines or their lymphatic system, you know, all the organ systems so they're supported so that the drains are open. And you start slow because as you dissolve that excess soluble fibrin in that glob of sludge and Debris. You can have all kinds of what Gary Klepper used to call hot potato toxins. You can have heavy metals that have been locked away, and the body just sort of grooves the fibrin up around it to get it out of the system. Right. You can have mold toxins, you can have infectious agents, you can even have thrombin. And if you go too quickly, you can overcome the body's ability to get the toxins out. And then that can in turn stimulate more hypercoagability. So you just have to go slow, take your time, and then push it and make sure that you're going to have a hard time treating anybody if they're still living in mold, if they're mold patient, they've got to get out of mold. They've got to change their diet. They're not going to stop eating gluten, if they're not going to stop eating sugar, if they're not going to stop eating regular standard American diet, which is the SAD diet, really is SAD diet. And they're not going to make those lifestyle changes, reduce some of the EMFs, then it's going to be very hard to help them. So it's relatively easy to, when somebody is doing what they need to do to then open up their excretory pathways, stimulate the detoxification, support them with whatever herbs and enzymes and everything you need to do that. And then you can really grind away at this excess soluble fibrin and then deal with these skeletons that come out of the closet. Also looks, you know, your virus really flared because we just let it loose. And so you have to be prepared. And when people all of a sudden start to have a symptom, then they've got to know they need to contact you and deal with it. But it's not difficult. It's actually fun to do that as long as you are aware of the fact that it can happen.

So we're talking about detoxification potentially triggering hypercoagulation. We also have the potential for detoxification or for toxins moving in the body to trigger mast cell activation syndrome. And so is there a connection between the mast cell activation and the hypercoagulation, or is it independent in that the toxins are triggering each of them, but that the mast cell activation and hypercoagulation are not directly connected in some way?

I myself am not aware of a direct correlation where mast cells, you know, actually directly influence coagulation. They may. That's just my lack of knowledge. But it's part of how each individual responds to inflammation Some people's mast cells are turned on more than others. And once they get all turned on and all the heat's on, then they just. It's just this, you know, positive feedback cycle. It just keeps going. So they're probably co passengers on the bus who take turns driving the bus of the illness. I'm not sure about direct relationships one way or the other. I just don't have that knowledge. But not everybody who's hypercoagulgable will have mast cell problems, and not everybody who has mast cell problems are horribly hypercoagulgable. You would need to treat with enzymes in just about everybody. But you know, there are going to be varying degrees of hyperpritability in mast cell patients. But a large proportion of our patients have really turned on dysfunctional mast cells. And those manifestations are a whole other talk. Right.

Talk to us about the three systems that control coagulation and how do they fit into this whole conversation?

Okay, well, you've got fibrin formation, you've got fibrin degradation, you have platelet activation. Okay, so those are the three main systems. So platelets really are the ones that help to plug holes in vasculature. They let clump around areas of real high toxicity. You have infectious foci. White cell blood cells call them to come in. And platelets can either be acutely activated, which often happens when a clot ruptures or a plaque ruptures. And then you get a heart attack when a platelet bug all of a sudden forms in some sort of irritation of a plaque in a coronary artery. Or you could have a low level activation of platelet aggravation and adhesion and secretion of the platelets make a whole lot of things which then stimulate the coagulation cascade. So platelet behavior is one thing, and we can talk about that. Then the next is the fibrin formation and that really, it's turned on. You have activation of the coagulation, you get excessive soluble fibrin deposition or production. And then there's fibrin degradation, which is called fibrinolysis. And if you don't break down the fibrin enough, hypofibrinolysis, then you tend to have too much soluble fibrin. And a lot of the genetic weaknesses are in the weakness in breaking down the fibrin. So a lot of the genetic tendencies are a hypofibrinolytic tendency.

Let's talk then about some of the factors that impact platelet activation and aggregation.

Platelets tend to aggregate and Stick in response to trauma of the blood vessels when the immune system activates them from either toxins or infections. The immune system is responding to white blood cells produce pro inflammatory cytokines which then cause platelets to aggregate. Activation of platelets can be a sign of viral infection. A lot of viruses cause an acute activation of platelets. Then junk food, having a sedentary lifestyle that all contributes to platelets activation and aggregation. And then again the platelets give you the, you know, they make the clotting factors that then help you to produce more fibrin. So you know, cardiovascular disease really, you know, one of the inducers of that is low level activation platelets. So you know, these are the things that are very common in our patient population. And you have to think about platelet aggregation and when people have persistent poor capillary refill, persistent cold hands and feet, ongoing modeling, a lot of pain, still a lot of fatigue and they don't really improve with the enzymes. Always think about the platelets and then deal with the platelets.

So let's then talk about the formation and degradation or breakdown of fibrin. What are some of the factors involved in the formation formation side versus the degradation side of this really important balance?

Thrombin formation drives the production of fibrin. You have tissue factors, you've got the platelet factors we talked about. You have things like plasminogen activase inhibitor 1, you have lipoprotein A which is a molecule that drives it, Alpha 2, any plasmin. These are all things that help to drive the production of cybofibrin. And it's a complex biochemical process that has both the intrinsic and the extrinsic pathways and there's all these checks and balances in it. And I would refer you to David Berg's lectures that he gave in 2011 to really understand that. So those are the factors that help to drive the production of the factors that help to break it down. The fibrinolysis side are our own natural proteins. We have antithrombin, we have protein S and protein C. We have other heparins, the heparin sulfates on the, on the lining endothelial membrane and the glycosaminoglycan, the gags out in the extracellular matrix. And then we can actually those are anticoagulant, those help to block the production of the pro coagulant cascade of proteins that makes fibrin. And then the things in our own blood that actually break down fibrin, the fibrinolytic Things are our plasmin, we have TPA tissue plasminogen activator, because plasmin is the enzyme which breaks down the fibrin. And we measure the breakdown products of fibrin with the D dimer. We also have lumbrokinase navakinase which are external to us. So there's this wonderful checks and balances.

So what are some of the factors then that impact the creation or the formation of fibrin? And what are the consequences of excess amounts of fibrin? Some of it we've covered. But are there other factors or consequences that we should know about?

Formation is really determined by the thrombin level and the rate of thrombin formation. So if you have something that's driving a lot of thrombin and you have evidence of that on your testing, then you've got to figure out what that is and lower that because you can keep giving people enzymes till the cows come home, but you're still going to be making it. You're still making it if you're driving thrombin. So each step has its both activators and inhibitors. And you want to support what's low. If you see that the protein S is incredibly low or the protein C is incredibly low, then you're going to need to have the enzyme support to do that. And again, fibrinogen, which is the precursor protein for the making of fibrin, fibrinogen is cleaved into fibrin. Those levels can be raised by increased production by the liver. In any acute or chronic inflammatory disorder, fibrinogen levels are increased in pregnancy, in cancer, estrogen therapy, and then you can have a pro coagulate environment, self perpetuating positive feedback cycle as a result of infection along the endothelial cell lining, anything like that. So those are some of the major determiners that are important in our patient population.

I know you have a very extensive panel of tests that practitioners can order to get a sense for whether or not hypercoagulation is an issue. We aren't going to be able to deep dive into that, but maybe you can talk to us about some of the key tests that you use to explore the potential for hypercoagulation. Which of these tests are your biggest guides?

Unfortunately, it's important to do the whole panel, but what I find most commonly is that when people are making a lot of thrombin, you'll see elevated tats, T AT complexes. That's the thrombin antithrombin complexes. Since thrombin has such A short lifespan. We can't measure it in the blood, but we can measure its breakdown products. You can measure prothrombin fragment 1 and 2, which is one of the degradation products when thrombin is made. And you can measure thrombin antithrombin complexes. So those two tell you about whether you're making too much thrombin. And if that's the case, then you better get rid of the infection, get rid of the virus, get rid of the toxin or whatever is really causing the thrombin to be made. Then I always look at the antithrombin protein S activity, protein C activity. Those three should be within about a 10 point range of each other. And if they're off, say even if they're in the normal range of the laboratory, but they're not in a one to one to one ratio, then you know you've got a stress in the system. You could have everything completely within normal ranges. And you could have the protein s be say 70 and the protein C being 150 and the antithrombin being 110. You know that that person has chronic hyperpragmatial stress because the protein C, protein S I mean, is either being consumed and it's so low, or they have a genetic weakness which is not allowing them to mount the response they need because the protein C is dramatically elevated in comparison. So those are very important. The D dimer can be up when your body is actively trying to break down soluble fibrin. So that's evidence that you've got too much and you break it down, your D dimer's up, right? Then if you've got high tax and high prothrombin fragment 1 and 2 and a high D dimer, you know your body's working really hard. It's making too much thrombin, but man, it's trying to break down the fibrin. Now if you have a high lipoprotein a, a high alpha 2 aneoplasmin, those can be genetic set points, they can be high in inflammation, but they can also be high as a genetic set point and they just stop your protein S, protein C, any thrombo cold, so that they are dramatically responsible, you know, for a lot of hyperparagus stress when they're elevated, right? So those are some of the ones that you can look at. That's why it's important to see all of them. The activated protein C resistance is what you look at to see if there's a factor V Leiden mutation that's not that common. I don't see that many of them. What I normally see is I normally see some sort of aberration of protein S, some elevation of lipoprotein A, pi1alpha2 antiplasmin, you know, as the genetic ones.

So where should people actually get these lab tests done then? Is there one panel that can be ordered or do they need to do it with a specific lab?

Well, it's best to do LabCorp. And the reason is when David Berg developed all of his this testing, he had a lab called Hemex Labs. Hemex was bought by Esoterics and then Esoterics was bought by LabCorp. So they have all of the protocols now. One thing that we can't get anymore, which I really is horrible, they used to have a test, it was ADP tested, another test that used to tell us whether the platelets were activated. So we used to actually have a platelet activation test where you could see whether they were a problem or not. Now you have to sort of figure it out clinically because they don't do that anymore. And it's sad. But LabCorp is the best place and I really would recommend that people do all of them. You can always do them. Part of the panel is also a fasting lipid panel and a lipoprotein A. Just because if the cholesterol and LDL are up, then you know you've got a lot of inflammation going and that can really help guide you. But you can always do it in two separate blood draws. It's not that whole lot of blood, but it's complicated for the lab. So I urge people to make an appointment with the lab or present lab slip to them ahead of time so that they can get all the tubes ready. So when you go in to have it drawn, you're not sitting there for a long time. Timely.

And so for listeners, we will in the show notes for this episode, you'll be able to find that list of tests that you can share with your practitioner as well. So how do you determine how abnormal the tests need to be before you decide to treat it? And do you treat a single abnormality or do you need to see several different indications that point you in the same direction?

You don't really need to have anything abnormal. As long as the balance is off, you can have all the tests within a normal range and still have somebody who's hyperpragable. Because our body has such an incredibly redundant, beautiful, God given system that helps to protect us from clotting too much or not clotting enough. So it's the balance of the test that's important. And I treat the patient, I don't treat lab tests. So if the patient has symptoms and get better with the enzyme treatments, then you've got your diagnosis. So even one abnormality is of significance. Even an imbalance is of significance.

How often would you recommend retesting after someone's been put on a protocol that would help address hypercoagulation?

It depends on what you're trying to follow. If somebody has a really high prothrombin fragment 1 and 2 or TATS complex, then probably every three to four months I check those abnormals or if the D dimer was high. But if it's just a little bit of a stress, an abnormal protein sc, a little bit of high lipoprotein, you know, I could wait anywhere from four to 10 months, depending upon their clinical situation. When it's not clear whether a abnormal result is a normal physiological adaptation to the hypercoagulation stress or whether it is a genetic snp, normally I wait even longer. I can wait up to a year because I want to make sure that patient is stable, they're improved, they're detoxified, they're feeling better, and then you repeat it. And if they still have a really low protein S in compared to protein C and an thrombin, then you can say, well, listen, you most likely have a weak protein S production in your body, and you have to be aware that the rest of your life, when you have a stressful situation of any kind of stress, then you should take extra fibrolytic enzymes because of your protein as weakness. So that's when I would check that. So it depends upon what you're following. You don't do it every single time, but you can do it in sequential several months at a time in order to follow what it is you're to trying, trying to treat. If your fibrinogen is up, you want to make sure that it's come down. So that would be three, four months. So if you really got dramatic abnormalities, maybe three to four months, check those abnormalities again, and then if you're thinking about a genetic weakness, then you can wait longer. I always, though, when patients are feeling better, repeat tests that were abnormal to document that they've improved always.

And when you're doing the repeat testing, are they still on the enzymes that were supporting the hypercoagulation or do you have them stop for a period of time to see if that, if that still is something that's necessary for them?

I generally don't stop unless clinically I feel that they can. Usually people in my practice are almost always on enzymes until they're ready to stop treatment completely. So if that's the time when we're testing it, it would just depend upon what they're taking or I don't withhold enzymes in order to do the blood testing.

So let's jump then into treatment. So part of treating hypercoagulation is reducing the systemic inflammation. What are some of the strategies that you implement to help reduce systemic inflammation?

Well, we've talked about some of that already. You know, you really need to normalize people's omega fats. And normally we're so overwhelmed with bad, toxic omega 6 fats that you really need to load them up with pure Omega 3s for a couple of years and you just give them high dose. I mean, I use 3, 4 grams of omegas a day with food, two huge ones twice a day to get somewhere between 3 to 4 grams. I always do that. And that's a wonderful treatment for platelet aggregation. So often I think I'm preempting a problem of platelets by the way, I treat inflammation. Then of course, you've got to optimize your liver detoxification pathways. You got to fix your gut dysbiosis. That's probably one of the main things you got to do first. If someone's really got a bad gut, you're never going to fix their liver until you fix the gut. And then once you work on the gut, you work on the liver, they're getting good fat. Sometimes they need phospholipids too. I use a lot of phosphozylserine, phosphatidylcholine, phosphatid combos of the phospholipids. Then you really need to, once the gut and liver doing a little bit better, clean up the extracellular matrix and that's also cleaning up the organs. That's when your drainage medicines, your lymphatic drainage, your kidney drainage, all of your organ systems need to be helped to be cleaned up. And then you really want to start getting at the infections that you have. Drinking good, clean water and being adequately hydrated is also very, very important, important. And I like to have people have a clean, good diet, organic diet. If they eat meat 100% grass fed, they need to just be very careful about glyphosate intake. They need to have their multivitamin on board, their extra trace minerals, all the essential minerals on board, enough antioxidants and then appropriate Physical exercise too, even if you can do just a little bit, you've got to move your body. Move motion is lotion. Trying to reduce stress, which can be very difficult when you just discovered your whole house is moldy. You've got to do something about it. But also thinking about the electromagnetic radiation in your environment. So those are the things that I address when I'm trying to reduce overall systemic inflammation. And of course, I use all kinds of nutraceuticals and things to reduce inflammation and help the body. As well as those things above, I use a lot of combination nutraceuticals and herbals to do that.

Yeah, and I love the trace minerals too, because you were mentioning the sulfate deficiency. And my understanding is that products like Quinton trace minerals actually can also be a source of sulfate for the body as well. So kind of all kinds of sources.

Of sulfate that I use that are helpful.

So let's talk then about the balance of the omega 3 and sulfate. Do you tend to feel that fish oils are appropriate? I know there's some people that feel that seed oils are better. Is there some balance between the two? And what are some of the healthy omega 6 fats that you recommend? Or do you recommend completely avoiding even the healthy omega 6 fats until the omega 3s have been replenished?

Well, that was the way Gary Klepper taught us way back in 15 years ago, was load them up with their Omega 3s for a couple of years and then go to your combos. So it really depends upon the patient and what they need, what their diet's been like, what their stresses have been. But the clean omega fats, the six fats, if you want to use an oil, I really like the cleaner nut oils like walnut or sesame, or use a combination 369 or 3679, you know, that's pre made. So the problem is a lot of these safflower sunflower oils, these things that cottonseed oil, there's very, it's very, very hard to find clean ones. Even foods that have organic safflower, the safflower oil doesn't seem to be right. So I try to avoid that completely. And I'm not a big fan of olive oil, although some people swear by it. I guess it just depends upon, you know, your body and your physiology. But I tend to, if they're not going to be taking an Omega 6, I generally don't use them alone. I'll use them in a combination. If I go to it, I generally start with the Omega 3s and then I shift to something that's got a mixture. But if they really want to be able to cook with omega 6 fats and things like that, I'll go to the cleaner nut oils.

You were probably one of the early voices that I learned about drainage remedies from and the importance of drainage REM remedies. I think it's also an area that probably is underutilized in treating chronic conditions. And so we're talking about the extracellular matrix here as well. So why are drainage remedies so important for unburdening the body of toxins that can be creating inflammation but also triggering this hypercoagulable state?

Well, you know, think about it. Don't you want to be playing around in this wing, pull this clean. You don't want to go jumping and playing around in a swimming pool that's full of mud, right? So your extracellular matrix is the communication highway. It is so important for the communication of the whole body, every cell to every cell. It should be that one little disturbance in the matrix in one spot of the body is immediately communicating to the entire body. That's what an acupuncture point should do. Right? So if you're all clogged up and your matrix doesn't have that fluidity to it and you don't have the exchange of all these important nutrients and communication molecules and tissue factors, then you got to get rid of that gunk. And what does the body do when it's got a toxic load? Well, it'll first. Well, it's got to get it out of the bloodstream. So it tries to put it out in the extracellular matrix and it'll dump it in there. If it's water soluble, it'll stay there and it'll be a little bit easier to move and get out of the body. If it's fat soluble, it'll put it in your fat tissues. So it's so important to get these toxic metals and these toxic things out of our extracellular matrix so our body works. Otherwise it just won't. And then you have all of these abnormal things there that keep setting off the fire alarms and setting off the immune system so that you create inflammation. I mean, it's sort of a no brainer. You gotta clean up, you know, all of the streets if you want your cars not to be clogged in traffic. Right.

And that's where some of the products, like the products from Picana like Apo Heat Pad and Renelix and Iteros and Mundipur can be really fantastic. So such an important piece to think about. Drainage. Let's move on to hydration. You mentioned the importance of being hydrated. Many people with chronic illness week drink a lot, we pee a lot, but we still are cellularly dehydrated. So beyond just consuming more filtered pure water, are there some tricks for improving the body's ability to utilize that hydration at a cellular level?

There are homeopathic medicines that help with that. Energetics has one. Several companies do. But remember that in mold illness, you have an antidiuretic hormone problem and you cannot concentrate well. So you're always drinking because your kidneys can't hold on to excess. The water it needs to hold on to, and you're losing. And then when you have inflammation, you're losing a lot of minerals through your kidneys. And so you can't regulate your cellular hydration very well, especially when you're in mold. And then when you have hypercrigability, you know, you get all this stuff stuck out in the tissues, and you have sort of water in there, kind of like with the mud out in the tissues. But the cells themselves may not be getting, you know, clean water. And you get that, you know, the water layer is disrupted. So there's a lot of buzz about hydrogen water and different types of hydrogen waters. And some of the tablets that you add to water create hydrogen water to make it much more able to, you know, go intercellularly and hydrate yourself. And I would just suggest for people just to, you know, try a few of them and see if some of them work for you. Some people talk about that one called watah a w a t t a h h or something that seems to be good research Nutritionals has a hydrogen H2 tablet that seems to work for some people really well. So definitely. But sometimes you can drink and drink and drink, and you can't hydrate yourself because you have botoxin illness, or you haven't worked on getting rid of some of the heavy metal toxicity, or, you know, you haven't taken care of your extracellular sludge and your intravascular sludge.

Right?

So you can do all these things all together, but the detoxification and the hydration are all important to do simultaneously.

And for listeners, the product from energetics that Dr. Courson was referring to is called rehydration. One of the things that I did not know about hypercoagulation until I had heard you speak previously was the connection to insulin resistance. So that's also part of your approach to treating hypercoagulation, reducing insulin resistance. What's the connection and how do you approach the insulin resistant connection component of hypercoagulation?

You know, insulin resistance drives inflammation. You eat a real high sugar load and you have a spike of insulin and that releases a lot of cortisol. And then that stress also stimulates coagulation cascade. So that's part of the stress. Like you're frightened. You got to run away from that saber toothed tiger. Well, if that saber toothed tiger nicks you as you're running away, you want to make sure you, you stop bleeding, right? So the coagulation cascade and the immune system is put on hyper alert and then you get stickier. So that's the connection. Reducing insulin resistance is hugely the patient's responsibility. It's what they put in their mouth. Now one thing I do is I talk to them about how they can change their diet. And that's a whole other talk, a whole nother podcast, you know, and, you know, lowering the, you know, the foods that have a high, you know, production of insulin as, you know, the high glucose load, then you also have to use like a lot of cinnamon in cooking. That's a very easy way to do that. There are all kinds of herbs and things that help with it and chromium and other, all kinds of things. You just have to look up, you know, what herbs and nutrients and trace minerals help insulin resistance, but it's really the patient's diet. And if they can make the lifestyle changes, the insulin resistance fades away.

Let's talk now about how we decrease the activation of the platelets. In conventional medicine. We hear about aspirin or pharmaceutical medications. Is that a reasonable approach to this platelet aggregation or activation side of hypercoagulation? Or are there other tools in integrative medicine that might be more appropriate?

What allopathic medicine is, they usually give you 81 milligrams of aspirin a day or they use something like Kleavix or some other platelet inhibitors. And that's how they treat high plug ability. They don't even think about the soluble fibrin piece. There's no way. There's nothing they do. Except if you're using heparin intravenously, that can help getting, stopping the production of soluble fiber and helping to degrade that when you're using say low Vinox or you're using intravenous heparin. But they only do that if somebody already has a blood clot, so they're not very proactive. Now in Integrative medicine. The way we decrease platelet activation is using high dose omega 3s and I use a lot more than 1500 milligrams daily, but that's the minimum you need. I like to use between 3 and 4 grams daily. Using vitamin E, you can use things like ginkgo. There are other herbs, ani and fiber, inflammatory herbs, antioxidant nutrients. I like to use Donchen Supreme a lot. Donchen, it's like an herb. But I like the supreme nutrition products. Don Shen, that really helps nattokinase in and of itself also affects platelets. It doesn't just break down cycle fibrin. So that's a favorite herb of mine. Of course, a lot of the antioxidant nutrients help as well. And then you've got to treat and get rid of the underlying triggers. So if somebody's got an underlying viral infection or underlying Babesia infection or underlying heavy metal toxicity or glyphosate toxicity, you got to deal with that. So I prefer using that than to the aspirin because the aspirin blocks cycle oxygenates really up high in the whole production of cytokines and you get both good and bad cytokine production decrease. Remember, you've got always balance in the body. You've got good cytokines, you got bad cytokines and they're always in a balance. And aspirin blocks it really early in the formation of those, all of those proteins. So I really don't like to use non steroidals or aspirin.

So let's jump into the Don Shin. So you mentioned Don Shin supreme from Supreme Nutrition. Is that in the hypercoagulation realm? Is it primarily, primarily on the platelet side or is it also helping with the fibrin part of this discussion? Tell us a little about Don Shen and how you might incorporate that into a protocol.

Well, I use it for a lot of different things. I use Don Shen of course for Bartonella. And that's one of the main reasons that we use Dongen supreme in medicine is, you know, to help with Bartonella. But it does an awful lot of things. It's an herb that's been used, you know, it's salvi, it's red sage and it's been used in people who have heart disease. And if people have had heart attacks, it can actually work and protect the cardiovascular system by helping to vasodilate. It can inhibit the platelet aggregation, it can protect against the ischemia. And so, you know, it does an awful lot of things and that's why I love the herbs, because they have so many different actions on the body. It can help to increase dopamine levels. In traditional Chinese medicine, Don Shen has been used to treat people with hepatitis B, liver disease. And it's also broad spectrum antimicrobial and against bacteria and fungi as well. So there's lots of different things that it does and I just like it. It does a lot of good things. It also helps to work as an anti cancer agent. Anti cancer agent and also against hiv, which is a retrovirus. So I don't know whether it's also helping with a lot of the retrovirus problems that we're seeing in our patients, but I find it to be very helpful herb. It was used in myocardial infarction to treat ischemic stroke and hypertension and then, you know, to inhibit the platelet adhesion in people who are prone to hyperfagulation disorders. So it's a fun one and I enjoy using it.

So if we turn now to dissolving the excess soluble fibrin, how often do you find that the pharmaceutical options like heparin and Lovenox are really critical? How do you decide between the pharmaceuticals versus sticking with the natural enzymes?

Okay, I don't find that I need to use heparin or Lovenox a lot in the few situations where I've had to go to that. I think David Burke talks about its use a lot more than what I had needed to in my patient population. And it may just because of a lot of the other meat herbs that I'm using, like the Danshen when I've had to use Lovenox or heparin in my patients. For instance, one time I was detoxing lead out of a patient using intravenous edta. And man, that patient got so hypercriggable and that needed to put on heparin. I had a patient who was developing preeclampsia. She'd gotten pregnant sort of as an oops and she wasn't well at all. And her babesia flared terribly in the third trimester and she got really preeclamptic and she needs to go on heparin. I had another pregnancy where I had to have patient on Lovenox the entire pregnancy. And then the anesthesiologist changed her over to heparin right before delivery because she had multiple multiple misses and she had gone into eclampsia with her first and this was her second. So I've had it use it in pregnant patient and sometimes detoxing. Heavy metals. Some of the really chronic mold people that aren't really out of mold, they claim they are, but they're so chronically ill. You know, they're still in mold and they still have a lot of mold toxins in their body. Sometimes they're so sick that they've got to go to a Lovenox, but I honestly don't use it terribly much at all. And the caveat when you're using Lovenox is to remember that you've got to check the CBC within the first couple weeks of treatment because very rarely the low molecular weight heparin can drop platelets. It's more common with the regular IV heparin you get in the hospital to drop platelets. Seriously. But you should check if you're putting people on load Knox.

So let's then talk about the enzymes, the proteolytic, the fibrinolytic enzymes and how they're used in the treatment protocol. Are there specific brands that you clinically find most effective?

Well, yeah, well, I'm always using enzymes, some kind of enzyme. So how do you pick which one you're going to use? How? Why? When? Well, nattokinase works really intravascularly, the lumbrokinase. And I really think the only brand that works is the Canada RNA balloon and that's the original one. It's the one with patent. It's the Japanese company, the knockoff lumber kinases just don't work. I'm sorry about that, but that's just the way it is. The only really the nattokinase that I find is the most efficacious is the soft gel cap that allergy research makes in a 36 or 100 milligrams. The soft gel cap seems to enable better absorption. And sometimes there's a nattocerazyme, I think designs for health or a few other companies may have a combo nattocerazyme and that really helps in little kids when you have to open capsules. But generally I use just the gel caps of the nattokinase Phenomenology research group, either the 36 or the hundreds or just the Canada RNA brand of blue. If you're using other ones, you're just not going to get the same clinical efficacy. So nattokinase and BALUC are discussed or lumbrokinase is discussed in allergy research groups. Focus magazine, they put out a really nice one in 2003 about nattokinase and again in 2008, I think 2010 about blue nattokinase really works well in terms of people have a bad infection of the vasculature, they have a vasculitis, they have that distal numbness, tingling, poor capillary refill. They have autoimmune disease in the vasculature like antiphospholipid syndrome, anticardiolipinol antibodies. When they're in mold, when you want to start, especially in children, when you're uncertain of what to do and you think they're hyperagical, you always start with nattokinase. You're never going to hurt anybody with nattokinase. Okay? Now, the loop really is reported to work both intra and extravascularly. So that's very helpful. When somebody has that sort of boggy extracellular matrix congestion look to them. Also, when you first put somebody on nattokinase and they have a low dose and they have a bad initial Hirschheimer reaction, then you really need to go in there with the loop before you slowly increase the nattokinase, because sometimes it indicates you got a really bad genetic snip right off the bat or you've got a really horribly congested extracellular matrix and you just can't even tolerate, you know, any type of breakdown of the sludge that you've already got. So if somebody has a bad initial Herx to the NATO and you know that you went slow enough not to, you know, you don't start somebody off with 200 milligrams of nattokinase three times a day. You know, you're starting in case you're going to start with either 36 milligrams twice a day or 100 milligrams twice a day. And then if they have an initial bag hertz, just that low dose, then you add the loop one twice a day when they come back or when they call. And then you keep them with that and you give them good drainage medicine. Now, you can also, when they have a bad Herx initially, the nattokinase, if they do, then it usually means you don't have your drainage medicine, regulation medicines lined up properly. If you have everything lined up properly, then you're not going to have a bad dose. But also if they do have a bad reaction, something some bad hot potato toxin, I love the way Gary said that comes out. You don't expect sometimes in addition to the blue, you need to add a proteolytic enzyme like a serrapeptase or an interface or something like that, or a marcazine, sometimes even an interface with evpa like The Interface plus from Claire Labs. Sometimes you just need the proteolytic enzyme rather than blue and then that's again where you can add the Donchian, which is the really helpful herb. So that's where you sort of go about determining when to use things and when to add things. When you're trying to break up a lot of biofilms, often you need to combine one or two different proteases that either have or don't have EDTA with often a high dose nattokinase as well as other specialty biofilm busters. Beyond Balance has their BFMP, BFM1 Research Nutritionals has their biodisrupt. There are a lot of really good biofilm busters that you can use when you're really getting down in there. When you're in the middle portion of a treatment course and you're trying to really get down to the deep doo doo and get rid of these biofilm cream.

Have you seen any over thinning complications with these enzymes? So is it possible that there can be significant side effects when we start implementing hypercoagulation protocols with the natural interventions?

I rarely see any significant bleeding problems. I have only rarely seen nosebleeds with nattokinase. If you give too high a dose to some nattokinase to somebody who doesn't need it, you will often just say they got a nosebleed or two, it stops. I've never had a serious bleeding problem. Never ever, ever. Then sometimes if you've got blue and somebody doesn't really need the blue, they might get a little bit larger than normal bruise if they bang themselves. But I have, even with people who've been on enzymes and had to undergo emergency surgeries, I have never in 15 years had anybody have a bleeding diathesis from being on fibrolytic enzyme. The only thing that natto do is they break down soluble fibrin. Natto does help a little bit again, you know, with the platelets and whatnot. But no one has ever had a bleeding out problem like they would with Coumadin or with these other, you know, things like Plavix and these other Xeralto and all these horrible ones that are being used currently in allopathic medicine.

Let's talk about special considerations around treating hypercoagulation in children. What do we need to think about in the pediatric population from a hypercoagulation perspective?

Well, with kids again, you know, you just need to go low and slow and you'll know you've done too much. If they get nosebleeds or they fall down and get a big huge bruise. If children can't swallow the little football shaped pills of the nattokinase, usually children, you'll start with a 36 milligram dose of the algae research group softgels. If they can't swallow that, then if they have to ingest a powder, usually use something like the natocerazine powder. You really need to double the dose because if it goes right into the stomach, you're going to lose about half the enzyme. So if you think they're going to need, you know, 36 milligrams twice a day, then they would need double that dose of the powder. So, you know, allergy research group does have a 50 milligram capsule of nattokinase. So they would need more than one capsule. If you're going to be, you know, giving them a 36 milligram gel cap, you know, it's a little more than a capsule of the 50 milligrams, you know, to give them because they'll lose half of it in the stomach. In children, the hypercoagulable symptoms are a little bit different than in adults. They often present with leg pain, especially at night abdominal pain, they're irritable, they have sleep problems, they're oppositional, they have oppositional behaviors. They have, you know, they're just bouncing all over the wall, they can't sit still. And then the hypercoagulability really worsens any bartonelle or mold radiance that they have. So they can have worse rages and worse anger and worse temper tantrums. And of course then they get fatigued.

Given the complexity in patient protocols and taking lots of different supplements, do you find that the enzymes need to be taken away from food and other supplements or will they still convey adequate benefit? If they're taken with food, they really.

Should be taken at least 30 minutes before you eat the baluc. One time there was a study that's quoted in one of the allergy research group focused newsletters that only 10% of the Baluc is absorbed through the gut lining. So you really need your baluc so you're going to waste it if you take the food. They're going to be better absorbed if they're taken on an empty stomach.

Do you find that some patients that tend towards hypercoagulation maybe need to remain on enzymes indefinitely or be on them during stressful periods throughout their entire lifetime?

Yes. Some of the people that have significant genetic abnormalities say they have a really high lipoprotein A. They may need to be on, you know, lumber kinase for the rest of their lives or they may just need, they have low protein s, they may just need to have enzymes during. So that's part of your job as a, as a treating practitioner to teach them that.

How do we balance? Let's say we start introducing the enzymes, we start breaking down fibrin. It potentially has some biofilm effects as well, releases toxins, releases infections, maybe triggers inflammation, maybe even triggering some additional coagulation. So when people get worse, when the enzymes are introduced, then what direction do you take? Is it that they need more enzyme? Is it that they need less enzymes?

It usually is that you don't have enough drainage and regulation medicines on board and you usually need to go up on the enzymes. But I would get control over the symptoms before I would increase the enzymes. So that if you have started somebody on enzymes and they start to have Hirksheimer then you've got to make sure that you have enough anti inflammatory, inflammatory substances on board. You have to have enough drainage medicines so their liver can detox. They've got to be pooping, they need to be on binders, they need to be on kidney drainage, lymphatic drainage. It looks like one of their infections is flaring and you've got to hit that with whatever you need to hit it with. And then you can always use the immune modulating medicines, the isopathic medicines. The tremendous fan of the San Pharma and syntrion products. We can't get syntrion anymore. And it's just an incredible heartbreak for me. I would love to find somebody who would want to bring that into this country and help us make them because those immune modulating medicines are just invaluable. And in hypercoagulation, the one made from mucorbacemus or the sizer Q was just unbelievably helpful and I just heartbroken without it. So, you know, that's where you can use those things. You know, you chelate the metals, you know, make sure that you're. Because if somebody has a significant hircheimer to starting fibrilytic enzymes, you haven't done your job well enough. You're missing something.

You've said that if you're treating mold without treating hypercoagulation, you're not treating mold properly. And you've also said that you've never met a patient with POTS that was not hypercoagulable and usually from mold. Tell us a little bit about those statements and what you mean by them.

Well, mold and these, the toxins from mold. And the inflammation from the mold drives hypercoagulability, just because anytime you have inflammation, the coagulation cascade is activated. So if you're not taking care of the hypercoagulation issue and thinking of that in your treatment protocol, you're not treating the patient properly, you're not doing an adequate job for the patient. That's what I mean by that. And then so many of these patients come in and they've been diagnosed with POTS and they're on all these drugs for pots. Well, vast majority of those patients are still in mold and because of that they're hypercritable. And that's usually not ever been dealt with.

Beautiful. In light of our current world situation. Can you talk to us about the role of hypercoagulation in COVID 19 and do you have any thoughts on what people should consider to minimize complications if they do acquire coronavirus?

Well, as we've seen, a lot of the morbidity and mortality in this disease is because of micro coagulation, especially in the lung. So they have some sort of almost, you know, a DIC like thing. And so what is this from? It's from the cytokine storm. And why do they have a cytokine storm? Well, that's a good question. You know, these people get this coronavirus, but then what's really happening when they all of a sudden, a few days afterwards, go into this cytokine storm and then develop respiratory stress? You know, is it some other thing going on? We don't know that. But everyone should be on the fibrolytic enzymes if they're starting to get sick. As a prophylaxis. I was having people take high dose marcozymes, which is a proteolytic enzyme combo, which is very well absorbed, which is a great medicine from Marco Pharma up in Oregon. It's a Nestman product as a prophylaxis because that proteases, those proteases would actually help to deactivate the virus in the bloodstream before it even gets or in the mucous membranes and stuff, before it even gets into the lung cells from the ACE inhibitor. So I think that the people that actually get sick with COVID could benefit from dramatically from high dose fibritic enzymes as well as the people that are hospitalized should really all be put on heparin. And I think that they found that they really helped people in the intensive care units by treating them with heparin. I don't know a lot about the experience. I wish they would publish it unless you know some published study. I know that they found there's hypercoagulation happening in COVID 19 patients, but I think that they should be treated aggressively and actually use the enzymes as a preventative as well the proteases and maybe low dose diatrendiasis.

For practitioners that want to learn more about hypercoagulation, what do you recommend that they explore? Do you do consultations with practitioners to help kind of guide them in their hypercoagulation learning process? What would you recommend?

Well, first place they can start is they can look at the PDF of the PowerPoint that I gave for the form for Integrative Medicine. What's the fuss about Vibrant, which you have on your website in the course and corner? And then if they want to delve deeper into that, then I would suggest they go to research nutritionals products and get the Role of Hypercoagulation Biofilms and Chronic illness conference for DVD set which is the 2011 and then also get the Decoding Mystery of Chronic Illnesses 5 DVD set which was in 2012. Then they can look at the information on Nattokinase in the Allergy Research Group Focus Magazine 200320082010 and then there are a lot of other practitioners that talk about hypercoagulation and Lyme disease that you can read about. I can consult with practitioners to mentor them on specific cases. I can act as a consultant for practitioners if they want to do that formally. They set up appointments to do that and then I'm able to help them and teach them more.

Beautiful. The last question I have is always 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?

Oh, I think the most important thing is to do the Falun Dapa exercises because those five meditative exercises, the four standing and the meditation exercises are really one of the best ways to maintain your physical, emotional and spiritual health. And there's really not a lot else you need besides that. I'm sorry.

Beautiful. This has been such a great conversation. I hope that it will be informative and enlightening for patients and practitioners alike. Again in my own healing journey, this was such a critical part of that process and it really was Dr. Courson that brought this to my attention and really helped me to understand the importance of exploring hypercoagulation. Just want to thank you so much for your generous time today for sharing your wisdom. You are so passionate about helping other people and I appreciate and honor you Dr. Corson. So thank you much so you so much.

Well thank you Scott so much for having me. I greatly appreciate it. You take good care, okay?

You too. Thank you. To learn more about Today's guest, visit annfcorsonmd.com that's an F Coursen md.com annfcorsonmd.com thanks for listening to today's episode. If you're enjoying the show, please leave a positive rating or review as doing so will help the show reach a broader, broader audience. To follow me on Facebook, Instagram or Twitter, you can find me there as Better HealthGuy. If you'd like to support the show, please visit betterhealthguy.com donate and to be added to my newsletter visit betterhealthguy.com newsletters. This and other shows can be found on YouTube, iTunes, Google Play, Stitcher and Spotify.

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