Part 2 – Mold 102 – MycoTOX Profile™ & OAT: Treatments, Monitoring, and Additional Insights

Watch Dr. Neu’s Part One Presentation

The material contained within this presentation is not intended to replace the services and/or medical advice of a licensed healthcare practitioner, nor is it meant to encourage diagnosis and treatment of disease. It is for educational purposes only. Any application of suggestions set forth in the following portions of this article is at the reader’s discretion and sole risk. Implementation or experimentation with any supplements, herbs, dietary changes, medications, and/or lifestyle changes, etc., is done so at your sole risk and responsibility. Views expressed are those of the presenter and not necessarily those of Mosaic Diagnostics.

Webinar Transcript

This is an automated AI transcript of the Webinar video seen above. For the most accurate account of Dr. Woeller’s presentation, please watch the webinar video on this page.

Hi, everyone. Good afternoon, and thank you for joining us for this Mosaic Edge educational webinar. We today are going to be hearing from Dr. Neu on the Mold 1 0 2. Hopefully you were able to join us for Mold 101 last month, this month. The topic is mycotoxin oat, focusing on treatment monitoring and additional insights. We will be reserving sometime at the end for questions, so please do type any questions you have in the q and a section, and we’ll get to as many of those as we can throughout the webinar. Dr. Neu, we’re so happy to have you. The floor is yours.

Great. Thank you so much, Michelle. And welcome everybody. Let me get onto my slides here.

Okay. So just for those of you that don’t, don’t know me, I am an integrated physician in Ann Arbor. My technical name is James Robert Neuenschwanderr, MD. I’m also the president of the Medical Academy of Pediatric Special Needs. So we focus on integrative treatment of children. But my practice has been integrative for about the last 35 years. We focus mainly on chronically ill children and adults, and you’ll spend about five minutes treating these patients before you see your first mold patients. So it’s really important.

If you did not see my last webinar, I highly recommend you go back and review it. That was really all about identifying, patients that have, mycotoxin illnesses and then also how to work them up. So we’re gonna take this, one step further and say, once you have your mycotoxin patient, you’ve worked them up, what do you do about it?

So, official title, mycotoxin, oh, treatments monitoring, and additional insights. And hopefully you guys get, good information out of this. The idea behind this webinar series is not to be the most technical in-depth, detailed version of how to treat a MotoX patient, but just to give you a basic toolbox that you can use day in and day out in your practice, to get comfortable with these patients.

So, I’m gonna start with a treatment overview. I mean, the most important thing, and you’re, I’m gonna drill this into everybody’s head, hopefully in the next 45 minutes, that the most important thing is you, you need to eliminate the source. You’re wasting your time with everything else. If you do not eliminate the source, then work on detoxing the patient.

That first webinar I talked about, the visual contrast sensitivity test. This is a cheap test you can do online. It’s $18. You start detoxing the patient, you eliminate the source, you do that until that VCS improves. So that gives you an idea. Your patient is getting better.

And then you start looking at, okay, maybe we need to treat the, the pots syndromes, the vagus dysfunction, the mast cell activation syndromes, and then work on the hormones, manage the, oxidative stress, and then also work on the marks MMP nine, Ms. HVIP, all those things.

All right, so let’s start from the top. Eliminate the source.

So there’s basically, this is the most important thing you’re gonna do. And unfortunately, this is the thing that most of my patients have the hardest time doing. Everything we’re gonna talk about after this is secondary to, to what we’re doing here. And there’s basically three primary sources where you’re gonna get exposure. One is gonna be, from, buildings or cars. Second is gonna be from food and the person, the third is gonna be when the person is actually colonized. So we’re gonna look at each one of those.

And let’s start with buildings. Basically if you have water, so not just a leak, but just relative humidity, over 55% plus organic material, you’re gonna get mold growth. And unfortunately, buildings are full of organic material cars less so, but definitely buildings are full of them. So you wanna start, you know, you can do a visual inspection. You can start looking at the obvious places, humid basements, you know, you can get, it’s very easy to get a hydrometer to tell you what the relative humidity is. You look at sites underneath or next to plumbing. You look at, eaves roofing corners of foundation junction points where the roof meets the house. The house meets the foundation. You know, all these are common areas to find mold.

And sometimes it’s very easy to find, you know, you can inspect these areas vis, visually, but sometimes, you know, if you’re worried about something in a wall cavity, you have to start using fiber optic, cameras.

So in buildings, there’s three ways to test for mold. One is to do air sampling. The second is to do IRMI testing, and the third is to use agar plates.

Air sampling is what most of the mold inspectors are going to use. Basically, they’ll come in, they’ll blow air onto a slide for a fixed period of time. You then take the slide and you stain it. You look for any molds that might be there, and you do different rooms. And then you also do a sample outside just where you compare what’s going on in the house to what’s going on outside. And that can quantify the total amount of mold that’s in each space. You know, if one area, like the bedroom’s really high and the rest of the house is okay, well then there’s something going on in the bedroom.

But it can be a problem if everything’s moldy. I mean, if, if you got a house that’s built on the edge of a swamp and it’s moldy outside, and it’s moldy inside, and there’s no difference between the two, it doesn’t necessarily mean it’s okay. The other problem with this type of sampling is it doesn’t identify individual species. It’ll just identify families in general.

IRMI testing, this is what I will frequently use. I mean, this involves collecting dust samples on horizontal surfaces, so floors, bookshelves, windowsills, that sort of stuff. And then using PCR to identify specific mold species. And then it compares what this home has to a nation, nationwide database. So score is zero, doesn’t mean you don’t have mold, it just means your average. And we start worrying about it when the scores get in the positive zone of over two and a half or three, and you’ll see some very high, scores sometime. And this just compares the difference between the toxin producing molds and the non-toxin producing molds. So it’s not a, you know, you can have a moldy house, but, still have a low score. So you also have to be able to look at these and say, oh, gee, that looks pretty moldy because this uses PCR. You can identify specific species, and you can use those species to calculate what’s called a Hertz me score.

Hertz score looks at the six, worst, I’m sorry, the five worst, mos, when it comes to toxicity, and I’ve got the way they score on the right hand side, you know, in my neck of the woods, most houses are gonna have enough aspergillus, penicillium and versa of color to get, 12 points right out of the gate. So right away, a lot of these houses are moldy than, than they should be. And then it’s just a matter of how much ch ammonium black mold and emia that they have, that determines their score. A score over 16 means that a mold sensitive person really should not be living in that house. They really should move out until they can get it. Remediated.

Agar plates, this is the most low tech, the cheapest way to do it. Basically, you, you can buy these plates, they’re relatively cheap. You expose ’em for a certain amount of time, cover ’em up, wrap ’em in foil, throw ’em in a closet for a few days and see what grows. If something grows, you either identify it visually or you can send it off to be identified. The advantage of this is if you’re worried about a, a living area that has multiple spaces, you, this is a relatively inexpensive way to do it. I mean, you would put these plates in different rooms, and then whichever rooms have growth, well then maybe you go back to that room and do IRMI testing and you do air sampling to determine exactly what you have.

So once you’ve identified that there’s mold in a building, what do you do about it? Well, I think step number one is this. You know, you, you, you wanna have remediation done by somebody that knows what they’re doing.

There is an organization I-I-C-R-C, you can look ’em up online. They have standards, for how to do it. And these standards are based on input from multiple professional sources and not just, you know, remediation experts, but industrial hygienists and microbiologists as well.

You really need to isolate the area of contamination from the rest of the house. I mean, you run the risk. If you just go in willy-nilly, guns a blaze, and then start remediating, you potentially could spread that mold to the rest of the house. So it’s really important that you isolate the stuff off.

And then things that are, you know, hard surfaces like tile, those can be, just, disinfected. But the porous surfaces, particularly wood, like if you’re dealing with studs, they kind of need to be sand blasted. ‘Cause they’ll have a little hyphie that go into the wood. And if all you do is wash the surface, you haven’t gotten rid of the mold. So it’s important it’s done the right way.

And then ideally, you know, once you’re done with the remediation, you take in these industrial ozonator and you just ozonate the whole house without people in it. Ozone can be toxic at high concentrations, but, you know, typically people go away for a long weekend. They bring in the industrial ozonator, ozonate the whole house to get it cleaned out.

You know, when I moved into my current office, it was owned by a bank. The roof leaked for many, many years. First thing we did was replace the roof. Then we, ripped out the whole front wall of the building. ‘Cause apparently nobody knows how to flash a window. They were all flashed improperly and all leaking, and there was mold underneath each one of ’em. So when we sandblasted all that out, we remediated it all. We spent, three days. They put in these ozonator and ozonated the whole place before anybody came back in.

So if you can’t remediate the whole house, the other technique is to do a safe room. Now, I just wanna emphasize this is a temporary, fix. This is not something you wanna do long term, but it’s something you can do for somebody where it’s like, well, we can’t remediate the house. We don’t wanna move. But on the other hand, we’re not ready to remediate yet. Well, you can make a safe room or if we’re gonna move, but it’s gonna take us some time. You know, create that safe room for the person.

And the idea is you wanna have a place that’s sort of a harbor, that, that is a, a, a safe harbor for this patient. And you wanna go in there and take out anything that might have mold. So mainly these are gonna be cloth and paper items, books, cloth, furniture, draperies, carpeting, rugs, all that stuff needs to get out of there. And then you wanna deep clean the room.

You know, with the advent of Covid and, and, and, Zoom meetings and being able to see patients, it’s allowed me into a lot of people’s homes without having to do house calls. And it’s always, eyeopening to me, you know, when I’m dealing with a patient that, that has a mold problem, then here they are sitting on this, stuffed, wing back chair that’s cloth. And I can s you know, it’s got a, have half the time. It’s got an Afghan draped over the back of it. And I can see behind the purse, it’s a big bookshelf full of paperback books. And it’s just like, you need to get rid of all that stuff because all that stuff is harboring mold.

You can ozonate books and that sort of thing. But, you know, when you’re trying to create a, a safe room, just get it out of there. And you wanna make sure the beddings are washed regularly. I typically recommend using a detergent with borax. Borax is very toxic to the mold.

And then you actually have to isolate the heating cooling system for the house. Now, if you have hot water, you can leave that. But if you have registers for stair, you wanna plug those registers and bring in portable units for the heating and cooling. And it’s, like I said to the outset, it doesn’t, not a long-term solution, either the house needs to be remediated or the person needs to move.

And it’s always hard to tell somebody, hey, you need to spend tens of thousands of dollars to remediate your house, or you need to get outta your house, you know, based on testing. But people will not get better if they don’t get rid of the exposure. Everything else is secondary to that.

So other things, you know, when you’re evaluating the source, you wanna make sure it’s not just the home. You wanna look at, you know, the work environment, the relative’s homes, any stores that they frequent and also look at cars and trucks. I mean, they have less, you know, organic material. So they tend to be less of a problem. But it can be an issue. And it’s truly an issue with used cars where you might not actually know the history of the car. But you know, if this car was involved with a flood, just don’t, don’t buy the car, right?

Once a car is moldy, it’s nearly impossible to get rid of it. And RVs are also notorious for this. They tend to have a lot more organic material than cars do. They tend to not to be used as much. You know, people will just close ’em up and use ’em a couple times a year. So it’s easy for them to get moldy.

Alright, so moving on to food. This is the other source, is in our food supply. And basically growing food, you can get, mold on foods when they’re grown, when they’re harvested. But the biggest thing is if they’re thrown in silos. And a lot of our grains and legumes are, are stored in silos. They keep ’em there until the prices are better and then sell ’em. So they have these huge fans to ventilate the silos. But despite that, they’re, they’re notorious for growing mold.

I mean, I have a friend who, is a, a farmer and, you know, he has a co-op that he stores his corn in. And he says, when the trucks come and haul away that corn, frequently there’ll be a foot, foot and a half of, of, mold at the bottom of the silo. When they get rid of the corn, it’s kind of disgusting.

So the mold and the mold spores, you know, usually those are killed off by whatever we do to process the food. You bake bread, you, you know, make, crackers, whatever you’re doing, it’ll kill off the crop. It’ll kill off the mold and the mold spores, but it will not get rid of the mycotoxins. Typically, you have to heat something over 500 degrees, in order to kill the mycotoxin. Now it, the mycotoxins are removed with distillation. So, you know, if, if you’re, using corn, to make alcohol, it might be a problem with something like beer, but where it’s not distilled. But once you distill it, it actually gets rid of the mycotoxin. So, you know, those, like your basic, bourbons that are made from, moldy corn, the distillation will get rid of that.

So this is a, a chart of foods. And, I just want you to pay attention to, the last two columns. So the sec, the second to last column there, are the US FDA requirements for these, mold toxins. And the last column is the European Union. And you can very rapidly see I just put arrows next to three of ’em. But you can put, you can see for a lot of them, we have much more relaxed requirements for mold toxin, concentration in our food than they do in the European Union.

Either we don’t have anything set like for ritoxin or sirone. We don’t even have standards. And for something like the, CINs, it’s 10 times higher than what it is in the European Union. So, even the, the deoxy vallen all, you know, this is some nasty stuff, and it’s, it’s, five to 20 times higher standard in the US than it is in the European Union.

So just watch out for the foods and, and it gives you an example where a lot of these foods are. So, you know, there’s thought that a lot of the, the benefit from some of these mold diets, you know, that, that these autoimmune diets, maybe because a lot of them eliminate grains and eliminate, legumes, and these are the moldies of the foods, right?

So optimally, your, your patients that have mycotoxins, you wanna get them, avoid any food that’s stored in the silo or any products that are made from them.

And then it’s the same with meat and dairy. You know, you really, if I’m telling you, avoid corn, avoid, soybeans, I don’t want you eating an animal that was fed corn and soybeans. So these, you know, animals should be grass fed. They should be free range, because otherwise they’re gonna concentrate the mycotoxin that they consume.

And remember, grains that are too moldy for humans are fed to animals, and they have standards for animals as well. They’re just, higher than they’re for humans. And again, if they’re, if they’re too moldy for humans, then they sell ’em to make alcohol, right?

Colonization is, the other source. This is where the person becomes the moldy building. You know, if a person sits in a moldy environment long enough, eventually they themselves can become colonized by the mold and potentially produce the mycotoxins internally.

So you can identify this on the organic acid test, and you can also identify the mycotoxins on the MycoTOX to screen. Again, those of you that were part of my first webinar, we talked about the differences between colonization and mycotoxins. You know, that you need both. You have to do the organic acid test to see if a person’s colonized. And then you have to do the myco to see if they actually have mycotoxins in their system. ‘Cause if they’re colonized, it doesn’t mean they’re making mycotoxins. If they have mycotoxins in their urine, it doesn’t mean they’re colonized. So you kind of have to do both.

Now and again, this is where the anti mold medications come in handy. And the two that I use are itraconazole, or voriconazole. And both of these are generic now, so they’re not super expensive and they can be very, very effective.

And this is just an example of, of a moldy organic acid test. So again, you look at those, first nine markers, those are all yeast and fungal markers. They now have ’em listed. So 2, 4, 5, 6, and 9 are the mold ones. And for this patient, they have an elevation of number six, which is tartaric acid. Should be under four and a half, they’re at 12. And then they have an elevation of number nine. And that one is a marker for fusarium.

So again, this is a pretty moldy, looking, profile. And when we do our, case study, I’ll show you another one of these.

So, so if you actually wanna work up the colonization, I mean, the primary thing is you do the organic acid test. I don’t usually go beyond that. But again, if you’re getting, you know, sometimes you have to get into the weeds. And if you’re getting into the weeds, the other sources of colonization can be in the sinuses.

So you can do a nasal swab for a fungal culture. It’s frequently hard to grow these things out. So a negative culture doesn’t mean you don’t have it, it just means you didn’t pick it up on your culture. The other way to do this is to do something called deep genome sequencing. You know, this has been around for a few years. It’s getting more popular as more people use it. The price is coming down. It used to be cost prohibitive.

And then the other problem with this is, you know, when you’re sequencing DNA, it doesn’t necessarily tell you if something’s living or dead. And if you don’t subtract off the DNA, that’s contaminating the glassware, the tubing, the solutions you’re using, you know, you have to run a blank and sequence that. ‘Cause there’s gonna be DNA in it. You can frequently get really weird findings. So I think they’re getting better with that, technology.

We use it a lot for stool, because the stool testing I do right now is only looking at bacteria with genome sequencing. And you can look for viruses, mold, fungus, as well as the bacteria. So it can be very, very helpful.

So again, if you find that colonization, treat it with, either itraconazole or antifungal herbs. I mean, there’s a whole world of antifungal herbs out there, that can be effective at treating, you know, if it’s strictly, in the nasal swab, you can also use things like colloidal silver. There’s a povidone iodine nasal spray you can use. So there’s a number of different, alternatives there.

All right. So that’s step number one. And again, I don’t want you going beyond step number one until you’ve dealt with it. You have to eliminate the source, and then you work on detoxing the patient.

So again, you use a few different techniques to remove these mycotoxins. You know, the best one, the best known is to use binders. And we’ll talk in more detail about how binders work, but basically they bind the toxin in the gut, so you just poop it out.

The liver’s detox system is the second technique for body detox. And the liver has a phase one and a phase two detox system that helps us get rid of these things.

And then the third technique is not as obvious. I mean, the gut microbiome, the bacteria in the gut are involved with detox, and we don’t give them enough credit for what they do. They frequently have mechanisms and pathways that we don’t have, so they can detox compounds that we cannot. And so they also have enzymes that we don’t have. So again, you want to make sure that gut ecosystem is on your side. ‘Cause a lot of times when the patient is sick, you know, they’ve been, “Oh, I’ve been having these symptoms for the last 10 years.” Well, chances are they don’t have a very good gut microbiome either. So always keep that in mind.

You know, this is one of the things we teach in the conferences we do at MAPS is, how do you evaluate that gut biome? What do you do about it? How do you restore it to health?

So this is my schematic of your digestive system. You’ve got your liver, you got your bile ducts, you have your small intestine. And a small intestine, you know, the bile is gonna dump in the second part of the duodenum. It’s gonna go to the jejunum and then to the ileum and out, out the other end as stool.

So here you have your bile salt, and your bile salt is gonna be picked up by the liver, and into those bile ducts. It gets dumped into the duodenum and then transported down to the ileum. Now, once it gets to the terminal ileum, there’s two pathways. One is, it gets absorbed, and that’s about 95% of all the bile. And the other 5% gets excreted out in the stool.

Now, certain bile salts—we’re gonna talk about TUDCA—but certain bile salts don’t get reabsorbed every time; they go out in the stool. But most of them do. And part of the reason for that is we make bile from cholesterol. And biologically it’s very expensive to make bile, so it’s something we want to recycle.

So that’s a great thing. It allows us to be efficient, it allows us to digest fats and all that sort of thing. But the same system is a way for us to get rid of toxins. So we have a toxin floating around in the system, particularly a fat-soluble one. The bile is gonna bind it. That complex is gonna be taken up by the liver, dumped in the duodenum, off to the ileum.

And unfortunately, the same thing happens—95% of it’s gonna get reabsorbed and just keep it going round and round and round, and only 5% is gonna be sent out to stool. So we call that reabsorption, enterohepatic circulation. And it’s one of the reasons why toxins can stick around for a long time.

So some of our treatments here—you know, we’ve got our binder. Our binder will actually block the reabsorption. A lot of these binders will bind that complex and not allow them to be reabsorbed.

But the other thing we can use is a non-absorptive bile salt like TUDCA. TUDCA will displace the toxin from the bile and bind it itself. And then again, TUDCA is something that does not get reabsorbed. It’s a hundred percent excreted. But either way you do it, you’re gonna significantly increase the amount of toxin that’s excreted in the stool.

So the classic binders work by disrupting that enterohepatic circulation, and it allows you to just poop them out so you can get them out.

So the two prescriptive binders that we use, one is cholestyramine, and the second is Welchol. And they work by binding the bile salt with the toxin attached. So that’s one of their mechanisms. And by binding that complex, it does not allow that to be reabsorbed. It gets pooped out the stool and everybody’s happy. But these binders can also directly bind the toxin. They’re exchange resins. They’ll exchange an anion for the toxin and, and get rid of it. And cholestyramine is probably the most effective because it just has more binding sites than, the Welchol does.

Now, the natural binders—and I don’t want you to get like, “I’m gonna, you know, like activated charcoal works best for trichothecenes, bentonite’s best for aflatoxin, chitosan is similar to the cholestyramine in what it does”—and there’s a lot of combinations out there. I don’t want you to get obsessed about which binder to use for which toxin. They all have some activity against all of these mycotoxins. It’s only if you’re doing a broad-spectrum combination binder and it’s not working, then maybe you go back to the drawing board and start looking at, “Should I, you know, should I use bentonite instead of charcoal? Should I use, cholestyramine instead of, instead of one of the natural binders?”

So all of these are dosed the same way—30 to 60 minutes before a meal. You want them leaving the stomach as you’re releasing bile from eating the food. You want it to mix with the bile, and you take it three to four times a day.

So using bile salts is a little bit more controversial than the binders. I mean, there’s lots of literature on using binders to deal with toxins. You know, the absorptive bile salts are thought to help because they bind the toxins in the system and get the liver to, filter ’em out. But again, they’re absorptive so they can get reabsorbed through the enterohepatic circulation. So you want to make sure that you have something that’s going to block that if you’re using those for detox.

The non-absorptive bile salts—and the classic is TUDCA—can actually act in the intestinal tract, displace the toxin from the bile salt so it doesn’t get reabsorbed, and then it just gets pooped out. So it’s also, TUDCA is also a big liver detoxifier. There’s a medication based on TUDCA that we use for patients that have fatty liver, that have, you know, problems with their, bile, pathways in the liver. And it also inhibits this NLRP3 inflammasome. And again, that, you know, hepatic hepatocyte apoptosis—that’s what causes, it’s one of the causes of fatty liver.

So the binders—any of these binders—will cause constipation. So almost always when I start a binder, I start something for constipation. So I like to use, sodium ascorbate powder. This is, a, vitamin C salt that’s neutral. It’s not an acid. It’s also—vitamin C is a mast cell stabilizer. So it can help with MCAS symptoms.

And then the other is magnesium citrate. You know, the magnesium citrate, the sodium ascorbate—sodium ascorbate, I try to get half a teaspoon to a teaspoon a day. That’s around 5,000 milligrams if you do a teaspoon. And the mag citrate, you know, we start with half a teaspoon and we just adjust them according to patient’s symptoms.

And again, I’m gonna treat with the binders and eliminating the exposure until that VCS normalizes. And then once it does, then I’ll go back and repeat the organic acid test and the MycoTOX or whatever testing I want to do.

And again, I cannot emphasize this as much. None of this stuff is going to work if you do not get rid of the source. If you start binding somebody when they’re still living in a very moldy environment, you potentially can make them worse. So always keep that in mind. You need to remove that source or at least get them into a safe room before you start binding.

All right, what else do we have in the detox world? We have the liver. So this is the second part of it.

The liver detox has two phases. You start with these lipid-soluble non-polar toxins. They go to phase one. Phase one is gonna make things more reactive, more polar, and potentially more toxic. The idea is you want to get it to bind one of these phase two reactions more effectively.

These are the reactions: oxidation, reduction, hydrolysis, hydration, and dehalogenation. Those are all enzyme-mediated. And then these are the nutrients we use.

We also use the CYP enzymes to make hormones. So keep that in mind. When you see hormone imbalances, it may be because there’s a problem with phase one. But these nutrients—you’ve got B vitamins, glutathione, amino acids, flavonoids, and phospholipids, particularly phosphatidylcholine.

And then you have phase two. And the purpose of phase two is to make things more polar so we can get rid of ’em.

These are the reactions: sulfation, glucuronidation, the glutathione-based conjugation, acetylation, amino acid conjugation, and methylation. And these are the nutrients, primarily amino acids, that we’re dealing with.

And then once you have these polar derivatives, they’re either going to the bile or into the serum. Serum’s gonna go to the kidneys and out the urine, and the bile is gonna go out the feces, as we discussed.

All right? So you’ve got a whole bunch of things you can do to support that. A bunch of the B vitamins, glutathione, amino acids, and phosphatidylcholine to support phase one. You’ve got glycine, glutamine, taurine, NAC, and methionine to support phase two. And you have TUDCA to support overall liver inflammation and prevent toxin-induced apoptosis. And you’ve got a bunch of herbs and things that you can use as well.

So the glutathione—this is what glutathione looks like. It’s basically a trip, amino acid peptide. That’s glutamate, cysteine, and glycine that make glutathione.

You need genes to make this work and recycle it. Those are the genes. You don’t have to memorize that. Just be aware that there’s a lot of variation in how people make glutathione. And you can have some people that have very low levels and some people that have great levels.

Chances are your chronically ill patients are gonna have problems in one of these pathways.

So, in addition to what we were just talking about with phase one and phase two detox, the main function of glutathione is to deal with oxidative stress created by oxygen and normal cellular respiration. All right? And that uses this enzyme called GPx to do that.

And again, NAC and sulforaphane can increase production. Liposomal glutathione will increase levels temporarily. You know, all these supplements that are out there will increase the levels for a few hours. And they have to be liposomal or protected some way from digestion. ’Cause otherwise they just get broken down in the stomach.

So the microbiome again—when you’ve got a patient that’s ill, frequently the microbiome is ill.

The key to a healthy microbiome is diversity. That comes from diversity of the diet, as well as avoiding foods that are inflammatory or reactive. And again, the same foods we talked about—the grains, the legumes—but also dairy, potentially eggs, potentially seeds, potentially nuts—those all can be inflammatory.

So I like using a low lectin diet. Lectins basically are in seeds, and they tend to be inflammatory. But at the very least, I’m going to do a food sensitivity panel and try to get rid of the foods that a patient is sensitive to, to decrease the reactivity the food’s creating.

So the other thing with the microbiome—the best way to alter it is to use specific fibers. There’s a lot written out there about the relationship between the different fibers and the bacteria in the microbiome.

For example, butyrate producers are fed by partially hydrolyzed guar gum. Bifidos is fed by acacia. Glucomannan will feed acidophilus. And frequently I’ll also use a spore-based probiotic to optimize that gut health. These are organisms that survive the stomach acid and will work to alter that gut environment and support the growth of beneficial bacteria.

You know, one of the things about probiotics that we know is they do not usually—I mean, I suppose it happens—but almost never do those probiotics set up a colony in the colon. They work by altering the gut environment, either directly, which is what these spore-based probiotics do, or by interacting with the immune part of the gut.

So they can interact—immune signaling will alter the gut environment and promote the growth of the bacteria that you want.

All right, so now we’re gonna move on to, mast cell activation and, and POTS.

So, you know, unless a person has a significant genetic issue with, histamine digestion or breakdown—and that’s gonna be in this ABP1 gene for digestion, HNMT is the big gene that breaks it down—or if they have mast cell dysfunction, and it’s a KIT gene that is involved with that process—normally MCAS is gonna be secondary to chronic immune activation from the mycotoxins.

And so that means that a lot of the interventions we use with MCAS don’t work all that well until you do all the things that we just talked about.

So, you know, if you have a patient who walks in the door and they’ve got all these mast cell symptoms—“I’ve got hives, I’m itchy, I’m rashy, I’ve got all this brain pressure,” and blah blah blah—and the first thing you jump in and say, “Oh, we need to treat your mast cell activation syndrome.” Well, great for identifying it—’cause most doctors have no idea what that is—but, you know, if you start treating that before you’ve dealt with the underlying issue, I always say it’s like treating anemia caused by a bullet wound to the liver by giving a patient a transfusion. It’ll help, but not for very long. You gotta fix the problem. You gotta remove the bullet and repair the liver. In this case, you gotta remove the source and detox those, mycotoxins.

But it’s one of the most challenging things to address. But again, there is logic to all the things you read about with MCAS, so don’t get overwhelmed with this stuff.

I mean, basically, you’ve got two things you can do.

One is decrease the amount of histamine that’s coming into that patient, and that’s with mast cell stabilizers, this DAO enzyme which helps with improved digestion, and then a low histamine diet which decreases the amount of histamine a patient’s taking in.

So these are the mast cell stabilizers: cromolyn sodium is a prescription. Ketotifen, or ketotifen—however you pronounce that—is a prescription, but it has to be formulated by a compounding pharmacy ’cause it’s only available as an eye drop. Luteolin and quercetin, and then vitamin C—those are all supplements that anybody can get. These things can be helpful. They’re really hit and miss as to whether they help the patient, but to me they’re always worth trying.

The DAO just helps you break down histamine in the food. I mean, the low histamine diet makes more sense. There are foods that are inherently high in histamine. But just remember, every time you ferment the food, you can increase the histamine content.

So you can have a meal that’s perfectly fine, you throw it in the fridge, you have it the next day, and it’s setting off all kinds of MCAS symptoms.

So if you have somebody that wants to eat leftovers and they’ve got histamine issues, what they need to do is take the food when it’s fresh, freeze it, and then when they’re ready for the leftovers, thaw it out and eat it. That’s really the only way they could do it. But I encourage people just not to do leftovers.

DAO is expensive, and you have to use it consistently. So people usually are not doing that because of the expense.

And the other thing you can do is increase the rate at which you’re breaking down histamine. And so typically we’re gonna support this histamine N-methyltransferase—this, again, HNMT methylation. So you need to support methylation, and these are some of the ways you can do it.

Try and improve the methylation by adding in methylfolate, methyl B12—those feed into the methylation cycle. You can use DMG or TMG as an alternative way to methylate. Homocysteine and methionine. You can add in SAMe. SAMe is the actual methylator. But some people get really wiggy on SAMe. So it’s not my favorite supplement. It can really help some people, but make a—you know, as many people get worse as get better with SAMe. So you gotta use it carefully.

And then the final one is creatine. I mean, this is something people don’t remember—that about half of our methylation goes to making creatine. So if you add creatine in as a supplement, you’re not necessarily increasing the amount of methylation you’re doing, but you’re decreasing the amount of methylation that you need. So the net effect is you have more methylation available for things like breaking down histamine.

The other thing you can do with histamine is block the receptors. So that’s—you have your H1 agents and your H2 agents.

Your H1 agents—I like to divide them up into things that cross the blood-brain barrier, and these are the older antihistamines that are out there. And then things that don’t cross the blood-brain barrier—these are all the non-drowsy, newer antihistamines that you see advertised every allergy season.

And then you’ve also got the H2 agents—these are the things that were originally developed for the stomach, the cimetidine and famotidine. You know, they do block the production of stomach acid, but they are also H2 blockers. They do that by blocking H2 receptors. And frequently we can combine those two together.

And then there’s a lot of natural agents that do this as well. The other thing to remember—there’s a lot of psychotropic drugs that have antihistamine side effects. That’s not what they were designed for, but sometimes they’re sneaking those in because they’ll have very potent antihistamine effects.

All right, the POTS and then the vagal dysfunction. Again, this is a form of dysautonomia, and because of that, it’ll affect the gut. The gut is very sensitive to the autonomic nervous system, and everything about it is affected by it. So that’s gastric acid, stomach emptying, motility, gallbladder and pancreatic issues.

But there’s also part of the vagus that affects sound and light sensitivity, smell and sensitivity, dysphagia, swallowing issues. You know, these patients that say, “I feel like there’s something stuck in my throat all the time,” and they don’t have a blockage—frequently, this is what it’s all about.

And like the MCAS, you know, you gotta address the underlying cause. You have to deal with the mycotoxin to expect them to get better.

You can treat some of the symptoms with beta blockers and with salt replacement, or there’s a medication called fludrocortisone that increases fluid retention. So all of these things can help with the symptoms.

I’m a big fan of just putting people on a boatload of salt, like a teaspoon once or twice a day, because that can help with a lot of their symptoms.

Now, that treats the tachycardia that’s involved with POTS. But if you really want to address a lot of the other symptoms, you have to do these autonomic retraining programs. And there’s a few of them out there. I put down websites for a couple of them.

You know, it takes advantage of this idea that our brains are plastic and you can change them. So if you can change the brain’s conditioned response, then you change the stress response and you improve the autonomic response.

So these are really critical, and they can make the biggest change in your patient’s lives. Highly recommend these programs.

So everything else we’re gonna talk about is of lesser importance. I call this getting into the weeds.

Hormones—you get a lot of mold-toxic patients who are going to have problems with the hormones. They can, particularly the reproductive, adrenal, and thyroid hormones. And it’s important that this is not a problem with the end organ. It’s not a problem with the adrenals, the thyroid, or the ovaries or testes. It’s a problem with signaling from the pituitary. And that signaling is usually an issue because the MSH is low.

So you always want to check the pituitary component of whatever axis you’re looking at. Don’t look at estrogen and testosterone without looking at FSH and LH. Don’t look at cortisol without looking at ACTH. And obviously don’t look at T3 and T4 without looking at TSH.

So supporting—if you’re gonna have somebody on some sort of hormone support, remember: as they improve, things will shift, and they may not need that anymore. So just be on the lookout. You know, if you’re giving somebody thyroid medication and they’re getting better from their myco symptoms, and all of a sudden they start having tachycardia and they’re agitated—well, maybe they’re hyperthyroid. Maybe they don’t need that thyroid replacement anymore. So just be aware of that.

MARCoNS—this is going to be difficult to manage. This is multiple antibiotic-resistant coagulase-negative staph. The reason why we worry about it is because it breaks down MSH. So if the MARCoNS is positive and the MSH is low, it might be worth treating.

There is BEG nasal spray. Frequently I throw itraconazole in the nasal spray. It can reduce MARCoNS. The trouble is, as soon as they stop it, it frequently will return. So doing regular sinus hygiene programs like saline rinses with or without an agent like colloidal silver in it is probably more useful than the BEG spray in my experience.

I mean, you could use BEG spray for a couple months to get the numbers down and then switch them over to some sort of hygiene program.

Oxidative stress—again, you know, detox and supporting those liver pathways frequently eliminate the need for it. And you also want to make sure you’re dealing with oxidative stress and not necessarily oxidative shielding. And basically, you do that by looking at your patient.

You know, if you start antioxidants and the patient gets worse, it’s not a healing crisis. Most of the time it’s because you’re inhibiting that oxidative shielding. You might want to back off till they’re better.

So in addition to the antioxidant vitamins, there’s a bunch of phytonutrients that I use. The most common ones I use are curcumin, resveratrol, and black seed oil. Just with curcumin, watch out for the oxalates. It’s on your organic acid test. If you start them on curcumin and all of a sudden the oxalates go through the roof, they might have a sensitivity.

MMP-9, C4a, VEGF, TGF-beta—people get really confused about this stuff. But most of these will get better just with those initial steps and normalization of the VCS.

MMP-9—if it’s not better, we use pioglitazone. Use the low-amylose diet that Dr. Shoemaker talks about. You can get information on that online.

C4a—if it stays high, usually it means persistent exposure. You can use this epoetin alpha to lower it, but most of the time it’s high because they’re still being exposed. Epoetin is an agent that we use to increase blood counts for chemotherapy patients. And we use low doses—we use about a tenth of the vial—to get the levels up.

TGF-beta—losartan, which is a blood pressure medication (angiotensin II receptor inhibitor), can lower TGF-beta. But again, all these things usually get better with treatment of the underlying cause.

MSH—you know, this can be a booger. Because you have to get rid of everything else if you want to try and raise the MSH. There’s something called VIP nasal spray. It has to be compounded. It’s not gonna work if you still have mycotoxins present, either in the patient or in the environment, or if the patient has a significant amount of MARCoNS. So you gotta deal with that before VIP is gonna do anything.

PT-141 is a peptide that stimulates MSH production. So I’ll use that frequently as well.

Again, I don’t want you to get too confused with all these other things. Because the key element is: get rid of the exposure, detoxification, and do the basics for MCAS and POTS. And most of your patients are gonna get significantly better.

Case Study

Let me do a case presentation to take us out, and then we’ll open things up for questions.

So this is a patient who, 70-year-old woman, had a non-small cell lung cancer resected from her left lung. She was treated with platinum-based chemo successfully. But that resulted in a low lymphocyte count. She had fatigue, she had persistent chemo brain. Any of your chemo patients are gonna complain of chemo brain because it actually gives you a lot of brain fog. And she also developed anxiety, which was not a usual symptom for her after the chemo.

We saw her, evaluated her. She had high levels of lead and platinum. Remember, platinum’s a heavy metal—it’s a toxic heavy metal. That’s why we use it for chemo. We actually chelated her and she got a whole lot better. About 90% of her symptoms went away just by chelating and improving some of her nutrition.

So she did well for a couple years. Then she started to see her symptoms come back. We repeated the urine testing for metals and just didn’t see much of anything there. She denied any changes in her environment, lived in the same house, hadn’t changed her supplements, her diet. She was cancer-free. She gets the evaluations every six months and they’ve all been great.

So when in doubt—and I say this over and over and over again—any medically complex patient, any chronically ill patient, any patient where you’re scratching your head, start with the organic acid test.

And this is what hers looked like. For starters, you know, the first page of the organic acid test—you can just go, “Okay, that’s pretty moldy,” right? She’s got markers 2 and 4—that’s aspergillus—and marker 9, which is fusarium. What’s interesting about this is she does not have the high arabinose that would suggest yeast. The other markers—the yeast markers—are normal. The bacterial markers are normal. And even the clostridial markers are normal.

So this is a definite mold colonization problem.

Second page: glycine was a little elevated, but oxalic acid was fine—again, that would vote against yeast. She has some issues with mitochondria. I know in the first lecture I talked about high succinate. She actually had low succinate and high malate. So that’s another toxin pattern that we’ll see. Basically, any time the mitochondria are disrupted, we worry about it.

Under the neurotransmitter metabolites, she’s got high HVA, which is the marker for dopamine. And she doesn’t have the appropriate VMA. So that conversion of HVA to VMA—that’s the dopamine beta-hydroxylase—that’s being inhibited. And so the ratio is very high. She’s doing okay with DOA, meaning her methylation is pretty good. And she’s doing okay with the other neurotransmitters.

Third page: she’s low in folate, she’s low in B6, she’s low in vitamin C—remember, that’s a mast cell stabilizer—so she’s got some issues there. She’s also got one of her ketones elevated. Doesn’t appear to have a problem with glutathione or methylation, which is not surprising. And her gut markers are okay as well.

This is her MycoTOX. She’s got an ochratoxin of 42.7. When it’s that high, it almost certainly is coming from water damage somewhere—it’s probably not coming from food. And she also had a citrinin level that was 186. So again, very high levels of both of these toxins. They both could be coming from the same source—citrinin can come from aspergillus, as can the ochratoxin A.

So here’s what we did: we did ERMI testing of her house. Most of the house was fine, but she had high levels in her bedroom. I always have people do your bedroom and then do some common area in the house like the living room, dining room, or family room. Turned out the bedroom was very moldy.

She got a mold inspector in there and it was pretty straightforward. She had a window over her bed that was leaking into the wall. She had a big headboard that hid the damage. They remediated all that, replaced the window, the drywall, sandblasted the studs, and got rid of the mold.

We treated with eight weeks of itraconazole. It took four weeks to do the remediation, so I wasn’t going to stop it while they were still remediating. We put her on a charcoal-based binder three times a day. Put her on phosphatidylcholine and some TUDCA. Treated the nutrient deficiencies—the folate, B6, vitamin C—and gave her some mitochondrial support, although I think the mitochondrial issues were because she had the toxicity.

Encouraged her to get a more diverse diet and include some fiber-rich foods. We treated the gut with pre- and probiotics. We added these fibers—partially hydrolyzed guar gum for spore butyrate, acacia for bifidos, dragon fruit powder for akkermansia—all based on a 16S rRNA stool analysis. We did some probiotics with a spore-based combination, and then a broad-spectrum probiotic that had lactobacillus and bifidos in it. And added Saccharomyces after she got done with itraconazole. I don’t use Saccharomyces with itraconazole because it is a yeast, and itraconazole will just kill it.

The results—it took her about three months to get back to her baseline. She continues with the prebiotic fibers. They made a big difference with her gut and her overall sense of well-being. She stayed on the spore-based probiotic, and she also remains cancer-free.

So this is a—you know, we never present our worst cases, by the way—always the best one. So this is a great case.

In summary:

It’s easy to get lost in the weeds when you’re dealing with these patients because they can drive you nuts, right? They have all these symptoms. Very sick. Just always remember the basics:

• Remove the exposure.
• Detox the mycotoxins directly with binders.
• Support the patient’s detox pathways.

That’s gonna get you way ahead of the game. Most of the time, that’ll get your patients well. Sometimes you have to go after the POTS and the MCAS separately. Remember the DNRS—patients will think it’s silly, but it’s very life-altering for most patients.

Many of your patients are going to have hormone problems because they have problems with pituitary signaling. Those potentially can get better after they detox. And it’s only if your patient isn’t improving that it might be time to get into the weeds.

And always remember: when you hit a wall, stop and reevaluate. What are you missing?

Keep in mind that most of these guys with mold toxicity—they don’t detox well in general. That’s why they get into trouble. So they may very well have other toxicities. They might have heavy metals, they might have chronic infections, they might have some of the other things that we talk about.

So always remember to check those as well. You sort of have to become a very good functional medicine doctor to deal with these patients. But the things we talked about today will help the majority of the people you’re seeing.

And with that, I think I am out. So I would thank you. And I’m gonna open things up for Q&A.

If you missed Mold 101, Watch Dr. Neu’s Part One Presentation