Watch Dr. Neu’s Part 2 Presentation
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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.
Hey everybody, it’s Dr. Neuenschwander. We’re gonna be talking about mold toxins today. Glad to have you guys with us. I’d like to thank Mosaic for sponsoring this whole academy. I think it’s really important to get the information out to folks and what I’m gonna try and do today and what Mosaic asked me to talk about.
You know, when you start talking about molds and mycotoxins, people can sort of glaze over. There’s a lot of information out there, and it can be very confusing as to how to approach the patient with mycotoxins. So, what I thought I would do is break this up into two parts. So this is Mycotoxins 101. We’re gonna talk about how to identify the patient with mycotoxin illness, sort of the process that I go through to say, “Hey, is this a mold patient or not?” And then we’ll have a second session where we’re gonna be talking about how to actually treat that patient. So let me go to a share screen here.
Okay. This is Mycotoxins 101, identifying the patient with mycotoxin illnesses. And we’re going to be talking about some mycotoxin basics to start out with here.
And so we’ll start with just the question of what are mycotoxins? So molds make these things. These toxins are primarily a defense mechanism for the mold to protect itself from the environment that it’s in, to discourage growth of competitors. Primarily it’s only a certain set of molds that’ll make these, and these are molds that will make these under certain circumstances.
So even if you have a mycotoxin-producing mold, it isn’t necessarily making those toxins unless it’s under certain circumstances. Again, these toxins are designed to inhibit the growth of a competing colony. It’s essential that you want to differentiate the toxin from this idea of a mold spore or a mold itself.
People can have allergies to mold spores. They can have allergies to molds, but that’s very different than actually having a reaction to a mycotoxin. And mycotoxins are much smaller than molds or mold spores. So again, when you’re looking at air purifiers and that sort of stuff, you have to make sure that these things are going to take care of the toxin, not just the mold or the mold spore.
And remember, a mycotoxin is never gonna cause a colonization. If somebody’s colonized with a mold, that’s one thing, but the mycotoxin itself doesn’t colonize. Also, there’s only specific molds that make these mycotoxins. Basically, if the conditions are right, meaning if you’ve got some moisture source and really relative humidity over 55% is a moisture source. You don’t necessarily have to have a leaking pipe or leaking roof, and some kind of growth medium.
And the problem with houses is they’re full of growth medium. It can be the wood, the paper, the drywall. Any of these things can be growth mediums for mold. And the presence of mold, again, you want to remember having mold doesn’t mean you’re gonna have mycotoxins.
The other big thing about mycotoxins: not everybody reacts. You could have two people in the same environment. One person is sick as a dog and the other person’s fine. It’s mainly because that person that’s sick has genetic predispositions that allow them to react to these mycotoxins that can make them ill.
So obviously there’s just some basic principles, but there’s a lot of confusion behind this stuff.
So what are some of the sources? As we already mentioned, mold’s gonna grow if there’s adequate moisture and organic material. It means any building with a water leak or relative humidity where it’s not over 55%, where it’s not addressed within a few days, it’s gonna have mold in it. And the same is true of vehicles.
Now with cars, there’s less organic material in a car. It can be a real problem for RVs because they have a lot of organic material in there, and building methods are part of why we have the problems that we have. So, you know, we’re trying to build houses that are energy efficient, and there’s always a trade-off. The best buildings are these houses built in the 1800s. Nobody gave a damn about energy efficiency. And they’re drafting. Well, almost none of those houses are moldy.
And the worst houses are the ones that were built in the eighties where they actually wrapped houses in plastics. And almost all of those houses inevitably develop mold. And remember also that molds can tolerate freezing, particularly mold spores.
So the other source of mycotoxins is our food supply. The growing and harvesting of crops can result in contaminated crops fresh from the field. All this stuff is made worse when we throw things in a silo. And most of these silos have the gigantic fans to circulate air through the crop. But despite that, these crops are notorious for having mycotoxins.
These molds and the mold spores are frequently killed with the processing of the crop. So if you take a crop and you bake it, you’ll kill the mold, you’ll kill the mold spore, but usually those things will not destroy the mycotoxin. Most of the mycotoxins have to be heated over 500 degrees in order to be destroyed. And just none of our processing does that.
Mycotoxins do get eliminated with distillation. So if you take a moldy crop of corn and you make bourbon out of it, well, the process of distilling that bourbon will get rid of the mycotoxin, but it will persist in beer and wine.
So this is an example of foods and sources of mycotoxins. Aflatoxins can be in almost any grain. They’re in spices, they’re in tree nuts, ground nuts. The aflatoxins can be in milk and milk products.
Now, what’s interesting with this is, the two right hand columns there: one is the US FDA limits to these mycotoxins, and the other is the European Union limit to these mycotoxins. I’m just gonna point out three of them.
Okra toxin—we don’t even have a set limit in the US for ochratoxin in foods. And the European Union, it’s relatively low. It’s two to 10 micrograms per kilo is all that’s allowed.
With ZENs, US does have limits, but it’s 2000 to 4,000 for the upper limits. For the EU, it’s 1000. So ours is two to four times higher.
For ZON (Zearalenone)—again, that’s from Fusarium as well—in the US it’s not set. European Union, it’s 20 to 100. So these are places where they can sneak a lot of mycotoxins into our food, and we don’t even have regulations to determine what the upper limit should be.
So what do mycotoxins do? These are some of the mechanisms of mycotoxin injury. We can have this mitochondrial-induced apoptosis. You can actually lose cells as a result of mycotoxins.
You have disruption of the liver detoxification pathways. We’ll talk about that a little bit. You have this whole idea of neuroinflammation and brain atrophy as a result of the mold toxin.
You have something called a cell danger response that we’ll talk about. This is very, very important. A lot of the symptoms that manifest as a result of mold toxin are from that cell danger response. You can have chronic immune activation. You can have autonomic dysfunction. You can have mast cell activation, DNA damage and repair disruption. That tends to cause increased cancer risk.
You can have malabsorption and nutrient deficiencies, and then also you can have hormone disruption. So if you look at that list, that’s gonna cover a whole lot of organ systems and a whole lot of systems. So mycotoxins should really always be on your radar when you’re dealing with any chronically ill patient.
Now, what we’re gonna do is talk about the cell danger response for a little bit right now, because like I said, a lot of the symptoms that we see in patients that are mold toxic are actually from activation of that cell danger response.
So the way the cell danger response works, you have your cell, there’s gonna be some danger signals. Primarily this is either injury or this is infection. The cell will release these danger signals, and that’s what the danger signals look like.
There are certain things in there like ATP. You’ve got histamine. You’ve got these pattern-associated molecular—pathogen-associated molecular patterns. You have mitochondrial DNA—things that really shouldn’t be in the circulation. When they’re sensed by other cells, that just tells them that there’s danger afoot.
Now, the immune system itself sends out danger signals. And then toxicity can affect this in two ways. One, it can affect the cell and cause the cell to release danger signals. But the toxins themselves can be danger signals. And then that will tell all the neighboring cells, “Warning, Will Robinson, there’s danger afoot.”
As a result, the cells will disconnect from their neighbors. Most of these cells are very tightly connected with each other, forever sharing cytoplasm and nutrients and all that sort of stuff. When they disconnect from their neighbors, it prevents all that stuff from happening.
It also prevents them from converting these hydrogen ions into making ATP. If you remember the process of how we make energy, we run activated electrons through our electron transport chain. At every step, we’re pumping a couple of hydrogen ions out into that space between the inner membrane and the outer membrane.
We create this big gradient of hydrogen ions. Then at complex five, those hydrogen ions come back into the cell and they make ATP. So the cell danger response actually blocks that step and allows those hydrogen ions to build up. That creates this very hostile environment. It looks very oxidative, but we don’t call it oxidative stress—we call it oxidative shielding.
The idea is you’re trying to destroy any foreign invaders that come in. The prototype would be viruses. And again, because the mitochondria are ubiquitous—they’re everywhere except red blood cells—you’re going to get a myriad of symptoms as a result.
So as a result of this, you end up having three stages to this cell danger response. The first stage is the idea of just: we’re gonna destroy the invaders, we’re gonna destroy infected cells. It’s kill, kill, kill. So you have a lot of this oxidation going on.
Stage two is the replacement. This is where the main goal of the mitochondria is to make new cells. So they’re actually gonna use what’s called glycolysis, but they’re gonna use it in the presence of oxygen. So we call it the Warburg effect that we see in cancer cells. But normal cells—we use it to replace cells. It’s very, very quick, not particularly efficient, but it’s a very rapid way to replace cells.
And then stage three is where you take all those new cells that you just created in stage two, and you reconnect and differentiate them into what they’re supposed to be. The mitochondria are in different phases in each one of the different stages. So they’ll be in M1 phase in that oxidative shielding mode. They’ll be in M0 for that aerobic glycolysis, Warburg mode, and they’ll be in M2, which is the normal state of a mitochondria.
The disease develops when things get stuck. So this is a visual of your three phases. You’ve got your CDR1, CDR2, and CDR3, and the various things that happen there. These are the diseases that develop when things get stuck.
Now, my intention here is not for you to memorize these lists, it’s just to understand that different disorders can be manifested as issues with the cell danger response. And the big thing is stress, injury, and toxins, as well as infections, are things that can set this off—as can adjuvants for vaccines, heavy metals, and pollutants. So again, there’s a lot of environmental things that’ll set this off.
So what happens if this system doesn’t get shut down? First of all, you divert glutathione into these regulatory detox reactions, and you also divert cysteine into hydrogen sulfide, chlorine, and sulfate excretion. So you end up having low levels of glutathione and cysteine, and that’s going to impair methylation.
So when you look at your chronically ill patients, how many of them have low glutathione and cysteine, right? It’s pretty much everybody. So you always want to think about cell danger response as a possible cause.
You’re going to reduce vitamin D because you’re reducing the CDR enzyme. You’re also going to increase histamine production because you have the cell danger response–induced histamine carboxylase activation. Too much of that, and you end up with mast cell activation syndromes, or MCAS.
And you’re also going to alter thyroid hormone effects. So again, you end up with clinical hypothyroidism as a result of this. And then you can sicken the microbiome. If you have a sick host, you have a sick microbiome and vice versa. So we end up with dysbiosis.
And because those bacteria are real important when it comes to detox pathways, you further impair your ability to detox and make everything worse. So many of the symptoms that we see in mycotoxin-induced illness can be explained by chronic activation of the cell danger response.
This includes things like fatigue, brain fog, gut dysfunction, oxidative stress, chronic immune activation. And it’s always important to consider the cell danger response when you’re addressing any patient with chronic symptoms, regardless of whether the mycotoxins are the underlying cause.
All right, so how do we recognize the mycotoxin patient? I mean, this is really important. Clinically, we want—you know, that patient walks in the door, they’re chronically ill—how do we know?
So according to the literature, these are the times that you should suspect mold toxin illness. Anybody with any of these findings: intestinal permeability, food sensitivity, mitochondrial issues, atopy in pregnancy, disrupted microbiome, neuroinflammation, cerebral folate deficiency, oxidative stress, blood-brain barrier disruption, microglial activation, inflammatory bowel disease—you can read the list there.
And then anything with an asterisk next to it is probably related to cell danger response activation. So again, this is a pretty exhaustive list, which sort of tells you that probably you should be thinking of this with almost everybody, right?
So here are some of the clues that you might have a hidden mycotoxin illness:
Somebody that has unexplained psychiatric symptoms, particularly if they’re new—somebody with anxiety, panic attacks, even hallucinations. If they’re new onset, if they’re happening at an inappropriate age, or if they’re happening in the absence of any kind of family history for psychiatric issues.
Any kind of syndrome patient, you should be thinking about this. Chronic fatigue syndrome, patients with ill-described chronic illness. Chronic Lyme patients that aren’t getting better with treatment or are plateauing without actually resolving their symptoms.
Any immune activation syndrome. Any mystery illness. Any non-specific change in cognition, particularly in memory—particularly in the absence of family history or personal history of APOE4. That’s the SNP that’s associated with dementia.
Any unexplained respiratory symptoms—especially weird ones like air hunger. I mean, what the heck is that? You start worrying about, is that the whole symptom? There are other things that can do it, but that’s one of the things we worry about.
Any onset or progression of electromagnetic field sensitivity. Any onset or progression of food or inhaled allergies. Any recurrent or chronic bronchitis, sinusitis, otitis, asthma—any of these things can give you an idea that it’s a mold problem.
And then any recurrent and new onset rashes, hives, or itching. Any unexplained paresthesias, neuropathy. Any muscle or joint pain. Any person that gets better when they’re away from home.
The classic is: I went on vacation for a couple of weeks, felt like a million bucks, came back home, felt like crap within two days. That should make you suspicious.
Frequent urination—we’ll talk about that a little bit, particularly at night. Issues with dizziness on standing, high heart rate, orthostasis—these are your POTS symptoms. And because this covers almost everybody that’s chronically ill, this should always be on your radar.
You know, all of us—me included—have been burned by mold and mycotoxins. I’ve been in practice for over 35 years, and I can’t tell you how many times I’ve been burned because I didn’t check for it.
All right, so some of the regular labs—I mean, we’ll get into more detailed labs—but because they impact our physiology in a bunch of different ways, there are clues on routine blood work that should alert you that maybe there is a mycotoxin issue.
One big issue is electrolyte balance. So how many times do you get a comprehensive metabolic panel and the sodium’s a little bit low? Most of these labs list the normal down to 135, but it really should be 140 or higher. So if you’ve got a sodium level that’s like 137, you’ve got a low chloride along with it, and then you also happen to have high serum osmolality and very dilute urine—that would be classic markers for brain dysfunction from mold toxins.
Again, because you get this mitochondrial dysfunction, you can have low creatinine. Usually, we don’t worry about low creatinine when we’re looking at a metabolic panel. But again, if that creatinine is less than 0.6, something’s going on.
If for any reason you’re measuring amino acids, a high alanine-to-lysine ratio—if it’s over two and a half—that’s a sign of mitochondrial dysfunction.
Because these mycotoxins can mess with MSH in the brain—and that will affect pituitary function, sort of the master regulator of the pituitary hormones—you can create issues with the downstream endocrine organs: the thyroid, the adrenals, the gonads.
It’s important to remember that, you know, you have somebody walk in the door and they have adrenal dysfunction. They have low DHEA, low cortisol, low pregnenolone, and you’re blaming the poor adrenal gland. Check their ACTH. If they have low cortisol and they have low or normal ACTH, that’s not primary adrenal dysfunction—that’s brain signaling problems. And that’s usually what you’re going to find.
Same with thyroid. You can have low T3 and T4 with normal TSH or low TSH. So again, with all these chronically ill patients, checking TSH is not adequate to determine hypothyroidism. You have to check the free T3 and free T4 levels in all these patients.
All right. Organic acid tests—this is sort of the backbone of a lot of what I do. I tend to order these things on almost everybody who’s ill, mainly because it’s going to give you a lot of information on multiple fronts. And it’s one of the things that I order on pretty much every chronically ill or complex patient.
It’ll give you information on those multiple fronts: the gut biome, the mitochondrial function, toxicity, brain chemistry, nutrient deficiencies—all that will be part of that report. And the OAT will also tell you if a patient has become colonized with molds, primarily because it identifies the metabolites of those molds.
It’s important to differentiate this from mold toxins. The OAT does not tell you if a patient has mold toxins. And that’s very, very important to differentiate. It’s a point of confusion. It sounds simple, but I can’t tell you how many people will look at an OAT and say, “Oh, this person has mycotoxins.” No—you can say the person has mold colonization, but you cannot necessarily say they have mycotoxins.
So again, you want to make sure that when you do this thing, you want to make sure the creatinine is adequate. A lot of these patients are chronically ill, they have screwed up brain signaling, they can’t concentrate their urine. If the urine is too low, all the tests on the OAT are indexed to the creatinine. So if the creatinine’s low, it means it’s going to skew everything down high side.
So, yeah, with Mosaic, they will not run tests if the creatinine is too low. So that’s to their credit. There are other labs that will run it even if the creatinine is low. So if you’re using somebody else’s lab—which obviously you shouldn’t—but if you are, just make sure if everything’s high, go back and look at the creatinine. Chances are the creatinine is low.
So this is an example: an 87-year-old with a history of Parkinsonism that is developing new onset memory loss and cognitive dysfunction. They’re racking it up to the Parkinson’s, but maybe not so much.
This is his organic acid test. He’s got a marker for mold—that’s number five. He’s got the yeast marker at number seven. And interestingly, he’s also got high DHPPA. Now, that is a marker for disrupted bacteria. And he’s got a high 4-cresol, which is a marker specifically for C. diff.
So this guy probably has fermentation with Clostridia. He’s got fermentation with yeast. And it looks like he’s colonized with mold.
This is some of the rest of his organic acid test. He’s got high oxalates. Usually, that is going to be from gut dysfunction. Don’t put this guy on a low-oxalate diet—fix his gut. He’s got a high pyruvate. The other mitochondrial intermediates look pretty good. A lot of times, you’ll see a high succinate or a high citrate with these patients. His are normal.
When you look at his brain chemistry, he’s got a very high dopamine marker—that’s HVA. He’s not converting it to norepinephrine—that’s VMA—very well. So the ratio of those two is high. And he’s not breaking it down through DOAC very well, which usually is a methylation problem. So the ratio of dopamine to DOAC is high as well.
Then when you look down at numbers 38 and 39: 38 is the marker for serotonin, 39 is the marker for quinolinic acid. Now, these are tryptophan products. I always say with tryptophan, there’s two pathways. One’s the happy pathway—that’s going to make serotonin and melatonin. You’re happy, you’re chill, and you’re sleeping. The breakdown product from that is 5-HIAA.
The other pathway is not so happy—where you make quinolinic acid and kynurenic acid. That’s the not-so-happy pathway. What determines which pathway it goes down is inflammation.
So anytime you have this—and they don’t calculate it anymore—but if you look at the ratio between quinolinic and 5-HIAA, that ratio’s pretty high. That tells you that there’s probably brain inflammation.
And then this is the rest of the OAT. He’s got low vitamin C. He’s got low B6. B12 is looking good. CoQ10 is looking good. Biotin is looking good. And then there’s your methylation marker—that’s high. Orotic acid is getting high—that’s usually because of the gut imbalance.
So the importance of succinate—this is the only part of the Krebs cycle that is actually part of the electron transport chain. So complex II in the electron transport chain is actually the thing that converts succinate to fumarate and creates FAD.
It’s influenced by a bunch of different factors. Obviously, if you’re low in riboflavin, you’re not going to make FAD. Some bacteria like Prevotella will make succinate. So the level can be high just because you have high Prevotella. Prevotella is a yeast marker—lives off of the breakdown products of yeast and mold.
Other bacteria like Clostridia—Clostridia is notorious for doing this—actually consume succinate. For this patient, he may actually be making more succinate, but the Clostridium may be eating it up. So the overall balance is that it’s normal.
The big thing is a bunch of toxins will influence the steps. So if you have toxicity, including mold toxins, you end up having a high succinate.
This is another example: a 15-year-old female with autism. She had worsening of her behaviors with an increase in aggression.
This is her organic acid test. There you can see very clearly the succinate is elevated. The rest of the Krebs cycle—if anything—they’re normal or even low.
And this is the rest of it. These are the ketones—all her ketones are elevated as well. She’s having quite a few mitochondrial issues.
This is a 17-year-old who has a history of lymphoma that was treated, that’s developing worsening fatigue and brain fog. This is his gut profile. So he’s got a bunch of markers for mold. He also has a marker for yeast, and he has a marker for strep and then Clostridia.
And this is what his profile looks like. He has high oxalates. Again, the oxalates are high probably because of what’s going on with his gut. And then he’s got that high succinate.
Now, he doesn’t seem to have as big a problem converting the dopamine to norepinephrine or DOAC. He doesn’t appear to have the methylation issues. But he does still have a relatively high quinolinic acid relative to his serotonin marker at 5-HIAA.
These are his ketones—he’s got a couple ketones that are elevated. These are his vitamins. His B6—getting on the low side. B2—again, anytime you see that asterisk, it means if the level’s high, then the vitamin’s low. So he’s getting low in B2.
His niacin is elevated, mainly because he’s taking it. And then there’s his methylation marker. So he’s got some methylation issues.
This is the summary of the OAT. Again, you want to make sure you know what it’s telling you.
It’ll tell you about: is there toxicity? The elevation of succinate will tell you if there’s toxicity. High or low mitochondrial markers will tell you about cell danger response. Signs of brain inflammation—particularly that high quinolinic acid. Do you have issues with detox? Again, the B vitamins, the vitamin C, the glutathione marker. Do you have issues with methylation?
That’s what the OAT’s going to tell you. The OAT will also tell you if somebody is colonized with mold and gives you a decent amount of information on the functional state of the gut.
What it doesn’t tell you is: does this patient have actual mycotoxins? Does this patient have immune activation? Does this patient have pituitary dysfunction?
And you need other testing for that.
So we’re gonna move on to the mycotoxin screen. This is one of the most helpful things that has come up. It’s one of my favorite tests from Mosaic—right behind the OAT. I do a ton of these tests.
Again, this is gonna look at 11 different mycotoxins in the urine. Most of these are specific to certain mold, and they include aflatoxin, which is aflatoxin, roridin, gliotoxin—these are all from Aspergillus.
It’s also going to include sterigmatocystin and mycophenolic acid. By the way, each and every one of us that talks about mold is gonna trip over one of these mycotoxins, and that’s the one I trip over. Both of those are from Penicillium.
ROA and verrucarins A are from the black mold Stachybotrys. Enniatin B and zearalenone are from Fusarium. And satratoxin A is from Stachybotrys as well.
Then you have citrinin, which is from a bunch of different mold species, including Aspergillus and Penicillium.
Related Tests and Panels
Like the OAT, the mycotoxin screen is done in the first morning urine. It’s indexed to creatinine. And again, because of the pituitary signaling problem, a lot of our patients are low in creatinine. So you just want to make sure patients are not drinking a ton of water. If the urine is too dilute, you may have to restrict fluids for the patient the day before to get good results.
And you always want to combine the mycotoxin with the OAT. Again, the OAT will tell you if they’re colonized, if they have activation of the cell danger response, if they have problems detoxing and nutritional deficiencies that could be interfering with recovery.
And the mycotoxin will specifically identify the toxins that are in that patient’s urine.
So this is a six-year-old with autism and worsening of behaviors. This is her OAT. She has a high level of number 3, which is a yeast marker. She has a high level of number 4, which is an Aspergillus marker. High level number 7, which is yeast. 10, which is strep. 14, which is bacteria. And 16, which is sort of your classic Clostridial marker that Dr. Shaw talks about being associated with autism.
This is what her second page looks like. She’s got the high succinate, citrate level is getting high. She’s got a problem converting dopamine to norepinephrine—so that ratio is high. She does okay converting it into DOAC. She’s got some ketones that are positive. She actually has high B5 but low B2, so that’s going to interfere with her Krebs cycle.
High vitamin C because she’s taking it. She doesn’t detox very well.
This is what her mycotoxin screen looks like. Now she’s got sky-high ochratoxin. She should be less than 7.5; she’s at 27.16. I couldn’t find her original one—this is actually a second one that she had—but in the original one, she also had high citrinin.
So again, this is a classic example of somebody who’s been exposed to mold and become colonized. They have significant dysbiosis. They have signs of cell danger response, both in the Krebs cycle and the fact that they have high ketones. They have disruption of normal dopamine metabolism with inhibition of that enzyme that converts dopamine to norepinephrine—that’s either from genetic glitches or from toxicity. And in her case, it turned out to be toxicity.
She has persistently high levels of ochratoxin. Like I said, on the first one, she also had citrinin, which suggests the presence of Aspergillus, which is what we’re seeing on her organic acid test.
Again, it’s likely that the gut dysbiosis is messing with her nutrition—particularly with low B2. She was already on methylation support that had B6, folate, and B12 in it.
Finally, the OAT shows problems with low glutathione. Either this is genetic or, again, this is low because it’s overused—because she’s too toxic.
But neither of these tests guarantee that these behaviors are coming from mold. You certainly would be suspicious, but you’d like to see more evidence for the brain inflammation.
But to me, this is enough to start treating. And this is also a patient that would likely benefit from actually treating the mold itself with anti-mold medication because she looks like she is colonized.
So this is a 44-year-old who has a history of chronic Lyme who’s not getting any better. Again, he’s got high aflatoxin, high ochratoxin, and high citrinin. So we’ve got three different toxins that are present. And he also has a little bit of mycophenolic acid there.
This is his organic acid test. Now in this case, he doesn’t have any of the mold markers. He does have a marker for yeast, and he’s got the elevated DHPPA, which is a bacterial marker. He does have oxalates—probably from the yeast. And again, he does have a high succinate level and a citrate that’s higher than it should be.
He’s got a little bit of a problem converting dopamine to norepinephrine—that ratio is a little bit high. But he doesn’t have a problem converting it to DOAC. He does not have high ketones. He does have a low B2 and a low vitamin C marker. He does not have the methylation marker that the other patients had.
So again, this is a similar pattern on the mycotoxin screen, but a very different OAT. This is a patient—he has high succinate and nutrient issues like the others—but he doesn’t have the mold markers on the OAT (2, 4, 5, 6, and 9 are not elevated). So it tells you he’s not colonizing mold.
And this is the type of patient that I would not use an anti-mold medication on.
All right, so these are some of the tricks to improve uptake on the mycotoxin test. You do all these the day before: a 24-hour fast or intermittent fasting if you’ve started it earlier—that improves release of toxins. Massage. Sauna—I put infrared, but any sauna will help mobilize toxins. Exercise. Pretty much anything other than glutathione that mobilizes toxins.
All right, so some other mold-specific labs—because you’ll start reading, especially some of Dr. Shoemaker’s work—and you start getting overwhelmed with these. I mean, start with the basics. You need to be comfortable with the OAT and the mycotoxin screen. That’ll give you a very good foundation on identifying which patients are potentially mycotoxin-affected.
But these are some of the other ones. So again, the OAT and mycotoxin screen will tell you:
- Are they colonized?
- Are there mycotoxins present?
- Do they have nutrient deficiencies?
- Is there toxicity or evidence of cell danger response activation?
What it doesn’t tell you is:
- Whether there’s immune system activation
- Whether there’s hormonal imbalance
- Whether the mold colonization or mycotoxins are actually causing the patient’s symptoms
Frequently, it’s pretty obvious from the clinical presentation, but there are other evaluations that are going to help you.
Visual contrast sensitivity is one of the big ones that I use. This is a pretty simple test. You can do it online. It allows you to distinguish the object from its background.
Basically, these are black and white lines. As you go from left to right, they get dimmer. As you go from top to bottom, they get closer together. At some point, you stop seeing black and white—what you see is gray. The point at which you see that determines whether you pass or fail the test.
It’s very different from visual acuity. You want to correct the acuity to do the test—you’ve got to do it with adequate lighting—but it’s not a test of visual acuity.
Basically, brain toxicity is the primary thing that screws up visual contrast.
This was actually developed by the military as a quick-and-dirty way to figure out which service members were getting toxic so they could be rotated out of those toxic situations.
So this is what a test result looks like. It basically answers the question: Is my patient neurotoxic?
Almost all mycotoxin patients will have an abnormal VCS to start out with. Now, this particular test is pretty good. You’re not going to have a mycotoxin patient with a completely normal VCS.
The red is the patient and the gray is the healthy. Typically, that red line is going to be a lot lower than the gray.
It’s inexpensive. It’s done online. You can buy packages of these tests. I mean, they’re $15 a piece. So I typically will have somebody do it along with other testing. And then this is the test that we’re going to do monthly.
And we typically don’t—we wait until this gets better before we start retesting. And also, if month to month they’re not getting better, you need to change what you’re doing.
You need to look at: Is there persistent exposure? That’s the number one thing that will cause this thing not to change.
Like, people are doing everything under the sun. They change their diet. They’re taking their binders. They’re doing their vitamins. They’re doing their bile salts and their phosphatidylcholine and all the other things I recommend—but they’re still living in a moldy house.
None of those things are going to work if you keep getting exposed. So this is the number one thing.
But if they got rid of the mold and they’re still not getting better and they’re doing all these things, then you may want to look at: Is there a secondary cause of brain toxicity?
High on that list would be things like heavy metals.
Once that VCS normalizes, then you can go back and repeat some of the testing that we’re talking about.
So Dr. Shoemaker is one of the pioneers of mycotoxin molds. He was the first one—he’s kind of crazy and very OCD—but he was the one that ran a hundred tests on his patients and showed that they were abnormal, would work on them to normalize, and then their symptoms would go away.
He would demonstrate resolution of the stuff on the bloodwork. And then when they went back to work in their moldy building and got sick again, he showed all these markers flared back up. So God bless him for doing all this testing because it really helps us now.
One of the big areas of his testing was this idea of abnormal brain signaling. And it’s all based on this hormone called MSH—that actually stands for melanocyte-stimulating hormone.
Now, with your skin, that’ll make you nice and tan. Your brain does not have melanocytes, so your brain is not going to get tan. But it’s a master hormone. It regulates the level of a bunch of other pituitary hormones like TSH, ACTH, FSH, LH, and all these other things that affect the end organs—like the thyroid, the adrenals, and the ovaries.
So you can get all kinds of hormonal symptoms because the MSH is not working the way it’s supposed to.
The classic patient would be somebody that has all these hypothyroid symptoms. You can run through 20 hypothyroid symptoms and they’re 20 out of 20, but they’ll have a normal or even a low TSH. And so the doctor will say, “Oh, they’re fine.” They’ll have low cortisol, but they’ll have a normal ACTH. “Oh, they’re fine.”
Again, you want to measure not just TSH. You want to measure the free T3 and free T4 to determine the actual function. If you’ve got a normal ACTH with a low cortisol, that’s not an adrenal problem—that’s a brain problem. It’s a signaling issue.
That’s the same reason why TSH never really correlated with clinical symptoms for most people—because it’s reflecting what’s going on with the pituitary and not necessarily what’s going on with the thyroid.
All right, so the other big pituitary hormone that we like to measure is arginine vasopressin hormone. This is the one that determines how much water the kidney is reabsorbing.
What’s supposed to happen is: as the osmolality goes up (the blood’s getting more concentrated), the arginine vasopressin hormone should go up to match it and get the kidneys to reabsorb more water. And as it goes down, the opposite should happen.
Dysregulation results in low AVP with high serum osmolality. These are your patients that are peeing all the time, but they have an osmolality of 300 or 305. And again, because they’re unable to reabsorb the water, they’ll have this dilute urine.
“I’m getting up four times every night to pee.” But they’ll have a high serum osmolality and the urine will be very dilute. Because this can affect the testing we do, you may have to fluid restrict some of these patients.
So immune testing—this helps determine whether the immune system is being activated by the presence of mycotoxins.
The classic lab tests are from Dr. Shoemaker: the C4a. This is activated complement. Normal is under 2,830. You have to order it from Jewish National Labs. It has to be drawn, spun, and frozen within 30 minutes. So work with your local lab to make sure they do it the right way. If you get a result of 60,000, they probably let it sit in the water bath for too long.
TGF-beta: normal will be less than 2,380.
MMP-9: normal will be 85 to 332.
The other area of immune function you can test is actually looking at lymphocyte numbers. I do an immune phenotype (IP) flow, which is CD4, CD8. CD3 is not on that list—that’s all T cells. CD19 are your B cells. CD15, 60, 16, 56, and 57 are your killer cells.
And then I also look at immunoglobulin levels—IgG, IgA, IgM, IgE—along with IgG subsets.
Typically the CD8 and CD57 numbers will be affected. They’ll either be too high if it’s an acute toxicity, or low if it’s chronic. Then also the helper-suppressor ratio—the CD4:CD8 ratio—can be helpful as well.
And the immune system—if it’s activated in the presence of a positive mycotoxin screen—then it’s almost certain that the mold toxins are causing the problem.
MARCoNS: this is a nasal swab. Looks for the multi-antibiotic-resistant coagulase-negative staph. This is the coagulase-negative cousin of MRSA.
MARCoNS will keep the MSH low, so it’s important that you treat this if it’s high. If MSH is low, it’s important to treat this because it’s going to be hard to recover MSH otherwise.
VEGF: this is vascular endothelial growth factor. It’s typically low in mycotoxin patients. It’s high in patients with cancer or clotting issues—like patients with long COVID or vaccine injuries—but it tends to be low in mycotoxin patients.
NeuroQuant MRIs: this is the idea of looking at the brain in a very standardized way. You get a standard MRI, but the patient is set up so that every MRI is the same. So my slice three is the same as your slice three.
Then they have a computer—use a little AI—to evaluate the imaging and say, “Where’s the caudate? Where’s the pallidum? Where’s the cerebellum?” and then compare your MRI to other people of the same age and same sex. So it’s always sex- and age-matched.
The classic findings in the mold-toxic patient are decreased volume in the caudate and increased volume in the pallidum. You’ll see decreased volume in the caudate all the time. The increased volume in the pallidum—I don’t see as much. But again, NeuroQuant is one way to quantify where that is at.
All right, mast cell testing—these are the patients that are rashy. They develop hives, they’re itching, they’re miserable. These are your allergy patients that have normal IgE or normal allergy testing. And they can be some of your sickest patients.
They’ll have all these histamine symptoms, but they have normal allergy panels. So you can measure histamine and tryptase levels. I always give patients an order for it and tell them: go to the lab on a really bad day—because most of the time, it’s going to be normal.
You can do 24-hour urines to look for prostaglandin D2. You can do IgE levels—if the IgE levels are really high, then maybe it is an allergy and you should be doing that type of testing. If the MMP-9 is very high, that would be another sign of mast cell problems.
But usually, this is more of a clinical diagnosis. And the treatment usually involves resolving a mold issue. Again, the mast cell is there because the immune system’s activated. The immune system is activated because of the mold issue. So doing all the mast cell things can help the symptoms, but it’s not necessarily going to deal with the underlying cause.
Autonomic testing—again, this is classic with any chronic immune activation.
The evaluation can be as simple as just checking orthostatics in your office. Typically, what’s going to happen is the pulse is going to go up, but you don’t necessarily have a significant drop in the blood pressure.
Or you can do formal tilt table testing where they can quantify all this stuff for you.
So all of this stuff can be very overwhelming. So I usually simplify my approach based on the person sitting in front of me.
But this is sort of how we go. I’m going to start—the patient tells me their story. I call it their “tale of woe.” They’re going to tell me their tale of woe. And then, based on that, I’m going to look…
Okay, I’m going to order an OAT on almost everybody because, again, this is—you know, anybody that’s chronically ill—you’re going to want to look and see where they’re at from an organic acid test point of view.
And then, the next thing is: based on that, you may want to order a mycotoxin screen. But even just based on their history, you want to order a mycotoxin screen.
And then from there, you may go directly to treatment just based on those two. And you can forget about everything I talked about in the last four or five slides.
But if that’s not enough information, you’re not really sure—I know that they have mycotoxins, they have evidence of toxicity on the OAT, or maybe they’re colonized—but do they have some of these other things?
So you start and say: do they have the immune activation markers? Well, if that’s present, then absolutely you would move to treatment right from there.
But if that’s not clear for you, then you can go look: do they have MCAS? If they do, then you would move to treatment.
Do they have the brain markers? And from the brain markers, we’re going to be going to the three things we talked about with the brain, which are:
- the visual contrast sensitivity test
- the NeuroQuant testing
- the POTS testing (autonomic testing)
And again, if any of that stuff is positive, we’re going right back to the treatment leg there.
You want to try and simplify this. You want to have a very low threshold to determine whether or not you’re going to be testing your patients and whether or not you’re going to be treating your patients.
Sometimes it’s worth just doing a month of treatment to see if these patients get better. Because obviously, if they do, then toxins had something to do with that.
Related Tests and Panels
And a lot of the treatments we talk about—it’s not just mold toxins—they can work for mycotoxins as well.
So again, you always want to have mycotoxins on your radar any time you’re addressing the health concerns of any chronically ill patient. They’re going to be one of the frequent things that are overlooked. You can use clues from your organic acid test along with evidence from your history, and that should decide whether or not you’re going to do the mycotoxin test.
Sometimes just from their history alone, that’s enough to justify ordering the mycotoxin screen.
I always ask my patients: Where do you live? What’s the environment like? Do you have a swamp out the back door? Has there ever been a roof leak? Has there ever been a plumbing leak? What’s the humidity like in your basement?
Because you’d be surprised how many patients will basically tell you, “Yes, I have a mold illness,” just based on their history. So frequently I’ll jump right to the mycotoxin screen based on that.
So these two tests, along with the history, are frequently enough to justify treatment. And then you don’t have to go down this road of very expensive testing.
Now, again, I frequently will throw the VCS in there because it’s not particularly expensive and it’s a great monitoring test. You don’t necessarily want to do an organic acid test every month. I’m sure Mosaic would love it if you did that, but it gets a little expensive for the patient.
But you can certainly do VCS testing every month. And then when that gets better, then you go back to your OAT, you go back to your mycotoxin screen to see what those are looking like—and they will change.
Other testing will just help you in designing a treatment program or trying to definitively nail the diagnosis—particularly if they have signs and symptoms of MCAS, POTS, or any hormone deficiency.
I’ve been harping on the thyroid and the adrenal, but the gonadal stuff is really important too. These are women with irregular menses. These are men that have low testosterone.
I can’t tell you the number of patients who are—you know—they’re 30 years old, they go to the doctor, they feel like crap. To their credit, their doctor measures a testosterone level—it’s low. And the first thing they do is put them on testosterone injections.
It’s like, dude—why? Why would a 30-year-old have a low testosterone level? I mean, come on. Let’s take it a step further and ask why.
And this is one of the big things. I didn’t show it on here, but if you look at how mycotoxins impact the way we make hormones—it’s a very complex pathway—but we hit that pathway in three or four different spots, and it just screws up our ability to make hormones.
A lot of this information we have on mold actually comes from animals. Because, you know, we take better care of our animals than we take care of ourselves, right?
So a lot of this—because if these animals don’t grow and reproduce, that’s money out of the bank. So a lot of the information comes from ranchers that are interested in the health of their animals. They’re very much into this.
So I’m going to leave you with this: once you have all this figured out, what do you do with these patients?
Well, this is your teaser—stay tuned for Mycotoxins 102.
So we’ll be talking about treating patients with mycotoxin illness. That is a brief three weeks away. We’ll be looking at, once you figure out you’ve got a mycotoxin patient, what do you do with them? And we’ll be talking about that in a lot of detail.
So that’s my contact information. For those of you that don’t know me, I’ve done a lot of speaking for Mosaic. I do a lot of speaking on autism. I’m president of the Medical Academy of Pediatric Special Needs, which is basically integrative pediatrics.
We deal with kids on the autism spectrum, kids with ADHD, other neurodevelopmental delays. But we also deal with kids that have autoimmune disorders, asthma, recurrent ear infections—all the chronic pediatric stuff you hear about—we deal with that stuff.
I have a practice in Ann Arbor. That’s my address there. That’s my email. That’s my office phone. We do see both children and adults in my practice. I work with four other nurse practitioners who are outstanding.
A big part of my practice is dealing with mycotoxins. I learned mycotoxins really from treating patients that had chronic Lyme. These patients came into my office, they’d test positive for Lyme, we’d start treating them, they’d start getting better—and then they would stall. They wouldn’t get any better.
And it’s like, what the heck is going on? The Lyme markers are looking better, the immune system’s looking better, but the patient isn’t.
And it turned out a lot of those people had mold toxicity. It’s a big problem in Michigan, but Michigan’s not unique—it’s a big problem all over the United States, even in supposed dry states like Arizona and New Mexico. It’s a problem there too. So it should always be on your radar.
And hopefully today gave you an idea of how to identify those patients, not make it too complicated, and understand that this is a big deal—regardless of age.
And then we will talk in a few weeks and go over exactly how you treat your patients.
So with that, I will open things up to Q&A, and I certainly appreciate your attention.
Michelle:
Thank you, Dr. N. That was a really wonderful lecture.
We’ve already had multiple people on our chat saying that this was the best lecture they’ve ever attended. It was extremely educational. So thank you so much.
Dr. Schwer:
Well, I’d like to thank my mother, my daughter, and my wife for commenting. I appreciate that.
Michelle:
I know that the next one is going to go into treatments, right? And not surprisingly, we’ve had quite a few questions about that. I’m wondering if you can give just a tiny little, like 30-second teaser to some of that?
Dr. Schwer:
Right, so I’ll give you my overview. Actually, you know—I wonder if I can do this right from my computer… maybe not… no, that’s going to be too complicated. No, sorry.
So the number one thing we want to do with treatment is eliminate the source. People get really bored with this. They get really tired of me talking about it.
But you are wasting your time doing any of this other stuff. I have people come into my office, and they’re taking their binder four times a day, they’re doing their TCA, they’re taking their PC, they’re on the right diet, we’re fixing their biome, they’re doing their fibers and probiotics—and they’re still living in a moldy house.
If you have a bullet wound in your liver and you have a low blood count and you’re getting transfused for your low blood count—yeah, it’ll help, but not for very long. You’re just going to bleed it right back out and need another transfusion. Fix the bullet hole. That’s the moldy building or the moldy environment.
And it’s very difficult. We have techniques—if you can’t remediate your house, you can create a safe zone. You can do various things to try and optimize it. And we’ll talk a lot about that in part two.
So that’s number one. The second thing is binders—things to remove this from your body. A lot of these molds are bound to bile salts and they just get reabsorbed. They get into the small intestine, and instead of being pooped out, they just get reabsorbed. Ninety to ninety-five percent of all the bile gets reabsorbed, and the toxin gets reabsorbed with it.
Binders disrupt that. Non-absorbable bile salts like TUDCA can disrupt that. So that can help get rid of the toxin.
Those two steps—get rid of the source and use a binder—that’s 90 to 95% of the battle. All the other stuff is really dependent on that.
So we use things for autonomic dysfunction. There’s something called DNRS that I really encourage patients to use—but again, you’re not going to fix the autonomics if you haven’t gotten rid of the toxin.
There are a million things you can do for MCAS—none of them work very well, because again, you’re still bleeding from a bullet in your liver. You gotta get rid of the mycotoxins before that stuff’s really going to take effect. And then you can change things around.
So the basics—the really basics that anybody can do:
- Get rid of the exposure
- Test your house however you want
- If you have mold, get somebody in there that knows what they’re doing to remediate it
- Create a safe place
- Put a mold toxin–rated air purifier in your bedroom
- Get rid of your books, papers, upholstered furniture, draperies
- Get rid of carpeting—make everything hard surface
These are things you can do to try and improve where you’re at. And everything will domino off of that.
Those two things—get rid of the source and detox the body—that’s fundamental. First things first.
Michelle:
Yep, absolutely. Get rid of the bullet in your liver.
Dr. Schwer:
Yeah. And then we’ll give you blood.
This session is continued in Part 2, Mold 102
