EP238: Two Perspectives, One Mission: Mold and CIRS - Neil Nathan, MD and Ritchie Shoemaker, MD
In a Nutshell
Dr. Shoemaker and Dr. Nathan present two distinct approaches to mold illness/CIRS: Shoemaker's protocol relies on HLA-DR genetic testing, blood biomarkers (C4A, TGF-β1, MSH, MMP9), and treating actinobacteria/endotoxins as primary causes in 90% of cases, while Nathan uses urine mycotoxin testing to identify specific toxins and prioritizes binders, antifungals, and addressing limbic/vagal/mast cell dysfunction first. They diverge significantly on HLA-DR utility, urine mycotoxin testing validity, MARCoNS treatment, and the role of mycotoxins versus other biotoxins. Both agree that removing ongoing exposure is essential, that 80-95% of patients can recover with proper treatment, and that mold illness is an epidemic the medical community continues to dismiss.
These notes were generated by AI and may contain inaccuracies.
Welcome to the Better Health Guide podcast, where we take a deep dive into complex chronic conditions and explore ways to build resilience, improve vitality, and achieve better health. The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing discussed on this podcast should be considered medical advice.
Episode 238 of the Better Health Guide podcast explores two perspectives, one mission, advancing the conversation on mold illness and CIRS. The special guests are Dr. Neil Nathan and Dr. Richie Shoemaker. Dr. Nathan is a leading clinician in the treatment of mold illness, Lyme disease, chemical sensitivities, and other complex chronic conditions, and is the author of several books, including Toxic and The Sensitive Patient's Healing Guide. Dr. Shoemaker is a pioneer in the field of biotoxin illness and the developer of the chronic inflammatory response syndrome or CIRS model. He is the author of several books including Mold Warriors and Surviving Mold.
Scott, the host, personally thanks both Dr. Nathan and Dr. Shoemaker for their meaningful impact on his own recovery from complex chronic illness. Scott first learned about Dr. Shoemaker's work around late 2005 reading the book Mold Warriors. At that time, he had been diagnosed with Lyme disease but had never thought of mold, and that was the first time that concept entered his awareness. Mold Warriors was published in 2005, and subsequently extended his knowledge through Dr. Nathan's book Toxic, which was published in 2018 for the first edition.
Today's conversation is not a debate. There will be no winner. The goal is for listeners to hear each of their perspectives on specific topics that have been previously agreed upon. Each will respond to a given question and then move on to the next question, and listeners can decide which perspective they resonate with the most. The goal is to give listeners a look at the lens through which each doctor looks at these conditions, how they approach diagnosing and treating patients, and to show that while they might have two different perspectives, there can still be one mission.
Dr. Shoemaker states that today's discussion is going to be a restart of what they've been doing for the last 25 years, with experiences from Gordon's group, Ratna Lang, and spending time in his office looking at what Neil's doing and what he's doing. He references a nice bound book of information from Santa Rosa in 2011 where Neil was doing Shoemaker for dummies. Dr. Shoemaker mentions that he has chosen a path that he thinks is different than Neil's. He accepted writing a forward to one of Neil's books and was very impressed with it, realizing that Neil had been holding his hand and talking about life in general as an unknown discussant. Dr. Shoemaker states that he likes Neil and feels they can be compatible, though they may have arguments that are going to be distinctive. He mentions having added a lot of new stuff since he last talked with Neil.
Dr. Shoemaker sent a paper a couple days ago about triple positives and Parkinson's and VIP. He states it's incredibly exciting, and now they're looking at the worst patients of all having a recognizable diagnostic process and treatment protocol. He mentions it's a happy day for some of the worst people before.
Dr. Nathan honors Dr. Shoemaker as the one who brought him into the field. He went out to Pocamoke, Maryland to spend time with him in the beginning. They became friends, lectured together for a while, and then began to see this whole field through a different lens. Dr. Nathan's number one goal is to raise the consciousness of the medical profession that mold toxicity is a serious epidemic and that they need to be looking for it, diagnosing and treating it. There are millions of Americans going undiagnosed, untreated, and this is a travesty. Worse, they're being gaslighted by their health care practitioners and being told there's no such thing as mold toxicity or CIRS. Dr. Nathan states both he and Dr. Shoemaker agree that you can't treat patients if they're ongoingly being exposed to mold at work, home, or in their car. Both use binders to a certain extent. He wants listeners to be aware that they may not be so far apart as it's been portrayed over the internet.
The host finds comfort in the different opinions and perspectives. It would concern him more if everyone agreed and still did not have solutions that worked for the vast majority of patients. The fact that each doctor is looking at different tools is likely to lead to more advances than if everyone agreed and no one was still working hard to find better tools and better solutions.
The underlying process with mold toxicity is inflammation. The goal is to get enough toxin out of the body that the immune system reboots itself. Removing the mold toxin is key as it's a root cause. Dr. Nathan has learned that mold toxin has triggered in many patients limbic, vagal, and mast cell issues. Many of the sickest patients have a limbic system and vagal system that has become dysfunctional. Also, mast cell activation has been set forth in many of those patients. Often treatment cannot even begin until first looking at limbic, vagal, and mast cell dysfunction.
Dr. Nathan views treatment as three-fold: first, removing the patient as best as possible from the source in which they're getting exposed; second, using binders that are specific for the toxins that are found in them; and third, using antifungals because a large percent of patients colonize, particularly in their sinus and gut areas. If the colonized mold is not treated, patients often won't get better.
When Dr. Shoemaker first got involved with people exposed to water damaged buildings was 1998. He had been working on biotoxins and dinoflagellates and ciguatera and pfiesteria and looking at blue green algae and microcystis and cylindrospermopsis in Florida, aphanizomenon in Florida as well. It wasn't until 1998 that they finally had a test, visual contrast sensitivity, that could be added to symptoms and then symptom clusters. It wasn't until 2001 and 2002 they were able to add HLA DR, MMP9, PCR, and the genetic basis of susceptibility. The visual contrast sensitivity, symptom clusters, and genetic markers have been keepers. MSH deficiency and MMP9 increase were ones that Dr. Shoemaker stumbled upon mostly, and he was about the only person doing this kind of work back in 1996.
Dr. Shoemaker made a case definition in 2003 that was replaced by GAO in 2008. He has added the approach of hypometabolism or suppression of ribosomal activity, looking at manifestations as well as mitochondrial genes that migrated from the mitochondria to the nuclear area for transcription. They're looking at proliferative physiology with insulin substrate 2 and aerobic glycolysis following along the pathway of Dr. Warburg years ago.
Dr. Shoemaker identifies eight elements of causation. The fourth element is metabolic acidosis, and if there is metabolic acidosis, there will usually be pulmonary hypertension, insulin resistance, gray matter nuclear atrophy in the brain, and T-regulatory cell deficiency. The fifth element is looking at HLA, especially with 4353 and 11352B, which is a tremendous tool for looking at progression within a family and relatives. The sixth element is immune dysregulation, seen mostly in patients worried about what their exposure could be, whether it's beta-glucans, fungi, actinobacteria, or endotoxins. The seventh element is T3, which has the addition of three separate immune markers with clusterin being one, coagulation being another, and dysfunctional passage of ions and nutrients in neurons. The eighth element, still in progress, is looking at neurosciences as a general category, but now looking at a vascular source.
Dr. Shoemaker mentions he will be following up with Dr. Nathan's comments because he has different things to talk about with autonomic dysfunction and mast cell activation syndrome.
HLA DR testing has historically been discussed in relationship to susceptibility or propensity to developing CIRS, possibly influencing recovery potential. Many are familiar with terms like mold susceptible, Lyme susceptible, multi-susceptible. In recent years, there's been discussion around the role of actinobacteria, endotoxins, and beta-glucans beyond mold. Dr. Shoemaker explains the approach to HLA was a stumble and guess approach to medicine. He had 10 people on Williams Point on the Pocomoke River who were water skiing during an outbreak of pfiesteria when a bloom was going on and fish kill was going on, but people were swimming along. Of the 10 people that were water skiing and falling into the water, seven got sick and three didn't. HLA was the first marker associated with illness and routinely not found at all in non-illness.
HLA DR does not change as opposed to biomarkers. HLA changes, but we know where mom and dad come from and brother and sister come from. If one person is ill or someone is contemplating having a family, HLA might be present. It helps understand whether one should be cautious about moldy buildings or not. Dr. Shoemaker states that if you don't have HLA, it's 99% of the time you will have MSH deficiency. MSH accounts for the rest of susceptibility. 24% of people get sick in a water damaged building, and that number has stayed for nearly 30 years. That correlates with HLA. HLA DR testing is useful for family answers about why someone got sick. The two genotypes Dr. Shoemaker worries most about are 4353 and 11352B. The third is 14552B. Dr. Shoemaker states that he is a 4353 himself, so there is still hope if that's the situation someone is in.
Dr. Nathan started using HLA DR on all his patients initially after training with Dr. Shoemaker. However, he did not see a correlation between how patients responded to treatment and what their HLA DR showed. Given that patients' limbic systems tend to be compromised because of mold toxicity, hearing that they have a 4353 scared patients, and many took that to mean they were basically going to be unable to heal properly because of their genetics. Dr. Nathan stopped doing HLA DR testing because he did not see a connection between whatever their HLA status was and their clinical response. He had patients with 4353s who responded beautifully to treatment and patients who had no supposed genetic predisposition who were really sick.
Dr. Nathan reframes the immune system concept through his lens. When looking at families or offices where people are being exposed to mold and some get sick and some don't, he looks at how robust their immune systems are, not measured by HLA DR, which he didn't find corresponded with that. If someone had a robust immune system, they could live in a moldy environment and be minimally ill. This is true for Lyme as well. But if the immune system took a hit, which could have been COVID, a flu, a serious infection, a surgical procedure, or an emotional upheaval, the immune system lost containment. Dr. Nathan views the process as intrinsically needing to remove enough toxin that the immune system could reboot itself.
The biotoxin blood markers discussed include C4A, TGF beta 1, MSH, MMP9, and others. Dr. Shoemaker states these markers were in wide use in his practice by 2003. TGF beta 1 was added in 2008. The illness was multifactorial with abnormalities and deficiencies of regulatory neuropeptides. MSH and later VIP, inflammatory cytokines, MMP9 was the first, C4A was the third looking more at complement. When symptoms and visual contrast are part of the case definition, labs seen in published peer-reviewed literature are also wanted.
Dr. Shoemaker made a list of biomarkers that he's published over the years that people have used and reproduced. Reproduction of science is what it's all about. He looked at groups of symptoms, clusters of symptoms, visual contrast, anion gaps, TGF beta 1 before and after treatment, MMP9, C4A, VEGF, MARCoNS, ACTH and cortisol, ADH and osmolality. These were all in wide use by 2008. When using transcriptomics in 2013, there were eight gene groups from molecular hypometabolism. IRS2 is controlling about glucose transport. Hypoxia inducible factor 1A is important for pulmonary hypertension and hypoxia. TUBA4A and TUBB1 are looking at the cytoskeleton again before and after. Immune systems are looked at before and after with a Parkinson's fingerprint with eight genes. Clusterin coagulation has 10 genes. Defective apoptosis is remarkably important. Specific causation cannot be underestimated. The role of fungi, actinobacteria, endotoxins, and beta-glucans can give specific findings to groups of genes that can be watched treating successfully and returning to normal.
Dr. Shoemaker mentions gray matter nuclear atrophy, cortical gray atrophy, forebrain parenchyma, and spiral ventricle. He and Dr. Nathan were going to do a talk in Norway in 2015, and Dr. Shoemaker presented the data on neuro QOL at that time. T-regulatory cells have a tremendous role in the T-cell synapse looking at antigen presentation. Without antigen presentation, antibody production doesn't occur. Actinobacteria can be isolated from skin and blood. The idea that blood is sterile is wrong. Actinobacteria are in blood all the time. Defensins, Lyme, acute Lyme treated, the molecular biology of Lyme acute and positive coming from John Aucott and Charles Chiu at UCSF. Cytokine CD14, CD4, CD12, gliadin antibodies are the new players. AKT and toll 2 are huge. These are now prodromal illnesses that can be recognized before they become terribly important.
Dr. Nathan started his training with Dr. Shoemaker and used visual contrast, having a visual contrast in his office. He used all those markers routinely on every patient. In the early days, those were the only measures that would help define people who had mold illness or didn't. Over time, when urine mycotoxin testing came about, that for Dr. Nathan was a game changer. From his perspective, that was the game changer that allowed knowing exactly which toxins were in that patient at that time. It gave the opportunity to be specific about which binders would be used to bind those toxins.
When Dr. Nathan began to apply visual contrast and TGF beta 1 and C4A and all the other markers, he saw that visual contrast would go back to normal long before urine mycotoxins were cleared. TGF beta 1 and C4A would normalize long before they were clear. He began to see that patients hadn't quite completed their healing journey perhaps at a different point in time than Dr. Shoemaker has. Dr. Nathan states that for him, those markers are useful but they represent a non-specific measure of inflammation in the body. Those markers can be elevated with Lyme disease, Bartonella, and several other types of infection.
Dr. Nathan points out what he thinks is a super important distinction between their practices. One of the things that has struck him over the years is that patients choose practitioners based on their perception of them. Both Dr. Shoemaker and Dr. Nathan have written books and done podcasts for many years, and patients are attracted to their
Dr. Nathan notes that different practitioners see different patient populations, which shapes their expectations and treatment approaches. He sees significantly more Lyme patients than Dr. Shoemaker, making certain markers less useful for his practice. Specifically, TGF beta 1, C4A, and visual contrast testing are affected not only by mold but also by Lyme and mercury toxicity, both of which he encounters frequently.
Dr. Shoemaker recently authored a paper discussing challenges and limitations surrounding urine mycotoxin testing. Dr. Nathan finds these tests clinically useful despite agreeing with Dr. Shoemaker's concerns about lack of appropriate controls and validation. He has performed tens of thousands of urine mycotoxin tests across all three companies and has found fair correlation between them despite their different methodologies (ELISA technology versus real-time mass spec used by Mosaic and Vibrant Health).
Dr. Nathan finds urine mycotoxin testing helpful for making diagnoses and determining which specific toxins are present, enabling more targeted treatment with binders. He uses these tests for follow-up monitoring and considers a RealTime test showing "not present in any category" as evidence that treatment is complete. He has a mentorship program for over 300 physicians, and the group has collectively seen value in urine mycotoxin testing for both diagnosis and patient follow-up.
Dr. Nathan expresses more concerns about blood-based mycotoxin antibody testing compared to urine testing. He finds positive Ig antibody tests helpful in indicating ongoing or acute exposure, but follow-up testing results have been inconsistent and less helpful than urine mycotoxin testing.
Dr. Shoemaker emphasizes that tests looking at causation must follow Koch's postulates and cannot skip proper validation simply because controls are inconvenient. He points out that assumptions based on six to eight mycotoxins found in urine may not account for proper handling from home to lab. He references his 2019 paper critiquing mycotoxin testing, which cited 21 studies involving 2,756 healthy controls, none of whom were sick. He notes that European criteria for safe food consumption frequently find mycotoxins in urine, with one person rarely lacking one of 50 different fungi.
Dr. Shoemaker cites Dr. Michael Soyok from Austria, who found 1,500 antigen formers in urine using mass spec among 2,000 people in water-damaged buildings. He emphasizes that the chance of correct findings with multiple mycotoxins in urine approaches zero without proper case-control studies.
Dr. Shoemaker explains that mycotoxins including aflatoxin, ochratoxin A and D, zearalenone, T2 toxin, and fumonisin are low molecular weight secondary metabolites that function as haptens rather than complete antigens. Without covalent conjugation to a carrier protein, these compounds cannot elicit class-switched IgG immune responses. He states there are 20 papers demonstrating this limitation and emphasizes that haptens lack biological plausibility for generating class-switched antibodies.
The discussion addresses other laboratory assessments beyond traditional CIRS biomarkers. VCS (visual contrast sensitivity) is acknowledged as non-specific but useful as an initial indicator. Dr. Shoemaker emphasizes that GENIE and NeuroQuant work together for assessing brain injury mechanisms, with GENIE providing specific causation information and NeuroQuant revealing patterns of brain injury. Endotoxin patients show cortical gray atrophy or superior lateral ventricle enlargement with four or more findings of gray matter nuclear atrophy.
Dr. Shoemaker notes that GENIE has identified 19 different pathways with potential for more information. He criticizes organic acid testing for omitting actinobacteria, which he considers one of the most important sources of bacterial interaction with fungi, actinomycetes, and gram-negative rods.
Dr. Shoemaker references a paper published October 23, 2020 by Matt Brad Hayyatt, finding that mycotoxin testing references primarily involve food studies, cell culture, or treatment rather than proper validation. He notes Dr. Hope's work with cholestyramine and various clay treatments.
Dr. Nathan references Dr. Joe Brewer's 2013 paper in which 92% of 112 chronic fatigue syndrome patients tested positive for urine mycotoxins. Dr. Brewer subsequently published papers in 2014 and 2015 involving 100 consecutive patients treated with different antifungal nasal sprays, finding 94% success with amphotericin B nasal spray and 89% response to nystatin, with binders and oral antifungals included in the protocol.
Dr. Nathan references a 2019 Townson Letter publication by Great Plains Laboratory (now Mosaic) comparing 82 controls and 112 mold toxicity patients. Among controls, only ochratoxin appeared in urine, while mold patients showed significantly higher levels. Controls had ochratoxin levels of 1.6 nanograms per gram compared to greater than 18 nanograms per gram in mold patients. As a result of this study, Great Plains Laboratory adjusted their acceptable ochratoxin threshold from 3.7 to 7.5 nanograms per gram.
Dr. Nathan conducted a pilot study with eight mold toxicity patients who avoided moldy foods (dried fruit, aged cheese, mushrooms, coffee, beer, wine, processed meats, tomatoes, fermented foods) for 10 days, then consumed them for 10 days. Surprisingly, seven of eight patients showed decreased mycotoxin levels when eating the supposedly moldy foods, though this was not statistically significant and requires larger IRB-approved studies.
MARCoNS (Multiple Antibiotic Resistant Coagulase Negative Staph) has been a significant focus since 1999, with work involving Harold Butts and Tim Roberts from Newcastle, Australia. They demonstrated that MARCoNS produces antibodies that lyse MSH, creating MSH deficiency. When MSH replacement was unavailable due to FDA restrictions, antibiotic preparations including BEG spray with EDTA and gentamicin were used.
Since 2015, there has been a significant increase in antibiotic resistance in MARCoNS, including vancomycin resistance. This resistance correlates with aal compound use from Hopkinson Drug and antifungal use, with Mayo Clinic finding 33% of antifungal users developing intolerance.
EDTA at 0.25% concentration with 12 doses daily for one month helps eradicate organisms, while lower doses of two sprays twice daily activate biofilm formation by competing organisms. Peggy DuLio published research in Frontiers in Endocrinology in April 2026 showing that clearance of multiple antibiotic-resistant coagulase-negative staph is selectively associated with higher circulating alpha-MSH.
Joe Musto found that polycyclic ether toxins are produced by MARCoNS when grown in well assays, particularly in patients with prior fungal antibiotic use. The mean number of antibiotic resistances for antifungal users was 5.1 out of six. These polycyclic ethers had no known molecular library when mass spec was performed. Using GENIE analysis of mitochondrial ribosomes (both large and small), organisms with a z-score of 0.94 or greater do not produce polycyclic ethers and do not require treatment.
Dr. Nathan initially treated MARCoNS aggressively with triple antibiotic treatment and BEG spray but found many patients could not clear the organisms. Clinically, he observed only mild improvement in sinus symptoms without global improvement in patient response. He has stopped measuring MARCoNS and finds treating it unhelpful for his patients.
Dr. Nathan continues using BEG spray but removed gentamicin years ago due to systemic reactions. He believes the spray helps through broader sinus effects rather than specific MARCoNS treatment. He references Dr. Donald Dennis, an ENT surgeon, who has found mold colonization in sinuses of many patients and uses amphotericin B nasal washing, with some patients requiring surgical removal of fungal balls.
Evaluating homes, workplaces, cars, churches, and other frequently occupied spaces is considered crucial. The approach includes using mold plates as an initial, inexpensive method to test every room in a house.
Hermy testing is considered the most accurate method currently available for determining whether a place is safe. The HERTSMI-2 process developed by Ritchie Shoemaker is valuable for determining whose place is safe and who isn't, with less than 5% false positives for treatment. Air testing is found highly inaccurate as a major component of the building industry. Licensed mold evaluators often have only 10 hours of training, which is insufficient. Finding an indoor environmental professional (IEP) who knows what they're doing is essential because if mold is present, the exact location must be known for proper removal. The source of mold needs to be found and surgically excised rather than sprayed with various treatments, which doesn't work well.
Treatment of CIRS requires an additional source beyond using medications from a physician. Working with highly skilled indoor environmental hygienists is beneficial, and there are fantastic series of lectures before the SIRS X conferences with three or four layers of testing and training available. Everyone involved with treatment of abnormal indoor environments should consider taking time to get up to speed with state-of-the-art lectures on treating water damaged buildings.
With current tools available, big differences can be made in cleaning houses and keeping them clean without burning down houses or tearing them down. There is value in doing a HERTSMI-2 even if the score isn't taken as the indicator of health of a building. Air sampling in the middle of the room is discouraged as it won't give the right information and chances are it will give the wrong information.
The patient's nervous system is critically important in influencing the success or failure of treatment when working with mold and CIRS. The limbic system and vagus nerve are two different parts of the brain that speak to each other and are all about safety. Both neurologically scrutinize stimuli inside and outside of the body from the perspective of safety, and if they don't think the body is safe, they will literally shut it down and not allow people to take the kinds of treatment they need.
A huge percentage of patients have some degree of limbic and vagal impairment - greater than 90% in some patient populations. Often treatment needs to begin not with binders but with getting patients' limbic and vagal systems rebooted, which is absolutely central to their ability to heal. In 2016 with the publication of "Never Bet Against Occam," mast cells entered the picture with a profound interaction between the limbic, vagal, and mast cell systems. These same patients often needed to treat mast cell activation as well before they could even begin to really respond to the right treatment.
Dysautonomia from the Cleveland Clinic should be considered and offered to patients. Sometimes there's a lot of discussion about brain injury and limbic system injury when the problem is just MSH deficiency, so the differential diagnosis of dysautonomia needs to be rigorous. Since the textbook of CIRS medicine was written in 2021, a low-dose VIP protocol has emerged for people with drug sensitivity, chemical sensitivity, food sensitivity, and extending it to dysautonomia. Starting with dilutions of 1 to 10,000 to 1 to 100,000 and working up very slowly can treat dysautonomia without much more intervention than just buying time.
With ability to give VIP, time can be bought, then adding in Wellchol or cholestyramine. Cholestyramine is not used for anyone with dysautonomia. A team approach including a coach or someone who spends time looking at dysautonomic factors is beneficial. Fatigue and muscle weakness and difficulty performing physical tasks are often simply due to inflammatory problems when they're due to dysautonomia.
40% of patients were overproducing histamine because of a gene CCL5 or histidine decarboxylase. They were making histamine routinely and most commonly were diagnosed as having mast cell activation syndrome. Physical exam involved drawing a tic-tac-toe board on a patient's back and it would turn red with an urticarial response. To diagnose mast cell activation syndrome properly requires showing a normal C4A, negative CCL5, and negative HDC.
Working with David Berg who was big in coagulation in the late 90s led to using his testing and treatments on many patients, but they weren't very impressed with results. Coagulation issues are coming up more in medical conferences, but from one perspective they haven't seen it be as much of a player as some colleagues have.
Dr. Shoemaker notes it's important to think about what's coagulating. Looking at von Willebrand's profile shows more acquired von Willebrand syndrome than anybody else in the world, which is a bleeding problem. Paradoxically, clotting problems can also occur. Factor V and Factor V Leiden are found at a rate of one in 150,000. The vascular hypothesis of Alzheimer's and Parkinson's involves GP6 glycoprotein 9, B3 integrin, 2B platelet factor 4, SP thrombospondin, and thrombospondin. These are platelet-derived clotting factors that interact with white blood cells and clotting elements including fibrinogen.
If more than two of 10 genes are upregulated, there's probably T3 with cluster and cytoskeleton abnormalities, which are now known to be fixable. Coagulation parameters are on the standard GENIE profile. Fibrinogen shows significant abnormality with ties to coagulation and Alzheimer's. Some coagulopathies in COVID were acquired, and COVID is super-acting on white blood cells to make positive endotoxin founding foundation as well as actinobacteria. Some of the coagulation problems seen may not have been thought of because nobody asked about water damaged buildings anymore.
Cholestyramine was found by luck when a lady had terrible secretory diarrhea. Clay was tried for Pfiesteria but found no benefit. Charcoal wasn't a great idea and nobody got benefit from it. Kaolinite comes from Cambridge where they're taking crab shells and grinding up the chitin. Kaolinite is a fantastic treatment if the pH of the stomach can stay over nine. If the stomach can't get that alkaline, kaolinite won't help. Dennis Case is trying to come back with kaolinite that gets around the problem of alkaline stomachs.
Wellchol has fewer binding sites than cholestyramine. Zeolite binds metals and positive charges so it's not going to work for negative charges. When first working with Dr. Shoemaker, cholestyramine was the first binder used and it worked great for many patients. Dr. Brewer did a deep dive into medical literature and found certain mycotoxins were bound preferentially by certain binders. Joe Mather developed a table available on page 66 of the book "Toxic" that goes over all binders shown in literature to bind specific mycotoxins.
Wellchol is preferred over cholestyramine as it has less side effects and works quite well, specifically best for ochratoxin and zearalenol. For trichothecene, aflatoxin, or gliotoxin, other binders are needed such as bentonite clay, activated charcoal, chlorella, and Saccharomyces boulardii which is particularly good for gliotoxin and zearalenone. Binders should be used based on urine mycotoxin test results, with close correlation between effective use of binders reducing urine mycotoxin test results and clinical response. When not enough binders specific to what's seen on testing are used, patients often make limited response.
The world is incredibly polluted with 350,000 new chemicals in the environment in the last 70-80 years, with the vast majority never studied for effects on human beings. When done with treatment, continuing light doses of one charcoal, one clay, and one chlorella forever helps the liver deal with toxic load.
In some patient populations, 90% have colonization. It's not easy to make the diagnosis - almost a diagnosis of exclusion. OAT testing gives a slight hint that colonization has occurred but is only somewhat accurate. Diagnosis is based primarily on response or lack of response to binders alone. If patients get well with binders alone, they don't need antifungals. If antifungals aren't given after binders, the vast majority won't get better.
Azoles aren't used alone - increasingly inclined to use amphotericin B both nasally and orally. It's safe given that way because it's not absorbed. IV amphotericin B has tons of side effects, but taken nasally and orally it's pretty safe. Itraconazole is also used quite a bit. Resistance to antifungals is almost never seen after giving them to 4,000-5,000 people.
Dr. Shoemaker is adamantly opposed to antifungals for theoretical reasons. In actual practice, patients often can't get well unless they go on antifungals. A fellow at Mayo Clinic was using amphotericin B and creating lots of intolerances. The literature on fungicides shows Dupont making benomyl for years creating horrible mutations. Substituted benzamidazoles are problematic because they impair delivery of pyruvate into the outer membrane of mitochondria. What's in the nose is not what's in the sinuses. Using medications that are bioactive where they're not necessary is not good medicine.
Dr. Shoemaker's position is both that antifungals are unnecessary and there are concerns with the type being used. This is not an infectious disease - it's an inflammatory problem. Mucus in the nose is probably the best antibacterial and best antifungal approach in the human body, and ignoring what the body provides naturally is a mistake.
What many people call mold illness is far more than mold alone. The broader concept is not new - that soup in a water damaged building. What's newer is discussion around contributors such as actinobacteria and endotoxins potentially playing a much larger role in CIRS causation than previously understood. Emerging data suggests mold and mycotoxins may represent a very small part - 7% of the overall causation picture.
In 2015-16, working with people in Finland looking at approaches to remediation of wet buildings showed fantastic remediation results where fungi or HERTSMI-2 was zero or four or eight or ten, yet people weren't better. Looking at actinobacteria, which has been discussed since 2002, showed actinomycetes are motile and move from place to place, making them more likely to cause trouble from one room if they got it in another. They grow well in alkaline environments and not acidic environments.
Treating for acidic conditions when there were alkaline conditions, isolating one room and quick cleaning it worked, but a week later it was recolonized. This became a problem, then looking at what else was wrong showed endotoxins and gram negative rods. Plumbing problems were found through smoke tests, finding places of water in the inner sanctum - bedroom, bathroom, and closet were all moist areas holding secondary organisms, not fungi.
Actinomycetes are nearly ubiquitous. Gram negatives are close to ubiquitous. They're making illnesses 48% for actinomycetes, 42% for endotoxins. Those numbers haven't changed over the past four years. When measuring skin extracellular mycetomes, there's more problem to pay attention to. Fungi can't be ignored - 7% is not zero. It's not unusual to find fungi and actinomycetes or fungi and endotoxins, but endotoxins and actinomycetes together are the most commonly found.
Every single patient has an 80% chance of having a non-fungal source of their illness. Learning to deal with actinomycetes doing actin skin and actin mycetomes or endotoxins allows getting ahead of people and keeping them healthy without relapsing when visiting neighbors with wet buildings.
In clinical experience, the mold issue and mycotoxins specifically are by far the biggest percent - 90% rather than 7%.
Neil Nathan reports that the vast majority of his patients recover using urine mycotoxin testing to address mold issues, with very few requiring specific treatment for actinomyces or endotoxins. Most patients are already receiving treatment for endotoxins through cholestyramine. In cases where patients worked with Shoemaker-trained practitioners, Nathan found that focusing on actinomyces did not lead to complete recovery—patients only became fully well after mycotoxins were addressed. Nathan acknowledges he may not be treating actinomyces adequately and mentions colleague Jill Crista, who treats actinomyces in 30-40% of her patients for optimal response. Both practitioners agree there is an inflammatory soup involving actinomyces, endotoxins, mannans, and proteins.
Shoemaker testified before the FDA in 2016 to keep VIP on the compounding list, presenting documentation of benefit and meeting FDA requirements. He warns that new peptides being promoted as miracle drugs carry allergy risks, referencing issues with erythropoietin that prompted FDA scrutiny of VIP. He emphasizes that practitioners must understand FDA safety requirements before using peptide hormones like KPV or BPC-157, as malpractice exposure exists if patients experience allergic reactions.
Nathan began using VIP in 2010-2011 but found it helpful in only some patients, not to the extent Shoemaker observes. He notes VIP was originally reserved for patients without ongoing mold exposure or active mold toxicity. Nathan attributes poor peptide response to patients being in Cell Danger Response 1 (survival mode), where peptides often worsen symptoms. As patients improve, they become more responsive. He mentions colleagues finding GLP-1 helpful in very low doses for all patients, though he has observed unacceptable side effects when timing is wrong. Other peptides helpful later in treatment include BPC-157, KPV, and MASI. Dr. Randy Haymon's mitochondrial markers may indicate when patients reach Cell Danger Response 2 or 3 and become more responsive to these interventions.
Nathan uses urine mycotoxin testing as the final arbiter of when mold is gone, but patient symptom resolution is the ultimate measure. He observes a direct correlation between clear urine mycotoxin tests and being well. Once symptoms are completely resolved and urine is clear, patients are considered cured—they can function normally, including staying in potentially moldy hotels. Many patients who undergo limbic retraining, mast cell retraining, and vagal retraining find that old traumatic injuries resolve and they become healthier than before their illness.
Shoemaker previously avoided the word "cure" but now reports 95% of patients become functional and 85% are happy with their outcomes. He notes the high cost of VIP treatment—20 doses costs $10,000. He acknowledges that patients adapt to illness and must learn to function despite limitations.
Shoemaker left ILADS in 2002 due to frustration with diagnostic approaches for babesia that ignored red cell inclusions under microscopy. He notes multiple apicomplexans (including malaria, babesia, sarcocystis from birds, pigs, chickens, toxoplasmosis from kitchens and cockroaches) share GPI or glycerol phosphotyl as toxin inducers. He questions reliance on single-test results for babesia when 28 organisms may test positive, and criticizes the Lyme community's failure to examine TGF beta 1, thymus-derived T-regs, and inducible T-regs as critical inflammatory markers.
Nathan reports Lyme and co-infections coexist in a huge percentage of his mold patients, with each condition weakening the immune system and predisposing to the other. He finds treating mold first is essential, as patients respond infinitely better to shorter antibiotic courses once mold is cleared. Newer tests like immunoblots detect more species of babesia and bartonella than older Western blot methods.
Nathan identifies three most common inflammatory root causes: mold, Lyme with co-infections, and longhaul COVID. Bruce Patterson's 14-panel cytokine test reveals distinct patterns for longhaul COVID, Lyme, and mold (with RANTES and sCD40L particularly elevated in mold patients). This allows identification of what the immune system considers primary threat. Many patients were "unmasked" by COVID—the inflammation triggered immune system weakening, allowing previously contained mold or Lyme to emerge. Nathan published a 2021 paper showing patients who recovered from COVID but worsened at six weeks had gene activation for actinomyces (63%) and endotoxins (54%), coinciding with symptom relapse. COVID induced activation of previously benign cells, revealing underlying mold toxicity or Lyme that had been contained.
Shoemaker keeps interventions in mind when they have experimental databases, make sense, and carry low patient risk. He stresses the need for proper IRB-approved studies and publication of treatment protocols. Nathan acknowledges his organizational limitations in data collection but is now working with Jill Crista on a validated questionnaire for mold toxicity, funded and IRB-approved for peer-reviewed publication. Through his mentorship program with hundreds of physicians, they will catalog every treatment aspect using AI computations to document which interventions work best for which patients.
Both practitioners report being significantly better at treating mold illness than in 2005, with more tools and greater understanding of its complexity. The majority of patients heal using either approach. Nathan's current research includes cytokine panel work with Bruce Patterson for streamlined diagnosis, and work with Jill Crista on validated questionnaires. His number one hope is that the medical profession will embrace this field and stop gaslighting patients. Shoemaker's research includes identifying a Parkinson's fingerprint showing peripheral injury rising to microglial cells, then linking peripheral to central injury as a prodrome with treatment mechanisms. He is now pursuing the vascular hypothesis for Alzheimer's disease, examining coagulation elements and the link between peripheral injury, inflammation, and beta-amyloid changes.
Nathan's takeaway message is that mold illness is real, diagnosable, and treatable. More research is needed to explore pieces of the field in greater detail, but enough is known to help many patients. Shoemaker expressed appreciation for the discussion and shared his daily practice of telling his wife how much he loves her, noting these are the best three years of his life following his first wife's death from breast cancer.
Both Dr. Neil Nathan and Dr. Ritchie Shoemaker share a common mission despite their different perspectives: advancing the conversation around mold illness and CIRS while improving the quality of life for those who have been impacted by it. Their life-changing work, unwavering commitment to pursuing new understandings, new tools, and new answers continues to move the field forward and brings hope for so many people on their healing journeys.
The episode closes with thanks to listeners of the Better Health Guide podcast. Listeners can learn more about today's guests, including relevant links and resources, in the show notes. The podcast may provide community discounts and occasionally share links from affiliate partners. Episodes are available on YouTube, Spotify, Apple Podcasts, Amazon Music, iHeart, and more. For information about Scott's personal journey to better health, visit betterhealthguide.com. The next episode invitation is extended to join the Better Health Guide podcast again.
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