Mold Illness and Mycotoxin Protocol

The Invisible Plague

Mold illness is the great masquerader of modern medicine. A patient presents with crushing fatigue, brain fog so thick they can’t remember the word for “fork,” joint pain that migrates without pattern, sinus congestion that never resolves, anxiety that appeared from nowhere, hormones in freefall, and a dozen other symptoms that don’t fit neatly into any diagnostic box. They’ve seen the rheumatologist, the neurologist, the psychiatrist, the endocrinologist. Every specialist runs their panel, finds nothing definitive, and sends them on. The patient begins to doubt their own sanity.

Meanwhile, behind their bathroom wall, Stachybotrys chartarum — black mold — is silently producing trichothecene mycotoxins that suppress their immune system, inflame their brain, and disrupt every hormonal axis in their body. The building is making them sick, and nobody is looking at the building.

Dr. Ritchie Shoemaker, a family physician from Pocomoke, Maryland, was the first clinician to systematically document and treat what he termed CIRS — Chronic Inflammatory Response Syndrome. His work, spanning two decades and thousands of patients, established that biotoxin illness is not psychological, not “just allergies,” and not rare. It is a genetically mediated inflammatory cascade triggered by biotoxins that approximately 24% of the population cannot clear through normal immune mechanisms.

Understanding Mycotoxins

Mycotoxins are secondary metabolites produced by molds — chemical warfare agents that fungi deploy against competing organisms. They are among the most toxic naturally occurring substances on earth. Unlike mold spores (which trigger allergic responses), mycotoxins are molecular toxins that cause direct cellular damage, immune dysregulation, and neuroinflammation.

Common Mycotoxins in Water-Damaged Buildings

Aflatoxin (produced by Aspergillus flavus and A. parasiticus): The most potent natural carcinogen known. Classified as Group 1 carcinogen by IARC. Aflatoxin B1 is the most toxic variant. Damages DNA through epoxide formation, causes liver cancer (hepatocellular carcinoma), suppresses immune function. Also found in contaminated grains, peanuts, and corn. Metabolized by CYP1A2 and CYP3A4 in the liver — genetic variants in these enzymes affect susceptibility.

Ochratoxin A (OTA) (produced by Aspergillus ochraceus, A. carbonarius, Penicillium verrucosum): Nephrotoxic (kidney-damaging), immunosuppressive, and possibly carcinogenic. Has a remarkably long half-life in humans — approximately 35 days — meaning it accumulates with chronic exposure. Found in water-damaged buildings and in coffee, wine, dried fruits, cereals, and cocoa. OTA inhibits mitochondrial ATP production and protein synthesis.

Trichothecenes (produced by Stachybotrys chartarum — “black mold,” also Fusarium species): Among the most toxic mycotoxins. Inhibit protein synthesis at the ribosomal level. Extremely potent — trichothecenes were investigated as biological warfare agents (Yellow Rain in Southeast Asia, 1970s-80s). Symptoms include hemorrhage, immune suppression, skin irritation, and neurological damage. Satratoxin H from Stachybotrys is particularly neurotoxic.

Gliotoxin (produced by Aspergillus fumigatus): An immunosuppressive epipolythiodioxopiperazine toxin. Directly kills immune cells (macrophages, neutrophils, T-cells) by inducing apoptosis. Suppresses NF-kB signaling. A. fumigatus is the most common airborne fungal pathogen in immunocompromised individuals. Gliotoxin also disrupts the gut barrier.

Zearalenone (ZEA) (produced by Fusarium species): A mycoestrogen — structurally similar to 17-beta-estradiol. Binds to estrogen receptors and causes estrogenic effects: gynecomastia, early puberty, menstrual irregularities, infertility, endometriosis exacerbation. Found in contaminated grain (corn, wheat, barley) and in water-damaged buildings where Fusarium colonizes.

Citrinin (produced by Penicillium citrinum and some Aspergillus species): Nephrotoxic, synergistic with ochratoxin A for kidney damage. Often co-occurs with OTA in contaminated buildings and foods.

The Symptom Landscape

Mold illness is multisystemic because mycotoxins affect virtually every organ. The symptom cluster is distinctive once you know what to look for:

• Neurological: Brain fog (cognitive impairment, word-finding difficulty, poor short-term memory), headaches, light sensitivity (photophobia), vertigo, tremors, seizures (rare but documented), numbness and tingling
• Fatigue: Profound, unrefreshing — not improved by sleep. Distinct from depression-related fatigue in that patients WANT to do things but physically cannot.
• Musculoskeletal: Migratory joint pain (not consistent with any rheumatological pattern), muscle cramps, morning stiffness, ice-pick pains
• Respiratory: Chronic sinus congestion, recurrent sinusitis, shortness of breath, cough, asthma exacerbation
• Gastrointestinal: Abdominal pain, diarrhea, appetite changes, nausea
• Psychiatric: Anxiety (often new-onset and severe), depression, irritability, mood swings, depersonalization
• Autonomic: Temperature dysregulation, excessive sweating or inability to sweat, orthostatic intolerance (POTS-like symptoms)
• Endocrine: Hormone disruption across axes — thyroid, adrenal, sex hormones, ADH (antidiuretic hormone), MSH (melanocyte-stimulating hormone), VIP (vasoactive intestinal peptide)
• Unusual symptoms: Static shocks (from elevated MMP-9 affecting charge distribution), metallic taste, frequent urination with excessive thirst (ADH dysregulation), ice-pick pains, red eyes, blurred vision

Testing

Mycotoxin Urine Testing

Measures mycotoxin metabolites excreted in urine. Several labs offer panels:

• RealTime Laboratories: Tests for aflatoxins, ochratoxin A, and trichothecenes (macrocyclic). The original mycotoxin urine lab.
• Great Plains Laboratory / Mosaic Diagnostics: GPL-MycoTOX Profile — tests for 11 mycotoxins from 40 species. Can be combined with the OAT (Organic Acids Test) for broader metabolic picture.
• Vibrant Wellness Mycotoxins panel: Tests for 31 mycotoxins — the broadest panel currently available.

Provocation: Some practitioners recommend glutathione loading (500-1000mg liposomal glutathione) and sauna session before urine collection to mobilize stored mycotoxins and increase test sensitivity. This is debated but commonly practiced.

CIRS Biomarkers (Shoemaker Panel)

The following blood markers define the inflammatory cascade in CIRS. They are not routinely ordered by conventional physicians and require specific lab requests:

• MSH (melanocyte-stimulating hormone): Reference range 35-81 pg/mL. In CIRS, typically LOW (often <35, sometimes undetectable). MSH is a master regulatory peptide — it controls cytokine production, antimicrobial peptide production (defensins in the gut and nasal mucosa), pituitary hormone release, and endorphin production. Low MSH = chronic pain, poor sleep, GI dysfunction, susceptibility to MARCoNS, hormonal disruption.
• VIP (vasoactive intestinal peptide): Reference range 23-63 pg/mL. In CIRS, typically LOW. VIP regulates pulmonary artery pressure, inflammation, and neurotransmitter production. Low VIP = shortness of breath with exertion, exercise intolerance.
• TGF-beta 1: Reference range <2,380 pg/mL. In CIRS, typically ELEVATED (often 5,000-15,000+). Drives fibrosis, autoimmunity, and remodeling. Elevated TGF-beta 1 is associated with restrictive lung disease, tremor, and autoimmune activation.
• C4a: Reference range 0-2,830 ng/mL (Quest Diagnostics — lab matters). In CIRS, typically ELEVATED. C4a is a complement split product indicating ongoing innate immune activation. Correlates with capillary hypoperfusion (reduced blood flow to brain, muscles, and other tissues).
• MMP-9 (matrix metalloproteinase-9): Reference range 85-332 ng/mL. In CIRS, typically ELEVATED. MMP-9 delivers inflammatory cytokines into subintimal spaces of blood vessels, brain tissue, and joints. Correlates with brain fog, joint pain, and cognitive impairment.
• VEGF (vascular endothelial growth factor): Reference range 31-86 pg/mL. In CIRS, can be LOW (impaired tissue oxygenation — fatigue, muscle cramps) or HIGH (angiogenic response to hypoxia).
• ADH (antidiuretic hormone) and osmolality: ADH dysregulation is common in CIRS. Low ADH with high osmolality = excessive urination, dehydration, excessive thirst. High ADH with low osmolality = fluid retention.
• Leptin: Reference range male 0.5-13.8 ng/mL, female 1.1-27.5. In CIRS, often ELEVATED — leptin resistance develops, contributing to weight gain resistant to diet and exercise.

HLA-DR Genetic Susceptibility

HLA-DR genes encode part of the Major Histocompatibility Complex Class II, which presents antigens to T-helper cells. Specific HLA-DR haplotypes are associated with inability to recognize and clear biotoxins — the immune system cannot “tag” mycotoxins for removal, so they recirculate indefinitely, causing chronic inflammation.

Approximately 24% of the population carries susceptible HLA-DR haplotypes. Shoemaker identified specific “dreaded genotypes”:

• 4-3-53: Multi-susceptible — reactive to multiple biotoxins (mold, Lyme, dinoflagellates). The most broadly susceptible haplotype.
• 11-3-52B: Mold-susceptible. Common in severe mold illness cases.
• 12-3-52B: Mold-susceptible.
• 14-5-52B: Mold-susceptible.
• 7-2/3-53: Lyme-susceptible (also relevant as mold and Lyme frequently co-occur).

Testing: LabCorp or Quest HLA-DR DQ panel. Interpretation requires knowledge of Shoemaker’s haplotype classifications.

Patients without susceptible haplotypes CAN still develop mold illness — the HLA system is not binary. But susceptible individuals develop CIRS at lower exposure levels and have more difficulty clearing it.

Visual Contrast Sensitivity (VCS) Test

A screening tool that detects neurotoxin-mediated capillary hypoperfusion in the visual cortex. The patient views a series of images with decreasing contrast and identifies the direction of line patterns. CIRS patients fail specific rows corresponding to impaired contrast detection. Free online version available at SurvivingMold.com (Shoemaker’s site). Sensitivity approximately 92%, specificity approximately 89% for biotoxin illness. Takes 10 minutes. Excellent for tracking treatment response over time.

Environmental Testing

ERMI (Environmental Relative Moldiness Index): Dust sample analyzed by MSQPCR (mold-specific quantitative PCR) for 36 mold species. Produces a single score. ERMI >2 is concerning. ERMI >5 is high.

HERTSMI-2 (Health Effects Roster of Type-Specific Formers of Mycotoxins and Inflammagens): A subset of ERMI focusing on the 5 most clinically relevant mold species: Aspergillus penicillioides, Aspergillus versicolor, Chaetomium globosum, Stachybotrys chartarum, Wallemia sebi. Score >10 is concerning for CIRS patients.

Air sampling and tape lifts: Traditional methods that detect airborne spore counts and surface colonization. Less sensitive than ERMI/HERTSMI-2 for hidden mold but useful for identifying active growth areas.

The Shoemaker Protocol (Sequential)

Shoemaker’s protocol is sequential — each step must be completed before moving to the next, because later steps won’t work if earlier ones are skipped.

Step 1: Remove from Exposure

This is the foundation. Nothing else works — no supplement, no medication, no protocol — if the patient remains in a moldy environment. This is the hardest step because it often means leaving a home, an apartment, a workplace. It means potentially discarding possessions that harbor mycotoxins (porous materials — clothing, furniture, books, mattresses — can be contaminated beyond remediation).

Remediation of the building is an option if the source is identified and contained. Professional remediation by an ACAC or IICRC-certified company is required — not a handyman with bleach. Bleach does NOT kill mold effectively on porous surfaces and generates toxic chlorine gas in combination with some mycotoxins. Proper remediation involves containment, HEPA filtration, removal of contaminated materials, treatment of structural elements, and post-remediation verification testing.

Some patients must leave without remediating — especially renters, or when contamination is extensive (whole-house involvement, HVAC contamination).

Step 2: Cholestyramine (CSM) or Welchol

Cholestyramine (CSM): A bile acid sequestrant originally designed for cholesterol. Dose: 4g (one packet) mixed in water, taken 4 times daily, 30 minutes before meals and at bedtime. CSM binds mycotoxins in the GI tract that have been excreted in bile, preventing enterohepatic recirculation. This is the most effective pharmaceutical binder for mycotoxins.

Side effects: constipation (manage with magnesium and fiber), bloating, and it binds medications and fat-soluble vitamins. Take all medications and supplements 1 hour before or 4 hours after CSM.

Welchol (colesevelam): Alternative bile acid sequestrant for patients who cannot tolerate CSM. Dose: 625mg capsules, 3 capsules twice daily. Less potent than CSM for mycotoxin binding but better tolerated. Does not require mixing in liquid.

Duration: typically 1-3 months on binders, guided by VCS improvement and symptom response.

Step 3: Correct MARCoNS

MARCoNS (Multiple Antibiotic Resistant Coagulase Negative Staphylococci) is a deep nasal colonization by antibiotic-resistant biofilm-forming Staphylococcus species. Found in approximately 80% of CIRS patients (low MSH allows colonization because MSH normally stimulates antimicrobial peptide production in nasal mucosa). MARCoNS produce exotoxins that further suppress MSH, creating a self-perpetuating cycle.

Testing: Deep nasal culture with API-Staph identification and sensitivity testing. Lab: Microbiology DX (formerly DiagnosTechs).

Treatment: BEG spray — a compounded nasal spray containing Bactroban (mupirocin 0.2%), EDTA (1% — disrupts biofilm), and Gentamicin (0.5%). Spray 2 sprays each nostril twice daily for 30 days. Reculture 4 weeks after completing treatment. Some patients require multiple courses.

Alternative/adjunct: colloidal silver nasal spray, xylitol-based nasal spray (Xlear — disrupts biofilm), nasal rinse with povidone-iodine (Betadine), probiotic nasal spray (Lactobacillus sakei — experimental).

Step 4: Correct Androgens and Address Gluten

Low MSH and chronic inflammation suppress sex hormone production. DHEA-S, testosterone, and estradiol may be low. Replace as indicated by labs. Gluten sensitivity is nearly universal in CIRS patients — implement strict elimination.

Step 5: Correct ADH/Osmolality

If ADH is low and osmolality is high (dehydration picture despite adequate fluid intake), intervention is needed. DDAVP (desmopressin) 0.2mg at bedtime can be used short-term. Electrolyte support and adequate salt intake help.

Step 6: Correct C4a

Elevated C4a indicates ongoing complement activation. High-dose omega-3 fish oil (4g EPA+DHA daily) reduces C4a. Some patients require statin therapy (atorvastatin or rosuvastatin) to reduce vascular inflammation and C4a. Erythropoietin (EPO) in refractory cases.

Step 7-8: Correct VEGF and C3a

Low VEGF: exercise helps (paradoxically difficult for fatigued CIRS patients — start extremely gently). High-dose fish oil continues. C3a: usually corrects as upstream steps are completed.

Step 9: Correct TGF-beta 1

Elevated TGF-beta 1 drives fibrosis, autoimmunity, and tissue remodeling. Losartan (angiotensin receptor blocker) 25-50mg daily reduces TGF-beta 1 effectively. Must monitor blood pressure and potassium. Some patients use this for months.

Step 10: Replace VIP

VIP (vasoactive intestinal peptide) nasal spray is the final step — only after all previous steps are completed and markers are normalizing. Dose: 50mcg per spray, 4 sprays daily. VIP is the master regulatory peptide that restores immune balance, reduces pulmonary artery pressure, improves exercise tolerance, and consolidates the gains from previous steps. Must be compounded. Must confirm no MARCoNS present before starting (VIP promotes biofilm growth if MARCoNS is active).

Naturopathic and Complementary Approaches

For patients who cannot access a Shoemaker-trained physician, or as adjuncts to the sequential protocol:

Binders (Always the First Priority After Removal from Exposure)

• Activated charcoal: 500mg-1g between meals, broad-spectrum. Excellent for trichothecenes.
• Bentonite clay: 1 teaspoon in water between meals. Strong affinity for aflatoxins.
• Chlorella (broken cell wall): 3-6g daily. Binds multiple mycotoxin classes, provides chlorophyll and nutrients.
• Modified citrus pectin: 5-15g daily. Gentler binder, well-tolerated, also reduces galectin-3.
• Saccharomyces boulardii: 250-500mg twice daily. This probiotic yeast binds mycotoxins (particularly ochratoxin A and aflatoxin) and supports gut barrier integrity. Dual mechanism — binding plus immune modulation.

All binders: take 30 minutes away from food, supplements, and medications.

Glutathione Support

Mycotoxins deplete glutathione — and glutathione is required for mycotoxin conjugation and elimination. The cycle is vicious: exposure depletes the very molecule needed for clearance.

• Liposomal glutathione: 500-1000mg daily on empty stomach
• NAC: 1200mg daily (600mg twice daily)
• Glycine: 3-5g daily
• Alpha-lipoic acid: 300-600mg daily (recycles glutathione)
• Milk thistle (silymarin): 200mg three times daily (upregulates glutathione S-transferase)

Nasal Protocols

Mold colonizes the nasal passages and sinuses, creating a persistent local source of mycotoxin exposure and inflammation even after the patient has left the contaminated building.

• Colloidal silver nasal spray: 10-15 ppm, 2 sprays each nostril twice daily. Antimicrobial, anti-biofilm.
• Xylitol-based nasal spray (Xlear): Disrupts biofilm, moisturizes nasal mucosa, osmotically unfavorable for bacteria.
• Nasal rinse with Betadine: 2-3 drops povidone-iodine in 8oz saline sinus rinse (neti pot or NeilMed). Use for 2-3 weeks, then cycle off. Broad-spectrum antimicrobial.
• Nasal ozone insufflation: Practitioner-administered. Ozone gas gently insufflated into nasal passages kills mold and bacteria. Requires trained provider with proper equipment.

Ozone Therapy

Major autohemotherapy (MAH): patient’s blood drawn, mixed with ozone gas, reinfused IV. Ozone (O3) is a potent oxidizer that enhances oxygen delivery, stimulates antioxidant enzyme production (SOD, catalase, glutathione peroxidase), modulates immune function, and has direct antimicrobial effects. Typically 10-20 treatments for mold illness. Also available as rectal insufflation (home-based), ozone sauna, and ear insufflation for sinus issues.

IV Phosphatidylcholine

Phospholipid exchange therapy. Mycotoxins are lipophilic — they embed in cell membranes and disrupt membrane function. IV phosphatidylcholine (PC) replenishes damaged membranes, supports bile flow (PC is a major bile component), aids liver detoxification, and facilitates mycotoxin release from cellular membranes. Typically 1-2 treatments weekly for 10-20 sessions.

Sauna Therapy

Infrared sauna (preferred over conventional): 20-40 minutes, starting at 110-125 degrees Fahrenheit, gradually increasing to 135-150 degrees. Begin with 15 minutes and increase slowly — mold patients are heat-sensitive and detox-reactive. 3-5 sessions weekly. Shower immediately after to wash off excreted toxins. Replace electrolytes. Studies (Genuis et al., 2011) document mycotoxin excretion in sweat.

Start SLOW. Many mold patients crash from aggressive sauna protocols. Begin at low temperature and short duration. If symptoms flare, reduce. The sauna must be mold-free itself — a moldy gym sauna defeats the purpose.

Limbic System Retraining

This is the intervention that separates patients who recover fully from those who plateau at 70-80% improvement. After prolonged biotoxin exposure, the limbic system (amygdala, hippocampus, insula, anterior cingulate) becomes hyperactivated — stuck in a threat response loop. The immune system, nervous system, and endocrine system remain in fight-or-flight mode even after exposure has ceased and biomarkers are improving. This is not psychological — it is neuroplastic maladaptation. The brain has literally rewired itself to maintain the inflammatory state.

DNRS (Dynamic Neural Retraining System): Developed by Annie Hopper, who recovered from severe chemical sensitivity and mold illness. A neuroplasticity-based program using visualization, incremental neural exercises, and limbic system calming techniques. Self-administered (DVD/online program or 5-day live seminar). Practiced 1 hour daily for minimum 6 months. Results in CIRS/mold patients have been remarkable — symptom reduction, normalization of inflammatory markers, recovery of chemical tolerance.

Gupta Programme: Developed by Ashok Gupta. Similar neuroplasticity approach targeting amygdala hyperactivation. Online program with video-guided exercises, meditation, and neural reconditioning techniques.

Both programs share core principles with ancient practices — meditation, visualization, and conscious rewiring of habitual neural patterns. The yogic tradition understood that the mind shapes the body’s inflammatory landscape. Modern neuroscience confirms this through PET and fMRI imaging showing limbic activation patterns in CIRS patients.

Recovery Timeline

Mold illness recovery is measured in months to years, not weeks. A realistic timeline:

• Weeks 1-4: Remove from exposure, begin binders. Some patients feel improvement within days; others feel worse initially as binders mobilize stored mycotoxins.
• Months 1-3: Binder therapy, nasal protocols, glutathione support. VCS begins improving. Brain fog starts lifting.
• Months 3-6: Address deeper inflammatory markers. Hormone recovery begins. Energy returning.
• Months 6-12: Limbic retraining consolidating. Biomarkers normalizing. Return to exercise tolerance.
• Months 12-24: Full recovery in most cases. Some severe cases (10+ years of exposure, dreaded genotype) require longer.

The body wants to heal. Remove the toxin, open the pathways, calm the immune system, retrain the brain — and the body does what it has always known how to do. The practitioner’s job is to remove the obstacles and provide the raw materials. The healing belongs to the patient.