Mold, CIRS & Dr. Andrew Campbell | Lyme & Associated Diseases Alliance

Start here

Use this page as a clear map through mold/CIRS evaluation, protocols, and Campbell's work.

The page is organized from the broad clinical frameworks first, then MARCoNS and colonization, clinician-supervised protocols, testing details, Campbell source materials, and patient-safety notes.

1. Main frameworks

Compare the Shoemaker CIRS model, Nathan's sensitive-patient model, Campbell's mold/mycotoxin approach, and practical remediation sources.

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2. MARCoNS and colonization

Separate bacterial nasal colonization, fungal testing, mycotoxin testing, and broader mold/CIRS theories.

Go to MARCoNS

3. Protocols and testing

Review clinician-supervised Shoemaker, Nathan, Campbell, and testing tabs in one structured protocol area.

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4. Campbell source materials

Review Dr. Andrew Campbell's MyMycoLab testing model, mold/mycotoxin themes, Lyme-overlap claims, and safety context.

Go to Campbell materials

Clinical frameworks

Shoemaker, Nathan, Campbell, and the CIRS recovery manuals point to the same first priority: stop exposure.

These frameworks should be discussed with trained clinicians and qualified environmental professionals. They are included for patient advocacy and appointment preparation, not as instructions to self-treat or self-remediate.

Shoemaker's CIRS-WDB model

Dr. Ritchie Shoemaker frames CIRS-WDB as a chronic inflammatory response after exposure to the interior of water-damaged buildings, with symptom clusters, VCS screening, HLA-DR susceptibility, biomarkers, binders, MARCoNS evaluation, and late-stage VIP readiness.

Nathan's mycotoxin and sensitivity lens

Dr. Neil Nathan emphasizes mycotoxin burden, sinus or gut colonization, glutathione and detoxification capacity, binder tolerance, MCAS-like reactivity, and the need to move slowly enough that treatment does not make the patient worse.

Campbell's mold and mycotoxin model

Dr. Andrew Campbell's work is presented as a major clinical perspective on mold and mycotoxin illness, with emphasis on exposure correction, MyMycoLab serum IgG/IgE testing, carefully supervised itraconazole discussion, and targeted nutritional support.

Recovery manual environmental standards

Mold Illness: Surviving and Thriving adds practical CIRS-specific guidance for IEP-led remediation, HVAC and duct review, contents decisions, carpet and dust reservoirs, post-remediation clearance, ERMI/HERTSMI-2 interpretation, and cross-contamination prevention.

MARCoNS, mold and nasal colonization

For a focused explanation of MARCoNS as bacterial nasal colonization, how nasal culture differs from fungal PCR and mycotoxin testing, and how to discuss disputed CIRS-related theories with a clinician, see the subsection below.

Jump to MARCoNS subsection

Dr. Andrew Campbell's work

See the dedicated section below for his mold and mycotoxin lecture themes, MyMycoLab testing model, Lyme-overlap editorial, and source summaries.

Jump to Dr. Campbell section

Mold/CIRS subsection

MARCoNS, mold colonization, and nasal testing

MARCoNS is a bacterial nasal culture question that often appears inside mold/CIRS conversations. It should not be used as proof of mold colonization or as a stand-alone explanation for every symptom.

What MARCoNS means

MARCoNS stands for multiple-antibiotic-resistant coagulase-negative Staphylococci. The result usually means a deep nasal culture grew resistant coagulase-negative Staphylococci, which are bacteria that commonly live on skin and mucous membranes.

Colonization versus active infection

Colonization means bacteria are present without necessarily invading tissue or causing acute infection. Active infection is more likely when symptoms, exam findings, fever, purulent drainage, or imaging support bacterial or fungal sinus disease.

Why testing needs context

A positive MARCoNS culture may matter in some CIRS-informed practices, but it does not diagnose mold illness, fungal sinusitis, mycotoxin exposure, or building safety by itself. Specimen quality and clinical context matter.

MARCoNS, fungal testing, and mycotoxin testing answer different questions

Test	What it looks for	What it cannot prove by itself
MARCoNS nasal culture	A deep nasal swab is cultured for bacteria, especially coagulase-negative Staphylococci, and the lab may report whether the isolate meets that lab's resistance definition.	It does not diagnose mold illness, mycotoxin illness, fungal sinusitis, or the location of any fungal colonization.
Antibiotic-susceptibility testing	The cultured bacteria are exposed to antimicrobial agents in the lab and reported as susceptible, intermediate, or resistant.	It does not prove the bacteria are causing symptoms, and it does not mean every positive culture should be treated.
Fungal culture or PCR	These tests look for fungal growth or fungal DNA in a specimen from the nose, sinuses, sputum, tissue, or environment.	They do not prove that a detected organism is invading tissue or explaining every symptom on their own.
Mycotoxin testing	These tests try to measure toxins, metabolites, or immune responses associated with mycotoxins.	They do not locate mold in the nasal passages, sinuses, gut, tissues, home, workplace, or belongings.

The proposed MARCoNS, mold exposure, and CIRS relationship is still evolving.

Some CIRS-informed clinicians view MARCoNS as persistent sinonasal bacterial colonization that may interact with neuroimmune markers such as melanocyte-stimulating hormone. That is a proposed framework, not settled medical consensus.

Symptoms people may report

Nasal congestion, postnasal drip, sinus pressure, throat irritation, headaches, smell changes, fatigue, brain fog, sleep disruption, mood changes, dizziness, and pain flares are all nonspecific and can also come from allergy, migraine, asthma, reflux, viral illness, bacterial sinusitis, MCAS, or other conditions.

Questions to discuss with a clinician

Does this look like colonization, infection, allergy, or a broader sinus problem?
How should MARCoNS results be weighed alongside symptoms and exam findings?
Should fungal culture, PCR, allergy evaluation, or imaging be considered?

Full guide

Use the full MARCoNS page for the longer testing and red-flag discussion.

Open full MARCoNS guide

Clinician-supervised protocols

Protocol paths: Shoemaker, Nathan, Campbell, and testing.

Three major clinical perspectives guide this section. Shoemaker's protocol is a sequential, biomarker-driven approach to Chronic Inflammatory Response Syndrome after water-damaged building exposure. Nathan's framework is a sensitivity-first model for patients who flare from ordinary doses. Campbell's source materials add a separate mold and mycotoxin treatment discussion centered on source removal, MyMycoLab testing, itraconazole, and targeted support. All require trained-clinician supervision.

Ritchie Shoemaker, MD — sequential CIRS protocol

Shoemaker 12-Step Protocol for Chronic Inflammatory Response Syndrome (CIRS-WDB)

Dr. Ritchie Shoemaker's protocol is the most widely referenced structured approach to CIRS from water-damaged building exposure. Each step builds on the last; skipping steps or proceeding without meeting criteria is a common reason for treatment failure. The protocol should be administered by a CIRS-trained clinician with appropriate lab monitoring.

Shoemaker 12-Step CIRS Protocol

Step	Action	Details & Criteria
Step 1	Remove from exposure	Confirm water-damaged building (WDB) exposure. Must leave or remediate the exposure source before other steps can succeed. Re-exposure after treatment causes relapse.
Step 2	VCS testing	Visual Contrast Sensitivity test as a screening and monitoring tool. Repeat after exposure change, binder therapy, and MARCoNS treatment. Improvement in VCS score correlates with clinical response.
Step 3	HLA-DR genetic testing	HLA-DR haplotype determines susceptibility. Approximately 25% of the population has a "dreaded" haplotype that impairs biotoxin clearance. Not diagnostic alone but supports CIRS diagnosis when combined with exposure history and symptoms.
Step 4	CIRS biomarkers	C4a (complement activation), TGF-beta1 (inflammatory cytokine), MMP-9 (tissue remodeling), MSH (melanocyte-stimulating hormone — typically low in CIRS), VIP, VEGF, ADH/osmolality, leptin, ACTH/cortisol. Labs require special handling (ice, spin, freeze).
Step 5	Binders (sequestering agents)	Cholestyramine (CSM) 4g 4x/day is the primary binder. Welchol (colesevelam) as alternative if CSM not tolerated. Must be taken 30+ min away from food/meds/supplements. Constipation prevention essential. Goal: reduce circulating biotoxins.
Step 6	ERMI / HERTSMI-2 testing	Quantitative PCR dust testing for 36 mold species (ERMI) or 5 key species (HERTSMI-2). Used to verify building safety before re-entry. HERTSMI-2 score <10 considered safe for re-exposure in most CIRS patients.
Step 7	Reassess VCS	Monitor VCS improvement after binder therapy. If VCS is not improving, recheck exposure status and binder compliance. Non-improvement suggests ongoing exposure or missed step.
Step 8	Treat MARCoNS	Multiple Antibiotic Resistant Coagulase-Negative Staphylococci (MARCoNS) in nasal passages. Diagnosed via deep nasal culture (Microbiology Dx or equivalent). Treated with compounded nasal sprays (EDTA, silver, antibiotics per sensitivity). Must be addressed before VIP.
Step 9	Recheck biomarkers	After MARCoNS treatment, reassess CIRS biomarkers. C4a and TGF-beta1 should be normalizing. MMP-9 may still be elevated. MSH recovery is a favorable prognostic sign.
Step 10	VIP (Vasoactive Intestinal Peptide)	Nasal spray (compounded). Dose: typically 50 mcg 4x/day, titrated up. Prerequisites: out of exposure, VCS passing, normal C4a/TGF-beta1, MARCoNS-negative, normal labs. VIP restores neuroendocrine-immune regulation. Monitor for adverse reactions.
Step 11	Correct hormone imbalances	Address low MSH (controls pituitary axis), ADH/osmolality disturbances (thirst, frequent urination), leptin resistance, androgen/aromatase issues, and adrenal insufficiency. Hormone replacement requires careful monitoring in CIRS patients.
Step 12	Re-evaluate at 6 months	Full reassessment. If symptoms persist despite protocol completion: recheck for re-exposure, MARCoNS recurrence, new exposure source, or missed co-existing condition (Lyme, Bartonella, MCAS).

Shoemaker CIRS symptom clusters (13 clusters)

Cluster	Symptoms	Biomarker correlate
1. Fatigue	Profound, unrelenting exhaustion; post-exertional malaise	Low MSH, elevated C4a
2. Cognitive	Brain fog, memory loss, difficulty concentrating, confusion	Elevated TGF-beta1, low MSH
3. Respiratory	Cough, shortness of breath, wheeze, sinus congestion	Elevated C4a, MMP-9
4. Musculoskeletal	Muscle aches, joint pain, morning stiffness, cramps	Elevated MMP-9
5. Neurologic	Headaches, dizziness, vertigo, numbness, tingling, tremors	Low MSH, elevated C4a
6. GI	Abdominal pain, diarrhea, nausea, bloating	Elevated TGF-beta1
7. Ocular	Eye irritation, redness, blurred vision, light sensitivity	Low MSH, low VIP
8. Urinary	Frequent urination, excessive thirst (ADH dysregulation)	Low ADH, high osmolality
9. Skin	Rash, itching, sensitivity, static shocks	Elevated C4a
10. Temperature	Temperature dysregulation, night sweats	Low MSH
11. Mood	Depression, anxiety, mood swings	Low MSH, low VIP
12. Hormonal	Menstrual irregularity, low libido, adrenal issues	Low MSH, low ACTH
13. Vascular	Palpitations, blood pressure instability, easy bruising	Low VIP, elevated MMP-9

* Shoemaker protocol requires CIRS-trained clinician supervision. Biomarker labs require specific handling (ice, spin within 30 min, freeze). VIP should not be started until all prerequisites are met. Do not self-administer. *

Neil Nathan, MD — sensitivity-first model

Nathan Sensitive-Patient Protocol for Mold Toxicity and Mycotoxin Illness

Dr. Neil Nathan's framework is designed for patients who cannot tolerate standard doses, binders, supplements, or treatments without flaring. His model begins with tolerance rather than intensity, and it is the preferred approach for patients with MCAS, chemical sensitivity, severe fatigue, or limbic system dysregulation. Nathan co-authored Toxic and Mold and Mycotoxins.

Nathan Sensitive-Patient Protocol — Six-Phase Framework

Phase	Focus	Key Interventions
Phase 1: Stabilize	Build baseline tolerance before any detox	Sleep restoration (melatonin 0.5-3mg, magnesium glycinate). Pain control (curcumin, LDN 0.5-4.5mg). Hydration + electrolyte balance. Limbic system retraining (DNRS, Gupta Program). Vagal tone support (humming, gargling, deep breathing). Address constipation before binders.
Phase 2: Confirm Exposure	Environmental assessment	ERMI/HERTSMI-2 dust testing. Mycotoxin urine testing (Great Plains, RealTime Labs, or MosaicDX). Visual inspection + moisture mapping. Remediation plan with IEP. Air testing alone is insufficient (misses fragments and sticky molds). Ensure exposure is fully resolved before proceeding.
Phase 3: Gentle Binders	Start binders at ultra-low doses	Start low: Charcoal 100-250mg (1/4 capsule) or clay (bentonite/zeolite) or chlorella. Or CSM at micro-dose (1/64 packet = ~60mg). Titrate up over weeks. "If a patient flares, the dose is too high or the patient is not ready." Treat constipation first (magnesium, vitamin C, hydration). Space 2+ hours from meds/supplements.
Phase 4: Address Colonization	Sinus and/or gut fungal colonization	MARCoNS evaluation (nasal culture). Sinus colonization: compounded nasal sprays (amphotericin B, itraconazole, EDTA, xylitol, colloidal silver). Gut colonization: Saccharomyces boulardii, antifungals (nystatin/fluconazole per sensitivity), biofilm disruptors (interfase, NAC). Treat only after binders are tolerated.
Phase 5: Support Detox Pathways	Enhance cellular clearance capacity	Glutathione: start liposomal 100mg or nebulized. NAC 300-600mg bid as glutathione precursor. Phosphatidylcholine for cell membrane repair. Far-infrared sauna (start 5-10 min, low temp). B vitamin support (methylated). Milk thistle for liver support. Stop if symptoms worsen.
Phase 6: Reassess & Maintain	Monitor and adjust	Repeat VCS and biomarkers every 3-6 months. Re-test mycotoxins if symptoms return. Check for re-exposure (new water damage, cross-contaminated belongings, workplace, vehicle). Address MCAS (quercetin, vitamin C, ketotifen, cromolyn) if mast cell activation persists. Nathan: "Unique responses are the norm, not the exception."

Nathan Binder Options for Sensitive Patients

Binder	Starting dose (sensitive)	Target toxin	Notes
Activated charcoal	100-250 mg 1-2x/day	Broad-spectrum; aflatoxin, ochratoxin A	Gentlest binder. Safe starting point. Can cause constipation. Available OTC.
Bentonite clay / Zeolite	1/4-1/2 tsp 1-2x/day	Aflatoxin, heavy metals	Mineral-based binder. Good tolerability. Monitor mineral status with long-term use.
Chlorella	500-1000 mg 2-3x/day	Ochratoxin A, heavy metals	Nutrient-rich freshwater algae. Also supports detox pathways. Well tolerated by most patients.
Cholestyramine (CSM)	1/64 - 1/4 packet (60-1000mg)	Ochratoxin A, trichothecenes	Prescription. Shoemaker's primary binder. Can be harsh for sensitive patients. Nathan recommends micro-dosing.
Welchol (colesevelam)	1/4-1/2 tablet (625-1250mg)	Ochratoxin A, trichothecenes	Prescription. Alternative to CSM. Better GI tolerability. Less constipation. Does not bind thyroid meds.
Saccharomyces boulardii	250-500 mg 2x/day	Gut mycotoxin binding	Probiotic yeast. Binds mycotoxins in gut lumen. Also addresses Candida overgrowth. Well tolerated.
Modified citrus pectin	5 g 1-3x/day	Heavy metals, some mycotoxins	Gentle binder. Also supports immune function. Good for patients who cannot tolerate other binders.

* Nathan's framework: "Start low, go slow." A flare may mean the sequence, dose, mast-cell state, or nervous-system state needs adjustment, not that the entire approach is wrong. Treatment should never make the patient worse. *

Andrew W. Campbell, MD — source-summary protocol themes

Campbell's mold and mycotoxin protocol themes for clinician discussion

Dr. Campbell's materials describe a four-part framework: identify and correct the environmental source, use MyMycoLab serum IgG and IgE testing, consider prolonged itraconazole when clinically appropriate, and support recovery with targeted supplements and diet. This is a source summary for education and clinician discussion, not a universal consensus protocol or a self-treatment plan.

Protocol at a glance

Remove the exposure. Correct roof, plumbing, window or foundation leaks, flooding, condensation, HVAC problems, wet basements, crawlspaces, and contaminated porous materials. Ask whether symptoms improve away from the building and return after re-entry.
Use MyMycoLab serum testing in context. Campbell's materials emphasize serum IgG and IgE reactivity to 14 mycotoxin targets. MyMycoLab reports one IgG and one IgE result for each target, for 28 total results.
Discuss itraconazole only with supervision. Campbell-associated material describes itraconazole, often around 200 mg per day for about six months in selected cases. That is off-label for chronic mold illness and requires liver, cardiac, and medication-interaction review by a qualified prescriber.
Support recovery. Targeted supplements, an anti-inflammatory diet, low-histamine adjustments when needed, and gut support are used to improve tolerance rather than replace source control.

Environmental investigation priorities

Detailed visual inspection, moisture-meter readings, indoor humidity measurements, thermal imaging when helpful, and HVAC/condensate review.
Borescope or limited destructive inspection when hidden damage is suspected.
Do not treat a brief air sample or species count as proof that a building is safe.
ERMI or other dust-based testing can be supplementary, but Campbell treats them as part of a broader building assessment, not a stand-alone answer.
Repair the moisture source first, then remove heavily contaminated porous materials, use containment and dust control, and confirm the space is dry before re-entry.

Review fields

Last reviewed: July 9, 2026
Medical review: Educational summary only; physician supervision required
Editorial review: LAADA web editorial pass
Evidence status: Controversial; not universal consensus

* Mycotoxin-antibody testing is not a stand-alone diagnosis. A positive result does not prove invasive fungal infection, and prolonged itraconazole should never be self-started. *

Evidence and controversy

Campbell's framework emphasizes exposure correction, MyMycoLab IgG/IgE testing, itraconazole, and targeted nutritional support. The full combination has not been validated as a single treatment package in high-quality trials for illness attributed to indoor mold exposure, so the page should describe it as a proposed protocol rather than established consensus care.

MyMycoLab serum IgG and IgE panel

Mycotoxin target	MyMycoLab-associated organism(s)	Result reported	Interpretive note
Satratoxin	Stachybotrys ("black mold")	Satratoxin IgG and IgE	MyMycoLab treats this as one target category even though both antibody classes are reported.
Verrucarin and verrucarol	Fusarium and Aspergillus	Verrucarin/verrucarol IgG and IgE	Grouped target name; do not expand it into extra targets without a matching lab report.
Ochratoxin A and B	Aspergillus and Penicillium	Ochratoxin IgG and IgE	Grouped heading on the current panel.
T-2 toxin	Fusarium	T-2 toxin IgG and IgE	Single target category with two antibody classes.
Vomitoxin / deoxynivalenol (DON)	Fusarium	DON/vomitoxin IgG and IgE	Panel uses a toxin name rather than a mold culture result.
Cladosporium toxin / HSP 70	Cladosporium	Cladosporium toxin/HSP 70 IgG and IgE	HSP 70 is the label used in the panel description.
Stachybotrys trichothecene	Stachybotrys and Myrothecium	Trichothecene IgG and IgE	MyMycoLab groups this as one category.
Alternaria toxin / alternariol	Alternaria	Alternaria toxin/alternariol IgG and IgE	Reported as a toxin-focused immune-reactivity pattern.
Aspergillus hemolysin	Aspergillus	Aspergillus hemolysin IgG and IgE	One of the 14 current target categories.
Sterigmatocystin	Aspergillus versicolor	Sterigmatocystin IgG and IgE	Single target with both IgG and IgE results.
Mycophenolic acid	Penicillium	Mycophenolic acid IgG and IgE	MyMycoLab includes this under the current panel.
Gliotoxin	Aspergillus fumigatus and Trichoderma	Gliotoxin IgG and IgE	Panel target is a toxin-associated category, not a culture result.
Fumonisin	Fusarium	Fumonisin IgG and IgE	One of the 14 antibody categories.
Zearalenone	Fusarium	Zearalenone IgG and IgE	Current panel target reported as one IgG and one IgE result.

* 14 targets, 28 total antibody results. MyMycoLab interprets the pattern as exposure or ongoing response, but the panel does not prove mold colonization or invasive fungal infection on its own. *

Campbell-associated treatment and follow-up timeline

Phase	Focus	What to review
Before treatment	Build the baseline	Take a detailed exposure and building history, correct active moisture problems, consider professional inspection and targeted sampling, review alternative diagnoses, obtain baseline liver testing and interaction screening, consider conventional fungal/allergy/pulmonary/infectious testing where indicated, and discuss MyMycoLab limitations before ordering it.
Months 0-1	Start carefully	Begin environmental correction, start physician-supervised treatment only after contraindications are reviewed, introduce nutritional support gradually, record baseline symptoms, and watch closely for medication intolerance.
Months 1-3	Monitor response	Continue exposure avoidance, repeat clinical and liver-safety assessment, review adherence and absorption, and reconsider the diagnosis if the patient is worsening or not responding.
Months 3-6	Stay selective	Continue only when risk-benefit remains favorable, avoid automatically extending antifungal therapy, reassess the building and possible continuing exposure, and review diet and supplements for unnecessary complexity.
Around month 6	Reassess the plan	Do a full clinical reassessment, repeat environmental review, repeat laboratory testing only when it will meaningfully change management, and decide whether to stop, modify, or continue treatment based on the entire picture.

Targeted supplement support

Supplement	Campbell-associated amount
Melatonin	3 mg at bedtime
Complete B-complex	Once daily
Magnesium complex	240 mg twice daily
Vitamin D3	5,000 IU daily
Vitamin C	1,000 mg three times daily
Phospholipid complex	500 mg daily; includes phosphatidylserine, phosphatidylcholine, and phosphatidylethanolamine
Curcumin	500 mg daily; standardized to about 18% curcuminoids
Spore-based probiotic	4-8 billion CFU daily

Additional agents and safety notes

Earlier Campbell presentations also discussed N-acetylcysteine, glutathione, vitamin A, vitamin E, quercetin, zinc, and lycopene as additional support agents.
Vitamin D should be considered alongside blood levels, calcium status, and kidney disease.
Magnesium may cause diarrhea and can affect medication timing.
Curcumin may increase bleeding risk in susceptible patients.
High-dose vitamin C may be inappropriate in certain kidney disorders.
B-complex products vary substantially in dose; probiotics need caution in severely immunocompromised patients; melatonin may cause sedation and add to other sedating drugs.

Diet and gastrointestinal support

Campbell commonly recommends an anti-inflammatory diet.
A low-histamine approach can be considered when histamine intolerance or mast-cell symptoms are present.
Reduce highly processed foods and maintain adequate protein and micronutrient intake.
Gut support may include the spore-based probiotic listed above.

Binders and detoxification

Binders are not usually the central feature of Campbell's current protocol.
MyMycoLab materials have cautioned against routine binder use.
Binders can reduce absorption of medications and nutrients, so any use should be individualized and separated from other therapies.
The evidence for routine binder use in chronic indoor-mold illness remains limited.

Balanced evidence statement

Damp buildings and indoor mold can aggravate asthma, allergic disease, and some respiratory conditions. The broader claim that indoor mycotoxin exposure commonly causes a chronic systemic illness requiring prolonged antifungal treatment remains disputed. Mycotoxin-antibody testing and six-month itraconazole treatment are not universally accepted standards of care. Patients should receive a conventional medical assessment and should not begin systemic antifungal therapy without physician supervision.

* Campbell's materials are included for education and source transparency. Mycotoxin-antibody testing remains controversial, the full supplement combination has not been validated as a single treatment package in high-quality trials, and prolonged antifungal use requires qualified supervision. *

Diagnostic and monitoring tools

CIRS and mold illness testing — lab panels and interpretation

CIRS Diagnostic Biomarkers

Test	Normal range	CIRS finding	Clinical significance
C4a	0-2830 ng/mL	Elevated	Complement activation marker. Indicates innate immune response to biotoxins. Should decrease with successful binder therapy.
TGF-beta1	<2380 pg/mL	Elevated	Inflammatory cytokine. Drives fibrosis and tissue remodeling. Elevation correlates with symptom severity.
MMP-9	85-332 ng/mL	Elevated	Extracellular matrix enzyme. Delivers inflammatory cells to tissues. Elevated in acute and chronic inflammation.
MSH (alpha-MSH)	35-81 pg/mL	Low (<35)	Master regulatory hormone. Controls inflammation, pain perception, sleep, and hormone production. Low MSH = widespread dysfunction.
VIP	23-63 pg/mL	Low (<23)	Neuropeptide. Regulates pulmonary, immune, and neurologic function. Low VIP correlates with shortness of breath and immune dysfunction.
ADH / Osmolality	1.0-13.3 pg/mL ADH	Low ADH, high osmolality	Anti-diuretic hormone dysfunction. Explains frequent urination, thirst, and electrolyte disturbances in CIRS.
Leptin	0.5-13.8 ng/mL (men); 1.1-27.5 (women)	Elevated (leptin resistance)	Obesity-associated hormone. Elevated leptin drives inflammation and weight gain resistance in CIRS.
VEGF	31-86 pg/mg	Low	Vascular endothelial growth factor. Low VEGF impairs capillary repair and oxygen delivery. Contributes to fatigue and poor healing.
ACTH / Cortisol	ACTH 8-37 pg/mL	Variable (low or high)	Adrenal axis disruption common in CIRS. Low ACTH contributes to fatigue, inflammation, and poor stress tolerance.
HLA-DR	Variable by haplotype	Susceptible haplotypes	Genetic predisposition. 15-6-51, 11-3-52B, 4-3-53, 14-5-52B among the "dreaded" haplotypes. Does not diagnose CIRS alone.

Environmental Testing Methods

Test	Method	Strengths	Limitations
ERMI	qPCR dust sample (36 species)	Comprehensive; settled dust captures chronic exposure history. Used for initial assessment and post-remediation clearance.	Requires professional interpretation. Score affected by cleaning, vacuuming, and dust accumulation patterns.
HERTSMI-2	qPCR dust sample (5 key species)	Simplified, focused on the most pathogenic water-damage molds. Score <10 considered safe for CIRS patients. Cost-effective.	Fewer species tested than ERMI. Designed for re-entry assessment, not initial diagnosis.
Air sampling	Spore trap, viable culture	Useful for detecting airborne spores during active water damage. Quick snapshot of current air quality.	Misses mycotoxin fragments, sticky molds (Stachybotrys), and reservoirs. Inadequate alone for CIRS assessment.
Mycotoxin urine testing	ELISA or LC/MS-MS	Directly measures excreted mycotoxins (ochratoxin A, aflatoxin, trichothecenes, gliotoxin, etc.). Useful for monitoring treatment progress.	Reflects excretion, not necessarily tissue burden. Provocation testing may be needed. Results vary with hydration and kidney function. Labs discussed by clinicians include Great Plains, RealTime Labs, and MosaicDX.
VCS (Visual Contrast Sensitivity)	Online visual test	Quick, inexpensive screening. Positive in ~92% of CIRS patients. Tracks treatment response. Repeatable without lab draw.	Non-specific; can be affected by other neurologic conditions. Not diagnostic alone.

Detailed clinical picture

Mold/CIRS care is often about exposure control, nervous-system tolerance, and careful sequencing.

Water-damaged building illness can overlap with Lyme, Bartonella, Babesia, MCAS, POTS, chemical sensitivity, migraine, asthma, sleep disorders, trauma physiology, and medication intolerance.

Exposure history to document

Musty odor, visible mold, leaks, flooding, roof or plumbing damage, HVAC contamination, basement dampness, condensation, old carpets, workplace exposure, school exposure, vehicle exposure, or storage-unit exposure.
Symptoms that improve away from a building and return after re-entry, including headache, sinus symptoms, cough, wheeze, brain fog, fatigue, dizziness, anxiety, pain, rash, or chemical sensitivity.
Past remediation quality, whether the water source was corrected, whether porous materials were removed, and whether belongings or HVAC systems may be causing re-exposure.
Environmental testing already done, such as professional inspection, moisture mapping, air samples, ERMI, HERTSMI-2, dust testing, or mycotoxin-related testing.
Whether there was post-remediation clearance, whether rooms were kept isolated while dust settled for qPCR dust testing, and whether contents were returned before the building was cleared.

CIRS and sensitive-patient markers

VCS screening, HLA-DR genetics, C4a, TGF-beta1, MMP-9, MSH, ADH/osmolality, VEGF, VIP, MARCoNS, inflammatory markers, and mycotoxin testing may fit selected cases.
MCAS, histamine intolerance, constipation, sleep deprivation, dysautonomia, limbic threat response, and adrenal or thyroid issues often need stabilization before binders or antimicrobial treatment.
Binders need medication spacing, constipation prevention, and clear signals for when the plan is moving too fast.
Clinicians should distinguish detox flares, mast-cell reactions, medication toxicity, mold re-exposure, infection flares, and unrelated medical problems.
Acute respiratory symptoms, mold allergy, asthma, and fungal sinusitis need conventional evaluation in parallel with CIRS-style workup when present.

Mold/CIRS testing and sequencing guide

Area	What the sources emphasize	Safe action criteria
Environment	Water source correction, IEP assessment, containment, negative pressure, HEPA cleaning, HVAC/duct review, contents sorting, carpet removal decisions, and post-remediation clearance.	Responsibility for proving the space is safe enough for a CIRS-sensitive person and endpoint criteria should be defined before re-entry.
Building tests	ERMI and HERTSMI-2 are emphasized for settled dust and health-risk interpretation; short air samples can miss fragments, reservoirs, and sticky molds.	Dust-based qPCR testing and HERTSMI-2 scoring may be needed when air testing is too narrow for the exposure history.
CIRS screen	Symptom clusters, exposure history, VCS, HLA-DR susceptibility, and inflammatory markers can help decide whether CIRS-WDB is plausible.	Findings should be sorted into CIRS-supportive evidence and competing diagnoses such as asthma, allergy, infection, migraine, or sleep apnea.
Biomarkers	C4a, TGF-beta1, MMP-9, MSH, VIP, VEGF, ADH/osmolality, leptin, ACTH/cortisol, and sex-hormone/aromatase issues may show inflammatory, endocrine, vascular, and fluid-balance disruption.	Labs should be ordered when results will change the plan, with specialty handling requirements confirmed before collection.
Binders	Shoemaker emphasizes cholestyramine or Welchol; Nathan also discusses charcoal, clay, chlorella, Saccharomyces boulardii, phosphatidylcholine, and glutathione tolerance in selected patients.	Binder choice, medication spacing, constipation risk, bile reflux, sensitivity, and symptom worsening need a monitoring plan.
Colonization	Nathan and Brewer-style discussions include sinus/gut colonization, antifungal tolerance, biofilm, and careful sequencing after binders are tolerated.	Colonization testing should precede antifungal or nasal treatment when exposure control and tolerance are not yet stable.
MARCoNS and VIP	Shoemaker sources place MARCoNS evaluation after initial binder work and VIP as a later step with prerequisites and safety monitoring.	MARCoNS treatment and VIP require prerequisites, VCS/lab tracking, exposure control, and re-exposure monitoring.

Recommended Mold/CIRS tests to discuss

Testing category	Shoemaker / Nathan / Lyme-MSIDS focus	Common tests and labs to discuss
Building and exposure testing	Shoemaker and the recovery-manual sources put exposure control first; Nathan also warns that treatment fails if the patient remains in a contaminated space.	IEP inspection, moisture mapping, HVAC/duct review, visible mold and water-source documentation, ERMI, HERTSMI-2, dust sampling, post-remediation clearance testing, and contents/cross-contamination assessment.
CIRS screening	Shoemaker-style workup starts with symptom clusters, exposure history, and VCS as a practical screen before deeper biomarker interpretation.	VCS testing, 13 symptom-cluster review, HLA-DR/DQ susceptibility testing, exposure timeline, symptom-away-from-building tracking, and prior remediation or re-exposure records.
Shoemaker biomarker panel	Used to document innate immune activation, vascular dysregulation, endocrine disturbance, and readiness for later protocol steps such as VIP.	C4a, TGF-beta1, MMP-9, MSH, VIP, VEGF, ADH with osmolality, leptin, ACTH/cortisol, sex-hormone/aromatase markers when indicated, CBC/CMP, inflammatory markers, and specialty handling instructions before collection.
Nathan mycotoxin and sensitivity workup	Nathan's model uses mycotoxin testing and tolerance markers to choose binders slowly enough for sensitive patients.	Urine mycotoxin testing such as LC/MS-MS or ELISA panels from labs such as Great Plains, RealTime Labs, or MosaicDX; glutathione status or oxidative-stress markers when available; liver/kidney function; constipation assessment; medication/supplement sensitivity history; and binder tolerance tracking.
Colonization and MARCoNS	Shoemaker places MARCoNS later in the sequence; Nathan also evaluates sinus or gut colonization when symptoms and mycotoxin patterns persist.	Deep nasal MARCoNS culture with antibiotic resistance/sensitivity, nasal/sinus evaluation, fungal culture or PCR when clinically indicated, stool/gut fungal evaluation when GI colonization is suspected, and biofilm/tolerance planning before nasal or antifungal treatment.
Overlap with Lyme, MCAS, POTS, and allergy	Horowitz and Kinderlehrer place mold/CIRS inside a broader complex chronic illness map; not every mold-reactive patient has CIRS alone.	Lyme/co-infection testing when exposure history fits, serum tryptase, histamine or N-methylhistamine, prostaglandin D2 metabolites, IgE/allergy evaluation, thyroid/adrenal labs, autonomic/POTS assessment, sleep apnea screening, and conventional asthma/sinus workup when present.
Binder and VIP safety labs	Binders and VIP should be monitored; moving too quickly can worsen sensitive patients or obscure ongoing exposure.	CMP/liver/kidney markers, lipids when bile-acid binders are used long-term, medication spacing review, constipation plan, VCS and biomarker retesting, MARCoNS-negative status and exposure control before VIP, and pregnancy/medication review when relevant.

* Mold/CIRS testing should follow a sequence. Building safety and exposure control come before aggressive detox; lab abnormalities must be interpreted with symptoms, exposure, and competing diagnoses. *

Herbal & nutritional support

Detoxification and immune support for mold-exposed patients.

For mold/CIRS patients, the priority is exposure control and tolerance. Brownstein's iodine protocol supports detoxification by displacing toxic halides and mycotoxins, while Zhang TCM herbs support organ function during remediation and binder therapy.

Brownstein Iodine Protocol — detoxification for mold illness

Mold-exposed patients accumulate toxic halides (bromide, fluoride) alongside mycotoxins. Iodine competitively displaces these from cellular receptors and supports the body's natural detoxification pathways.

Iodine/Iodide (Lugol's or Iodoral): 12.5–50 mg/day. Antifungal, antibacterial. Concentrates in glandular tissue. Displaces bromide from flame retardants and fluoride from water supply. Use only after exposure is controlled.
Vitamin C: 3,000–6,000 mg/day. Potent antioxidant; supports phase I and II liver detoxification. Reduces oxidative stress from mycotoxin exposure.
Selenium: 200–400 mcg/day. Required for glutathione peroxidase which neutralizes oxidative damage. Frequently deficient in mold/CIRS patients.
Unrefined salt: 1–1.5 tsp/day. Chloride competitively inhibits bromide reabsorption. Essential for halide detoxification.
Magnesium: 400–800 mg/day. Supports mitochondrial function and energy production. Relaxes bronchial smooth muscle for mold-reactive airway symptoms.

Testing: 24-hour iodine loading test before treatment. Brownstein reports >96% of 6,000+ patients are iodine deficient.

Zhang TCM — organ and detoxification support

Zhang Clinic protocols for environmental toxin exposure focus on supporting liver, kidney, and lymphatic clearance pathways alongside binder therapy (cholestyramine, charcoal, clay).

Liver Support formula: Zhang Clinic hepatic detoxification herbs to support phase I and II pathways during mycotoxin clearance. Particularly important when binders mobilize stored toxins.
Kidney Support formula: Supports renal clearance of mobilized toxins. Hydration and electrolyte balance essential during detoxification.
Lymphatic Support: Herbal lymphagogues to improve lymphatic drainage, which is frequently stagnant in CIRS patients with fluid retention and edema.
Adaptogenic herbs: Adrenal and nervous system support during the stress of remediation and treatment. Zhang uses Reishi, Cordyceps, and Eleuthero in customized formulations.

Note: Herbal detoxification should only begin after acute exposure is controlled and the patient is stable. Sensitive patients should start with micro-doses and titrate slowly, consistent with Nathan's "start low, go slow" principle.

Research and clinical sources

Mold and CIRS source references.

These sources inform the clinical frameworks on this page. They are references, not treatment instructions.

When mold symptoms need urgent care

Seek urgent care for severe asthma or trouble breathing, anaphylaxis, chest pain, fainting, confusion, suicidal thoughts, severe dehydration, uncontrolled vomiting, or rapidly worsening neurologic symptoms.

Bring building exposure details, medication list, and supplement list.
Do not assume every flare is detox. Rule out toxicity, allergy, infection, and unrelated medical emergencies.

Source stack used on this page

Ritchie C. Shoemaker, MD, Matthew C. Hudson, and Patti Schmidt, Surviving Mold: Life in the Era of Dangerous Buildings
Ritchie Shoemaker, State of the Art Answers to 500 Mold Questions
Neil Nathan, MD, Mold and Mycotoxins: Current Evaluation and Treatment 2016
Neil Nathan, MD, Toxic, 2nd Edition
Paula Vetter, Laurie Rossi, Cindy Edwards, and Ritchie C. Shoemaker, MD, Mold Illness: Surviving and Thriving
Andrew W. Campbell, MD, 2018 lecture extraction on molds, mycotoxins, testing themes, and treatment claims
Andrew W. Campbell, MD, 2019 editorial extraction on Lyme disease and mycotoxicosis overlap
EPA: A Brief Guide to Mold, Moisture and Your Home
Health Canada: Guide to addressing moisture and mold indoors
Health Canada: Residential Indoor Air Quality Guideline - Mold
CDC: Use of Unvalidated Urine Mycotoxin Tests
ACMT 2025 Position Statement on Mold-Related Inhalation Exposures

Dr. Andrew Campbell's work

Dr. Andrew Campbell's mold, mycotoxin, and Lyme-overlap materials.

These materials summarize Dr. Campbell's clinical perspective. They are included for source transparency and should be weighed against current public-health guidance and independent verification.

Official and affiliated resources

* MyMycoLab is associated with Dr. Campbell's testing approach and is not an independent evaluator.

What the source bundle emphasizes

Damp buildings, hidden growth, and water intrusion as the exposure starting point.
Overlapping, nonspecific symptoms that can resemble Lyme disease, mold-related illness, or both.
Serum IgG and IgE antibody testing for mycotoxin exposure as his favored lab strategy.
His criticism of urine mycotoxin testing, which he argues can be confounded by background dietary exposure and assay interpretation.
Historical treatment themes including exposure removal, intranasal amphotericin B for chronic rhinosinusitis examples, antifungals, immunotherapy, melatonin, vitamins, binders, and IVIG for selected neurologic illness.

Overlapping symptom groups in the 2019 editorial

Constitutional: fatigue, sweats, fevers, chills, weight change, and general flu-like illness.
Neurological/cognitive: brain fog, memory trouble, dizziness, balance problems, neuropathy, headaches, and mood changes.
Respiratory/cardiac: cough, shortness of breath, palpitations, and other chest or airway complaints.
Immune/sensitivity: allergies and chemical, food, or medication sensitivity.
Gastrointestinal: nausea, abdominal discomfort, and bowel changes.
Other: rashes, bruising, sores, urinary discomfort, hair loss, nosebleeds, pelvic or testicular pain, menstrual changes, and alcohol intolerance.

Lyme testing and coexistence claims

The editorial says the right lab method matters and favors multi-peptide ELISA over Western blot.
It says that approach can detect different Lyme life-cycle patterns and Borrelia subspecies, and it discusses Babesia and Ehrlichia co-infections.
The author argues that some patients treated for Lyme can improve when mycotoxicosis is addressed, and the reverse can also happen.
The paper treats Lyme disease and mycotoxicosis as potentially coexisting conditions rather than mutually exclusive explanations.

Testing and treatment themes in Campbell's materials

Topic	Dr. Campbell's clinical perspective	Context for readers
Symptom overlap	His editorial argues that Lyme disease and mycotoxicosis can look very similar and that some patients may have both.	Symptoms are nonspecific and need differential diagnosis; overlap does not prove either condition on its own.
Lyme testing method	The editorial favors multi-peptide ELISA rather than Western blot and says it can better capture multiple Borrelia species and selected co-infections.	That is the author's position and should be checked against current independent Lyme testing guidance.
Serum mycotoxin antibodies	The lecture describes blood-serum IgG and IgE antibody testing as the preferred way to evaluate mycotoxin exposure in his framework.	That interpretation reflects his clinical perspective and is not universally accepted as diagnostic consensus.
Urine mycotoxin testing	The editorial argues that urine levels can be misleading because trace mycotoxins may appear in food and healthy people.	CDC and ACMT caution against over-interpreting unvalidated urine mycotoxin tests.
Exposure routes and mechanisms	The lecture discusses inhalation, ingestion, dermal absorption, nasal mucosa and olfactory-nerve transport, and lung surfactant/alveolar pathways for mycotoxin movement.	These are proposed mechanisms described in the source material, not universally accepted clinical proof.
Other tests he discusses	Immune function tests, neurological autoantibodies, pulmonary function testing, SPECT imaging, and selected neurophysiologic testing appear in the lecture extraction.	Availability and clinical utility vary by setting and indication.
Treatment themes	Source material discusses exposure removal, intranasal amphotericin B examples, antifungal medication, immunotherapy, melatonin, vitamin D3, vitamin C, B-complex support, IVIG for demyelination, and adsorbent or antioxidant approaches.	These are historical/source summaries only; they are not LADA recommendations or individualized treatment advice.
Adsorbents and antioxidants	The lecture warns that adsorbents are not selective and may cause adverse effects with long-term use; it discusses cholestyramine and sodium bicarbonate for ochratoxin, then names NAC, glutathione, vitamin C, vitamin E, vitamin A, quercetin, zinc, and lycopene as supportive alternatives.	Read as source-summary language only. Clinical choice, safety, and appropriateness depend on the patient and prescriber.

* Long-term antifungal use can carry liver, cardiac, and drug-interaction risks and requires supervision by a qualified prescriber. This page is describing source material, not recommending a protocol. *

Questions to discuss with a qualified clinician

Could the symptoms fit asthma, allergy, infection, migraine, MCAS, POTS, medication effects, or another diagnosis?
Is there enough exposure history to justify building inspection, remediation review, or dust testing?
What test is being ordered, what question does it answer, and how would it change care?
What are the risks of antifungal, binder, or immune-based treatment in this particular patient?
How should results be interpreted if Lyme disease or another tick-borne illness may also be present?

Evidence context

Broad agreement: dampness and visible or concealed mold should be corrected, and wet materials should be dried promptly.
Dispute: whether typical indoor inhalation causes chronic systemic mycotoxicosis in the way some clinics describe it.
Dispute: clinical validity of serum mycotoxin antibody testing and urine mycotoxin testing for diagnosis.
Public-health guidance: EPA, Health Canada, CDC, and ACMT all support caution around damp buildings and emphasize validated evaluation and remediation.

Patient safety

Do not push treatment faster than the patient can tolerate.

For sensitive patients, a flare may mean the sequence, dose, exposure load, mast-cell state, or nervous-system state needs adjustment. LADA encourages clinician-guided care with clear stop rules.

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