Frequently Asked Questions

We are a dedicated non-profit organization committed to addressing the critical issues surrounding mould and related health issues in Australia. Our mission is built around four core objectives:

1. To support and guide comprehensive studies on dampness and mould, focussing on its health impacts and implications for building design. MAC’s goal is to contribute to a safer and healthier environment for everyone.
2. To educate and engage various stakeholders, including building professionals and medical practitioners, about the risks and consequences of dampness and mould exposure. By fostering a community of informed advocates, MAC aims to drive meaningful change.
3. To offer essential resources and support for those affected by mould-related illnesses, whether localized or systemic, acute or chronic. MAC aims to empower practitioners and individuals with the knowledge and tools needed to navigate and overcome mould-related challenges.
4. To strive to provide much-needed credibility to the area of dampness and mould and its connections with health problems, to assist with the general perception of mould-related illnesses in the community.

The British English spelling used in Commonwealth Countries is “mould” and is the one used throughout this FAQ. American English spelling omits the “u”, and this is also the case in most non-Commonwealth Countries.

Mould is a type of fungus that grows in multicellular filaments called hyphae, forming a fuzzy or powdery-looking colony. It thrives in warm, damp, and humid environments and reproduces by releasing microscopic spores into the air, which can spread and settle on surfaces where moisture is present.

Fungi are a group of organisms that include:

1. Moulds
2. Yeasts
3. Mushrooms

Moulds play an important role in nature by breaking down organic material like dead plants and animals. They have also been a source of many important medicines—including penicillins, cephalosporins, mycophenolic acid, cyclosporin (immunosuppressants) and several statin drugs including mevastatin (a substrate for creating other statin drugs). Recently there has been renewed interest in the fungal byproduct psilocybin for use in depression and other psychiatric conditions. However, when mould grows indoors—especially in homes, workplaces, or buildings with water damage—it can become a serious health concern.

As people don’t get sick from mould by walking in a forest where there are high levels of mould, many people don’t understand why mould in a water-damaged building can cause illness.

Mould in nature:

• Mould is a natural part of the environment, primarily functioning as a decomposer that breaks down organic material like leaves, wood, and dead animals.
• It exists in a balanced ecosystem, where it competes with other microorganisms and is naturally regulated by environmental factors such as sunlight, wind, and microbial competition.
• As a result of this, there is a tremendously diverse fungal (and bacterial) ecosystem, which prevents pathogenic strains from becoming dominant.
• Outdoor air provides dilution, preventing mould spores from accumulating at high concentrations.
• It typically does not pose a significant health risk unless there is an occupational exposure (e.g., working with compost, potting mix, or decaying wood in a closed space).
• There may also not so much need for the production of mycotoxins outside, because they’re not competing over small damp spaces like they are indoors.

Mould overgrowth in a built environment:

• In buildings, mould can become a problem when moisture levels rise due to leaks, flooding, condensation, or poor ventilation.
• Indoor environments lack the natural checks and balances found outdoors (such as UV light exposure, diversity in the ecosystem, and natural air circulation), and also includes unfavourable elements such as fungicides (which cause natural selection of more pathogenic moulds) and chemicals, allowing mould to overgrow rapidly if conditions are favourable.
• Mycotoxins and mould fragments can become highly concentrated in enclosed spaces, leading to chronic exposure and potential health issues, especially for individuals with mould sensitivity, asthma, allergies, or mast-cell activation syndrome
• Indoor mould growth often involves species that thrive in damp, cellulose-rich environments (like gyprock, wood, and carpets), including Stachybotrys, Aspergillus, Cladosporium and Penicillium species, which can produce harmful mycotoxins.

Essentially, mould in nature is a necessary and regulated part of the ecosystem, while mould in a built environment can become an unchecked health hazard due to poor ventilation, excessive moisture, and the lack of natural balancing factors.

Given the propensity of indoor pathogenic mould to cause human illness, what are the mechanisms whereby this can occur?

MAC uses the term Mould Illness as an umbrella term to cover four types of conditions caused by mould, bacteria, their toxins, and other toxicants in water-damaged buildings.

1. Mould allergy: Allergic responses to mould can give rise to a variety of illnesses, primary affecting the respiratory system. Allergic responses can give rise to asthma and wheezing, particularly in children. Allergic rhinitis is also linked to allergic responses to mould as is hypersensitivity pneumonitis or “farmer’s lung”. Further, the condition known as allergic bronchopulmonary aspergillosis is related to a more severe allergic reaction to aspergillus species, leading to lung inflammation. This mechanism of mould-related illness is most widely accepted, but separate to these common diagnostic labels, mould allergy can be more nebulous and contribute to a more systemic illness presentation such as fibromyalgia or ME/CFS.
2. Innate immune activation: While the innate immune response is intended to be a short-lived immune response heralded by the production of cytokines, in mould-related innate immune activation, it persists as the dominant immune response resulting in persistent inflammation and release of cytokines. These cytokines are released by various white blood cells in the systemic circulation and by activated microglia in the central nervous system. The result is a systemic inflammatory response, similar to that described as “chronic inflammatory response syndrome” (CIRS) by Shoemaker & colleagues.
3. Fungal colonisation/infection: As the name implies, this is where the mould itself (or alternatively yeast, a related form of fungus) is growing in, or on, the body, either in the gastrointestinal tract, nasal and/or sinus cavities, skin, lungs, and/or occasionally bloodstream. Culture tests (sinus, nasopharynx, lungs), organic acids testing, and stool testing can be used in diagnosis. Symptoms may be single system (localised to the system of colonisation), or, if the fungus is producing mycotoxins or inflammatory proteins, multisystem. Colonisation generally indicates the organism is not triggering an immune response that leads to symptoms, while infection implies that it is actively causing an immune response, and therefore symptoms. Treatment usually involves antimicrobials to reduce the fungal burden and pro/pre-biotics to improve the terrain, but binding and inflammation reduction therapies are often used in conjunction.
4. Mycotoxin toxicity (Mycotoxicosis): For this subtype, the mycotoxins produced by fungi causing a toxicity in the body, whether inhaled or produced by internal fungal colonisation, are seen as driving the illness. Symptoms can be similar to subtypes #1 and #2, although sometimes less severe. Diagnosis can involve urinary mycotoxin testing or serum mycotoxin antibody testing. Some of the specific effects of various mycotoxins include the following:
   • Ochratoxin A—Kidney damage, neurotoxicity
   • Aflatoxins—Liver toxicity, increased cancer risk (hepatocellular carcinoma)
   • Trichothecenes (e.g., T-2 toxin, DAS)—Neurological symptoms (e.g., headaches, brain fog, anxiety/depression, dizziness, vertigo, and peripheral neuropathy), respiratory and mucosal damage (including chronic sinus congestion, chronic cough, and irritation of the throat or eyes)
   • Zearalenone—Estrogenic effects (eg triggering of oestrogen sensitive pathology such as fibroids or endometriosis), hormonal imbalances, reproductive issues
   • Gliotoxin—This can cause gastrointestinal and microbiome disruptions, neurological symptoms (eg fatigue, brain fog, mood disturances and peripheral neuropathy) and respiratory and sinus-related issues.

1. Ritchie Shoemaker, MD / Andrew Heyman MD:
   • Dr Shoemaker from Pocomoke City, Maryland in the USA is the primary researcher for the Center for Research on Biotoxin-Associated Illness, a tax-exempt organisation in the USA. Groomed as a rural general practitioner in Pokemoke, Maryland, USA, he stumbled across what he would later coin biotoxin-related illness in the late 1990s due to a pfiesteria outbreak on the Chesapeake Bay. By happenstance, he found that giving cholestyramine for secretory diarrhea in a patient resolved multiple symptoms across multiple systems. In the early 2000s, he published studies showing that biotoxins from water-damaged buildings (then called sick building syndrome) caused a similar type of syndrome that he later labelled CIRS-WDB. This stands for “chronic inflammatory response syndrome due to exposure of the interior of water-damaged buildings”. He developed a series of biomarkers to look at the inflammatory changes that occur in this illness, which is primarily related to mould and bacteria such as actinobacteria. His primary treatments included cholestyramine, silver/EDTA nasal spray, and a nasal spray of vasoactive intestinal polypeptide (VIP). Dr Heyman is one of the most well-known proponents of the Shoemaker protocol but introduces additional steps at the start of the protocol including the use of phosphatidylcholine, RG3, curcumin, BPC-157, magnesium, and various herbal therapies.
2. Neil Nathan, MD/Jill Crista, ND
   • Drs Nathan and Crista have a holistic medicine approach for systemic mould-related illnesses. Nervous system dysregulation plays a huge role in chronic illness, and rebooting the system can be a key part of recovery. Drs Nathan and Crista utilise multiple avenues such as brain retraining and vagal stimulators, etc to assist with rebooting the nervous system. They both address mast cell activation as a primary mechanism for mould-related inflammation. For diagnosis, they primarily use urinary mycotoxin testing and their treatment involves targeted binders based on which mycotoxins are elevated. If sinus/nasal fungal colonisation is diagnosed, then antifungal medications (Dr Nathan) or herbs (Dr Crista) are prescribed intranasally and oral antifungal medications (Dr Nathan) or herbs (Dr Crista) are often used for gastrointestinal fungal colonisation. They may also use multiple other therapies, including ozone therapy plus phosphatidylcholine and other membrane stabilisers.
3. Andrew Campbell, MD
   • Dr Campbell.is a Mexico-trained MD who primarily ascribes mould-related illness to be due to mycotoxins and fungal colonisation. His preferred testing is serum mycotoxin antibodies done via the laboratory MyMycoLab, which he is the medical director of. His treatment protocol does not use binders; instead, he uses the pharmaceutical antifungal itraconazole orally, plus various natural supplements such as vitamin D and B complex, vitamin C, Omega 3s, CoQ10, melatonin, and spore-based probiotics. These treatments are individualised according to the specific case.

1. Ritchie Shoemaker, MD (CIRS/Shoemaker Protocol)
   • Dr Shoemaker from Pocomoke City, Maryland in the USA is the leader for the CIRS subtype of Mould Illness, having discovered biotoxin illness in the late 1990s due to a pfiesteria outbreak on the Chesapeake Bay. By happenstance he found that giving cholestyramine for secretory diarrhea in patient resolved all symptoms. In the early 2000s he published studies showing that biotoxins from water-damaged buildings (then called sick building syndrome) caused a similar type of syndrome, that he later labelled CIRS-WDB.
2. Neil Nathan, MD/Jill Crista, ND
   • Drs Nathan and Crista mostly align with the fungal colonisation and mycotoxin toxicity subtypes of Mould Illness, acknowledging that these subtypes can cause chronic inflammation as well. They primarily use urinary mycotoxin testing for diagnosis and treatment involves targeted binders based on which mycotoxins are elevated. If fungal colonisation is suspected they also use pharmaceutical or herbal/natural antifungals orally and/or intranasally.
3. Andrew Campbell, MD
   1. Dr Campbell also aligns with the fungal colonisation and mycotoxin toxicity subtypes of Mould Illness. His preferred testing is serum mycotoxin antibodies done via the laboratory MyMycoLab, which he is the medical director of. His treatment protocol does not use binders, instead he uses the pharmaceutical antifungal itraconazole orally, and various supplements such as vitamin D and B complex, Omega 3s, CoQ10, melatonin and spore-based probiotics.

All of the main thought leaders advocate removing oneself from exposure to environmental dampness and mould as the most important step in recovery. The Shoemaker protocol currently focuses more on bacteria in the environment. However, this tends to go hand-in-hand with dampness and mould in most cases.

Two out of the three major protocols (Shoemaker & Nathan) include the use of binder medications and/or supplements, and two of of the three major protocols (Nathan & Campbell) include use of antifungal therapies (pharmaceuticals and/or herbal antifungals).

All the protocols involve some form of therapy to reduce inflammation whether it be pharmaceutical (Shoemaker) or a combination (Nathan) or primarily natural supplement-based (Campbell).

A summary of an integrated protocol might look like this:

© Mold Illness Mastery course

For fungal colonisation and mycotoxin toxicity, yes mould, yeast, or their byproducts (e.g., mycotoxins) are the cause.

However, innate immune activation may be caused by the toxigenic microbial soup found in water-damaged buildings and includes mould fragments, mycotoxins, mannans and beta-glucans from mould, endotoxins and exotoxins from bacteria (including gram positive and gram negative bacteria, mycobacteria and actinobacteria), microbial volatile organic compounds (mVOCs) from bacteria and mould, VOCs from building materials that are broken down through microbial activity, and many more compounds. Mould is just the most visible, most researched and easiest microbe to test for.

Until recently, the below are what are generally considered the mainstream medical viewpoints on how mould/fungi/yeast affect human health, and are not the main focus of MAC.

1. Mould allergy:  Usually seen as inhaled mould causing an allergic response in the upper respiratory system, causing asthma and/or rhinitis. Doctors will usually test for mould allergy via IgE blood tests or skin prick tests. Treatment is centred on exposure reduction and/or immunotherapy.
2. Candidiasis: An overgrowth of the yeast Candida. It can affect the skin, mouth, throat, vagina, and joints. Invasive candidiasis occurs when Candida spreads to the bloodstream creating a more serious illness. This is generally only diagnosed in immunocompromised individuals (e.g., those on chemotherapy or transplant immune suppressant medications).
3. Fungal infection (Mycosis): Invasive fungal infection of the blood or organs. Subtypes include:
   • Tinea: Fungal infection of the skin that causes itching and rashes. Usually treated by topical antifungals.
   • Aspergilloma/cryptococcosis: This is when the mould Aspergillus (or the yeast Cryptococcus) causes fungal balls in the lungs. Symptoms include a cough bringing up blood, wheezing, shortness of breath, weight loss, and fatigue.
   • Invasive aspergillosis/cryptococcosis: When the fungal infection from #2 spreads to the brain, heart, kidneys or skin, usually in people with weakened immune systems such as those having cancer chemotherapy/other immunosuppressant drugs, bone marrow transplantation, HIV, or other diseases of the immune system. Usually serious and, if untreated, can be fatal.
   • Fungal meningitis: Similar to #3, but the fungus/yeast spreads to the areas around the central nervous system (e.g. brain or spinal cord).

Common conditions that Mould Illness is associated with include:

• Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
• Fibromyalgia
• Multiple Chemical Sensitivity (MCS)
• Inflammatory Bowel Disease (IBD), Irritable Bowel Syndrome (IBS), SIBO, Leaky Gut (webinar)
• Alzheimer’s Disease (webinar)
• Mast Cell Activation Syndrome (MCAS) (webinar)
• Multiple Sclerosis (MS)
• Depression
• Post Traumatic Stress Disorder (PTSD)
• Allergies.

The VCS is a simple visual test used to screen patients to see if they are affected by biotoxins/toxicants, as these cause inflammation that results in hypoperfusion (lack of blood flow) throughout the optic nerve. The test measures your ability to distinguish between finer and finer increments of light versus dark (contrast).

Further details of the VCS test can be found on the Medical Testing page.

A summary of relevant blood markers are presented in the table below.

BIOMARKER	AUS LAB (NATA)	MEDICARE	FASTING	RANGE (Shoemaker)	NOTES
α-MSH	N/A			35-81 pg/mL
ACTH	Local lab	Y			Interpret with cortisol
Anti-gliadin antibodies	Local lab	Y		0-19 (IgA, IgM)	Sometimes elevated in CIRS
Anti-phospholipid antibodies	Local lab	Y		0-12 (IgA), 0-10 (IgG), 0-9 (IgM)	Sometimes elevated in CIRS
C4a	N/A			0-2830 ng/mL
Copectin (ADH surrogate marker)	Local lab -> RPA	N - Out of pocket cost varies		1.0-13.3 pg/mL	NSW Health Pathology page | Common pattern is low copeptin with high osmolality
Cortisol (AM)	Local lab	Y			Pattern can be low ACTH and low cortisol but sometimes high ACTH, high cortisol
DHEA	Local lab	Y			Sometimes low in CIRS
Estradiol	Local lab	Y			Sometimes high in CIRS
HLA DR/DQ	Sonic Group or NutriPATH	Y (66695)			Sonic page
Leptin	Local lab -> RPA	N - Out of pocket cost varies	Y	NR 2-5.6 ng/mL (M), 3.7-11.1 ng/mL (F)	NSW Health Pathology page
MMP-9	N/A			85-332 ng/mL
Serum Osmolality	Local lab	Y		280-300 mmol/kg	Interpret with ADH
Testosterone	Local lab	Y			Sometimes low in CIRS
TGF-β1	N/A			344-2380 pg/mL
VEGF	Local lab -> Peter MacCallum Cancer Centre	N - Out of pocket cost varies		31-86 pg/mL	Transport on ice / store refrigerated | Only performed infrequently
VIP	Local lab -> RPA	Y (71151)	Y	6.8-18.6 pmol/L	NSW Health Pathology page

See the Medical Testing page for in-depth information.

NutriPATH offers biotoxin/mould blood panels that test many of the core CIRS biomarkers. However, apart from HLA DR/DQ genetic testing and the MARCoNS nasal swab, these tests cannot be recommended at this time due to inaccuracies compared to US laboratories.

(These inaccuracies were discovered by Dr Sandeep Gupta, who compared biomarker testing from Quest Diagnostics against NutriPATH’s results. Ref: Mold Illness in Children webinar (35m) and Low Tox Life podcast episode 55.)

No other accurate Australian diagnostic testing for TGF-b1, C3a, C4a, MMP-9, and MSH is currently available. (However, testing for VIP and VEGF is available from other Australian pathologies.)

2.4.1 What is the HLA DR/DQ Genetic Test (a.k.a. Mould Genes)?

In unpublished research conducted by Dr Shoemaker of his 10,000-size patient population, approximately 25% of the general population have Human Leukocyte Antigen (HLA) genes that are mould, Lyme or multi-susceptible (i.e., susceptible to toxins from mould/WDB, Lyme, and dinoflagellates). Dr Shoemaker’s hypothesis is that when these genes are primed (see 2.4.5) and a person is exposed to a high level of toxins/toxicants from water-damaged buildings, the immune system does not make the appropriate antibodies to clear them due to a defect in antigen presentation, which creates a state of chronic inflammation and upregulation of the innate immune system.

Critically, this research has not yet been replicated. While there may be a role for the HLA system in antigen presentation of biotoxins, further research is needed to establish such a link.

Note: The HLA genes merely indicate a potential genetic susceptibility to CIRS and having them does not automatically mean you have/or will develop CIRS.

2.4.2 My partner/child has HLA-susceptible genes but they don’t get sick with exposure to water-damaged buildings. Why is this?

Dr Shoemaker found that HLA genes generally need to be primed by an inflammatory illness, or event, that causes a cytokine storm. Possible priming events include influenza, Coxsackie virus, Lyme disease, mononucleosis (Epstein Barr Virus/glandular fever), ECHO virus infections, intense inflammatory lung responses, and unusual conditions such as Kawasaki disease. (Berry, 2014, p14). In 2021 Shoemaker et al published a paper that a small cohort (n=21) of Post COVID Syndrome (a.k.a. Long COVID) patients shared proteomic (blood protein) similarities to CIRS patients.

However, if there is a great deal of inflammagens, biotoxins and toxicants in a water-damaged building that can be enough to prime the genes and cause CIRS by itself.

2.4.3 Getting the HLA gene test in Australia

Further details on how to get the HLA DR/DQ genetic test are on the Medical Testing page.

2.4.4 Does 23andme or similar genetic testing show these HLA genes?

No. 23andme does not show all the HLA haplotypes and not in a format that correlates to Dr Shoemaker’s table.

2.4.5 HLA susceptibility in other disease states

MAC staff have put together a Google spreadsheet that summarises many disease susceptibilities, and also disease protection, corresponding to Dr Shoemaker’s HLA haplotypes found in the scientific literature. Autoimmune conditions in particular are prevalent.

NeuroQuant® is a software program from Cortechs Labs that measures microscopic volumetric changes in defined areas of the brain from a magnetic resonance imaging (MRI) scan. Dr Shoemaker’s research found microscopic interstitial oedema, a.k.a. neuroinflammation, and atrophy, a.k.a. neuronal loss, in brain areas in two small studies (2014, 2017) of CIRS patients. Additionally, Professor Dale Bredesen also published a paper (2016) on a case series of patients suffering an early-onset form of cognitive decline he dubbed “Inhalational Alzheimer’s Disease”, which involved a subet of CIRS patients.

A limitation of volumetric MRIs is that it cannot show the volume of the brain before the illness. However, NeuroQuant can also be a tool to track inflammatory and atrophic changes at baseline and throughout treatment. Successful treatment can sometimes demonstrate the reversal of neurological atrophy.

Further details on obtaining a NeuroQuant scan are on the Medical Testing page.

Multiple Antibiotic Resistant Coagulase Negative Staphylococci (MARCoNS) are bacteria that colonise the nasopharynx area forming biofilms and creating exotoxins. The underlying research was based on studies associating membrane-damaging toxins from coagulase-negative staphylococci that colonised the sinuses with chronic orofacial muscle pain (1998).

MARCoNS form due to low levels of MSH in mucous membranes, which is antimicrobial and anti-inflammatory. MARCoNS can themselves further lower MSH levels. Dr Shoemaker reports MARCoNS colonisation in 80% of CIRS patients, although further research is needed to replicate these results.

See the Biotoxin pathway diagram to see how hormones and immunity are affected in CIRS.

• Berry, Y. (2014). A physician’s guide to understanding & treating biotoxin illness. Surviving Mold.
• Shoemaker R, Lipsey R. (2006). Results of health screening and visual contrast testing. St. Bernard’s Parish, Louisiana. Surviving Mold. Full-text
• Shoemaker R., McMahon S, Heyman, A., Lark, D, van der Westhuizen, M., & Ryan, J. (2021).Treatable metabolic and inflammatory abnormalities in Post COVID Syndrome (PCS) define the transcriptomic basis for persistent symptoms: Lessons from CIRS. Medical research archives, 9(7). https://doi.org/10.18103/mra.v9i7.2493

Two laboratories, Realtime (available via NutriPATH) and Mosaic (formally Great Plains, available via RN Labs) currently offer urine mycotoxin testing in Australia.

Realtime in their Mycotoxin panel use enzyme-linked immunosorbent assay (ELISA) technology while Mosaic in their MycoTOX profile use liquid chromatography tandem mass spectrometry (LC-MS/MS) technology.

See the Medical Testing page for more details, including research studies, on both of these tests.

Dr Shoemaker does not recommend these tests for a number of reasons:

1. Mycotoxins make up < 10% of the burden of inflammagens in a WDB.
2. These tests only look for one to two dozen mycotoxins when there have been four hundred discovered so far.
3. These tests are polyclonal and have never had specificity of their antibodies confirmed (Realtime test).
4. Urine mycotoxins are generally confounded by mycotoxin ingestion from common foods such as grains, corn, peanuts, tree nuts, chocolate and coffee.

See Dr Shoemaker 2015's Hopkinton Lecture (2:24:53. Thoughts on Realtime Labs) and Dr Joseph Brewer: Nasal fungi, anti-fungals and junk science.

Physician and researcher Dr Andrew Campbell believes mycotoxin antibodies in the blood are the best measure of the toxic burden from mould exposure.

His company MyMycolab provides testing of IgG and IgE antibodies of 12 different types of mycotoxins in blood serum. He believes the IgE response occurs when there is a large exposure to that particular mycotoxin, and has mast cell involvement, while IgG responses are indicative of lesser amounts of exposure. Unlike antibodies to mould spores mycotoxin antibodies are short lived and should reduce after 6 months of avoiding exposure.

Testing (USD $380) can be ordered and drawn by those in Australia and shipped back via FedEx.

See the Medical Testing page for more details, including research studies, on this test.

Mould allergy testing tests for an IgE allergic reaction to certain species of mould spores, usually a mould mix, and not mycotoxins. This is usually done via skin prick testing or blood RAST testing. This is a common test offered by most laboratories, covered by Medicare, and often the only mould-related test most GPs or allergists will know of and worth doing.

As stated previously mould allergy is an adaptive immune system antibody response and is different from CIRS which is a chronic innate immune system response. It is possible, but not that common, to have both mould allergy and CIRS.

ArminLabs in Germany, known for their Lyme (Borrelia) and co-infection testing also offer EliSpot testing for Aspergillus Peptide Mix 1 & 2. This tests for the cell-mediated, rather than the humoral (antibody), arm of the adaptive immune system.

Reducing or, ideally, eliminating exposure to mould and other biotoxins/toxicants from water-damaged buildings is the first step in any treatment protocol for any kind of mould-related illness. Before spending money on any other form of treatment, patients need to avoid the source of their illness. While this step is of paramount importance, it is often the most difficult, because places of residence (home), work, education (school, university), and even vehicles all need to be considered. These locations and vehicles will need to be either adequately remediated (which can be costly), or the patient will need to relocate to a safer environment or replace the vehicle.

Many Mould Illness patients develop an environmental sensitivity, whereby they react to even small amounts of biotoxins and toxicants in water-damaged buildings and vehicles. Some of the most extreme reactors often resort to camping in dry locations in tents, caravans (RVs), or converted trailers. Patients monitor how their symptoms fluctuate to deduce what locations or (potentially) even possessions are exacerbating their illness.

This form of extreme mould avoidance originated with Erik Johnson, who was a prototype for chronic fatigue syndrome during the original outbreak of the syndrome around Lake Tahoe, Nevada in the mid-1980s. Erik became largely symptom free with using extreme mould avoidance. For more on Erik’s story and mould-avoidance techniques, please read Back from the edge by Lisa Petrison (see resources).

The use of binding medications or supplements to adsorb mycotoxins and other toxins/toxicants in the intestines is suggested by most Mould Illness practitioners, except for Dr Andrew Campbell and those strictly following his protocol.

Side-effects

Binders can have some gastrointestinal (GI) side-effects such as constipation, gas, and acid reflux. Constipation can usually be ameliorated with magnesium citrate, vitamin C, and/or soluble fibre (chia seeds, flax seeds, and psyllium). Long-term use of binders can deplete fat soluble vitamins (A, E, D, K, CoQ10), so many practitioners suggest to supplement these, taking them at a different time of day to binder dosing.

How long do I stay on binders?

This is highly individualised but typically varies between three and twelve months. Duration of binder use is dependent on improvement in lab work, symptom reduction, and absence of exposure to further water-damaged buildings.

Some people stay on a lower maintenance dose of binders on a continual basis, or increase them short term when re-exposed to a water-damaged building (e.g., take a full dose for 3–7 days after exposure).

Worsening of symptoms (intensification reaction)

Dr Shoemaker hypothesised that binders, especially cholestyramine, can cause an intensification reaction (a general worsening of symptoms)—commonly but incorrectly referred to as herxing/herx—especially in Lyme patients. This is because as biotoxins detach from cell receptors, they can enter the bloodstream and cause a rise in inflammatory cytokines.

Symptoms will generally be exacerbated, along with a worsening of visual contrast sensitivity (in columns D and E). The protein biomarker MMP-9 will also increase.

Dr Shoemaker suggests an inflammatory-lowering mini-protocol using fish oil. Start at least ten days before starting cholestyramine. If symptoms intensify, either lower or stop the cholestyramine dose, and then follow the interventions below for 5–10 days before restarting.

• No-amylose diet:
  • A no-amylose diet enhances the effectiveness of Actos or fish oil.
    Amylose is found in most grains, vegetables grown below the ground (root vegetables), and bananas. Similar diets include low carbohydrate, grain free, paleo diets such as the Bulletproof diet, Wahls Diet, or Doug Kaufman’s Phase I diet for at least the duration of CSM treatment.
• High-dose fish oil:
  • High-dose fish oil can lower inflammatory cytokines and other inflammatory markers. Dr Shoemaker suggests a dose of fish oil where the daily total of EPA at least 2.4 grams per day and DHA is 1.8 grams for ten days, with cholestyramine started on day six. Many people stay on this high-dose fish oil for longer.

Two pharmaceutical binders are available by presciption only.

Cholestyramine (CSM)

Cholestyramine (CSM) is a sixty-year-old cholesterol lowering medication that has been extensively studied with a good safety profile. This negatively charged binding resin attracts positively charged toxins/toxicants from bile and excretes them in the faeces. It is not absorbed systemically but only passes through the gastrointestinal tract. CSM is available in Australia either as Questran Lite, which contains aspartame, or as a pure compounded version. The compounded version may contain stevia and various forms of cellulose, which are harmless excipients for most people. (See resources for compounding pharmacies.) The full dosage is four grams four times per day (QID), thirty minutes before meals/medications or one-two hours after meals/medications. Many clinicians suggest starting with a small dose (1–4 grams) and working your way up to the full dose.

CSM is the only binder tested in clinical trials in humans that demonstrates efficacy in lowering associated inflammatory biomarkers.

Colesevelam (Welchol)

Colesevelam (brand name Welchol) is a medication similar to CSM. It generally causes less GI side effects, and can be taken with food. It is the binder recommended by Dr. Shoemaker for sensitive patients who can’t tolerate CSM. One caveat is that colesevelam only has 25% of the binding capacity of CSM. Like CSM, colesevelam can only be obtained at a select number of compounding pharmacies in Australia. Dosage is two tablets (625mg) up to three times per day.

Non-systemic binders (these stay in the GI tract)

• Activated charcoal—A broad spectrum binder that has been used successfully in animal mycotoxin and endotoxin (bacterial toxin) studies. It can also bind pesticides and VOCs but may bind with nutrients so, as with CSM, activated charcoal is best taken away from other supplements and medications. Suggested dose: 500–1000mg, 2–4 times per day. Suggested brands: Bulletproof, Blants (powder form) and Nature’s Way. Caveat: it will cause darkening of stools.
• Chitosan—Similar in structure to CSM and Welchol, Chitosan has a similar effect to those medications of lowering cholesterol, but it may also have anti-microbial and anti-cancer properties. Caveat: Derived from shellfish. (1, 2, 3). Suggested dose: 500–1000mg, 2–4 times per day. Suggested brands: Now, Nutricology, and Natural Balance.
• Bentonite clay (aka montmorillonite)—Binds to mycotoxins (1, 2), bacterial toxins (1, 3), pesticides (1), and heavy metals (1). Suggested dose: 1–3 grams, 2–4 times per day. Suggested brands: Blants, also widely found on eBay (make sure it is marked for human consumption/internal use).
• Zeolite clay (aka clinoptilolite)—Similar to bentonite clay. Established as a mycotoxin binder in animal studies (1, 2, 3). Suggested dose: as per bentonite. Suggested brands: Vita Pure (LavaeVitae), Zeolith MED, Toxaprevent, ZeoBind (BioPure)

Systemic (these are absorbed into the blood stream)

• Nanoised zeolite—This is a form of  zeolite small enough to be absorbed into the blood stream and cells from the gut. As with normal zeolite, it is mainly thought of as a heavy metal chelator. (No peer reviewed studies are found for nanoised zeolite and chelation or binding; refer to zeolite research above.)
• Modified citrus pectin—A fibre from citrus peel that is known to bind to heavy metals (especially lead) and environmental toxins. It also has anti-cancer/anti-galectin 3 effects. Brands include Pectasol-C and Now (among others). (1, 2, 3, 4).
• Glutathione—The body’s master antioxidant. It can also aid in the detoxification of toxins including mycotoxins, and heavy metals. Gluthathione can be used in various forms including liposomal, intravenous, intranasal, N-acetylcysteine (a precursor) and L-glutathione.

Combination formulas

• Ultra Binder (Quicksilver Scientific)—This formulation combines bentonite clay, activated charcoal, chitosan, aloe vera, zerolite, and acacia gum.

• Shoemaker, R. C., & House, D. E. (2006). Sick building syndrome (SBS) and exposure to water-damaged buildings: time series study, clinical trial and mechanisms. Neurotoxicology and teratology, 28(5), 573-588. PMID 17010568
• Shade et al. (2018). A Push-Catch System That Enables Effective Detoxification. The Townsend letter, February/March 2018. Link.
• Huwig, A., Freimund, S., Käppeli, O., & Dutler, H. (2001).  Mycotoxin detoxication of animal feed by different adsorbents. Toxicol Lett, 122(2):179-88. PMID 11439224
• Wilson, T. (2017). Are you detoxing with the correct binders. Sophia Health Institute. Link.
• Rudd, C. (2024). The Binder Compendium. Google doc.

A popular treatment protocol for Mould Illness (CIRS) is the Shoemaker Protocol, named after its originator, researcher Dr Ritchie Shoemaker. This is an eleven-step protocol designed to restore immune homeostasis. Parts, but not all, of this protocol have been trialled in published studies on CIRS, unlike some other Mould Illness protocols.

According to the Shoemaker Protocol, after removal from mould exposure/WDBs and at least one month of binders, MARCoNS should be treated if tested positive.

• Current Recommended Treatment—EDTA plus colloidal silver nasal spray
  • If positive for MARCoNS, a patient will be begin a nasal spray of EDTA/colloidal silver nasal. EDTA helps break down the biofilm and the colloidal silver is an effective antimicrobial with some anti-biofilm activity as well. The duration of this treatment can be between one and several months.
• Past Treatments
  • Previously, BEG nasal spray was used which contained Bactroban, EDTA, and Gentamicin. With the increase of antibiotic resistant MARCoNS strains and studies done by Dr Joseph Musto of Microbiology DX showing the effectiveness of colloidal silver, the protocol has been changed.
• Alternative treatments
  • Neti pot or nasal spray of water with iodine or salt or xylitol (e.g. xyclear).
  • Colloidal silver nasal spray by itself may help.
  • Nebulised PVP-iodine may be effective according to Greg Muske of Biotoxin Journey. Read his detailed MARCoNS, More MARCoNS, and Even more MARCoNS blog posts for more details.
• Follow up testing
  • After one to several months of treatment, patiensts should repeat the MARCoNS test. If still positive, consult with your health practitioner for treatment options.

After removal from WDB exposure, pharmaceutical binders, and treatment of MARCoNS, patients will undertake a number of mid-level steps aimed at both reducing inflammatory biomarkers and restoring affected hormones to normative levels.

Vasoactive Intestinal Polypeptide (VIP) is a neuropeptide hormone that is predominately made in the hypothalamus. Along with MSH, VIP is critical in controlling inflammation and the immune system. In a 2013 study and in clinical practice, Dr Shoemaker found that VIP:

• Increased plasma VIP levels
• Reduced symptoms to the level of healthy controls
• Reduced inflammatory cytokines (TGF-b1, C4a, MMP-9)
• Increased VEGF
• Balanced Treg immunity
• Increased 25-Vitamin D levels
• Normalised low testosterone levels in Males
• Normalised high estradiol (estrogen) levels in Males
• Increased tolerance to water-damaged buildings

Intranasal VIP has also been shown in a small clinical trial and case studies to correct multinuclear atrophy of grey matter in the brain, although further research is needed to confirm these findings.

However, the caveat to VIP therapy is that if you’re still being exposed to biotoxins from water damaged buildings or MARCoNS,  then instead of reducing inflammation—such as TGF-b1 and C4a—VIP can potentially increase it. Thus, the following conditions must be met before using VIP spray.

• You live, work, and study in buildings with a HERTSMI-2 score of < 11
• You pass the VCS test
• You test negative for MARCoNS
• You have normal lipase levels.

My VIP level is normal, can I still benefit from VIP spray?

Yes. VIP has wide ranging effects apart from repleting VIP plasma levels. If you still have symptoms even with a normal VIP level, VIP may help.

For the fungal colonisation subtype the eradication or reduction of fungal and yeast colonies is usually recommended using herbal/natural and/or pharmaceutical antifungals. This may also involve biofilm eradication (biofilm busting) as these fungal/yeast colonies are often protected by biofilms.

Some protocols and doctors also aim to balance the nasal/sinus, oral, gut or skin microbiome(s) to improve a person’s external or internal microbiome terrain.

Removal from mycotoxin exposure is the the first step in the mycotoxin toxicity Mould Illness subtype. Either via removal from exposure to water-damaged buildings/vehicles and/or reduction of internal fungal colonisation.

Most practitioners, except for Dr Andrew Campbell, generally suggest that binding supplements/medications is then needed to bind (adsorb) mycotoxins in the GI tract after being released in the bile. See Part 4.3-4.5 above for more information on this.

Dr Shoemaker discourages the use of nasal antifungals for two main reasons:

1. The rates of fungal colonisation in the nasal passages in CIRS patients is the same as healthy controls
2. Anti-fungal use can cause antibiotic resistance to nasal bacteria such as MARCoNS as fungus and bacteria can transfer genes to one another.

See Dr. Joseph Brewer: Nasal fungi, anti-fungals and junk science.

There are several professions that inspect buildings for water damage and mould, who may also do sampling for mould/microbial growth including Building Biologists, ACAC certified inspectors, Mycologists/Microbiologists and Occupational (Industrial) Hygienists. The IICRC S520 Mold Remediation standard uses the umbrella term Indoor Environmental Professionals (IEPs) for these professions. These professionals are able identify the source and extent of water damage, moisture and, if necessary, amount and location of microbial growth via sampling. They can also determine the required scope of works to return the property to pre-event condition, and after remediation,  provide post-remediation verification. They may send mould samples to microbiologists or other laboratories for analysis and quantification.

Please see the Mould and Building Inspection page.

Yes, ideally. According to the IICRC S520 Standard for Professional Mold Remediation:

4.2.1 Assessment
When a preliminary determination indicates that mold contamination exists or is likely to exist, an assessment should be performed prior to starting remediation. An independent IEP who has no business affiliation with the remediator should be used for this purpose. In circumstances where an entire building or system is fully involved as a result of Condition 3 mold contamination or when the scope of work can be determined without sampling or independent IEP inspection and assessment, engagement of an IEP for assessment may not be necessary. Notwithstanding the foregoing, if health issues are discovered or apparent that seem to be related to the actual or suspected mold contamination, an IEP or other appropriate professional should be engaged by the property owner and the extent and Condition (1, 2 or 3) to which areas of the structure, systems and contents are potentially mold contaminated should be assessed, documented, and reported to the client.

Likewise according to the ACAC code of conduct:

Note on Conflicts of Interest:

The American Council for Accredited Certification strongly discourages its certificants from performing both assessment services and contracting services on the same project. Certificants who offer both services to the same client create a perceived conflict of interest regardless of their integrity. Nevertheless, as circumstances sometimes prevent the employment of multiple professionals on the same project, ACAC does not prohibit the practice, nor does ACAC make compliance with this policy a condition of continued certification.

MAC does not favor one group of professionals over another for the investigation and remediation of water damage and microbial growth in buildings. Neither can we personally vouch for any of the professionals on the Mould and Building Inspection page — do your own due diligence and research.

Yes, the international standard is the ANSI/IICRC S520 Standard for Professional Mold Remediation (Fourth edition, 2024).

Mould Illness/CIRS patients may need a higher level of remediation than the IICRC standard. The Surviving Mold protocol to achieve this level is outlined in Schrantz, et al. (2021).  Indoor Environmental Professional Panel of Surviving Mold Consensus Statement for Microbial Remediation 2020. Medical Research Archives, 9(1). https://doi.org/10.18103/mra.v9i1.2327

IICRC and ACAC also offer certifications in mould remediation.

Please see the Mould Remediators page.

Yes, ideally. See Part 7.3 of this FAQ.

Please see the Mould 101 – Preventing, Removing and Remediating page.