*Last edited: May 2021 by Eric Chan, ND

Mold Illness and Mycotoxin Illness

Mold toxicity is a very new, evolving science, and the diagnosis and treatment is still in its very early stages. Approaches and treatments differ from even a couple of years ago. Diagnostics and treatments evolve as new information and experience is acquired.

Some of the data from this approach apply to the extremely sensitive patients, such as those that have aggravations from single drops of medication.

Persistent inflammation has been linked to many illnesses, CFS, lyme, ME, etc. Mold toxicity can trigger mast cell activation, porphyrias, methylation dysfunction, and especially reactivation of viral, bacterial and parasitic infections. Especially important is the trigger of limbic system dysfunction, vagal nerve dysfunction - if these are not addressed first it is very difficult to help patients. The sequence as well as identification of factors to treat is very important.

New models are in development:

1) Cell danger response

2) Horowitz 16 point differential diagnostic map

3) Dr Bredesen 36 point ReCODE program (Alzheimer's)

4) Biotoxin pathway from Dr Shoemaker

There is no single treatment protocol though, no algorithm as each individual patient situation and chemistry is different.

What is Mold Toxicity?

"Mold" includes fungal organisms, actinomycetes, mycobacteria, VOC, beta glucans - a highly diverse antigenic stimulation and trigger for the immune system. Mycotoxins are one of the ones that are readily measurable. We should note that this is different from the concept of the usual mold "allergies" - but rather a toxicity. Roughly 25% of the population is sensitive to mold toxicity as they have difficulty processing the toxins. This leads to the development of the cell danger response.

Other molds do not affect us as much. Out of doors mold usually affects allergy. It is usually indoor molds that grow without competition that affect subsets of patients. In the outside world, the toxins that the molds make keep each of the other species in check, and thus most patients tolerate this well. Inside buildings, if there is no competition then the production of certain toxins can go unchecked and then affect patients.

These patients have inflammation and activation of innate and acquired immunity - in some patients you have to treat mold allergy and toxicity concurrently.

There are significant interactions between mold mycotoxin effects with lyme disease and viral infections, MCS, food allergies, mast cell activation, electromagnetic dysthymia / electromagenetic sensitivity - ie molds make many illnesses worse.

Symptoms of Mold Toxin Illness

Mold toxin symptoms are widespread: the inflammation crosses many systems in the body (which often leads patients to be told that they need an anti-depressant). Fatigue, weakness, especially lightning bolt sensations type of pain, joint pain, muscle pain, cognitive impairment, anxiety unrelated to stressors (eg a physical anxiety without a life trigger), depersonalization / derealization, depression, skin sensitivity, emotional lability, thermal lability, vertigo, dizziness, nausea, vomiting - and more. Mold toxicity may look like fibromyalgia, myalgic encephalitis also. The problem is that many of the symptoms, especially things like fatigue, can be caused by many conditions, but there are some keynote symptoms that make us consider mold.

Unique symptoms include electrical shocks, ice pick pains, non specific and central paresthesias (that may be related to autonomics), internal vibration / tremor, increased sensitivity / reactions due to limbic system involvement.

History taking would involve environmental history, including water damage history. Lab testing would include urine mycotoxin testing, visual contrast testing, and testing for biochemical / inflammatory markers such as TGF beta 1, c4a, MSH, VEGF, VIP, MMP9 - but these are not as specific and are markers for the inflammation. The mycotoxins found would dictate the type of treatment or binders being used for treatment. Usually the binding protocol should involve combinations to address each mycotoxin found.

Mold Toxin Testing

The mycotoxin testing is most useful. The positive test confirms the diagnosis. (Hooper et al). Mycotoxin testing can be done by ELISA testing at Realtime labs; mass spectrometry can be done by Great Plains Lab. Mass spectrometry only measures for what we are looking for, whereas ELISA can also cover metabolites of the toxins we are looking for.

In testing of mycotoxins, sometimes the sample is unprovoked (eg a first morning urine) and in other cases provocation can be useful for assessment. The toxins themselves can interfere with excretion into the urine, and thus in some cases provocation initially with glutathione for 7 days, and then some form of sauna / hot bath the evening prior to the first morning urine can be useful. For initial testing, if patients are on binders, these can be with-held. Of note - many patients can not tolerate any provocation especially with glutathione, as the mobilization is too much for the body to properly excrete. This can help the body to provoke toxins into the urine. We should also note that the first test is often the "tip of the iceberg" - and often on subsequent testing the levels increase since excretion capacity has improved. Thus - urine testing measures both the presence of toxins as well as the ability to excrete.

With repeat testing, higher results thus do not necessarily mean the patient is worse. While it can be re-exposure to molds, it can also be improved detoxification, and can also be excessive binding of toxin, and be excessive killing of mold. There can even be an issue of stimulating mold to make more mycotoxins. For example, charcoal adsorbs toxins as opposed to tightly binding toxins. If there is a toxin that is "loosely bound" then some of the toxins can then "fall off" later in the GI tract and become reabsorbed. Thus, the difficulties in treatment are related to finding the correct dose for an individual patient. Usually, if a patient has difficulties with the treatment, the proper thing is to reduce the dosage. Patients who can only tolerate small dosages actually respond very well to low dosages. The same will apply to the killing of mold - many patients can have colonization of mold in the airways as well as the GI tract. In many cases patients will have difficulty if any antimicrobials are given before the full binding protocol has been implemented. Stimulation of mold to make more toxins can occur (especially with gliotoxins) when mold is stressed, particularly with antifungals.

An easy way to distinguish between a second test showing higher mycotoxins being the result of improved detoxification vs an increase in toxicity is what the patient response is. If the patient is improving, it is not an issue. If the patient is getting worse then toxicity is a concern.

With regards to the testing, some have discussed that all patients have mycotoxins and thus testing is not useful. In one study of 103 mold patients versus 82 controls - showed that 51% of controls did have ochratoxins but the average amount in controls was 1.6, while the average in patients was 18. The other mycotoxins were trivial - only ochratoxin was a possible issue but was very quantity dependent.

A negative mycotoxin testing can mean that the patient is not mold toxic, but can also mean that detoxification is so compromised that excretion in the urine is not possible. It can also be that the testing is not measuring a particular mold toxin that is making them sick.

The other testing mentioned above, including the visual contrast sensitivity, inflammatory marker testing can be useful to follow, but it is not diagnostic of mold as other conditions likely contribute to the same abnormalities. Infection, lyme, bartonella, toxicity such as mercury and other heavy metals likely can affect this also.

MARCoNS can be useful but there is disagreement in terms of which patients seem to benefit from this. Some practitioners find that treatment is essential as the organism can cleave compounds such as MSH (important for the immune system) whereas others find treatment does not affect them.

Treatment of mold sensitive and mycotoxin patients is multi-step and multi-factorial.

Evaluation of the environment of the home, work and car is important as patients can improve in a toxic environment but it is very difficult to get them well. This is difficult due to the cost, as well as disagreement between experts on evaluation and remediation. Some inexpensive ways of testing the home include mold plates, where you open the plates from Immunolytics for example, let it sit for 2 hours, and then replace the top. The plates are evaluated for any significant growth over 3-5 days (usually growth happens after 3 days). Of note, it has to be analyzed as many of the molds are non toxic. An especially useful aspect of this test is that individual rooms can be evaluated.

ERMI (environmental relative moldiness index) is a dust related test - looking at 5 grams of dust in the house and then a lab such as Mycometrics can evaluate for fungal DNA.

Urine mycotoxin can then guide binder treatment as well as antifungal treatment.

Specific mycotoxins are affected by different binders. Ochratoxin is affected well by certain medications, while gliotoxin by NAC, charcoal, s boulardii.

Binders should be taken away from food and other supplements, but can be taken together once or twice a day. Many can do this around 3 in the afternoon, or at bedtime for other patients. Constipation with binders can be managed with oral magnesium as well as oral vitamin C. Patients with "inflamed brain" respond well to 50/50 mix of medium chain triglyceride and coconut oil but has to be dosed every 6-8 hours.

A dietary trial of foods that are lower in mold could be tried. There is some mold in dried fruit, aged, cheeses, coffee etc, but Dr Neil Nathan had recently done a study with 8 days where mold rich foods were completely avoided and urine levels of mycotoxins checked, and then after 10 days of markedly increasing consumption there was no increase in mycotoxins.

Antifungal approaches to mold and mycotoxin patients may or may not be applicable. Many respond to the binders alone, but some patients who have had mold exposure for a long period may need an antifungal component of treatment. A silver hydrosol / colloidal silver can be used nasally, and a product such as argentyn23 orally can be done. Other patients can tolerate stronger antifungal nasal spray often with agents for biofilm. For gut colonization, the argentyn23 at low dosage daily or oral antifungals can be useful. For very sensitive patients, dosing can often be given very infrequently depending on the agent selected.

Allergy can also be an important treatment, and desensitization in many is important. Glutathione can be useful, but may also be a signal to the body that production is adequate and can be stopped. Some patients use LDI with the patients own nasal washings, but it is not useful when a patient is very ill. Hormonal assessment can be very useful clinically as well - assessing for any thyroid or adrenal imbalances.

Pretreatment before giving binders is very helpful, including herbal medicine support for detoxification. Limbic retraining such as DNRS (Dynamic Neural Retraining System), and rebooting strategies for the vagus nerve can be very useful - and in some patients has to be done for 3-6 months even prior to binders.

I have also found ozone therapy to be very useful in treating the biochemical and immunological changes associated with mold and mycotoxins.

Other Concurrent Factors and Illnesses in Mold and Mycotoxin Illness

Mold is often the first starting point in many patients who have comorbid diagnoses - with lyme being one common example. Mycotoxins can be a roadblock for other treatments being effective as well.

Mast cell activation is a very important component of treatment often. Even the connection from the vagus nerve and autonomics can affect mast cell activation - leading to an issue with persistent inflammation. There are many mediators released from mast cells, not limited to histamine and tryptase, though these can be measured more readily. Mast cell activation should be a consideration if symptoms from foods / drinks come within a few minutes to 15 minutes come on. Treatment can also be done empirically and often starts with quercetin 30 min prior to meals alongside DAO, mirica, antihistamines

In summary, the treatment of mold and mycotoxin associated illness is complex and the patients are generally quite sensitive to treatment as well. There is no one protocol that suits all, though a multi-factorial investigation and treatment approach is generally the rule rather than the exception.

Much of this summary comes from personal experience in treating such patients; the literature that is published on mycotoxin associated illness that is relevant in our patient cohort is new, contradictory, and is helping to revise treatment as time goes on. Dr Neil Nathan MD, has written an excellent book “Toxic” which is written in accessible language for most patients. Much of the approach described on this page has been presented by Dr Nathan at various conferences from which notes comprise the data on this page.

Selected references are below:

Recent Advances in Our Understanding of Mast Cell Activation - Or Should It Be Mast Cell Mediator Disorders? Theoharis C Theoharides, Irene Tsilioni, Huali Ren Expert Rev Clin Immunol. 2019 June ; 15(6): 639–656

Detection of Mycotoxins in Patients with Chronic Fatigue Syndrome. Joseph H. Brewer, Jack D. Thrasher, David C. Straus, Roberta A. Madison, Dennis HooperToxins (Basel) 2013 Apr; 5(4): 605–617

A Review of the Mechanism of Injury and Treatment Approaches for Illness Resulting from Exposure to Water-Damaged Buildings, Mold, and Mycotoxins. Janette Hope. ScientificWorldJournal. 2013; 2013: 767482

Nutritional supplementation and dietary restriction in the resolution of enthesitis-related arthritis. Stephen J Genuis, Anna-Kristen J Siy. JRSM Short Rep. 2011 Apr; 2(4): 32.

A Water-Damaged Home and Health of Occupants: A Case Study Jack Dwayne Thrasher, Michael R. Gray, Kaye H. Kilburn, Donald P. Dennis, Archie Yu J Environ Public Health. 2012; 2012: 312836.

Toxic effects of mycotoxins in humans. M. Peraica, B. Radić, A. Lucić, M. Pavlović Bull World Health Organ. 1999; 77(9): 754–766.

How Much Should We Involve Genetic and Environmental Factors in the Risk Assessment of Mycotoxins in Humans? Edmond E. Creppy, Serge Moukha, Hassen Bacha, Maria Rosaria Carratu Int J Environ Res Public Health. 2005 May; 2(1): 186–193.