Week of February 26, 2024

1/ Success rate of remediation

QUESTION: Do you have a sense of what proportion of your patients are unable to bring their ERMI/HERTSM/-2 scores to safe levels despite thorough cleaning, removal of contaminated building materials, and correction of moisture problems by a quality remediation company following IICRC 5520 guidelines? I ask because some of the mold docs in my area say that in addition to remediation, their patients often need to have HEPA systems installed and fogging to bring levels down enough.

ANSWER: I have not analyzed proportion of patients that cannot clean their homes. At one time I use to say that failed remediation was one word, meaning that cleaning never worked.

Having said that, strict attention to precise detail is required to clean. Fogging alone has no role to help rehabilitate homes. Think about it. Say you have some magical fog that kills all bacteria, fungi and actinomycetes with a single application (there is no such

product for sale). What will that action do to the fragments of fungi or bacteria? Nothing.

Where does the problem with WDB come from? Fragments by about 500 to 1. What possible logic supports trying to kill what isn't alive and then not cleaning compulsively?

We are looking at the need to clean down to computer room level safety for those who have HLA susceptibility. Trying to kill chemicals that are not alive is not logical.

2/ Sudden onset of severe symptoms

QUESTION: I had an exposure that resulted in severe abdominal pain and cramping with fast heart rate and profuse sweating. The illness onset caused me to pass out. Since then I have had a cough. My illness duration is now 13 years. I have severe weakness in

my quadriceps that has put me in a wheel chair though I sometimes can use two canes to move about. Could this be mold illness?

ANSWER: This is the kind of tragic case that demands every bit of clinical skill from the attending physician. The differential diagnosis for cough and severe weakness includes mold as well as many other different illness parameters. While the HLA that you showed me is

indeed mold susceptible (13-6-52A; 13-6-52C) there is far more in diagnosis than just HLA. If you have been sickened by exposure to water-damaged buildings for 13 years, it is more likely than not that you would have multiple disturbances in the chronic inflammatory response system such that laboratory parameters will help you understand your illness better.

Profound severe weakness that has resulted in becoming wheelchair-bound raises the issue of upper motor neuron disorders and must be ruled out. I trust that your physician has discussed this rather ominous possibility with you.

3/ Supplements

QUESTION: What supplements do you recommend people use on a daily bases?

ANSWER: I recommend that supplements that are shown to be beneficial be used. What I mean by this is that it is not unusual to see people taking anywhere from 10-60 different preparations every day but without any confirmation of benefit or known adverse interaction.

For people with untreated inflammatory responses that underlie their illness I recommend that the treatment protocols be applied. If at the end of the inflammatory response protocols a patient wishes to take supplements then I would recommend one supplement be taken one at a time for approximately two weeks to assess benefit. If there is no benefit I would not continue use of the supplement. If there is benefit I would then stop the supplement for two weeks to see if the benefit is lost. If that is the case I would restart the supplement and then use a similar approach to supplement 2, 3 and 4 for as many different products as many people might like.

Most commonly used supplements that have documented benefit include a daily vitamin that contains fat soluble vitamins A, D, E and K; Co Q10 and the omega 3 fatty acid preparations.

4/ Supplements to correct hair loss

QUESTION: I have suffered severe hair loss as what I think is due to the “ochratoxin dance” in my body. What supplements can I take to control hair loss?

ANSWER: I am not sure how the diagnosis of ochratoxin-induced injury is made as the causative agent in your case. The case definition includes the potential for exposure to an interior environment of a water-damaged building together with the presence of (i) a multisymptom, multisystem illness and (ii) typical labs found in published peer-reviewed papers. You may find the papers listed on the Surviving Mold website of use to you to see if your case meets published criteria.

Severe hair loss can be due to an injury from inflammation to the hair follicles. Growing hairs are called “anagen” hairs; hairs that are temporarily resting are called “telogen” hairs; and hair follicles that have stopped growing and may actually be dead are called

“catagen” hairs. We know that TGF beta-1 is highly associated with development of catagen hairs. So called alopecia universalis is due to rising levels of TGF beta-1.

There are no supplements to correct TGF beta-1 reported in any peer-reviewed literature or supported by any anecdotal data that I have collected. Reduction of TGF beta-1 is one of the most important steps of the treatment protocol. This protocol should be discussed

with your attending physician. It is available for review in the paper published in Health; it has been on this website since March, 2013.

5/ Serotonin, melatonin, dopamine

QUESTION: I am trying to see if there is a connection between mold exposure and low serotonin. Any insight in the connection between mold and serotonin and other neurotransmitters is appreciated.

ANSWER: The reason that we use drugs like serotonin reuptake inhibitors to treat depression is simple: taking serotonin by mouth will not result in increasing serotonin in the brain. Serotonin just does not cross the blood brain barrier. Similarly, orally administered melatonin does not cross the blood brain barrier. Many people have undeniably felt improvement with melatonin, using it to treat insomnia and jet lag, among other problems. I don’t argue with their reported improvement but would look towards documented answers. If someone can show (even in lab animals) that melatonin and serotonin can be given orally resulting in measurable changes in brain chemistry I think they will make a lot of people happier. Having said that, we know that in inflammatory conditions the blood brain barrier becomes more permeable (leaky) letting a variety of compounds traverse the normally “solid” blood brain barrier. Brain inflammation is enhanced in the presence of peripheral inflammation. I am fond of speculation and conjecture regarding use of neurotransmitters orally (or parenterally) in treatment of central nervous system diseases. Such speculation does not translate into testable hypotheses given our lack of knowledge of correction of neurotransmission with anything other than the medications that we use now. A notable example is Parkinson’s disease where dopamine deficiency is treated with a variety of medications to increase dopamine centrally. The atrophy of the caudate nucleus, one of the hallmarks of the mold fingerprint that we can see in the central nervous system using NeuroQuant, does suggest that there is a direct impact of mold on dopaminergic pathways. This is a hot item for research and I feel additional information will be forthcoming in peer-reviewed literature. Until we have good data I would suggest extreme caution relying on anecdotal-based opinions regarding treatment of central nervous system disease.

6/ “Sicker-quicker”

QUESTION: What is the biological mechanism involved with acceleration of CIRS to which you have given the jargon term “sicker, quicker?”

ANSWER: The enzyme that makes C4a is abbreviated as MASP-2. This particular receptor-based enzyme is important in activation of the complement cascade. There is a variety of sugar compounds that will activate this receptor provided the particular sugar moiety can be detected by the receptor. Both mannose and ficolin sugars will activate this receptor as will particular toxins too. Importantly, in mutations of fungal species acquired during the time in which benomyl was widely used as a fungicide there is good reason to suspect that the particular mutants are now ones that activate MASP-2 but the parents did not. Whether benomyl is the problem or not, however, has never been proven. The chapter in Surviving Mold on benomyl has a lot of information on this topic. Nonetheless, the marker for a mutant created by benomyl exposure is found in the beta tubulin-1 compound. The genes for beta tubulin-1 are liked to the genes that move a methyl- or acetyl-group from inside the hydrophobic area of a mycotoxin to outside the hydrophobic area such that now this structure will be recognized by ficolins. This movement of structures provides for fascinating speculation as to the emergence of inflammation related to exposure to mycotoxins following a man-made intervention and not a long term function of mycotoxins themselves. Once there is activation of ficolins, the MASP-2 develops the ability to autoactivate. We don’t see autoactivation in most people but those who have it will suffer from rapidly rising C4a after trivial exposures.

7/ Sicker-quicker, treatment

QUESTION: What can be done to down regulate MASP-2?

ANSWER: Ongoing removal from exposure is critical to accomplish this task. The use of VIP for extended periods of time certainly down regulates MASP-2. Whether that benefit is on a genomic basis or not is not clear at this time. Also treatment with erythropoietin in doses that require significant informed consent will be effective.