Mold, Mycotoxins, Anti-fungal treatment, Urine test/mycotoxins, Water damaged buildings/treatment

Response to Moldy Buildings, CIRS, Sick People and Damaged Brains

Matthew Pratt-Hyatt, PhD, and William Shaw, PhD

The latest research is proving that mold mycotoxin exposure is a silent epidemic across much of the developed world. The reasons behind the increase in mold mycotoxin exposure and its increased pathogenicity are complex and beyond the scope of this letter, but the amount of research going into mycotoxins is immense. Since the year 2000 there have been over 22,000 articles on mycotoxins according to PubMed. Since expanding our environmental toxicant testing platform, we have endeavored to increase the field of research into how environmental toxicants cause injury by collaborating with multiple academic institutions. We have tested over 150,000 samples with various types of environmental toxicants, which have been shown to be underlying contributors to multiple chronic illnesses.

We are writing this letter in response to Dr. Shoemaker’s five-part article seen last year in the Townsend Letter. While we greatly respect and appreciate Dr. Shoemaker’s contributions to understanding and treating patients with water-damaged building syndrome, we respectfully wish to refute three points that he claims in his article: 1.) Dr. Shoemaker states “we find scores of papers regarding healthy people with markedly abnormal levels of mycotoxins in urine.” 2.) Dr. Shoemaker downplays the need for anti-fungal therapy to treat mold exposure. 3.) Throughout the five articles Dr. Shoemaker advocates the need for expensive testing for genetic and chronic inflammatory response (CIR) markers. We advocate the need to find the underlying causes of mold-related illnesses, eliminate the mycotoxins derived from mold, and alleviate the cell danger response for proper treatment.

In part three of the series Dr. Shoemaker states “there is no published control group data (PubMed 4/9/2019) showing absence or simply a paucity of mycotoxins in urine in controls compared to cases.” Even though we had not published our results by the time of Shoemaker’s publication, our Townsend Letter article, “Biochemical Markers in the Urine Associated with Gastrointestinal Mold Overgrowth Are Associated with Elevated Urinary Mycotoxins in Patients with Suspected Mold Illness” shows that patients exposed to mold have significantly higher amounts of mycotoxins compared to healthy controls.¹ In addition, multiple papers had been previously published that demonstrate that mold exposed patients have higher values than controls.^2-4 Without any citations by Shoemaker to back up his claim that normal individuals have elevated mycotoxins, it is possible that he is referring to the background amounts in the urine of normal people from exposure to mold in food sources or outside air. Such exposures may be especially common for mycotoxins such as ochratoxin, fumonisins, and deoxynivalenol.⁵ However, from our published data we see a 23-fold increase in urine levels of aflatoxin M1, an 11-fold increase in urine levels of ochratoxin A, and a 38-fold increase in urine levels of sterigmatocystin in mold-exposed patients compared to controls.¹ These data indicate that mycotoxins are significantly elevated in patients that are exposed to water-damaged buildings.

In the first and third parts of the series Dr. Shoemaker argues against the importance of determining fungal infections and treatment in dealing with water-damaged buildings. His one point of evidence is a single study in Germany from 2003 which came to the conclusion that “Positive fungal cultures from nasal secretions have to be considered normal findings.”⁶ However, utilizing this one study simply ignores more recent studies which contradict this finding. One of the best recent findings was done by Joseph Brewer, which found multiple species of mold producing mycotoxins in chronically ill patients; but none in healthy controls.² In another study using an advanced DNA platform, the authors were able to determine that several species of Aspergillus were in significantly higher amounts in ethmoidal sinusitis compared to healthy controls.⁷ Shaw et al’s study on autism,⁸ published nearly 20 years ago, showed much higher amounts of mold metabolites in urine samples of children with autism compared to normal control children; these mold markers decreased significantly after treatment with the anti-fungal drug nystatin, together with reduced autistic symptoms. The reduction of these metabolites by a drug that is not absorbed from the intestinal tract indicated a colonization of the intestinal tract by mold that would not have resolved without antifungal treatment. In addition, a very recent study confirmed that autistic children have a high prevalence of Aspergillus fumigatus in blood samples compared to healthy controls.

Our own data demonstrates that, using an organic acids test, we can determine if a patient is colonized with either Fusarium or Aspergillus. Using the markers 5-hydroxymethyl-2-furoic acid, furan-2,5,-dicarboxylic acid, and tricarballylic we were able to determine which patients are more likely to have high mycotoxins. Patients with these values had elevated mycotoxins over 97% of the time.¹ In addition, using antifungals has been shown to be an integral part of treatment. Colonized patients could linger for years and rarely get better without antifungal treatment. After discussing treatment with hundreds of doctors and attending the International Society for Environmental Acquired Illness (ISEAI) conference, we believe it is a necessary part of treatment to check for colonization and to provide antifungals when necessary. Obviously, practitioners should be careful to only provide it when warranted to help prevent an increase in anti-fungal resistant species, but the agricultural use of anti-fungals is much more a driver of this phenomenon than medical use.⁹

The last point that we wish to make is to advocate against doing multiple tests to diagnose a chronic inflammatory response syndrome (CIRS). Many of the genes and cytokines upregulated in this pathway are very promiscuous and will be upregulated by a variety of stimuli. Some of these things include metals, pesticides, traumatic brain injury, and mycotoxins.^10-13 It seems better for the patient that practitioners determine the cause of upregulation rather than prove that upregulation exists. There seems to be at least three main parts of treatment that need to be followed: 1.) Identify if there is an environmental source of mold and, if there is, remove it. 2.) Assist in detoxification. 3.) Assist the body in eliminating the cell danger response.¹⁴ Treatment that assists in identifying and assisting with these aspects will provide the most personalized and effective treatment for the patient.

References

1. Pratt-Hyatt M, et al. Biochemical markers in the urine associated with gastrointestinal mold overgrowth are associated with elevated urinary mycotoxins in patients with suspected mold illness. Townsend Letter. 2019;436.

2. Brewer JH, Thrasher JD, Hooper D. Chronic illness associated with mold and mycotoxins: is naso-sinus fungal biofilm the culprit? Toxins (Basel). 2013; 6 (1): 66-80.

3. Brewer JH, et al. Detection of mycotoxins in patients with chronic fatigue syndrome. Toxins (Basel). 2013;5(4): 605-17.

4. De Santis B, et al. Study on the Association among Mycotoxins and other Variables in Children with Autism. Toxins (Basel.) 2017;9 (7).

5. Alshannaq A, Yu JH. Occurrence, Toxicity, and Analysis of Major Mycotoxins in Food. Int J Environ Res Public Health. 2017;14 (6).

6. Braun H, et al. [Incidence and detection of fungi and eosinophilic granulocytes in chronic rhinosinusitis]. Laryngorhinootologie. 2003; 82 (5): 330-40.

7. Zhang J, et al. Distinguishing the dominant species of pathogen in ethmoidal sinusitis by sequencing DNA dataset analysis. Exp Ther Med. 2018;16 (5),:4207-4212.

8. Shaw W, Kassen E, Chaves E., Assessment of antifungal drug therapy in autism by measurement of suspected microbial metabolites in urine with gas chromatography-mass spectrometry. Clinical Practice of Alternative Medicine. 2000;15-26.

9. Revie NM, et al. Antifungal drug resistance: evolution, mechanisms and impact. Curr Opin Microbiol. 2018; 45: 70-76.

10. Yang L, et al. Transcriptome profiling of malignant transformed rat hepatic stem-like cells by aflatoxin B1. Neoplasma. 2014; 61(2):193-204.

11. Martin TJ, Whalen MM. Exposures to the environmental toxicants pentachlorophenol (PCP) and dichlorodiphenyltrichloroethane (DDT) modify secretion of interleukin 1-beta (IL-1beta) from human immune cells. Arch Toxicol. 2017; 91(4): 1795-1808.

12. Kerr N, et al. Inflammasome proteins as biomarkers of traumatic brain injury. PLoS One. 2018;13(12): e0210128.

13. Marth E, et al. The effect of heavy metals on the immune system at low concentrations. Int J Occup Med Environ Health. 2001; 14(4): 375-86.

14. Naviaux RK. Metabolic features and regulation of the healing cycle-A new model for chronic disease pathogenesis and treatment. Mitochondrion. 2019;46: 278-297.