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Symptoms of mold and mycotoxins

Hello Everyone,

Welcome back to the RTL blog.  In today’s blog I will discuss common bodily damage that is associated with mold infections and mycotoxin exposure.

Because of genetic and environmental variation symptoms and damage can be quite different from person to person.  I have done thousands of consults with both patients and practitioners dealing with various types of mold and mycotoxin exposure.  Because of the variability of symptoms (even within the same family) mold and mycotoxin exposure can often go undiagnosed.  Common symptoms that can arise could be fatigue, headaches, poor memory, abdominal pain, vertigo, etc.

Even more problematic is that many practitioners are not aware that mycotoxins can cause many different types of ailments and can contribute to many different chronic illnesses.  I am going to focus on the major areas of problems.  In later blogs I will give more details on how mycotoxins affect these systems and what can be done to alleviate symptoms and reverse damage.  The bodily systems that are most affected are:  immune system, nervous system/brain, and gut. 

Through my studies and experience I have learned that most of the toxic mycotoxins effect the immune system in some way. Mycotoxins have even been commercialized  by the pharmaceutical industry as a immunosuppressant medication (CellCept and Myfortic), which can be used to prevent organ donation rejection and treat lupus, rheumatoid arthritis, and other autoimmune diseases (1). Many other mycotoxins can cause immune suppression such as gliotoxin, aflatoxin, and trichothecenes (2-4).  This suppression of the immune system can lead to other infections including bacterial, viral, and fungal.  These infections can occur throughout the body but are especially localized in the gut and respiratory tract (common spots of mold colonization) (5).  These infections can make the diagnosis of mold and mycotoxins even harder to pin down, because practitioners are distracted by these infections and don’t know to dig deeper for underlying causes.  I frequently consult with practitioners whose patients have had multiple cases of bacterial or fungal overgrowth before finding out the underlying problem of mycotoxins.  I suspect, however with no data to substantiate, that a significant amount of Lyme patients have significant mycotoxins.  It is my hypothesis that if we measured mycotoxins in a large population of Lyme patients, they would have higher amounts than the general public.  It is these higher amounts of mycotoxins that allow for the overgrowth of the pathogenic bacteria. 

Unfortunately, immune suppression is not the only immune response caused by mold and mycotoxins.  The immune system can be sent on an out of control cascade when mold and mycotoxins exposure increases circulating plasma chemokine and cytokine levels (6).  These reactions can be triggered by both allergen dependent and independent mechanisms (7).  Inflammation can lead to many of the symptoms associated with mold and mycotoxin exposure.  Some of the most important symptoms are associated with the respiratory tract.   Mold exposure has been linked to a nine-fold increase in emergency room visits among asthmatics (8).  These phenomena are tied to alterations in inflammatory system pathways.  Data indicate that several cytokines are elevated when patients are exposed to mold and mycotoxins.  These include IL-17, IL-10, TGF-α, and MIP-1β (6).  This inflammation has been referred to as CIRS (Chronic Inflammatory Response Syndrome). 

Probably the most common symptoms that drive patients to seek medical help when it involves mold exposure have to pertain to neurological symptoms.  Recent studies have tied exposure to mold and mycotoxins to many different types of neurological problems.  Some of the more common ones are headaches, migraines, Parkinson’s, multiple sclerosis, and Alzheimer’s (9-12).  However, this is nowhere near a complete list.  Many of these diseases have been tied to inflammation.  Mycotoxins trigger multiple different pathways which can lead to induced apoptosis. T-2 and trichothecenes enter cells and trigger expression of MEKK1 and c-jun and the downregulation of Nrf2(13, 14).  These changes will lead to increased oxidative stress and decreased detoxification.  Ochratoxin (OTA) has a much more complex method for damaging neuronal cells.  Multiple papers have given results that show a mixture of oxidative stress, inhibition of protein synthesis, and OTA induced DNA breaks can lead to damage to the neuronal system (15, 16).  As disconcerting as these results are, there is a lot of hope in the newest research.  There are now studies that have shown that neurological decline can be reversed if the toxin source can be located and treatment is performed (17). 

Last, I will briefly touch upon how mycotoxins affect the gut.  I won’t spend too much time on this subject because I want to do more justice to it in a later blog post.  The take home message is that gut issues are a common hallmark of mold and mycotoxin exposure.  I frequently consult with practitioners and their patients that suffer from leaky gut and increased food sensitivities.  Patients having frequent gut pain should look into mold allergy and mycotoxin testing.

I hope this blog helped you determine if your problems might stem from exposure to mold and mycotoxins. These issues can linger for years, and I know from talking to and testing thousands of individuals that these problems aren’t in your head, and we can help you find solutions to your problems. 

Note: The views in this blog are those of Dr. Pratt-Hyatt and not necessarily the views of RealTime Labs.

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2.         S. Konig et al., Gliotoxin from Aspergillus fumigatus Abrogates Leukotriene B4 Formation through Inhibition of Leukotriene A4 Hydrolase. Cell Chem Biol 26, 524-534 e525 (2019).

3.         Y. Jiang et al., Aflatoxin-related immune dysfunction in health and in human immunodeficiency virus disease. Clin Dev Immunol 2008, 790309 (2008).

4.         Q. Wu et al., Immune Evasion, a Potential Mechanism of Trichothecenes: New Insights into Negative Immune Regulations. Int J Mol Sci 19 (2018).

5.         W. P. Liew, S. Mohd-Redzwan, Mycotoxin: Its Impact on Gut Health and Microbiota. Front Cell Infect Microbiol 8, 60 (2018).

6.          J. H. Rosenblum Lichtenstein et al., Environmental mold growth and mycotoxin exposures elicit specific cytokine and chemokine responses. PLoS One 10, e0126926 (2015).

7.         M. Flamant-Hulin, I. Annesi-Maesano, D. Caillaud, Relationships between molds and asthma suggesting non-allergic mechanisms. A rural-urban comparison. Pediatr Allergy Immunol 24, 345-351 (2013).

8.         J. Blatter et al., Fungal exposure, atopy, and asthma exacerbations in Puerto Rican children. Ann Am Thorac Soc 11, 925-932 (2014).

9.         A. A. Inamdar et al., Fungal-derived semiochemical 1-octen-3-ol disrupts dopamine packaging and causes neurodegeneration. Proc Natl Acad Sci U S A 110, 19561-19566 (2013).

10.       L. D. Empting, Neurologic and neuropsychiatric syndrome features of mold poisoning and mycotoxin exposure. Toxicol Ind Health 25, 577-581 (2009).

11.       C. B. Purzycki, D. H. Shain, Fungal toxins and multiple sclerosis: a compelling connection. Brain Res Bull 82, 4-6 (2010).

12.       A. M. Ratnaseelan, I. Tsilioni, T. C. Theoharides, Effects of Mycotoxins on Neuropsychiatric Symptoms and Immune Processes. Clin Ther 40, 903-917 (2018).

13.       S. Sehata et al., Morphological and microarray analysis of T-2 toxin-induced rat fetal brain lesion. Food Chem Toxicol 42, 1727-1736 (2004).

14.       M. Chaudhary, P. V. Rao, Brain oxidative stress after dermal and subcutaneous exposure of T-2 toxin in mice. Food Chem Toxicol 48, 3436-3442 (2010).

15.       V. Sava, O. Reunova, A. Velasquez, R. Harbison, J. Sanchez-Ramos, Acute neurotoxic effects of the fungal metabolite ochratoxin-A. Neurotoxicology 27, 82-92 (2006).

16.       G. Dirheimer, E. E. Creppy, Mechanism of action of ochratoxin A. IARC Sci Publ, 171-186 (1991).

17.       D. E. Bredesen et al., Reversal of cognitive decline in Alzheimer’s disease. Aging (Albany NY) 8, 1250-1258 (2016).