Reviewing and Summarizing the recent Toxic Mold Summit Session by Dr. Amy Myers. Part 2 of 3
(Read this blog series’ introduction at end if you are catching up)
From the discussion of leaky gut, Dr. Myers bridges into how mold toxicity contributes to autoimmunity through multiple possible mechanisms. Like other toxins, mycotoxins likely work through direct effects on the immune system and through influencing the intestinal barriers directly. Through Dr. Shoemaker’s work, we know that mycotoxins disrupt the complement system (C4a test elevation) and the cytokine (TGF-Beta 1) pathway. We also know that patients with mold toxicity express a susceptibility to other chronic infections like EBV, yeast, and Lyme. Simultaneously, the immune system is upregulated and downregulated. Dysregulation would be the appropriate term as both immunosuppression leading to infections and hyper-activation leading to autoimmunity occur. On the autoimmune from we see elevated ANA’s (anti-nuclear antibodies associated with lupus and other autoimmune diseases), elevated antibodies against gluten, and anti-cardiolipin antibodies against our own lipids.
Besides the direct immune dysregulation, we see more food sensitivities in terms of clinical symptoms and measurable food antibodies. The presence of mold toxins is known to disrupt the intestinal barrier (……….). With this open border policy, protein antigens (antigens, meaning anything to which the immune system reacts) which would normally stay inside the intestinal lumen, now enter the prohibited areas where the immune system ramps up to prevent their further progress. Should the immune system to one of these food proteins cross react with one of our own proteins, an autoimmune process can ensue. Combine this cross-reactivity with the dysregulated immune system noted earlier and a recipe for autoimmune disaster may result in over disease.
Another point on which she elaborated was genetics and how some people have no apparent effect from mold exposure or even relatively high levels of mold toxins in their bodies. We see this in our patient’s families. We have several families in which both parents and children share in the toxicity, yet even in these families, we usually see each member affected differently. One may gain 30 pounds while another drops to 90 pounds. One may need to sleep all the time while the other cannot sleep more than 3 hours per night. Adults and children definitely respond differently (read my review of Dr. Shetreat’s presentation for more on these differences). However, in many families, only one or 2 family members suffer while others, especially spouses wonder what is the big deal about mold. Genetics is the obvious deeper answer, but recognizing how different two individual’s response can be to mold is important. A toxic patient may release no mold toxin into their urine on testing yet their immune system, hormones, and nervous system are off the charts in reactivity. A non-toxic patient may pump out high levels in their urine test, yet have neither symptoms nor lab changes of mold toxicity.
While we agree 100% with how different people respond differently to mold toxins, we do believe testing genetics provides useful information for diagnosis and treatment. We agree with Dr. Shoemaker that an appropriate diagnosis includes performing HLA genetic testing to see if the patient sitting in our office is predisposed to poor toxin elimination. We understand that this test adds to the cost of therapy, but this adds to several aspects of mold toxicity treatment. First, only rarely are mold toxic patients with good mold detox genetics found on testing. Other unknown genetic factors likely contribute. Before we embark on the cost and effort of detoxing mold from a patient’s life, having the genetics as a confirmation is goof for both doctor and patient. Second, when parents inevitably ask about their children’s potential for mold toxicity, we can answer their questions more definitively. Third, should we need to address a patient’s work environment, we can objectively state that our patient possesses genetics making them more likely to suffer from mold in their work environment. Finally, for our patients with HLA genetics indicating a predisposition to post-Lyme syndrome, we can sometimes focus more on Lyme therapy than worrying about mold in their home or work environments. In the end, we always want to make the most of a patient’s testing budget. The HLA genetics is nearly always worth the expense.
Return soon for Part 3 including the “Take Home Points”.
Until then … Thanks to those who collaborated and contributed to the Toxic Mold Summit. While I have a few nuanced different opinions here and there, the information one can glean from listening to this summit is empowering for those facing this disease. While some are able to handle the recovery process without formal care by a medical provider, I do believe it is wise for most to have a “trusted guide” of some sort who stands outside the tornado of active mold toxicity. Standing inside the mold tornado leaves one with a spinning sense of direction. Having a stable and fixed point of reference in a knowledgeable guide serves you well. Traveling the road to recovery is better done with someone who has walked it before. That is what we try to do at Sanctuary: working to restore healthier more abundant lives even after the tornado of mold toxicity.
To order the Summit from our affiliate link, click here (we receive a commission for this purchase): https://toxicmoldproject.com/order/?idev_id=25016
REFERENCES
A few academic resources supporting the blogs statements.
Mold and gut
Liew, Winnie-Pui-Pui and Sabran Mohd-Redzwan. “Mycotoxin: Its Impact on Gut Health and Microbiota” Frontiers in cellular and infection microbiology vol. 8 60. 26 Feb. 2018, doi:10.3389/fcimb.2018.00060
J. Toxicol Environ Health B Crit Rev. 2017;20(5):249-275. doi: 10.1080/10937404.2017.1326071. Epub 2017 Jun 21. Impact of mycotoxins on the intestine: are mucus and microbiota new targets? Robert H, Payros D, Pinton P, Théodorou V, Mercier-Bonin M, Oswald IP. https://www.ncbi.nlm.nih.gov/pubmed/28636450
Leaky Gut and Autoimmunity
Leaky Gut As a Danger Signal for Autoimmune Diseases. Qinghui Mu, Jay Kirby, Christopher M. Reilly and Xin M. Luo*……..https://www.frontiersin.org/articles/10.3389/fimmu.2017.00598/full
Megan Ciara Smyth; Intestinal permeability and autoimmune diseases, Bioscience Horizons: The International Journal of Student Research, Volume 10, 1 January 2017, hzx015, https://doi.org/10.1093/biohorizons/hzx015
Leaky Gut in General
Arrieta, M C et al. “Alterations in intestinal permeability” Gut vol. 55,10 (2006): 1512-20. …. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1856434/
SERIES INTRODUCTION
You may feel a little overwhelmed and stressed after the recent Toxic Mold Summit. A great line up of both clinical types and environmental remediator types took the stage for several day offering a smorgasbord of information about mold toxicity. Now, what do you do with all that information? Should you run out the door screaming in your underwear and leave everything behind?
Short answer….NO! You should simply keep coming back to Sanctuary’s Facebook Live sessions every other week about mold toxicity and read our regular blog posts about mold toxicity and a ton of other chronic health issues. Bring your questions. Hear from myself, Dr. Eric Potter Functional MD who has walked both sides of the mold toxicity line in caring for my family and for hundreds of patients. While I can’t diagnose or treat non-patients by Facebook, I will do my best to educate and empower you in the journey of healing from mold toxicity. Over the coming weeks, I will review several of the Mold Summit’s sessions with additional information from our experience and study.)
Sanctuary Functional Medicine, under the direction of Dr Eric Potter, IFMCP MD, provides functional medicine services to Nashville, Middle Tennessee and beyond. We frequently treat patients from Kentucky, Alabama, Mississippi, Georgia, Ohio, Indiana, and more... offering the hope of healthier more abundant lives to those with chronic illness.