Can You Clean Something With Mycotoxins and Use It Again

Tolle Causam

Lauren Tessier, ND

Mold illness comes in many different forms, with the nigh widely acknowledged forms being allergic and infectious, and the more controversial form existence mycotoxicosis and Chronic Inflammatory Response Syndrome (CIRS).

Molds and their secondary metabolites, mycotoxins, accept taken the medical customs past storm in recent years. This started with news of the pediatric pulmonary hemorrhaging cases in Cleveland in 1994, and was then followed by the evening news report of the Stachybotrys epidemic in Hollywood and the development of Dr Ritchie Shoemaker'south theory of CIRS in the late 1990s and early on 2000s.

Mold and their mycotoxins have been around for a long fourth dimension; even religious texts such as Leviticus take observe of the dangers of mold. There is even speculation that one of the 10 plagues of Egypt may accept been caused by mycotoxins, every bit well every bit Saint Anthony'due south fire. Mycotoxins are ionophores measuring approximately 0.03 microns in length and weighing approximately 500-1500 daltons. As airborne particles smaller than i.0 micron, they are easily inhaled. Man and beast studies have shown that toxicity^ane,two and increased body burden³ can result from inhaling mycotoxins. Their infinitesimal size and combined hydrophobic and hydrophilic nature allow them to pass easily into and out of cells, which makes them hard to eradicate from the living system. Thus, bioaccumulation can event. Toxicity from mycotoxins is compounded by mutations in detoxification genes; animal studies also advise that mycotoxins take an inherent power to hinder detoxification mechanisms by depleting glutathione (GSH), interfering with GSH pathways,^4-7 and downregulating the transcription gene, NRf2.⁸ Chronic infections should also be considered in such cases, every bit their presence tin can further complicate unwinding of the complex toxicology at paw.

Case Study

Patient History

A 43-year-quondam Caucasian female person presented with multiple symptoms following astute, severe mold exposure that had been preceded by low-level, chronic mold exposure. Minor allergy symptoms were commonplace for the patient when in the habitation, but ultimately had been well controlled with over-the-counter H1-blockers. During a kitchen remodeling project, she noted a conspicuous water stain on the wall backside her fridge. She decided to test the air for mold spores. Ambience room air-testing was comparable to the external air; however, an in-wall air sample was obtained that showed elevated spore counts from the Aspergillus and Penicillium family of molds.

Severe symptoms began when the patient attempted to self-remediate the presumptively small surface area of mold growth. Every bit a event of not using personal protective equipment (PPE), she was exposed to a high level of mold that was agitated and aerated following demolition of the h2o-stained wall. The patient reported developing neurocognitive complaints within moments of exposure, including brain fog, difficulty with word-finding and the ordering of steps, defoliation, and disorientation. Assuming at showtime that she was suffering from her recurrent hypoglycemia, she stopped working for the day and ate some nutrient.

The patient had returned to the workspace the following day, without any noticeable improvement, and one time again conducted the repair without PPE. Following approximately iii hours of exposure, she adult ataxia and dizziness then severe that she had to discontinue the remediation work for the day. By the 3rd twenty-four hour period, the patient removed herself completely from her third-story apartment, and indefinitely paused the cocky-directed remediation work. Despite doing so, her symptoms worsened by the twenty-four hour period.

Suspecting that the mold might have something to do with the sudden onset of her illness, the patient had a family unit member collect a sample for ERMI (Environmental Relative Moldiness Alphabetize) testing. The patient called a local repair company, and remediation was completed in the course of 1 week. Unfortunately, negative pressure containment was not used, water intrusion was not found or repaired, and hypochlorite cleaning solution was used as the sole remediation tactic. The patient, now living on the 2nd story of the family'south "Three Decker" home (typical of a New England domicile converted into apartments), noted the wafting of hypochlorite fumes throughout the edifice. Seemingly, as a effect, the patient developed sensitivity to all perfumes, scents, chemicals, and foods, which manifested as a called-for tongue sensation and an exacerbation of her dizziness. While maintaining tenancy on the 2nd floor apartment of her home, initial symptoms worsened over time, and new and curious symptoms arose.

Prior to the onset of her affliction, the patient was a triathlete and held a job requiring a high level of cognitive flexibility and problem-solving skills. She was assessed past her primary-intendance doc, who referred her to a neurologist without making a diagnosis. The neurologist also made no diagnosis, instead suggesting stress and depression as the crusade of her complaints. At the time she established care, the patient had been absent from her loftier-demand job for 2 months, and had self-implemented interventions of sauna therapy, increased slumber, avoidance of exposure, and omission of exercise. Sauna therapy notably worsened her symptoms. After attempting to cook with dish soap instead of oil, she reached out to establish care.

Symptoms

At the initial part visit, the patient reported the post-obit symptoms:

• General: temperature regulation difficulties, cold sweats, hot flashes, night sweats, severe fatigue, exercise intolerance, increased thirst
• Rima oris: bleeding gums, natural language paresthesia, metal taste in rima oris, hypogeusia, and glossodynia
• Head: headache
• EENT: sore pharynx, popping of ears, blurry vision, focal length changes, light sensitivity, post-nasal drip, coryza, dry eyes, maxillary sinus pain, loss of olfactory property
• Neurological: intermittent stabbing pain, dizziness, internal vibration awareness, rocking awareness when at rest, non-dermatomal numbness
• Psychiatric: "drunkard" feeling; disorientation; difficulties with short-term retrieve, concentration, pattern recognition, give-and-take-finding, and distinguishing between objects; mood swings; broken-hearted feeling; depressive mood
• Musculoskeletal: myalgia, intermittent and wandering articulation pain, fasciculations
• Gastrointestinal: gas, bloating, intestinal pain, appetite swings, nutrient intolerance
• Genitourinary: increased urinary frequency and urgency, nocturia
• Peel: itchiness, like shooting fish in a barrel bruising, hives, redness

The patient was adopted, is a nonsmoker, former triathlon runner, ultralight backpacker, and follows an organic paleo nutrition. She denied previous out-of-country travel, as well as known exposures to pesticides, heavy metals, and organic solvents. By medical history was unremarkable except for mononucleosis in her teens.

Physical Exam

Pertinent concrete exam findings included the following: orthostatic hypotension, oxygen saturation 94%, delayed capillary refill, positive hippus test, dermatographism, positive Romberg, anosmia (tested with lavender), failed 2-point discrimination on palms and shins, and failed vibration sensation (128 Hz) on right hallux merely. The patient failed the analogue visual contrast sensitivity (VCS) examination in both eyes, and failed the Montreal Cognitive Assessment (MoCA) (score of 24/30), with deficits demonstrated in memory, delayed think, and attention.

Laboratory Workup

Since the patient had a history of mononucleosis, presented with severe neurological complaints, and had abnormal neurological test findings, assessment for chronic infections in add-on to mold and mycotoxin exposure was considered. A CIRS workup was ordered, as it was requested by the patient and was also pertinent to her case presentation of multi-organization, multi-symptom complaints. An MRI with NeuroQuant analysis and SPECT scan were refused by the patient.

Laboratory Testing: CBC with differential was within normal limits except for a mildly elevated WBC count. Iron console was inside normal limits. Elevations of AST, ALT, GGT, and LDH were present. Preliminary Lyme and coinfection testing included IgM & IgG serology for Borrelia burgdorferi (ELISA & Western Blot, not reflex), Babesia microti, Bartonella (henselae & quintana), Mycoplasma pneumoniae, Ehrlichia chaffeensis, and Anaplasma phagocytophilum, all of which were negative. An EBV panel demonstrated positive results for VCA-IgG, EA-IgG, and EBV-NA, indicative of reactivation. HSV-1 IgM and IgG were both positive, and HSV-2 IgG and IgM were negative. Urine mycotoxin testing via ELISA demonstrated elevations in ochratoxin A, macrocyclic trichothecenes, and gliotoxin. CIRS parameters (VIP, VEGF, C4a, C3a, TGF-B-1, MMP-ix, a-MSH) were within normal range, while TGF-B-1 (transforming growth factor-beta-ane) was elevated. HgA1c was 5.4%.

Home Testing: ERMI (MSQPCR) testing from the wall cavity demonstrated elevated spore counts of Aspergillus fumigatus, Stachybotrys chartarum, Aspergillus ochraceus, and Aspergillus niger. All of these are producers of mycotoxins, specifically gliotoxin, ochratoxin A, and the macrocyclic trichothecenes.

Treatment & Follow-ups

As the patient'southward symptoms were manageable and the chronic infections were seemingly silent prior to the mold exposure, she was directed to adhere to strict abstention – the foundation of recovery. She sought residence in a friend'south habitation that had no history of water damage. As an added precaution, she was directed to leave most of her personal items in storage until she was well enough to address them. Use of a PECO air purifier was also implemented.

Equally the bulk of detoxification occurs in the liver, and bones treatments target enterohepatic recirculation, it was imperative that treatment start in the gut. The patient was placed on supplements designed to improve the integrity of the gut lining so equally to minimize the impact of mycotoxin mobilization during bile excretion. She was prescribed a lignite trace-mineral product in combination with a conservative dose of L-glutamine (5 grams), due to elevated liver enzymes.

The patient was instructed to maintain the paleo nutrition, avoid inflammatory foods, and increase inulin-rich foods and cobweb, with a goal of 50 grams per day. Dietary changes and gut support were well tolerated for 2 weeks; therefore, initiation of a therapeutic binder was prescribed. She reported that charcoal caused correct-upper quadrant (RUQ) pain, so information technology was discontinued afterwards 3 days. She was prescribed a cytidine 5′-diphosphocholine supplement to aid in bile production and secretion for 1 week prior to resuming charcoal. Some improvement in severity and occurrence of RUQ discomfort was noted, but sick effects continued. As a result, the charcoal was discontinued and a pharmaceutical bile acid sequestrant was prescribed. This was well tolerated and only caused minor constipation, which was remedied with magnesium citrate dosed to bowel tolerance.

Approximately one month later, an antiviral medication was prescribed (800 mg twice daily); however, worsening of her "internal vibration" symptom after two days acquired her to discontinue the drug. The patient was encouraged to try a combination, natural antiviral production (containing vitamins A and C, selenium, Melissa officinalis, Olea europaea, L-lysine, and lithium orotate), which afterward 1 month resolved the oral complaints of tongue paresthesia, metallic sense of taste in mouth, hypogeusia, glossodynia, and loss of smell. She was directed to maintain herbal antiviral agents indefinitely.

Oral liposomal GSH was then introduced at 500 mg per twenty-four hours, to exist held under the natural language for one minute before bedtime. This was poorly tolerated, equally it resulted in severe exacerbations of fatigue and myalgia. GSH was discontinued, and later on a 4-day washout period, was restarted at 1-2 drops daily. Despite this lower dose, the patient continued to have negative reactions, so the GSH was discontinued. N-acetylcysteine (NAC), a GSH precursor, was brought on both for its antioxidant potential too every bit its potential for lowering elevated TGF-B-1.^9-11 NAC was well tolerated, and afterwards 2 weeks, she was placed on an additional GSH precursor: glycine, at 1000 mg per day (other GSH precursors were already in use, including vitamin C, selenium, and L-glutamine).

Approximately four weeks subsequently, after the patient was stabilized on the to a higher place regimen, at that place was a noticeable difference in neurological and cerebral complaints: brusque-term memory had improved, word recollect was no longer a concern, and sharp wandering pains had diminished. Energy level had increased from i-2 out of 10 (10=maximum free energy), to a 4/ten, and she was able to tolerate gentle walking equally long as it was kept below anaerobic threshold.

Calendar week by week, the patient slowly improved, while maintaining abstention of exposure. At the 6-month betoken, some other ELISA urine mycotoxin test was ordered. Results demonstrated an increase in urine mycotoxin levels, inferring increased excretion (bold avoidance of exposure was adequately maintained). Additionally, AST, ALT, LDH, and GGT had normalized. GSH supplementation was reintroduced, using driblet doses, and was now tolerated. After a three-week titration, she was able to increment the oral GSH to 500 mg, taken at bedtime.

The patient was directed to continue treatment, with follow-up urine mycotoxin testing at 3-calendar month intervals. The next urine mycotoxin examination, occurring at 9 months, demonstrated a decrease in urine mycotoxin levels. This indicated a decrease in excretion, likely due to decreased toxic load. Since the body burden of the allowed-destabilizing mycotoxins was decreasing, it was now reasonable to retest TGF-B-1. Results demonstrated an improvement, but non normalization. To modulate TGF-B-1, the patient was placed on 20 mg/d of melatonin^12,xiii and 250 mg of epigallocatechin gallate (EGCG).¹⁴

At a 12-month follow-up, the urine mycotoxin test demonstrated clearance of all formerly elevated mycotoxins, also every bit normalized TGF-B-1. She was maintaining normal levels of AST, ALT, GGT, and LDH; VCS test was normal; and her MoCA score was thirty/30.

Discussion

The purpose of this case study is not to imply that treating mycotoxin exposure is like shooting fish in a barrel, or to demonstrate this physician'southward level of expertise. Rather, what is hopefully conveyed in this case study is humility on the role of the provider, and the value of avoiding dogmatic protocols. Admittedly, the same case resulted in a positive ending in a relatively short amount of time – approximately 1 year. It is non uncommon for people suffering from multifaceted and complex chronic disease initiated by mold exposure to continue to be ill for quite some fourth dimension; layer by layer, the issues arise and are addressed as the body slowly recovers. From this case, information technology is hoped that the reader volition have gleaned the following principles:

• Not all mold cases are CIRS
• Glutathione does not cure everything, and can brand things worse
• Binders can cause unintended ill effects, and different people volition tolerate them to unlike degrees
• Perfunctory use of antifungals should exist avoided and are not required in every mold-exposed patient
• What appears to be CIRS may be frank mycotoxicosis, and can exist more complex than what is taken at face up value.
• Mold exposure can suppress the immune system, leading to an awakening of chronic silent infections
• Multiple chemic sensitivity following mold and mycotoxin exposure is not uncommon

References:

1. Creasia DA, Thurman JD, Wannemacher RW Jr, Bunner DL. Astute inhalation toxicity of T-2 mycotoxin in the rat and republic of guinea pig. Fundam Appl Toxicol. 1990;xiv(one):54-59.
2. Creasia DA, Thurman JD, Jones LJ third, et al. Astute inhalation toxicity of t-2 mycotoxin in mice. Fundam Appl Toxicol. 1987;8(2):230-235.
3. Brasel TL, Campbell AW, Demers RE, et al. Detection of trichothecene mycotoxins in sera from  individuals exposed to Stachybotrys chartarum in indoor environments. Curvation Environ Wellness. 2004;59(6):317-323.
4. Guerre P, Eeckhoutte C, Burgat V, Galtier P. The effects of T-2 toxin exposure on liver drug metabolizing enzymes in rabbit. Food Addit Contam. 2000;17(12):1019-1026.
5. Huang L, Duan C, Zhao Y, et al. Reduction of Aflatoxin B1 Toxicity by Lactobacillus plantarum C88: A Potential Probiotic Strain Isolated from Chinese Traditional Fermented Food "Tofu." PLoS One. 2017;12(one):e0170109.
6. Yılmaz South, Kaya E, Comakli S. Vitamin E (α tocopherol) attenuates toxicity and oxidative stress induced by aflatoxin in rats. Adv Clin Exp Med. 2017;26(half dozen):907-917.
7. Choi KC, Chung WT, Kwon JK, et al. Chemoprevention of a flavonoid fraction from Rhus verniciflua Stokes on aflatoxin B1-induced hepatic damage in mice. J Appl Toxicol. 2011;31(two):150-156.
8. Chaudhary Chiliad, Rao PV. Encephalon oxidative stress afterward dermal and subcutaneous exposure of T-ii toxin in mice. Nutrient Chem Toxicol. 2010;48(12):3436-3442.
9. Sugiura H, Ichikawa T, Liu X, et al. N-acetyl-Fifty-cysteine inhibits TGF-beta1-induced profibrotic responses in fibroblasts. Pulm Pharmacol Ther. 2009;22(vi):487-491.
10. Qu 10, Li Q, Wang X, et al. North-acetylcysteine attenuates cardiopulmonary bypass-induced lung injury in dogs. J Cardiothorac Surg. 2013;8:107.
11. Felton VM, Borok Z, Willis BC. Northward-acetylcysteine inhibits alveolar epithelial-mesenchymal transition. Am J Physiol Lung Prison cell Mol Physiol. 2009;297(5):L805-L812.
12. Zonta Year, Martinez G, Camargo ICC, et al. Melatonin Reduces Angiogenesis in Serous Papillary Ovarian Carcinoma of Ethanol-Preferring Rats. Int J Mol Sci. 2017;eighteen(iv). pii: E763. doi: ten.3390/ijms18040763.
13. Shin NR, Park JW, Lee IC, et al. Melatonin suppresses fibrotic responses induced by cigarette smoke via downregulation of TGF-β1. Oncotarget. 2017;viii(56):95692-95703.
14. Chen 1000, Chen W, Liu SL, et al. Epigallocatechingallate attenuates myocardial injury in a mouse model of heart failure through TGF-β1/Smad3 signaling pathway. Mol Med Rep. 2018;17(6):7652-7660.

---

Lauren Tessier, ND, is a licensed naturopathic md specializing in mold-related illness. She is a nationally known speaker and is Vice President of the International Society for Environmentally Acquired Illness (ISEAI) – a non-turn a profit defended to educating physicians nigh the diagnosis and treatment of environmentally acquired illness. Dr Tessier's practice, "Life Subsequently Mold," in Waterbury, VT, draws clients from all around the world who suffer from chronic circuitous affliction every bit a result of environmental exposure and chronic infections. Dr Tessier'south eastward-booklet, Mold Prevention: 101, has been widely circulated and its suggestions implemented by many worldwide.

Advertisements

burrjamathand.blogspot.com

Source: https://ndnr.com/gastrointestinal/mycotoxicosis-a-complex-case-following-acute-mold-exposure/

Share this post