For those dealing with a complex chronic illness—such as chronic fatigue syndrome, fibromyalgia, frequent infections, neuroendocrine disorders, and autoimmunity—mycotoxins are often overlooked, yet significant, silent killers that deteriorate various systems in the body. The symptoms caused by mycotoxins are often nonspecific and overlap many other health issues, and it’s common for standard test results from screening labs to either be normal or borderline abnormal. The subsequent band-aid approach to managing these symptoms may cause delays in proper treatment, potentially resulting in worsened outcomes.
Mycotoxins are secondary metabolites of mold compounds that act as significant triggers of chronic immune activation. Mold toxicity—mycotoxin illness—reflects an immune response to mycotoxin exposure; this is different from mold allergy—immunoglobulin E (IgE)-mediated, immediate hypersensitivity reaction—and mycosis—mold infections.
Common and concerning sources of mycotoxins include Alternaria, Aspergillus, Claviceps, Fusarium, and Penicillium. Individuals become exposed to mycotoxins through dermal, inhalation, and ingestion routes, although exposure through water-damaged buildings, such as from flooding, can be particularly problematic.
It’s postulated that the systemic chronic inflammation associated with mycotoxin exposure relates to abnormalities of pro-inflammatory cytokines, complement activation, and cellular immunity,1 contributing to various negative health effects (Figure 1).2
Management of chronic inflammation, and the subsequent symptoms, is difficult to achieve with persistent mycotoxin exposure; hence, the primary goal is eliminating the source of exposure. In addition, it’s imperative to use binders to reduce mycotoxin burden while supporting detoxification and redox capacity to promote immune tolerance.
Signs/Symptoms of Mycotoxin Illness
Clinical presentation of mycotoxin illness can vary greatly from case-to-case, based on such factors as the nature of the exposure and genetic susceptibilities. These multisystem symptoms include but aren’t limited to the following types:
Mycotoxin Illness Management
Eliminate or Reduce Mold Exposure
Individuals should consider remediation of the affected space to whatever degree possible using experienced and trained professionals. Additionally, reducing the mycotoxin burden can be achieved with such methods as the use of a dehumidifier, with a relative humidity (RH) of 35-40%; use of a central air filter or portable air purifier; removal of all carpets; use of a high efficiency particulate air (HEPA) canister vacuum; and prevention of seasonal basement flooding.
Detox and Redox Support
Supporting phase 2 detoxification pathways, namely glutathione conjugation and glucuronidation, is important in promoting the elimination of mycotoxins, managing oxidative damage, and enhancing the threshold to toxic load. This is achieved with nutrients such as N-acetyl cysteine (NAC), vitamins C and E, selenium, and calcium D-glucarate. In addition, silybins from milk thistle are an excellent hepato-protectant that facilitates glutathione conjugation of xenotoxins, via the upregulation of glutathione S-transferase (GST).3
Sequestering Agents (Binders)
Sequestering agents are used to bind mycotoxins in the digestive tract to aid in elimination by preventing enterohepatic recirculation.
Figure 2 shows the three primary mechanisms of action that appear to be involved in the binding and degradation of mycotoxins by lactic acid bacteria (LAB)4: (1) degradation by LAB enzymes, (2) adsorption by LAB cells, and (3) the interaction of mycotoxins with LAB metabolites.
LAB degrade mycotoxins by production of proteolytic enzymes and prevent their absorption through the digestive tract,5 with several LAB strains being identified as having that capacity (Figure 3).6-9
Lactobacillus rhamnosus uses a variety of adsorption mechanisms, such as hydrogen bonding and ionic or hydrophobic interaction, to bind mycotoxins.10-12
Various LAB produce metabolites, such as acids; carbon dioxide (CO2); hydrogen peroxide (H2O2); phenyllactic acid; fatty acids; reuterin; and bioactive, low-molecular-weight peptides, that mitigate growth of mold and subsequent mycotoxin production.13,14
An RCT examining the effects of Lactobacillus rhamnosus LC705 and Propionibacterium freudenreichii subsp. shermanii strains on liver-cancer risk, mediated by alfatoxin exposure, found that a five-week intervention led to a statistically significant reduction in alfatoxin exposure in the intervention group and a decreased the risk of liver cancer.15
In addition to LAB, Saccharomyces boulardii (S. boulardii) has demonstrated mycotoxin binding effects,16 as well as the ability to reverse mycotoxin-induced injury by attenuating the “p38 mitogen-activated protein kinase (MAPK)” signaling pathway to modulate expression of inflammatory cytokines and apoptotic genes.17
Activated charcoal (AC) has also been found to bind several mycotoxins, including alfatoxin B1, deoxynivalenol, ochratoxin, and zearalenone.18-20 Due to possible concurrent adsorption of essential nutrients,21 AC should be taken at least two hours after ingestion of food, medication, or supplements. Concomitant use of an oral multimineral formula or IV nutrient therapy can be considered based on the duration of the treatment.
Conclusions
With the growing awareness of the multisystem health risks associated with mycotoxin exposure, probiotic therapy offers practitioners a valuable therapeutic tool in the management of mycotoxin illness, to be used in concert with detox and redox support and general exposure-avoidance strategies.
References
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