Trichothecenes are mycotoxins (secondary metabolites or chemicals) primarily produced by various species of Fusarium (T-2, HT-2 and DAS), Trichoderma and Stachybotrys (black mold). They are toxic to humans, other mammals, birds, fish, a variety of invertebrates, plants and bacteria. The effects of poisoning will depend on the particular toxin, the concentration of exposure, length of time and way the animal or plant is exposed. Even a small amount of a highly concentrated solution of the mycotoxin is likely to cause severe effect, including death.
Trichothecene mycotoxins can be absorbed through topical, oral and inhalational routes. Trichothecenes differ from other toxins since they can act through the skin by crossing cell membranes. As a dermal irritant and blistering agent, it is alleged to be 400 times more intoxicating than sulfur mustard (mustard gas). Exposure to nuclear material will initiate autoimmunity more quickly, but human data is sparse.
Trichothecenes are highly toxic at the sub-cellular, cellular and organic system levels. They appear to cause toxic injury to mucosal neurons, and leukocytes (white blood cells), creating a predisposition to fungal colonization or infection.
Exposure to trichothecenes:
1. Inhibits protein synthesis (plant chlorophyll and animal antibodies)
2. Induces cell destruction – apoptosis, which is the injury of the skin (sores) and mucosa (mouth, respiratory, gastrointestinal).
3. Damages nerve and immune cells
Based on a comparative analysis of clinical disability or deformity outcomes, the innate detoxification process is damaged or destroyed by immunosuppression (lowered immune system response), and impaired genetic changes that reduce the detoxification process. In other words, fungus or mold has gotten into DNA and RNA.
Mycotoxins are spread all over the world, and affect 25% of world’s grain production (FAO data). Moreover, most mycotoxins are very stable and resistant to different storage and processing conditions.
Trichothecenes are mycotoxins that frequently contaminate stores of grain products. Hazardous concentrations of trichothecenes have been detected in corn, wheat, barley, oats, rice, rye, vegetables and other crops, causing rot of the plants. Humans are susceptible to injury due to dietary intake. GMO foods, and genetically modified grains from Monsanto. To prevent consumption of GMO products, be sure to read food labels.
These toxins have also been identified in weather-delayed-harvest soybeans. Feed contaminated with these toxins must be handled carefully because these toxins can cause severe skin irritation. As with most other mycotoxins, the only control is to avoid contaminated feeds.
This makes trichothecene contamination a significant public health problem. There are no known direct antidotes to trichothecene exposure, so risk management and prevention demands that grains are stored in areas with a very low moisture content.
All domestic animals are susceptible to injury by dietary intake of trichothecenes. In poultry, T-2 toxins are closely related to the production of lesions at the edges of the beaks, abnormal feathering in chicks, a drastic and sudden drop in egg production, eggs with thin shells, reduced weight gains, and mortality. The same feed given to turkeys results in reduced growth, beak lesions and less immunity to infection.
T-2 and DAS (a secondary metabolite of Fusarium) in cattle feed results in lethargy, decreased feed consumption, slow growth, lowered milk production, and sterility. An outbreak of the bowel syndrome and death of some animals can occur in herds of cattle, swine and poultry.
In swine, infertility with some lesions in the uteri and ovaries result from consumption of feed contaminated with T-2 toxin. When sound feed was provided to all domestic animals, the troubles quickly disappeared. T-2 toxin and DAS in amounts sufficient to cause toxicoses have been found in corn still in the field, in silage, and in prepared feeds made in part from corn.
Urinary Trichothecenes disease severity is strongly correlated with MTHFR gene, which plays a role in processing amino acids, the building blocks of proteins. Mycotoxin exposure to individuals with mutations in this gene can cause hopeless, depression, anxiety, confusion. The only way you can check the severity is through urine testing.
The symptoms of a mycotoxicosis (toxic exposure to fungal poisoning by natural means) depend on the type of mycotoxin; the amount and duration of the exposure; the age, health, and sex of the exposed individual; and many poorly understood synergistic effects involving genetics, blood type, dietary status, and interactions with other toxic insults.
Congenital placental defects, disabilities and deformities are consistent with exposure parameters coupled with immune suppression, especially inuterio, pregnancy, malnutrition and steroids. Cutaneous or skin and mucosal bleeding (bloody noses) are extremely common.
The severity of mycotoxin poisoning can be compounded by factors such as vitamin deficiency, caloric deprivation, alcohol abuse, and infectious disease status and blood type. In turn, mycotoxicoses can heighten vulnerability to microbial diseases, worsen the effects of malnutrition, and interact synergistically with other toxins. The strongest diseases severity predictors are mucosal injury and hazardous activities in elevated IgG and IgE antibodies that protect against bacterial, viral and fungal infections.
Once the mycotoxin genes mutate, they cannot be detoxified from the system. The MTHFR variant factors – a1298c and c677t, cause a higher risk of hyperhomocysteinemia (risk factor for heart disease); nervous and parasympathic system problems; and recurrent pregnancy loss. Trichothecene toxins cause homosystene imbalance (body is out of balance).
How They Affect our Homes
Fusarium and trichodermia persist in fungal fragments – dust mites and feces. Readily airborne, they contaminate indoor environments, and remain hazardous despite disinfection (remediation efforts). In addition, in time they will morph, and become adjusted to chemicals efforts to destroy them. Biocides may transform them to even more toxic daughter particulates.
Stachybotrys produces toxic black mold mycotoxins. People with toxic black mold in their homes are mostly exposed to trichothecene mycotoxins through breathing them in. These are some of the most toxic and stable mycotoxins. Trichothecene mycotoxins from Stachybotrys can take several years to break down and can be nearly impossible to remove from homes.
There is no cure or antidote which can be taken for toxic black mold. The only solution is to remove the toxic black mold from your environment or remove yourself from the environment. Once you are away from toxic black mold, your body may start to recover and most of your symptoms should go away over time. Methylfolate helps reduce the impact of the MTHFR variant, which helps with the detox from black mold. However some of the damage from toxic black mold can be permanent.
Natural and Manmade Trichothecenes
Trichothecenes are an extremely cytotoxic (inert) nano particulate of stachybotrys. Trichothecene mycotoxins are categorized as either biological or manmade. Although it is still controversial, it is suspected that manmade T-2 mycotoxin have been used as a chemical warfare agent from the 1970s till the 1990s.
Elevated specific mold IgG and IgE antibodies are the strongest laboratory predictors for disease severity, and may indicate persistent fungal colonization or infection. Perspective observations can document contamination based on biostatic analysis of outcomes and exposure details for hazards and related illnesses. A mold doctor recommends treatment by a report of an individual’s health stats. In general, however, matching environmental and clinical fungi tests appears to give a clarity to the identification of hazardous exposures.