Mycotoxins

Main Fungi That Cause Disease

Several types of mold are known for their ability to produce mycotoxins that can harm human health. Here are the top culprits:

Aspergillus (Ocharatoxin A):

Found in moist environments and foods like grains, nuts, and spices.

Produces aflatoxins, which are highly toxic and carcinogenic.

Exposure occurs through inhalation, ingestion, and contact with contaminated materials.

Penicillium:

Commonly grows on water-damaged walls and spoiled foods like fruit and bread.

Produces ochratoxin A, which has been linked to kidney damage and immunosuppression.

Stachybotrys (black mold):

Thrives on cellulose-rich materials like drywall and wood in consistently moist conditions.

Produces trichothecenes, which are potent mycotoxins that cause respiratory and neurological problems.

Fusarium:

Found in crops such as corn, wheat, and barley.

Produces zearalenone and fumonisins, known to cause gastrointestinal and hormonal disorders.

Cladosporium:

Frequently found indoors in damp carpets, wallpaper, and HVAC systems.

Although less toxic, it can trigger allergies and asthma.

Alternaria:

Common outdoors and in damp indoor areas.

Can cause allergic reactions and respiratory symptoms.

 

Common contact points

Moist indoor spaces: Water damage from leaks, flooding, or poor ventilation creates ideal conditions for mold growth.

Food supply: Improperly stored crops and foods, such as grains, peanuts, and coffee, often harbor mycotoxins.

Outdoor exposure: Decaying leaves, compost, and soil are natural sources of airborne mold spores.

 

Why Your Genes Matter

Genetic variants in these detoxification genes can influence how well your body handles mycotoxins. For example:

Variants in GSTP1 can reduce the efficiency of glutathione conjugation, increasing susceptibility to oxidative stress.

Polymorphisms in MTHFR can impair methylation, affecting detoxification and long-term recovery.

Reduced activity of SOD2 or NQO1 increases vulnerability to oxidative damage.

Variants in CBS can affect glutathione production, reducing the body’s ability to effectively neutralize mycotoxins.

Reduced function of EPHX1 can impair the breakdown of reactive intermediates, increasing the risk of toxin-induced damage.

PON1 (Paraoxonase 1) helps protect against lipid oxidation and may indirectly support detoxification by reducing oxidative damage from mycotoxin exposure.

Variants in TNF-alpha can increase cytokine production, leading to an overactive inflammatory response that can cause additional cellular damage during mold exposure.

Variants in the CRP (C-reactive protein) gene can influence baseline levels of inflammation, potentially increasing the body’s response to mold toxins.

Polymorphisms in IL-12 may affect immune system signaling, potentially leading to prolonged inflammation and impaired recovery after mycotoxin exposure.

Variants in IL-6 may increase the inflammatory response, amplifying tissue damage and contributing to more severe symptoms during mold exposure.

 

Which pathway is more important: oxidative stress or methylation?

Both oxidative stress and methylation genes are essential, but their importance depends on the context:

Oxidative Stress Genes: Critical for immediate protection against cellular damage caused by mycotoxins.

Methylation and transsulfuration genes: Vital for ongoing detoxification, DNA repair, and systemic recovery from exposure.

A deficiency in either pathway may lead to increased sensitivity to mold toxins and long-term health consequences.

 

Final thoughts:

Understanding your genetic predispositions can empower you to take proactive steps to manage mold exposure. Testing genes such as GSTP1, SOD2, NQO1, MTHFR, CYP1A2, CBS, EPHX1, and PON1 provides valuable information about your detoxification capacity. Supporting these pathways through personalized nutrition and supplementation, such as increasing glutathione levels or increasing methylation, can help you mitigate the effects of mycotoxins and protect your health.