Mold Genes: How Do Mycotoxins Affect You?

We are all exposed to mold on a daily basis. Fungi are essential to life: they dwell on our skin, make our soil fertile, and help decompose organic matter. However, some molds give off microscopic toxins that can harm you.

For some people, exposure to specific types of mold can result in long-term health problems.

This article explores the research on mold toxins and how these molecules affect our health. I’ll explain the genetic variants involved in the body’s detoxification process before concluding with what  clinical trials reveal about supplements and lifestyle changes for mold toxicity recovery.

How can mold harm your health?

Molds are everywhere! From the green fuzz on an old loaf of bread to the essential fungi found throughout healthy soil, mold is a general term for the types of fungi that are filamentous. Yeast are also classified as fungi, but they are single-celled and don’t produce filaments.

Exposure to certain types of mold – the kind that produce mycotoxins – can cause chronic health-related problems, gut health issues, immediate injury, or even death.

What are mycotoxins?

Mycotoxins are microscopic mold metabolites that can cause harm. They are naturally occurring toxins produced by filamentous fungi (molds). They are classified as toxins because even at very low doses, they can cause ill effects or even death in humans and other animals.[ref]

They differ from the toxins found in poisonous mushrooms (which are the fruiting bodies of fungi). Instead, mycotoxins are found in trace amounts on moldy nuts, grains, coffee, and dried fruits. Molds growing on damp building materials can also produce mycotoxins.

Aflatoxins, ochratoxins, trichothecenes, zearalenone, fumonisins, and ergotamine are more commonly studied mycotoxins, but more than 300 mycotoxins are known to exist. Some of these mycotoxins are produced by more than one type of fungus, while others are specific to a single fungal species.[ref]

The World Health Organization estimates that up to 25% of crops are contaminated at some point with mold or fungal growth.[ref] Many human food processing methods, though, reduce mold or mycotoxin contamination.

How are we exposed to mycotoxins?

Mycotoxins are produced by fungi that grow on crops, in preserved foods, and in the soil. It’s a problem in areas with warm and humid conditions favorable for fungal growth.

The main routes of exposure to mycotoxins include:[ref]

  • ingestion (most common route of exposure)
  • inhalation
  • via the skin (dermal)

Food can be contaminated by mycotoxins either in the field or during drying and processing. In general, good quality control with harvesting, drying, and processing food prevents the formation of mycotoxins.

In other words, every ear of corn or coffee bean you consume isn’t going to be contaminated with mycotoxins. Instead, contamination with mycotoxins is more of a problem when agricultural processes and food handling procedures are poor.[ref]

Mycotoxins pose a two-fold problem: they are toxic at extremely low levels and are chemically stable, allowing them to survive food processing and cooking.[ref]

Specific mycotoxins:

Ochratoxin A is produced by Aspergillus and Penicillium species of mold. Ochratoxin A is toxic and likely carcinogenic, especially in the kidneys and liver.[ref]

Ochratoxin A is found in cereals, coffee, wine, dried fruits, beer, and grape juice. It also occurs in animal organs (kidneys, liver) of grain-fed animals. In humans, ochratoxin A can have a severe immunosuppressant effect at low and high exposure doses.[ref] Ochratoxin A also changes the absorption of nutrients in the intestines.[ref]

Zearalenone is produced by Fusarium species. It can bind to estrogen receptors (mimic estrogen) and is a reproductive toxin in animal studies. Additionally, zearalenone is toxic to the liver and leads to cell death.[ref]

One study describes zearalenone as: “It is a non-steroidal compound that exhibits oestrogen-like activity in certain farm animals such as cattle, sheep and pigs.”[ref]

Aflatoxins are produced by a couple of different Aspergillus species. There are multiple types of aflatoxins, with aflatoxin B1 being one of the most toxic and carcinogenic.

Aflatoxins are often found in peanut products and in milk from cows fed with contaminated grain. Aflatoxin B1 is also found in cottonseed oil.[ref]

“Aflatoxicosis is a toxic hepatitis leading to jaundice and, in severe cases, death.”[ref]

Chronic dietary exposure to aflatoxins is linked to liver cancer.[ref]

Fumonisins are metabolites produced by Fusarium species. Certain fumonisin subtypes are linked to an increased risk of esophageal cancer, and in general, fumonisins are considered a WHO class 2B carcinogen.[ref]

An interesting observation by researchers is that fumonisins interact with folate uptake in cells: “Because fumonisin B1 reduces uptake of folate in different cell lines, fumonisin consumption has been implicated in neural tube defects in human babies”.[ref]

Trichothecene mycotoxins encompass about 100 subtypes of metabolites from Fusarium species. Trichothecenes can contaminate corn, wheat, barley, oats, rice, rye, vegetables, and other crops. They are a common cause of poisoning in animals eating contaminated feed. Trichothecenes are easily absorbed and then distributed throughout the animal’s tissues. Human exposure comes from consuming meat, milk, and eggs from animals fed contaminated grains.[ref]

Consumption of trichothecene-contaminated foods can cause gastrointestinal issues. This mycotoxin affects actively dividing cells, such as in the intestinal or oral mucosa, and causes cell death.[ref]

Ergot alkaloids are compounds created by Claviceps species, which are fungal pathogens that attack grasses such as rye. Ergot poisoning has been known for centuries. It was described as a “slow nervous fever” that occurred in the summer after a wet winter in the Middle Ages. Modern grain processing methods eliminate ergot as a problem in human food sources, but it can still affect animals that graze on grasses or contaminated grains.[ref]

St. Anthony’s fire refers to an illness caused by consuming ergot-contaminated grain (usually rye). The symptoms recorded throughout history include convulsions, sores, hallucinations or mania, headaches, nausea, gangrene, and burning extremities.[ref] The gangrene occurs because ergot is a vasoconstrictor, and too much constriction cuts off blood circulation to the extremities. The neuroactive components in the ergot alkaloids are similar to precursor molecules for LSD. Interestingly, a couple of Parkinson’s drugs are derived from ergot.

Deoxynivalenol is a mycotoxin produced by Fusarium species. It is found on wheat, beans, and some spices. Deoxynivalenol causes severe gastrointestinal issues when consumed via contaminated foods.[ref]

What happens when you are exposed to mycotoxins:

Exposure to mycotoxins can produce various responses, depending on the toxin, exposure route, amount, and individual genetic differences.

Lung inflammation, mitochondrial function: An inflammatory response occurs when lung tissue is exposed to airborne trichothecenes. Il-1B increases in a manner dependent on NLRP3 activation. This mycotoxin can impair mitochondrial function and inhibit the synthesis of certain proteins.[ref]

Organ damage: From airborne exposure, the mycotoxins can travel to the liver, kidneys, and spleen. It causes inflammatory cytokines to increase in all of these organs. Specifically, researchers found higher levels of IL-1B, IL-6, and TNF-alpha.[ref]

Another mycotoxin that increases inflammation in the lungs is aflatoxin G1. It increases not only inflammatory cytokines but also induces specific detoxification genes.[ref]

Genetic variants can influence how strong the inflammatory response may be. For example, TNF-alpha variants may cause some individuals to produce more of this cytokine in response to a stimulus.

Read more about inflammatory genetic variants.

It is not as simple, though, as mycotoxin = inflammation.

Suppressed immune response: Zearalenone is a mycotoxin that suppresses the normal inflammatory response that cells should produce against pathogenic bacteria. Zearalenone exposure tamps down the proinflammatory cytokines (TNF-alpha, IL1B, IL6) that should be produced in response to gram-negative bacteria. This ‘tamping down’ suggests a reduction in the innate immune response, which could leave someone vulnerable to infections after exposure to zearalenone.[ref]

Kidney damage: Oral exposure to ochratoxin A from contaminated food is linked to kidney injury. Animal studies show that ochratoxin A increases inflammatory cytokines and up-regulates genes related to fibrosis in the kidneys. Blocking NLRP3, an inflammatory activator, was able to suppress the kidney injury.[ref]

Gut microbiome interaction:  Exposure to mycotoxins through foods can impact the gut microbiome in several ways. First, some gut microbes can metabolize mycotoxins – sometimes creating more toxic metabolites. Mycotoxins can also impact the composition of the gut microbiome. Interestingly, certain mycotoxins affect the way nutrients are absorbed.[ref]

Types of mold exposure:

Exposure to mycotoxins can be either acute or chronic:

  • Acute exposure will bring quick and severe poisoning symptoms for someone exposed to higher levels of mycotoxins at one time (e.g., eating a bunch of moldy nuts).
  • Chronic exposure is more common. Very low-dose exposure over long periods can result in various health consequences, including an increased risk of certain cancers.

Acute exposure by consuming foods containing mycotoxins can cause food poisoning type symptoms. Researchers think that a percentage of food poisoning cases each year are actually due to mycotoxins.

Mycotoxins often contaminate coffee beans and tea leaves at low levels. Drinking contaminated coffee or tea every morning is one way we can be chronically exposed to trace levels of mycotoxins.[ref]

In addition to being consumed in foods, mycotoxins can be airborne and enter your lungs when you breathe. Some mycotoxins can also enter through your skin.

Detoxifying mycotoxins:

We are all regularly exposed to mycotoxins at trace levels, and our bodies have ways of getting rid of mycotoxins. The key is to not overwhelm the detoxification system through either an excess of toxins or by not having enough of the cofactors needed for detoxification.

Let’s look at some examples of the pathways involved in mycotoxin elimination:

Aflatoxin can be combined in the body with glutathione, making it easy for the body to excrete. Having enough glutathione available to handle mycotoxins is essential, and the GST family of genes is important here.[ref]

Ochratoxin A increases oxidative stress. It can be counteracted on a cellular level by the Nrf2 pathway, which is necessary for upregulating genes that combat reactive oxygen species.[ref]

Glucuronidation is a phase II detoxification process by which a glucaric acid molecule is added to a toxin to make it more easily excreted and less reactive. Zearalenone mycotoxins are excreted via the glucuronidation pathway, specifically utilizing UGT1A1, UGT1A3, and UGT1A8.[ref]

Additionally, methylation, hydroxylation (addition of a hydroxyl group), hydrolysis, and sulfation reactions are utilized for transforming mycotoxins for excretion from the body.[ref]

My take-away: Knowing the specific mycotoxin involved is important for understanding which detoxification pathway to target.

“Mold Genes” — are the HLA types in 23andMe?

One question that I get asked fairly often is how to find the mold genes in 23andMe data… There is a lot of confusion and over-simplification being promoted on the internet about “mold genes”.

In general, some natural health websites write about mold genes and refer to certain HLA types. Practitioners identified these HLA types more than a decade ago as being likely to have mold reactions. Listed symptoms of mold illness include fatigue, muscle pain, headaches, sinus problems, vision problems, brain fog, mood swings, vertigo, joint pain, weakness, and more.

I’m going, to be honest here… I can’t find any quality research studies on this. There are research-backed links between asthma and mold sensitivity in children[ref], but asthma isn’t one of the ‘mold symptoms’ being talked about in alternative circles. There are thousands of research studies on the poisoning-type symptoms from mycotoxins. But the multitude of mold illness symptoms and common HLA types doesn’t have much in the way of published research.

Does a lack of peer-reviewed research mean that people don’t really have mold illness or mold toxicity? Of course not. Clinicians make valid discoveries about health all the time, and not everything is written in a peer-reviewed journal.

But, I am not a clinician, and thus I’m sticking with just explaining what high-quality research studies show us, which, in this case, is not a lot.

Could mold symptoms be related to mycotoxin exposure? Quite possibly. Instead of being able to tell you if you have ‘the mold gene’, I would rather invite you to read about the different ways your genetic variants impact your ability to handle mycotoxins.

Genetic variants related to mycotoxin reactions:


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XPC gene: encodes a DNA nuclear excision repair gene

Check your genetic data for rs2228001 Lys751Gln (23andMe v4, v5)

  • T/T: typical
  • G/T: increased DNA adducts (risk marker for cancer) with aflatoxin B1 exposure; increased risk of liver cancer with aflatoxin B1 exposure
  • G/G: increased DNA adducts (risk marker for cancer) with aflatoxin B1 exposure[ref] increased relative risk of liver cancer with aflatoxin B1 exposure[ref][ref][ref]

Members: Your genotype for rs2228001 is

Phase I Detoxification and Mycotoxins:

The following variants affect the activity of CYP450 enzymes involved in the detoxification of mycotoxins. Please note that some of these are not directly researched regarding mycotoxins. Thus, take this more as information in pathways that are likely involved — but without direct evidence to back it up.

Often molecules that are acted upon by phase I enzymes are then also made water-soluble and excretable using phase II enzymes. Thus, phase I detoxification needs to be in sync with phase II detoxification. 

CYP1A2 gene: encodes an enzyme involved in the metabolism of caffeine, polycyclic aromatic hydrocarbons, and mycotoxins such as aflatoxin B1.[ref]

Check your genetic data for rs12720461 (23andMe v4, v5; AncestryDNA):

  • C/C: typical
  • C/T: decreased activity (carrier of one CYP1A2*1K allele)
  • T/T: decreased activity (CYP1A2*1K )[ref]

Members: Your genotype for rs12720461 is

Check your genetic data for rs72547517 (23andMe v4, v5; AncestryDNA):

  • A/A: decreased activity or inactive (CYP1A2*8)[ref]
  • A/G: decreased activity (carrier of one CYP1A2*8 allele)
  • G/G: typical

Members: Your genotype for rs72547517 is .

Check your genetic data for rs72547515 (23andMe v4,v5; AncestryDNA):

  • A/A: decreased activity or inactive (CYP1A2*16)[ref]
  • A/G: decreased activity (carrier of one CYP1A2*16 allele)
  • G/G: typical

Members: Your genotype for rs72547515 is .

CYP3A4 gene: encodes an enzyme involved in phase I detoxification of aflatoxin G1 (as well as many other substances and medications).

Check your genetic data for rs4987161 (23andMe v4, v5):

  • G/G: CYP3A4*17, decreased function of enzyme[ref][ref]
  • A/G: carrier of one CYP3A4*17 allele
  • A/A: typical

Members: Your genotype for rs4987161 is .

Check your genetic data for rs4986909 (23andMe v4; AncestryDNA):

  • A/A: CYP3A4*13, decreased function of the enzyme[ref]
  • A/G: carrier of one CYP3A4*13 allele
  • G/G: typical

Members: Your genotype for rs4986909 is .

Check your genetic data for rs2740574 (23andMe v4, v5; AncestryDNA):

  • C/C: CYP3A4*1B, altered function of the enzyme[ref]
  • C/T: carrier of one CYP3A4*1B allele
  • T/T: typical

Members: Your genotype for rs2740574 is .

Check your genetic data for rs4986910 (23andMe v4, v5):

  • G/G: CYP3A4*3, decreased function
  • A/G: carrier of one CYP3A4*3 allele
  • A/A: typical

Members: Your genotype for rs4986910 is .

Check your genetic data for rs4986907 (23andMe v4, v5):

  • T/T: CYP3A4*15A, decreased function
  • C/T: carrier of one CYP3A4*15A allele
  • C/C: typical

Members: Your genotype for rs4986907 is .


Phase II detoxification:

The phase II detoxification enzymes make the metabolites from mycotoxins easily excretable via urine or feces.  Again, you want phase II detoxification to move at the same rate as phase I.

GSTM1 enzyme: This enzyme helps the body detoxify several types of carcinogens, drugs, toxins, and oxidative stress byproducts. Regarding mycotoxins, GSTM1 is important in the detoxification of aflatoxin B1.[ref] Not everyone has a functioning copy of this gene.[ref] The deletion is fairly common with  50 – 78% of people, depending on the ethnic group having the null genotype for GSTM1.

Check your genetic data for rs366631 (23andMe v4 only):

  • A/A: deletion (null) GSTM1 gene. increased risk of certain cancers[ref][ref][ref] increased risk of liver cancer with aflatoxin B1 exposure[ref] (note: this is a common genotype in many population groups)
  • A/G: GSTM1 present
  • G/G: GSTM1 present

Members: Your genotype for rs366631 is .

GSTA1 gene: Variants in the GSTA1 gene can reduce the enzyme function, which is associated with increased risk for certain cancers.[ref][ref][ref]  GSTA1*B (non-functioning) is also associated with a higher risk of asthma and allergies.[ref] GSTA1 is also important in eliminating ochratoxin A from the body.

Check your genetic data for rs3957357 (23andMe v4, v5; AncestryDNA):

  • A/A: GSTA1*B, low/ non-functioning enzyme; increased risk of asthma, allergies[ref], increased risk of kidney disease with ochratoxin A exposure[ref]
  • A/G: GSTA1*A/*B, somewhat lower enzyme function.
  • G/G: GSTA1*A

Members: Your genotype for rs3957357 is .

GSTP1 gene: GSTP1 is involved in estrogen metabolism as well as various toxicants.[ref]

Check your genetic data for rs1695 (23andMe v4, v5; AncestryDNA):

  • A/A: typical
  • A/G: typical risk
  • G/G: reduced function, increased risk of certain cancers[ref][ref][ref] increased risk of liver damage with aflatoxin B1 exposure[ref]

Members: Your genotype for rs1695 is .

SLCO1B1 gene: The SLCO1B1 gene encodes an organic anion transporter protein. It is important in the way the liver deals with substances such as bilirubin and estradiol, as well as certain drugs (statins).[ref]

Check your genetic data for rs4149056 (23andMe v4, v5; AncestryDNA):

    • C/C: increased risk of liver damage with aflatoxin B1 exposure[ref]
    • C/T: increased risk of liver damage with aflatoxin B1 exposure
    • T/T: typical

Members: Your genotype for rs4149056 is .

Lifehacks for mycotoxins:

The big picture with mycotoxins is avoidance and counteracting the effects of exposure.

Avoiding contamination:

Food sources of mycotoxins: Pigs that eat foods contaminated with ochratoxin A are a continuing dietary source of ochratoxin for people who regularly eat pork products.[ref] Many countries do periodic testing for contamination, so this isn’t a problem with all pork. But this is a reason to choose high-quality pork or pork from a known local farmer when possible.

In general, food production and storage are important in avoiding mold contamination, especially in humid climates. Coffee is frequently a source of mycotoxin contaminants.[ref][ref] Peanuts, especially in tropical regions, are a source of aflatoxin exposure.[ref][ref]

Check your environment: Water damage is notorious for causing mold growth. Moldy buildings can be a continual source of airborne mycotoxin exposure. Look for leaking plumbing, water from an air conditioner condenser, or roof leaks.

A study in a school found that more children had headaches, runny noses, and tiredness when in classrooms with higher levels of mycotoxins in the dust.[ref]

Wallpaper that gets wet can easily grow mold, and moving air, such as from a fan, can easily aerosolize the mycotoxins. [ref] Other wet building materials that support mold growth include gypsum board, chipboard, and spruce wood.[ref]

Drugs that may slow down detoxification:

  • UGT inhibitors include the drug class of kinase inhibitors[ref]
  • Clindamycin (antibiotic) inhibits GST enzyme activity[ref]

Blueprint for Members:

This member’s section contains information on specific supplements that have been shown in research studies to impact mycotoxin detoxification pathways. Please talk with your doctor if you have questions about supplements – especially if you are on other medications that may interact.

Supplement research on mycotoxin detoxification:

Targeting oxidative stress:

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About the Author:
Debbie Moon is the founder of Genetic Lifehacks. Fascinated by the connections between genes, diet, and health, her goal is to help you understand how to apply genetics to your diet and lifestyle decisions. Debbie has a BS in engineering and an MSc in biological sciences from Clemson University. Debbie combines an engineering mindset with a biological systems approach to help you understand how genetic differences impact your optimal health.