Mold Genes: How mold and mycotoxins interact with genetics

Key takeaways:
~ Some types of mold produce mycotoxins which can harm you.
~ We have detoxification pathways to eliminate many types of mycotoxins.
~ Some individuals have genetic variants in the detoxification genes that make them more susceptible to negative health effects from mold and mycotoxins.
~ Knowing your genetic susceptibility can help you target the right pathways to detox mold and mycotoxins.

Members will see their genotype report below, plus additional solutions in the Lifehacks section. Join today. 

How can mold harm 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. And for some people, exposure to specific types of mold can result in long-term health problems.

Mold is a general term for the types of multicellular 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 produces mycotoxins – can cause chronic health-related problems, gut health issues, immediate injury, mitochondrial dysfunction, or even death.

When people talk about the health effects of mold, they are usually referring to the consequences of mycotoxin exposure.

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] Mycotoxins differ from the toxins found in poisonous mushrooms, which are the fruiting bodies of fungi.

Mycotoxins are found in trace amounts on moldy nuts, grains, coffee, and dried fruits. The mold that grows in damp places, such as water-damaged 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 in their lifecycle, with mold or fungal growth. Some grains may have fungal problems in the field, while other products may grow mold during storage.[ref]

Food processing methods reduce mold or mycotoxin contamination in foods that are used for human consumption. Animal feed, though, is more often contaminated with mold.

How are we exposed to mycotoxins?

Mycotoxins are produced by fungi that grow on crops, in preserved foods, in wet homes, 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 of food prevents the formation of mycotoxins. To be clear – 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:[ref]

• they are toxic at extremely low levels
• they are chemically stable, allowing them to survive cooking

Specific mycotoxins:

Mycotoxin is a general term, and individuals are unique in how their body processes and eliminates different types of mycotoxins.

Genetic variants in the detoxification genes mean that some people may have little or no problem with mycotoxin exposure, while others may be very sensitive to low amounts of specific mycotoxins.  Understanding the different types – along with understanding your genes – can help you to identify what may be a problem for you.

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][ref] Ochratoxin A also changes the absorption of nutrients in the intestines.[ref]

Zearalenone is produced by Fusarium species that grow on corn or other grains.[ref] 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: “a non-steroidal compound that exhibits oestrogen-like activity”.[ref]

Aflatoxins are produced by a couple of different Aspergillus species. There are 18 types of aflatoxins, with aflatoxin B1 being one of the most toxic and carcinogenic.[ref]

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 the medical term for acute aflatoxin exposure that leads to liver damage, jaundice, and, in severe cases, death.[ref] Aspergillosis is a lung infection caused by Aspergillus infections in the lung. This mainly occurs in immunocompromised people. [ref]

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

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

An interesting observation by researchers is that fumonisins reduce 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 in wheat, beans, and some spices. Deoxynivalenol causes severe gastrointestinal issues similar to food poisoning when consumed via contaminated foods.[ref]

Patulin is a mycotoxin produced by Aspergillus, Penicillium, and Byssochlamys sp. It is most often found on apples, but can also occur on other moldy fruits or grains. The biggest dietary source is apple juice made from apples that aren’t fresh. Patulin can cause gastrointestinal problems and also organ damage.[ref] Patulin binds to thiol groups found in the intracellular antioxidant glutathione, which then causes oxidative stress, mitochondrial dysfunction, and cell death.[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: 
An inflammatory response occurs when lung tissue is exposed to airborne trichothecenes. Il-1B increases in a manner dependent on NLRP3 activation.[ref]

Mitochondrial dysfunction:
This mycotoxin can impair mitochondrial function and inhibit the synthesis of certain proteins.[ref] Even at very low levels, mycotoxins, such as aflatoxin, can cause mitochondrial dysfunction and cell death. In the mitochondria, mycotoxins can cause disruption in the respiratory chain, decreasing the production of ATP and leading to chronic diseases.[ref] Some mycotoxins, such as patulin, can bind to thiol groups in glutathione, thus decreasing this essential cellular antioxidant. Without enough glutathione, oxidative stress and mitochondrial dysfunction.[ref]

Organ damage and lung inflammation:
From airborne exposure to cereal grain fungi, the mycotoxins can travel from the lungs to the liver, kidneys, and spleen. Mycotoxins can cause inflammatory cytokines to increase in all of these organs. Specifically, researchers found higher levels of IL-1B, IL-6, and TNF-alpha.[ref]

Aflatoxin G1 airborne exposure significantly increases inflammation in the lung. [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 SNPs

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]

Atopic dermatitis (eczema):
Long-term exposure to visible mold during infancy increases the risk of atopic dermatitis.[ref]

2 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 symptoms. Researchers think that a percentage of food poisoning cases each year are actually due to mycotoxins.

Chronic exposure to mycotoxins can come from food or a moldy environment. For example, mycotoxins often contaminate coffee beans and tea leaves at very 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, mycotoxins can be airborne and enter your lungs when you breathe. Some mycotoxins can also enter through your skin. Homes that have been water damaged from floods, roof leaks, plumbing drips, or AC water leaks can develop mold in hidden places, leading to mycotoxin exposure through the air.

Detoxifying mycotoxins: pathways involved

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 of the detoxification pathways involved in mycotoxin elimination:

Aflatoxin detoxification:
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:
Exposure to 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]

Zearalenone:
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 takeaway: Knowing the specific mycotoxin involved is important for understanding which detoxification pathway to target.

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

I want to take a moment to do a bit of ‘myth busting’ here. 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” (sometimes from practitioners selling tests and supplements).

Some natural health websites write about mold genes and refer to certain HLA types — which are actually pretty common and found in over a quarter of the population. About 20 years ago, practitioners found that people with these HLA types were over-represented in having mold reactions. They explained the 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’m not finding a lot of high-quality research here – other than a couple of case studies.[ref][ref] There are research-backed links between asthma, HLA types, and mold sensitivity in children.[ref] There are thousands of research studies on the poisoning-type symptoms from mycotoxins, but the “mold gene” information on alternative health sites doesn’t seem to overlap with those studies.

Does a lack of peer-reviewed research mean that people don’t really have mold illness? Of course not. Clinicians make valid discoveries about health all the time, and not everything is written in a peer-reviewed journal. But here I’m sticking with just explaining what high-quality research studies show.

 

Let’s take a look at what research shows for genetic variants that do interact with mold and mycotoxins:

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Lifehacks for mycotoxins: Supplements, lifestyle changes, environmental factors

The big picture with mycotoxins is avoidance when possible and then counteracting the negative effects of exposure. Let’s look at multiple ways of doing this (backed by research studies).

Avoiding mold contamination:

First up, let’s look at what research shows about environmental factors for mold exposure from food, housing, and medications.

Sources of mold in your diet:

In general, food production and storage are important in avoiding mold contamination, especially in humid climates.

Coffee beans from tropical regions can easily become moldy. Coffee can be a source of mycotoxin contaminants, and older studies show that mycotoxin contamination was fairly common.[ref][ref] However, new testing shows that many organic brands of coffee are both mycotoxin and pesticide-free. Tested brands included Peet’s, DeathWish, Bulletproof, and 12 more.[article] A large 2022 study in Saudi Arabia found that 28% of green coffee beans (not roasted) had ochratoxin A contamination, but only 4% of the roasted coffees contained mycotoxin.[ref]

Peanuts, especially in tropical regions, are a big source of aflatoxin exposure.[ref][ref]

Pigs that are fed grains that are 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 in all areas. But this is a reason to choose high-quality pork or pork from a known local farmer when possible.

Research shows that the coffee pot reservoir and basket or pods with wet grounds are also sources of daily bacterial and fungal exposure, so be sure to clean your coffee machine regularly. Certain Aspergillus species thrive on caffeine.[ref][[ref][ref]

Pollen, such as bee pollen supplements, has been shown to harbor aflatoxins, ochratoxins, fumonisins, zearalenone, and other mycotoxins.[ref]

Check your environment for mold:

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.

Here are a few studies on airborne mycotoxins in buildings:

• A study in a school in Malaysia found that children had more 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]
• The washing machine, especially around the lid/door and the detergent tray, can be a big source of fungal and bacterial biofilms in the home.[ref] Sanitize your washing machine regularly.

Drugs that may slow down detoxification:

Mycotoxins may be impossible to avoid completely, but most people have no problem with low-level exposure. However, if you are impairing your detoxification pathways with prescription medications, it could be adding to your mold problems.

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

Supplement to improve mycotoxin detoxification pathways:

First, let’s look at some ways to generally reduce the oxidative stress in cells due to mycotoxin exposure. Excess ROS causes oxidative stress in cells and mitochondrial dysfunction, leading to a decrease in cellular energy.

Next, I’ll go through some specific mycotoxin pathway targets, if you know a specific mycotoxin exposure or to counteract your individual genetic susceptibility.

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Related Articles and Topics:

Mast Cell Activation Syndrome
Mast cells are essential to your innate immune system, defending against pathogens and allergens. For some people, mast cells can be triggered too easily, giving allergy-like responses to many substances.

Chronic Sinusitus Genes
Genetics plays a role in the likelihood of having chronic sinus problems. This article looks at the genetic reasons driving some people to have chronic sinus infections.

Rheumatoid Arthritis Genes
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