Celiac Disease and Mycotoxins

Celiac disease and Mycotoxins: Is there a relationship?

Short answer: there is no proven genetic link that directly connects celiac disease and mold (mycotoxin) toxicity, but there may be overlapping genetic susceptibilities that influence how some people respond to both.

Genetics of Celiac Disease: Well Established

Celiac disease has one of the strongest known genetic associations among autoimmune conditions. Over 95% of people with celiac disease carry one or both of the following HLA genes:

• HLA-DQ2

• HLA-DQ8

These genes affect how the immune system presents gluten peptides to T cells. Importantly:

• Having HLA-DQ2 or DQ8 is necessary but not sufficient to develop celiac disease.

• About 30–40% of the general population carries these genes, but only ~1% develop celiac disease.

• Environmental triggers (gluten exposure, infections, microbiome changes) are required.

These HLA genes are specific to antigen presentation and do not directly control detoxification of toxins like mycotoxins.

The Genetics of Mold / Mycotoxin Susceptibility are less clear

“Mold toxicity” is not a single disease and does not have a universally accepted genetic definition in mainstream medicine. However, research and clinical observations suggest that individual responses to mycotoxins vary, possibly due to differences in:

• Detoxification pathways

• Immune regulation

• Inflammatory responses

Genes sometimes discussed in this context include:

• HLA-DR variants (different from HLA-DQ2/DQ8)

• Phase I & II detoxification genes (e.g., CYP450 enzymes, GSTs)

• Inflammation-related genes (e.g., TNF-α polymorphisms)

Evidence here is inconsistent and incomplete, and no genetic test can currently diagnose “mold toxicity.”

Where the Overlap May Exist

While there is no single shared gene, overlap may occur at a functional level rather than a disease-specific one.

1. Immune Reactivity Bias

People genetically predisposed to autoimmunity (like those with celiac disease) often have:

• Heightened immune sensitivity

• Strong inflammatory responses to environmental stimuli

This does not mean mold causes celiac disease—but it may mean some individuals respond more intensely to immune triggers, including toxins.

2. Gut Barrier Genetics

Genes involved in:

• Tight junction integrity

• Mucosal immune regulation

may influence both:

• Susceptibility to intestinal damage in celiac disease

• Absorption and systemic effects of mycotoxins

In celiac disease, increased intestinal permeability is common—this could theoretically increase systemic exposure to dietary toxins, regardless of genetics.

3. Detoxification Capacity (Indirect Relationship)

Some individuals may have genetic variants that reduce efficiency of:

• Glutathione production

• Mycotoxin conjugation and excretion

If someone with celiac disease also has:

• Ongoing gut inflammation

• Nutrient deficiencies (e.g., zinc, B vitamins)

detoxification pathways may be functionally impaired, even without a clear genetic defect.

What Is Not Supported by Evidence

• A single “celiac + mold gene”

• Mold toxicity as a cause of celiac disease

• HLA-DQ2/DQ8 causing impaired toxin detoxification

• Genetic testing alone diagnosing mold illness

Claims that a specific HLA type proves mold sensitivity should be viewed cautiously.

Practical Takeaway

• Celiac disease has a strong, well-defined genetic basis.

• Mold/mycotoxin sensitivity does not yet have a clearly defined genetic basis.

• Some individuals may have overlapping vulnerabilities related to immune reactivity, gut integrity, and detoxification—but these are indirect and variable, not deterministic.

In other words: The genetics of celiac disease may make some people less resilient to additional environmental stressors, including mycotoxins—but they do not genetically link the two conditions.

If you suspect to have both or you are celiac and suspect to have mycotoxins, contact me. Let's see if there is something underneath!