Mould Exposure and Autoimmune Disease: What’s the Connection?
Photo by Kelly Sikkema on Unsplash.
I remember the first time I did a training with an American practitioner who talked about mould as a common issue in their mast cell activation syndrome (MCAS) clients, many of them with autoimmune issues. Though compelling, I thought mould toxicity was a fringe issue, likely affecting only a handful of people.
These days, I know better. Mould toxicity affects a large chunk of my client population, and I’m constantly finding new and surprising ways that symptoms of it can manifest.
Most people think of mould as something that smells musty or grows on old bread, but for many, mould exposure can have much deeper effects — particularly on the immune system. Increasing research links chronic exposure to water-damaged buildings and mould toxins (mycotoxins) to immune dysregulation and even autoimmune disease.
How Mould Affects the Immune System
Moulds like Aspergillus, Penicillium, Cladosporium, and Stachybotrys release microscopic spores and chemical by-products known as mycotoxins. These substances can act as irritants and immune disruptors, particularly when exposure is prolonged or occurs in poorly ventilated environments such as water-damaged homes.
When inhaled or absorbed through the skin, mycotoxins are recognised by the immune system as potential threats. The body’s “front-line defenders” — macrophages and dendritic cells — sense these toxins using molecular sensors called pattern recognition receptors (for example, Toll-like receptors). When these receptors are triggered, they switch on intracellular signalling cascades such as NF-κB, a key pathway that drives inflammation.
Once activated, these immune cells release messenger molecules known as cytokines, including interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β). These cytokines recruit more immune cells to the area, amplify inflammation, and can even affect how the nervous and endocrine systems function.
While short-term activation is part of a healthy defence response, chronic exposure to mould toxins can keep this alarm system switched on. Over time, this leads to oxidative stress, mitochondrial strain, and immune “priming” — where the immune system becomes hypersensitive and more likely to overreact to otherwise harmless stimuli. In genetically or environmentally susceptible individuals, this state of constant vigilance can tip the immune system into autoimmunity, where it begins to attack the body’s own tissues.
Mould and the Gut–Immune Axis
One of the key mechanisms linking mould to autoimmune disease lies in the gut microbiome. Mycotoxins such as ochratoxin A and aflatoxin B1 have been shown to damage intestinal tight junctions and alter gut microbial composition.
This process — often called leaky gut or increased intestinal permeability — allows antigens and microbial fragments to enter circulation, where they can trigger immune reactions. Once the gut barrier is compromised, molecular mimicry and bystander activation become more likely — both recognised mechanisms in autoimmune disease development.
For example:
Ochratoxin A increases gut permeability and provokes IL-6-driven inflammation.
Trichothecenes (from Stachybotrys chartarum) can suppress normal immune cell function, then cause rebound inflammation once exposure ends.
Gliotoxin from Aspergillus fumigatus directly impairs T-regulatory cell activity — the very cells responsible for maintaining immune tolerance.
On top of all this, many people exposed to mould also experience MCAS, leading to symptoms such as flushing, brain fog, fatigue, or food sensitivities. Mast cells are sentinel cells that respond to both infection and toxins, releasing histamine, tryptase, and inflammatory cytokines when activated. Many of them are located in the gut but they’re found around the entire body.
Chronic exposure to mould toxins has been shown to destabilise mast cells, making them hyper-responsive to even minor triggers. This ongoing histamine and cytokine release further fuels autoimmunity by perpetuating inflammation and oxidative stress.
The Role of the Liver and Detoxification
Because mycotoxins are fat-soluble, they tend to accumulate in fatty tissues and cell membranes, where they can interfere with mitochondrial energy production and cellular signalling. Unlike water-soluble toxins, which are easily flushed out through the kidneys, fat-soluble toxins must first be processed by the liver before they can be excreted.
The liver’s detoxification process occurs in two main stages. Phase I enzymes (primarily the cytochrome P450 family) convert these compounds into more reactive intermediates, and Phase II enzymes then neutralise them through conjugation pathways such as glucuronidation, sulfation, and glutathione conjugation. Once bound to these molecules, the toxins can be carried safely out of the body via bile or urine.
However, in genetically or nutritionally vulnerable individuals — for example, those with variants in GST (glutathione S-transferase), MTHFR, or CYP450 genes — these detoxification steps may not function optimally. Nutrient deficiencies (especially in B vitamins, magnesium, sulphur-containing amino acids, and antioxidants) can further slow these pathways. The result is a toxin backlog, which not only perpetuates oxidative stress but also maintains immune activation, a key factor in autoimmune disease progression.
Supporting detoxification requires a balanced and gradual approach. Providing the body with antioxidants such as vitamin C, glutathione precursors like N-acetylcysteine, and sulforaphane-rich vegetables (e.g., broccoli, kale, and rocket) helps buffer oxidative stress and enhance Phase II clearance. Ensuring adequate bile flow through hydration, movement, dietary fibre, and gentle liver support is equally important, since bile is the main route of mycotoxin elimination.
However, this process needs to be done slowly and carefully, particularly in those with existing inflammation or sensitivity. Mobilising toxins too quickly can overwhelm the body’s elimination capacity and temporarily worsen symptoms such as fatigue, brain fog, or joint pain. A stepwise approach that stabilises the gut, supports the liver, and restores nutrient reserves before promoting detoxification tends to yield the best outcomes.
Common Autoimmune Conditions Linked to Mould Exposure
While research is ongoing, clinical reports and case series suggest mould exposure may exacerbate or trigger:
Hashimoto’s thyroiditis
Multiple sclerosis
Rheumatoid arthritis
Systemic lupus erythematosus
Autoimmune autonomic ganglionopathy (particularly in people with POTS-like symptoms)
In each case, the underlying mechanism involves some combination of immune hyper-reactivity, molecular mimicry, oxidative stress, and impaired detoxification.
Taking a Holistic Approach
If mould exposure is suspected, testing can include:
Urinary mycotoxin testing (for exposure assessment)
Organic Acids testing (for exposure assessment, plus tracking biochemical impacts)
Environmental mould testing (e.g., ERMI or HERTSMI-2)
Microbiome analysis to assess gut health
But testing is only one piece of the puzzle. I also ask a series of questions in my initial intake session with clients to assess for potential mould exposure and symptoms. These questions then inform the type of testing we do and a recovery plan moving forward.
Meanwhile, recovery often involves:
Reducing or eliminating exposure
Supporting detoxification and liver function
Repairing the gut barrier
Stabilising mast cells and calming the nervous system
Addressing micronutrient deficiencies
Gradually rebuilding immune tolerance
In Summary
Mould exposure doesn’t just affect the respiratory system — it can reach deep into the immune network, altering how the body recognises “self” from “non-self.” For individuals with a genetic or environmental predisposition, this can be the spark that triggers autoimmune activation.
The immune system never acts out without a good reason for its activities. When we recognise how profoundly mould can influence immune function, energy, and wellbeing, it opens the door to deeper healing — restoring balance not just in the immune system, but throughout the entire body.
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