Environmental Health · Toxic Exposure · Functional Investigation
Mycotoxins — the toxic metabolites produced by mould — are an underdiagnosed cause of fatigue, brain fog, immune dysregulation, and hormonal disruption. They're largely invisible to conventional testing, and they affect some people profoundly while leaving others untouched. Here's the clinical picture.
There's a particular kind of patient I've seen more times than I can count.
They've been through the NHS. They've had the standard bloods — TSH, full blood count, liver function, maybe a CRP. Everything comes back "normal." They're told they're fine. But they are not fine. They're exhausted in a way that sleep doesn't touch. Their brain feels like it's wrapped in damp cloth. They react to foods they used to tolerate. They ache without obvious cause. They've been handed antidepressants, or a referral to a therapist, or simply a shrug.
Sometimes the missing piece is mould.
Not the mould you can see on a piece of bread. The mould you can't see — growing quietly inside a wall cavity, behind a bathroom tile, under a kitchen floor — producing chemical compounds that accumulate in your body and interfere with processes so fundamental that the symptoms look like almost everything else.
Mycotoxins are toxic secondary metabolites produced by certain species of mould — fungi of the genera Aspergillus, Penicillium, Fusarium, Stachybotrys, and others. They're not the mould itself. They're what the mould produces — chemical compounds that are, in many cases, extraordinarily potent biological disruptors. Some are carcinogenic. Some are immunosuppressive. Some are nephrotoxic. Some disrupt hormone signalling. Some cross the blood-brain barrier.
Produced by Aspergillus and Penicillium species. Found in water-damaged buildings, stored grains, coffee, dried fruit, and wine. Nephrotoxic, immunosuppressive, and neurotoxic. Has been shown to deplete glutathione, inhibit protein synthesis, and accumulate in kidney tissue.
Primarily Aspergillus flavus and Aspergillus parasiticus. Among the most potent naturally occurring carcinogens known. Found in groundnuts, tree nuts, spices, and maize. Aflatoxin B1 is classified as a Group 1 carcinogen by the International Agency for Research on Cancer.
Produced by Fusarium and Stachybotrys species. This group includes the notorious T-2 toxin and deoxynivalenol (DON). They inhibit protein synthesis at the ribosomal level and are profoundly immunosuppressive. Stachybotrys chartarum — "black mould" — is a trichothecene producer and is strongly associated with sick building syndrome.
A Fusarium mycotoxin with oestrogenic activity. It binds oestrogen receptors and disrupts the HPG axis. Clinically relevant in women with unexplained hormonal dysregulation, early puberty, or cycle irregularities.
There are two primary routes that matter clinically.
Inhalation from water-damaged buildings. Any building that has experienced water intrusion — a leaking roof, a burst pipe, rising damp, poor ventilation — can harbour mould colonies within 24 to 48 hours of moisture exposure. The mould grows invisibly inside wall cavities, beneath flooring, behind tiles. You don't need to see it or smell it to be exposed to its metabolites. The UK housing stock is particularly vulnerable.
Dietary exposure. Mycotoxins contaminate food crops globally. Ochratoxin A is found in coffee, wine, dried fruits, cereals, and cured meats. A person eating a diet high in processed grains, nuts, dried fruits, and conventionally grown produce is getting a daily mycotoxin load that regulators acknowledge but don't fully account for in combination.
A secondary dietary route: if you have gut dysbiosis, fungal overgrowth in the intestinal tract becomes an endogenous source of mycotoxin production. The gut becomes a mycotoxin factory from the inside.
The symptoms are non-specific. Fatigue, brain fog, joint pain, headaches, chemical sensitivities, mood disturbance, immune dysregulation, recurrent infections, poor sleep, digestive dysfunction — these are the symptoms of mycotoxin burden. They are also the symptoms of approximately forty other conditions.
Conventional testing doesn't look for it. Standard blood panels don't include mycotoxin markers. Your GP cannot order a mycotoxin urine test.
Mycotoxins also disrupt the very systems that would help clear them. Ochratoxin A depletes glutathione. Gliotoxin suppresses macrophage function. Trichothecenes impair protein synthesis. The result is a deepening spiral — mycotoxin exposure progressively undermines the body's capacity to deal with further mycotoxin exposure.
When I suspect mycotoxin involvement, I'm looking across several layers. On the OAT, I pay particular attention to arabinose and citramalic acid as markers of yeast and fungal activity in the gut. On the GI-MAP, I look at Candida species, Saccharomyces, and broader dysbiosis markers. On blood chemistry, I look at GGT (which rises with glutathione depletion and toxic load) and inflammatory patterns.
The MycoTOX Profile is the direct test — a urine-based panel measuring actual mycotoxin metabolites: ochratoxin A, aflatoxins, trichothecenes, gliotoxin, zearalenone, and others. It identifies which mycotoxins are present, which matters for the remediation and detoxification strategy.
Testing the patient is only half the picture. If someone has significant mycotoxin burden, the first question is where it's coming from. Without addressing the source, the clinical work is swimming against the tide. ERMI or HERTSMI-2 testing of the home environment gives objective data on building contamination.
Binders interrupt enterohepatic recirculation of mycotoxins. Cholestyramine has the strongest evidence base for certain mycotoxins. Bentonite clay, modified citrus pectin, and activated charcoal are used more broadly — timing matters, taken away from food and supplements.
Glutathione support is central given how comprehensively mycotoxins deplete it. Liposomal glutathione, N-acetylcysteine, and glycine as a glutathione precursor are the primary tools. Glycine specifically is underappreciated — inexpensive, well-tolerated, and its role in supporting phase II conjugation is clinically meaningful.
Liver support — phase I and phase II hepatic detoxification. Milk thistle, alpha lipoic acid, B vitamins, and adequate protein all matter here.
Mitochondrial support — mycotoxins, particularly ochratoxin and trichothecenes, impair mitochondrial function. CoQ10, B vitamins, magnesium, and ribose all have roles in supporting energy metabolism during recovery.
Not everyone exposed to mould gets sick. The HLA-DR gene variant is the most studied genetic susceptibility factor. Approximately 24% of the population carry an HLA-DR type that makes them poor at producing antibodies to biotoxins including mycotoxins. These individuals are disproportionately affected and often mount a prolonged, multi-system inflammatory response sometimes referred to as Chronic Inflammatory Response Syndrome (CIRS).
Being the sickest person in a household with a mould problem does not mean you're imagining it. It may mean you're the one with the least capacity to clear what everyone is being exposed to.
Mould illness is real, measurable, and treatable — but it requires someone to look for it. If you have a pattern of symptoms that has defied conventional explanation — particularly fatigue, brain fog, immune dysregulation, and chemical sensitivities — mycotoxin burden deserves serious consideration as a contributing factor.
The investigation starts with the right tests: the OAT for intestinal fungal activity, the MycoTOX Profile for direct mycotoxin measurement, and the full clinical picture. This is exactly the kind of detective work the TDG approach was built for.
MycoTOX Profile · Organic Acids Test · GI-MAP · TDG Five-Test Programme
The DH Clinical Concierge is a good first step — or explore the TDG Five-Test Programme for a full functional investigation.
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