I used to have two posts on this subject. Between them they said that a quarter of people carry genes that stop them clearing mould toxins, that toxins build up in your tissues for years, that a urine test confirms the problem, and that there is a correct sequence of binders to clear it. When I went back to the sources, most of that didn’t hold. So I’ve merged the two into this one and rewritten it. What changed is listed on the corrections page.
What is well evidenced: damp homes and breathing
A review of the epidemiological studies by Mendell and colleagues found that visible damp or mould indoors was consistently linked with asthma developing and getting worse, wheeze, cough, breathlessness, respiratory infections, bronchitis, allergic rhinitis and eczema, in people with and without allergies. The evidence “strongly suggested” that damp and mould cause asthma attacks in children (Mendell 2011). NHS inform says the same in plainer words: moulds produce allergens and irritants and can trigger asthma attacks (NHS inform, Damp and mould indoors).
The same review found that measuring particular moulds or microbes in house dust gave limited and mixed results, and concluded that current evidence doesn’t support measuring them to decide what to do. Damp and visible mould are the risk; fixing them is the action.
Damp/mould and breathing problems: strong and consistent across studies; causal for asthma attacks in children.
Mycotoxins from a damp building causing fatigue, brain fog or multi-system illness: not established. The details are below.
What mycotoxins are, and where most of them come from
Mycotoxins are compounds some moulds make. Most of the exposure people have comes from food, not buildings. In a Dutch study of 36 pregnant women, two mycotoxins (deoxynivalenol and zearalenone) were found in the urine of every woman, and ochratoxin A in the blood of every woman; the researchers judged the levels to be of low concern (McKeon 2024). Finding mycotoxins in a person is normal.
Ochratoxin A (OTA)
Mainly from cereals, coffee, dried fruit and wine. It does stay in the body a long time: in one volunteer the blood half-life was about 35 days (Studer-Rohr 2000). Kidney damage is shown in animals; EFSA judged the risk of non-cancer effects at usual dietary intake to be low concern for most people (EFSA 2020).
Aflatoxins
Almost entirely dietary: groundnuts, tree nuts, maize, spices. Aflatoxin B1 causes liver cancer at high dietary exposure (EFSA 2020). Building exposure is not the usual source.
Trichothecenes
Stachybotrys makes the macrocyclic ones (roridin, verrucarin, satratoxin); Fusarium makes deoxynivalenol in cereals. They block protein synthesis in lab and animal studies. Effects at the levels found in homes haven’t been shown.
Gliotoxin
Suppresses immune cells in the lab. A. fumigatus matters in people with weakened immunity or lung disease, and that is a medical diagnosis, not a urine test. What a urine level means is unknown.
Zearalenone
Oestrogen-like in lab and animal studies. Most exposure is from cereals. No study I’ve found links a urine level to a hormone problem in a person.
Citrinin and enniatins
Mostly food contaminants of grains. Kidney and cell effects come from animal and lab work.
What isn’t established
“Mould illness” as a mycotoxin disease
The German multi-society guideline on indoor mould (AWMF, updated 2023) is the most thorough clinical guideline I know on this. It covers allergy, irritation and infection from indoor mould, and it states that measuring mycotoxins in blood or urine has no indication in diagnosing people exposed to indoor mould and shall not be done (strong consensus) (Hurraß 2024, AWMF guideline). I hold a different view from that guideline only where I can point to evidence, and here I can’t.
CIRS
“Chronic Inflammatory Response Syndrome” comes largely from one clinician’s research group, with its own case definition and markers (MSH, TGF-beta-1, MMP-9, C4a, visual contrast sensitivity). I haven’t found independent studies validating that case definition. Grade: mechanistic and untested outside its originating group.
“24% carry HLA-DR genes that can’t clear mycotoxins”
I repeated this. I can’t find a population study behind the figure. What PubMed has is case reports: four people in one paper (Saghir 2024; the first author lists an affiliation with a mould-litigation firm) and one person in another (Gunn 2016). HLA-DR types are genuinely linked with mould allergy in children with severe asthma, which is a different thing. Grade: none for the 24% claim. I don’t recommend HLA-DR testing for this.
Glyphosate making mould toxicity worse
I said glyphosate impairs liver enzymes so mycotoxins build up. I found no human study testing that. Removed.
“Gut fungi make mycotoxins from the inside”
Not shown in people. No OAT or GI-MAP marker is validated as a sign of mycotoxin exposure.
Urine mycotoxin tests: what a result can and can’t tell you
A urine test shows exposure, mostly from food. It doesn’t diagnose illness, and there is no published validation of urine levels for that. The study most often quoted, where 93% of 112 people with chronic fatigue tested positive, used ELISA tests, had no control group tested at the same time (55 healthy people had been tested earlier by the same lab), and was co-authored by someone from the testing lab (Brewer 2013).
Sauna or exercise “challenges” before collection, which I used to describe as improving sensitivity, have no evidence behind them. The lab’s own preparation is what counts.
I used to offer the MycoTOX Profile for this. I stopped: it shows exposure, mostly from food, it doesn’t diagnose illness, and the German guideline above says it shouldn’t be used for that. If you already have a result, here’s how to read it. Otherwise I’d rather you spent the money on a surveyor.
What I’d do first
Places I see damp missed in Scottish homes, from practice rather than studies: stone walls where breathable lime mortar has been replaced with impermeable render; loft conversions and extensions without proper vapour barriers; flat roofs; under-floor voids in older buildings; and cars that have had water in them.
One question I always ask: do your symptoms ease when you’re away from the building for several days and come back when you return? It’s a useful clue that points at the building. It isn’t a test, and it can’t tell mould from anything else in that building.
Binders, glutathione and “detox” protocols
The only placebo-controlled data on cholestyramine for illness linked to water-damaged buildings is a two-week trial in 13 people at a single clinic, run by the group that defined CIRS (Shoemaker & House 2006). The German guideline lists cholestyramine “detoxification” among treatments without sufficient scientific evidence. Cholestyramine is a prescription medicine in the UK, and it binds other medicines.
Charcoal, clay, zeolite, glutathione, NAC and “drainage” for mould: untested. What a binder can and can’t do is in Binders: what’s actually evidenced. I don’t give doses or a “correct sequence”, because there isn’t one with evidence behind it.
If your home is damp, that matters for your health, especially your chest. Fix the building, look after your lungs, and be wary of anyone, me included, who offers a urine test as the answer to fatigue and brain fog. Those symptoms have many causes, and they deserve a proper look at all of them.