This interests me because in a previous life I used to know a bit about macrofungi – mushrooms etc. I find the mould theory difficult to get to grips with because of the gaps between what is known and what is proposed seem so large. Fungal toxicity in mammals, via dietary sources, from either mushroom poisoning or contaminated plant material requires ingestion of grams or kilograms respectively, of the source material to produce acute effects. There seems very little available data on the levels of ingestion required to produce chronic effects in humans, although chronicity is known to be associated with major organic harm (liver damage, cancer). I don’t understand how there could be continuous exposure to health impairing levels of mycotoxins without liver damage being evident in at least some cases.
There also seems to be confusion in some of the discussions, between spores and toxins, as well as some problematic views on the human facial sinuses . All fungi produce spores to sexually reproduce, we are surrounded by fungal spores all the time and while these can (like plant pollen) cause allergic responses, the amount of toxicity (if it exists at all ) that is inhalable is in most circumstance very, very small. Certainly some microfungi can produce serious infection, but that isn’t the same thing as toxicity, just because a fungus produces a mycotoxin under some circumstances, doesn’t mean that it is perpetually throwing out toxins. Also the idea that a fungus can set up home in a facial sinus, and then proceed to produce high levels of mycotoxins seems rather improbable. Certainly the vector by which the toxins enter the body isn’t by spores being aerosolised via the nasal passage. The volume of the skeletal cavity of the frontal sinus is about 10mls in an adult human, and this is largely filled with soft tissue and mucous, the passage between sinus and the back of the nose is less than a millimetre across and is mucous filled.
If a fungi are in the sinus and are producing mycotoxins, then it would seem more likely that the toxins are being directly absorbed into the soft tissue. Even were this to be the case the volumes needed to produce a health impact still seem mismatched to a low level of surface infection. It might be different if people had ballooning faces, tooth abscess style, but there just doesn’t seem enough infecting organism present to produce enough toxin to be disease causing.
The levels of toxins in urine set as being significant by Brewer seem to be in the order of 1 part per billion. This is as compared to a base of less than 2 parts per 10 billion in healthy controls. There seems to be no data on what levels of mycotoxin in urine are consistent with known disease, but in the US, 50 parts per billion of aflotoxin in food stuffs of is considered safe for human consumption, and it seems feasible that >50 ppb ingested orally would yield a small measure in urine. The differential between healthy controls* and declared chronically ill, would be explainable by differences in digestive function or immune system performance, so I’m unclear why these urine tests are considered significant.
I’m not suggesting that fungal exposure can’t be an issue in ME/CFS but I don’t understand why allergy is not sufficient to explain the symptoms involved (headache, nausea etc) rather than some arcane solution that requires novel behaviour (super mould ? ) and novel responses by the human body.
* Added: On further reading I see what others meant by lack of helathy controls. Brewer et al describe their controls as 'patients' but don't say what their health status actually was, but rather that the controls didn't have known mould exposure. This is a pretty unsatisfactory basis on which to build a treatment programme, moulds are ubiquitous in the environment and just because someone doesn't live in a building with obvious mould growth doesn't mean they are not exposed to 'infectious' spores. Even if the testing regime were to have identified a significant difference (debatable) between controls and 'non controls', there are numerous confounding elements that need to be addressed.