By the way, I have no scientific training beyond high school. Previously you indicated you "used to know a bit about macrofungi". You may have some training that would lend more credence to you opinion. If so, I think many people would want to know. Can you elaborate on that?
Credence to an opinion on a web forum ??? The phrase ‘used to know a bit’ was intended entirely literally, I’m not claiming professional insight and anyway post illness onset any such capacity becomes in doubt, particularly in the biological sciences where things are subject to rapid change and constant updating of knowledge is needed. What I do take from past knowledge though is that fungi are all around us and are part of us, and because of that identifying fungi as pathogens needs more than the coincident presence of their biological by products.
I really don’t think that Brewer’s work needs specialist appraisal to identify the short comings – you’ve identified an issue of concern yourself but gloss the significance:
I don't understand why some people say there were no healthy controls. In the paper it was stated that the controls were "healthy" with "no known toxic mold exposures in water-damaged buildings".
The CFS paper does indeed state ‘healthy controls’ but there were no controls at all in that paper. The ‘controls’ are referenced to a previous work where they are described not as ‘healthy’ but as ‘patients’, and their selection is based on reporting of non mould exposure. There was no randomisation involved. I’m not going to labour through why the methodology is dubious, but as I wrote in a reply on the CFSPatientadvocate Blog:
In Int. J. Mol. Sci. 2009, 10, 1465-1475; doi:10.3390/ijms10041465 Brewer and others, selected 55 patients (health status unstated) who were deemed not to have had toxic mold exposure (method unexplained) as a ‘control’ group. All 55 tested positive for mycotoxins, however Brewer et al arbitrarily set the results of these ‘non exposed’ controls as the base line between clinical and non clinical significance. There are some obvious problems with this approach, most particularly there is no means to associate a test result and a disease process.
As you’ve noted Re: aflotoxin, there’s a huge volume of research material, much of it in the public domain. The veterinary material (which is very extensive) may not be wholly applicable to humans but it certainly sets some parameters, and aflotoxin related liver disease in humans sets a measure of dietary exposure way beyond anything suggested as relevant in the various CFS mould hypotheses.
The logic of relating percentages of tiny amounts of something to percentages of absolutely vast amounts of something else (alcohol) escapes me entirely. Basically I just can’t see the relationship between known toxicity and what is being claimed. Mould as an allergen is well established and I don’t understand why anything additional is needed as an explanation of what has all the appearance of allergy symptoms in ME/CFS. Given the strong indications of B cell dysfunction (Rituximab etc.) in ME/CFS, if fungi do play a pathogenic role then allergy, which is notable for having responses in the parts per billion range, seems a far more likely vector than toxicity where exposures multiple orders of magnitude higher are required to produce recordable pathology.
I don’t think there’s anything I can add further to this thread, particularly noting the way the discussion is going. My take remains that as far as toxicity is concerned levels are so far below anything associated with known pathology that there’s a pretty profound lack of plausibility in mycotoxins causing disease at those levels. Rhinitis could be caused by non identified fungal infection but I don’t understand how in the absence of competitive trials that could be easily distinguished from ongoing allergy where recurrence is cyclical.
Anyway I shall leave this discussion to others, it certainly isn’t in the frame of the mycological discussions I’m used to.
