Dual-factor theory of ME/CFS
One argument that may
link mold, biotoxins and other chemical toxins
to triggering ME/CFS is the fact that ME/CFS can appear in severe yet
very localized infectious epidemic outbreaks.
The London 1955 Royal Free Hospital ME/CFS outbreak is one example of a very localized epidemic which afflicted 1 in 10 of the hospital staff, but affected very few people outside the hospital, in spite of the virus being pretty contagious; and the 1984 Lake Tahoe outbreak is another localized outbreak that was severe, but did not spread to the rest of the country.
I always found it very perplexing that infectious epidemic outbreaks of ME/CFS could cause such severe disease, and yet not spread much further than the localized environment, apart from perhaps some sporadic appearing as the virus spreads outwards. To me, that makes it
impossible that epidemic ME/CFS is caused by a virus alone, because if it were just a virus, then that virus would have spread to the whole region or country, and caused the same devastation throughout.
But it seems that as these viruses leave the vicinity of these outbreaks, they lose most of their ability to cause ME/CFS.
To my mind, that means there
must have been some local cofactor (such as a toxin) present only in the vicinity of the outbreak — a cofactor which in combination with the virus then causes ME/CFS. And as soon as the virus spreads further than the local area containing the toxic cofactor, the virus loses most of its ability to trigger ME/CFS.
So this argument presents the logical requirement for such a cofactor, and this then makes us consider the possibility of mold, biotoxin or toxic chemical cofactors being present only in the vicinity of the outbreak, acting in tandem with the virus to trigger ME/CFS.
In the case of Royal Free Hospital, there were investigations into possible toxic chemicals in the hospital environment (including investigations into the use of pesticides, chemicals used in the kitchen and catering, and the paints and materials used during renovations; ref:
1). These investigations came back negative.
However, I think back in 1955, nobody would have been aware of toxic mold (as there was no knowledge about mold toxicity then), and so would not have looked for it. Thus it is conceivable that there may have been water damage and a toxic mold growth in communal staff rooms in one or more of the hospital buildings, which in combination with the virus, caused the Royal Free outbreak. If the mold infested rooms were used by staff only, that could also explain why it was mostly only the hospital staff who contracted ME/CFS, with very few hospital patients being affected.
Or it could be that since patients do not usually stay that long in hospital, their exposure to the presumed toxins in the building would be minimal. But staff working in the hospital for years would be more heavily exposed, especially if the toxins were bioaccumulative.
Likewise, in the case of the Lake Tahoe outbreak, Lake Tahoe survivor
@Erik Johnson points out that in the year of the epidemic, a bright green cyanobacteria (toxic algae) started growing all over the beach of Lake Tahoe, which he found made him a little sick. Erik says that a toxic cyanobacteria called
Microcystis which periodically grows in the Boca Reservoir (located just north of Lake Tahoe) sometimes results in contamination of the water supplies of both Reno and Lake Tahoe. So this Microcystis toxic cyanobacteria may have been one of the biotoxins present during the outbreak.
Erik also points out that people who were living or working in buildings he knew to be moldy were more likely to get ME/CFS during the Lake Tahoe outbreak (Erik had had a lifelong mold allergy, so was familiar with which buildings in the area had a mold problem).
Erik Johnson has been championing the theory that toxic mold and biotoxins were the cofactors behind the Lake Tahoe outbreak ever since that outbreak occurred.
For Erik, it was mold avoidance that was key to recovering from his Lake Tahoe ME/CFS (but remember that Erik was mold sensitive anyway, so this treatment may not work for other ME/CFS patients).
Erik sometimes posts on this forum (see his posts
here).
So I think the localized nature of the above ME/CFS outbreaks suggests a
dual-factor theory for ME/CFS, where a virus may only cause ME/CFS in combination with some immune suppressing factor, such as a toxin.
One fact that tends to corroborate this dual causal factor theory is Dr John Chia's discovery that an acute viral infection + corticosteroids often triggers ME/CFS (see
this post for details of Chia's corticosteroid discovery).
Dr Chia investigated thousands of ME/CFS patients' case histories, and noted that ME/CFS was often triggered in these patients when corticosteroids were prescribed during the course of an acute infection. Corticosteroids weaken the immune response, so it seem that when the immune response is weakened during the time of an acute infection when you first catch a virus linked to ME/CFS, that creates the conditions necessary for the virus to trigger ME/CFS.
So with acute viral infection + corticosteroids, we see another example of the dual causal factor theory of ME/CFS.
I think to toxic algae or mold may have analogous immunosuppressive effects to corticosteroids, weakening the immune response in such a way that allows the virus to trigger ME/CFS.
A generalized and broader version of the Dual-Factor Theory of ME/CFS is outlined in
this post.
