A couple of years ago, I decided to contact one of the researchers whose name appears in this present editorial on microbes and Alzheimer’s disease.
I contacted this researcher because I wanted to inform them about
Dr William Pridgen's experimental antiviral protocol for treating herpes simplex I infections in fibromyalgia, as I thought this antiviral protocol might be worth trying for HSV-1-associated Alzheimer’s.
This researcher told me that unfortunately it would be almost impossible for their research team to obtain a grant to study the use of antivirals on Alzheimer’s patients, as some
influential people in the Alzheimer’s field regard the idea of microbes playing a causal role in the disease as heretical, and these influential scientists block all grant applications for studies on microbial associations to Alzheimer’s. I found that rather shocking.
So it is not just in the field of ME/CFS that the idea of micro-organisms playing a causal role in disease is routinely dismissed by many researchers.
I would like to know whether microbial etiologies of chronic disease are dismissed on scientific and evidential grounds, or merely just on philosophical or ideological grounds.
By "philosophical or ideological" grounds, I mean that researchers just simply do not feel comfortable with the idea that infectious microbes in common circulation can trigger and/or maintain chronic disease. Because accepting such an idea would of necessity lead to a radical re-evaluation of how we understand, prevent and treat chronic disease.
Thus I question whether there some kind of ideological dislike in the minds of many researchers against the idea infectious microbes could play a major role in disease.
Accepting the possibility of a microbial etiology in chronic disease does not of course imply that other etiological avenues should be ignored. For example, POTS (postural orthostatic tachycardia syndrome) often appears after viral infection, and preliminary studies show that POTS may be driven by autoimmunity. Thus these two (tentative) facts suggest that under certain conditions, infection might play a role in triggering and/or maintaining autoimmunity in POTS.
Now, it may well turn out that it's easier and more effective to treat POTS by treating the autoimmunity than by treating the viral infection (not least because medical science does not at present have much in the way of good antivirals). However, it would not seem a good idea to suppress research on the viral angle on POTS, just because the autoimmunity in POTS may be an easier route to treat this disease.