- Last Updated: 07 November 2015 07 November 2015
Current theories of pathogenesis
The "Why" behind the "What"
After this symptom review, Dr. Bell proceeded to a theory review: a look at the most popular current theories about the cause and nature of CFIDS/ME, and their strengths and weaknesses in explaining the illness fully.
First Bell addressed the theory of persistent subclinical infection. Historically (especially in the early and mid-'80s), this was the most prevalent hypothesis; with reactivated Epstein-Barr virus commonly considered the driving force behind the illness (which was, in fact, called chronic Epstein-Barr syndrome at that time). Myriad other agents have been proposed since then, with Human Herpes Virus 6 still under active consideration, as well as other herpes family viruses, a "stealth" virus, a retrovirus, Coxsackie virus, Chlamydia, and more—many more, as any issue of The UPDATE or The CFIDS Chronicle will demonstrate. Bell finds this theory unconvincing, since no single bodily area of infection and no single causative agent has yet been pinpointed, despite more than a decade of research. "This theory may be correct," he said, "but my hunch says otherwise."
Second is a related conjecture that CFIDS/ME results from agent-induced immune activation i.e., that some trigger (most likely a virus or bacterium) alters the immune system and keeps it habitually upregulated, with the bulk of CFIDS/ME symptoms stemming from the immune abnormalities rather than the triggering agent. While this remains the most prominent theory at present, it suffers from one deficiency also embodied in the first: the failure to identify a single infectious or other agent in a majority of PWCs. Moreover—and more significant—says Dr. Bell, "The sickest people should, but don't, have the worst immune-system activation. The immune activation is there, but we haven't been able to explain why, and if it were closely linked to the cause [of CFIDS], the severity of the illness should parallel the severity of the immune activation."
(In a humorous aside, Dr. Bell noted that he once subscribed to this theory but no longer believes it's correct: "If anyone here was misfortunate enough to purchase my book [The Doctor's Guide to Chronic Fatigue Syndrome], this theory is the whole second half of the book. I now think it's all wrong and I want to apologize for having wasted your money. ")
Three other theories that Bell quickly dispatched: abnormal adrenal function (it doesn't account for enough of the CFIDS/ME symptomatology); mitochondrial disease ("hard to study and hard to measure"); and the notion that CFIDS/ME is either psychosomatic or a form of malingering ("an attitude which, fortunately, is beginning to disappear, especially in the last five years").
Having provided his opinion of these theories and their shortcomings, Dr. Bell introduced his new hypothesis—still in the initial stages and requiring more research, still not an answer for every patient he's studied, but intuitively logical, consistent with a lion's share of the CFIDS/ME symptoms just listed, and quite promising in terms of identifying treatments: neurocirculaton asthenia.