I just read Hilda’s second blog which I missed when it was published.
A couple of points of interest which may have been noted elsewhere:
1. I see that
David Colquhoun (prominent pseudoscience buster) has posted a comment below the blog:
David Colquhoun said:
To what extent do you agree with the following summary?
1. ME/CFS is vaguely defined and probably very heterogeneous. Its diagnosis is therefore arbitrary.
2. Nobody has the slightest idea about what causes it.
3. There are no very effective treatments.
2. I was not previously aware of this part of Hilda’s disclosure which appears at the bottom of the blog:
Hilda Bastian said:
I was a health consumer advocate (aka patient advocate) from 1983 to 2003, including chairing the Consumers’ Health Forum of Australia (CHF) from 1997 to 2001, and its Taskforce on Consumer Rights from 1991 to 2001. I have not experienced CFS/ME and nor has anyone close to me.
However, at the time I first encountered CFS activists, I had a relevant personal frame of reference. I had to leave my occupation several years prior after a severe bout of repetitive strain injury (RSI) following a stretch of workaholism as a teenager. Then, RSI was regarded by some medical practitioners as malingering or psychological, rather than a physical condition. (You can read about the controversy around Australia’s RSI epidemic here, here, and here [PDF].)
As then editor-in-chief of a consumer health information website based on systematic reviews at the NIH, I was pressured about the inclusion of systematic reviews on GET and CBT and approach to CFS consumer information, but not by CFS activists.
I have just submitted the following responses to David Colquhoun’s comment which I assume will appear after being vetted:
“As an ME patient, I would say:
1. ME/CFS is probably heterogeneous, but that doesn’t mean that the diagnosis is arbitrary. It means that it is probably heterogeneous. There are different diagnostic criteria, some of which are more useful than others, and within those criteria there are likely to be different sub-groups and probably different illnesses. However, that doesn’t mean that the diagnosis isn’t useful. The recognition that there are significant numbers of people who are disabled by illness who meet specific diagnostic criteria (particularly post-exertional malaise, or PEM) is important and necessary for advocacy and research. Equally, I strongly agree with the NIH panel which concluded that “the continued use of the Oxford (Sharpe, 1991) case definition may impair progress and cause harm” (as quoted by Hilda above).
2. A bit like CFS, “cause” seems to be a heterogeneous term used to mean different things. There appear to be a number of triggers for ME/CFS, such as EBV, but knowing the triggers is less important than understanding the mechanism, identifying biomarkers, and developing effective treatments. There has been some limited progress made in identifying potential biomarkers (see, for example, this blog on evidence of “something in the blood”:
https://mecfsresearchreview.me/2019...avis-more-evidence-of-something-in-the-blood/) and hypothesising about possible mechanisms but there is still a very long way to go.
Unfortunately, the PACE trial and Cochrane reviews, along with the “collective ad hominem attack” on the ME community by a small group of influential researchers (referred to in Hilda’s previous blog:
https://blogs.plos.org/absolutely-m...-the-me-cfs-exercise-dispute-matters-so-much/) appear to have had a significant effect on inhibiting progress by perpetuating the myth that ME/CFS can be reversed by CBT/GET.
3. Agreed. Moreover, the FINE and PACE trials provide good evidence that CBT/GET are ineffective treatments for ME/CFS, even when using very broad and diagnostic criteria.
Thanks for taking an interest in this, David. And many thanks to Hilda for your blogs and for your ongoing efforts to try to help to resolve the issues which have been so harmful to patients.”
