How ME/CFS Progresses: A Framework for Research and the Prevention, Treatment, and Rehabilitation in ME/CFS Nacul et al 2019

Hi @Mithriel

Yes, chronic EBV was the flavour of the day; looks like the concept of post viral fatigue syndrome was involved in the mix.

Page 71 of the Health and Welfare Canada document (link below) added to the Holmes definition: "From the Proceedings of our workshop we can abstract the following recommendations:

1. Modifications to the case definition of Holmes et al. (Ann Intern med 1988; 108:387-9)
(1) We recommend that chronic fatigue syndrome (CFS) be considered as consisting of 2 types:

Type 1 - CFS with no pre-existing or co-existing major depressive syndrome.

Type 2 - CFS with (a) pre-existing or (b) concurrent major depressive syndrome as defined by the American Psychiatric Association (DSM-III-R).

(2) It is the experience of the workshop that one-quarter to one-third of CFS patients will qualify as CFS Type 1.

(3) We consider that in addition, CFS is a triphasic syndrome...." This quote continues as above under post #17.

http://publications.gc.ca/collections/collection_2016/aspc-phac/H12-21-1-17-S1-eng.pdf



You are probably more than aware of the 1980s reaction from NIH and CDC re EBV not being the cause.

Late activist, Craig Maupin did so much for our community, including requesting a copy of a letter from Dr. Stephen Straus to Dr. Kieji Fukuda about the concept of a "discrete form of fatiguing illness" evaporating.

Craig's website may have been taken down, however, I found a portion of this letter on Gabby Klein's website:

In this letter Dr. Straus says:

"Now that the definition is revised we could project at leisure what will come of it. I’d be very interested in your frank opinion on the matter when convenient. My own sense is that a few years of use in the field will once again verify that there is no demonstrable or reproducible differences between individuals who meet the full CFS criteria and those who can be said to suffer Idiopathic Chronic Fatigue. This would beg the question of whether additional revisions to the definition are warranted, or its entire abandonment.

I’ve felt for some time, Kieji, that those that have CFS are at a certain point along a continuum of illness in which fatigue is either the most dominant symptom or the most clearly articulated by virtue of impression on the part of the patient or physician that such a complaint is important. I predict that fatigue itself will remain the subject of considerable interest but the notion of a discrete form of fatiguing illness will evaporate. We would then, be left with Chronic Fatigue that can be distinguished as Idiopathic or Secondary to an identifiable medical or psychiatric disorder. I consider this a desirable outcome."

Here is a link to Gabby Klein's website.

https://relatingtome.net/2019/03/22/cdc-the-puppeteer-and-the-uk-bps-connection-to-bury-me/

 

It has never made sense to me why everyone was so keen to get rid of ME as a distinct disorder. Right from the start it had features that were unknown in any other disease - the variability of symptoms and the abnormal response to exercise.

 

https://twitter.com/user/status/1177568571322458112

 

1 remember finding this very useful.
Carol Sieverling

Carol Sieverling of the CFS & FMS Support Group of Dallas-Fort Worth wrote this article based on transcripts of another member's visit with Dr. Paul Cheney, transcripts of a presentation he gave at a conference in Orlando in October 1999, and the tape of his seminar in Irving, Texas in May 1999.


https://www.prohealth.com/library/t...fatigue-syndrome-dr-paul-cheneys-theory-20573

CFIDS: The Big Picture

Paul Cheney, M.D., Ph.D., has treated over 5,000 CFIDS patients in the last 15 years. As many patients were followed over time, Dr. Cheney began to suspect that the illness moved through three distinct phases. One of our members saw Dr. Cheney recently, and he brought up a diagram on his computer and offered a refined version of his theory of the 3 phases of CFIDS.

The main problem in CFIDS is cellular metabolic dysfunction. The body's cells do not work very well. And every cell is affected. As a result, intracellular acidosis develops – the cells become more acidic inside. This is true of any chronic illness. What is specific to CFIDS are the arrows on the diagram. These are CFIDS-specific mechanisms by which CFIDS disrupts cell function.

 

https://www.preprints.org/

 

Now published: https://www.frontiersin.org/articles/10.3389/fneur.2020.00826/full.

 

Glad they published, but I still didn't find this particularly enlightening with regards to any specific hypotheses.

The concepts like "aberrant homeostasis" and "multi-spiraling disease course" apply to pretty much all chronic diseases.
Doctors have long mistaken lesions (tissue damage) with disease, when in fact lesions are simply symptoms of an underlying disease process.

 

Merged thread

In retrospect I can recognize a prodromal phase.

I have also thought that the disease changes over time and that some of the observed heterogeneity may be due to patients being observed at different stage of progression.

 

Maybe because it seems to allow for any BPS interpretation?

A very bad argument, I´d say.

I found the paper very clear and balanced, and possibly instructive for people who don´t know much about this sadly odd and utterly sparkling disease.

They could, right, maybe they do both?

My hypothesis would be, it´s a (self-reproducing) miss-wiring in the basal ganglia and non-specific thalamus structures. And I find this paper very well in accordance to this, and therefore in its details enlightening (although they themselves don´t come up with any hypothesis).

May well be, though ME might be especially complicate in its presentation, and, therefore, difficult to interpret. Interesting is also the (small or limited, resp.) possibility of getting better, which they mention two or three times. I think they didn´t mention ups and downs, although it had been mentioned, which may also be a hint for the nature of the illness.

Yes, but the mistake here occurs at the end of a chain, and therefore doesn´t allow any judgement about the initial steps (impacts and/or disposition, maybe aberrant homeostasis en grand), where any differentiation may be necessary.


Taken together, I find this paper at least helpful, if not insightful, although it merely shows the limited knowledge (which they also estimate). Hopefully researchers reading it will come to the idea that any psychological interpretation is highly unlikely to become successful.