USA: Cornell Center for Enervating NeuroImmune Disease and Maureen Hanson

http://simmaronresearch.com/2017/12/simmaron-patient-day-summary-part-ii-hanson-report/

"Maureen Hanson has been making waves. An ace molecular plant biologist prior to entering the chronic fatigue syndrome (ME/CFS) field, Hanson has worked on mitochondrial and gene studies in plants dating back decades. Now, with her son ill from ME/CFS, she’s turned her talents to this field, and has made a difference in a hurry....."

The article presents her ongoing research, also with a background, and what is to come.

 

This is how lower respiratory capacity, mentioned in the article, was interpreted in a previous study:

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0186802

 

by Jackie Swift

https://research.cornell.edu/news-features/researchers-duality-plants-biomedical

 

To facilitate sharing:

https://twitter.com/user/status/1199823562233798657

 

https://twitter.com/user/status/1386901444708737026

 

Maureen Hanson's presentation, Searching Plasma for Clues to ME/CFS, from the Massachusetts ME 2021 Annual Meeting, can be found here, Webinar: Massachusetts ME/CFS & FM research update - 23 October 2021

 

Research update

https://www.youtube.com/watch?v=AomPPtzZHgc

 

It's a definitional problem, Long Covid Syndrome includes so many pathologies that there can not logically be a simple equivalence of LCS = ME/CFS. Occurrence of classic Post Viral Syndrome and long term ME/CFS following COVID19 infection is an important area of study but it needs to be conceptually separated from the amorphous thing that is LCS.

 

The problem with her argument is that it is not logically consistent - if no cases of LongCOVID are ME/CFS then ME/CFS itself probably isn't a single disease either.

 

Pathophysiological and cellular abnormalities for PEM would put us all in the same boat and then we can call it what it is.

I would personally like a new name for M.E b/c it doesn't really describe my illness.

 

Strongly agree—Yeah I saw this earlier (but didn’t comment) and thought it was problematic. I don’t know what she is thinking, but I really don’t think it’s helpful. The smaller you make your box, the worse your funding prospects are. I also think she is wrong.

 

I interpreted her statements as primarily political. I think she fears that with all the money going to LC in the US, funders will just say we don't need to give any more money to ME, those pwME can just sit there nice and quiet and wait for the LC results to roll in and hope for the best.
Sure, LC research may come up trumps for us but if it doesn't that'll be more years or decades wasted just waiting. Which is not a strategy I want to rely on.

 

Absolutely.

I don't see what Hanson said as being merely political, to me it sounds to be a logical parsing of the research challenge. Of course it depends on what the research objective is but I don't see at all problematic to say LCS and GWS do not offer useful populations for the investigation of ME/CFS, it's not as though data on LCS and GWS aren't available for comparison or that comparison studies can't happen.

Hanson isn't explicit but I take from what she says that she is allowing that post infection conditions (PVS etc) may not be pathophysiologically the same as ME/CFS - that seems to me to be an important consideration and is something that really does need to be made explicit. Although many PwME trace their illness back to an infection that in itself isn't evidence that the underlying pathology of PVS etc is the same as ME/CFS.

Hanson's point about a % of LCS patients meeting ME/CFS criteria is important because we can't know, merely on the basis of symptoms, whether COVID19 is substantially implicated in any individual's developing ME/CFS. The lack of incidence and prevalence monitoring of ME/CFS is major inhibition but tens of thousands of people develop ME/CFS every year, in a pandemic where over half the population has been infected at least once in a two year period it must be expected that at least a quarter of the expected annual incidence rate of ME/CFS will be comorbid with COVID19 exposure. If your study population is selected by COVID19 infection patients meeting ME/CFS criteria, what is it you are actually studying ?

 

Wonder if she was "selected" in the knowledge that would promote the ME/CFS cause but that seems ridiculous based on how excluded ME/CFS is ---- but yes, it's positive for a number of reasons 1 of which it makes it harder for those who challenge ME/CFS as a real (biological) disease.

 

Swedish ME expert doctor/researcher Per Julin, who works at a long covid clinic nowadays, was quoted in a (paywalled) news article yesterday:

"I don't equate ME with long covid, you don't get lung problems in ME for example. But there are some similarities."

I'd be very interested to hear more about his thoughts on this.

 

https://news.cornell.edu/stories/2023/04/95m-fund-cross-disciplinary-chronic-fatigue-research
$9.5M to fund chronic fatigue syndrome research

 

I doubt that the headline is the writer’s fault; the copy is otherwise unobjectionable and the news itself is of course great.

 

This $9.5 million grant (over 5 years) looks pretty much like a follow-on to the 2017 $9.4 million grant for the CRC.
This is just one of the NIH funded CRCs though. I wonder what the details are on the others and on the data center?