USA: Cornell Center for Enervating NeuroImmune Disease and Maureen Hanson

H

Helen

Senior Member (Voting Rights)
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:

Significantly altered mitochondrial stress test parameters in the CFS group compared with the healthy control group (Fig 3 & Fig 5) suggests that CFS patients may have systemic abnormalities in energy transduction, particularly when isolated PBMCs are put under mitochondrial stress. Lower reserve capacity observed in CFS patients are indicative of the cells of patients performing closer to their capacity in normal conditions without stress than healthy controls. Lowered maximal respiration suggests that the PBMCs of CFS patients are not capable of the same levels of respiration as healthy controls. Results showed that CFS patients can only increase their respiratory capacity 47% (±37%) from baseline when maximally stimulated by FCCP, which is significantly (p<0.001) lower than the 98% (±32%) increase in respiratory capacity achieved by control PBMCs. The consistently lower maximal respiration in the CFS cohort shows the inability of CFS patients to respire to the same extent as the control cohort when cellular stress is applied. The lower reserve capacity suggests that when CFS PBMCs come under stress they are less able to increase their respiration rate to compensate for the increase in stress leaving patients unable to fulfil cellular energy demands. Similar abnormalities in reserve capacity are thought to contribute to a range of other disease pathologies such as heart disease [49], neurodegenerative diseases in aging [50], and smooth muscle cell death [51].
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0186802
 
Wikipedia said:
The National Academy of Sciences (NAS) is a United States nonprofit, non-governmental organization. NAS is part of the National Academies of Sciences, Engineering, and Medicine, along with the National Academy of Engineering (NAE) and the National Academy of Medicine (NAM).

As a national academy, new members of the organization are elected annually by current members, based on their distinguished and continuing achievements in original research. Election to the National Academy is one of the highest honors in the scientific field. Members of the National Academy of Sciences serve pro bono as "advisers to the nation" on science, engineering, and medicine. The group holds a congressional charterunder Title 36 of the United States Code.

Founded in 1863 as a result of an Act of Congress that was approved by Abraham Lincoln, the NAS is charged with "providing independent, objective advice to the nation on matters related to science and technology. … to provide scientific advice to the government 'whenever called upon' by any government department."
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the NAS announcement linked in the previous post said:
WASHINGTON — The National Academy of Sciences announced today the election of 120 members — 59 of whom are women, the most elected in a single year — and 30 international members in recognition of their distinguished and continuing achievements in original research.

“The historic number of women elected this year reflects the critical contributions that they are making in many fields of science, as well as a concerted effort by our Academy to recognize those contributions and the essential value of increasing diversity in our ranks,” said National Academy of Sciences President Marcia McNutt. “I am pleased to welcome all of our new members, and I look forward to engaging with them in the work of the National Academies.”

Those elected today bring the total number of active members to 2,461 and the total number of international members to 511.
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It looks like quite an honour, and perhaps creates opportunities for Maureen to push ME/CFS and Long Covid forward as issues that need attention. I think Maureen is a deserving recipient of the honour - her team's research work is always sensible and solid, as is her advocacy.
 
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Thanks @Jaybee00, that's an interesting presentation; some things sound promising. The study that found that particular types of immune cells have drastically different gene expression for pwME and healthy controls is intriguing. (see at 25.30 minutes)

I'm a bit surprised that Maureen Hanson is so dogmatic about Gulf War Illness being different to ME/CFS. (see at 50.30 minutes) To my mind, the research on that has not been nearly good enough to say that so certainly.

And I was surprised at her reluctance to accept that people with Long Covid who meet ME/CFS criteria have ME/CFS. That seems to ignore the fact that ME/CFS seems to result from a range infections, including other coronaviruses. I can't help but wonder if her viewpoint is based as much on politics as biology. For example, she made the point that if the answer to Long Covid is found and that it is due to the virus hiding in some protected part of the body, then the solution to that is not going to be helpful to people with (pre-2020) ME/CFS, as they can't be infected with that particular virus. And so we should keep studying ME/CFS. Perhaps it's mostly that she wants to keep funds coming in for ME/CFS research and to keep her team studying it, and not completely jump over to Long Covid as the NIH seems to have done, leaving people with ME/CFS feeling abandoned. Maybe it's about not putting all the eggs in one basket.

(edit - Mango has just posted about Jonas Bergquist also saying he doesn't think ME/CFS and Long Covid are the same, although there are common mechanisms.
Long Covid in the media and social media 2022. I wonder if it's some OMF concerted approach to the question. It doesn't make sense to me. It's like ME/CFS is all the various types of apples, Granny Smith and Braeburn and whatever, and ME/CFS compliant Long Covid is a brand new type of apple - and then saying, oh, ME/CFS and Long Covid aren't the same.)
 
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Hutan said:
And I was surprised at her reluctance to accept that people with Long Covid who meet ME/CFS criteria have ME/CFS. That seems to ignore the fact that ME/CFS seems to result from a range infections, including other coronaviruses.
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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.
 
Hutan said:
And I was surprised at her reluctance to accept that people with Long Covid who meet ME/CFS criteria have ME/CFS. That seems to ignore the fact that ME/CFS seems to result from a range infections, including other coronaviruses.
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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.
 
Hutan said:
And I was surprised at her reluctance to accept that people with Long Covid who meet ME/CFS criteria have ME/CFS. That seems to ignore the fact that ME/CFS seems to result from a range infections, including other coronaviruses. I can't help but wonder if her viewpoint is based as much on politics as biology.
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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.
 
Hutan said:
And I was surprised at her reluctance to accept that people with Long Covid who meet ME/CFS criteria have ME/CFS. That seems to ignore the fact that ME/CFS seems to result from a range infections, including other coronaviruses. I can't help but wonder if her viewpoint is based as much on politics as biology. For example, she made the point that if the answer to Long Covid is found and that it is due to the virus hiding in some protected part of the body, then the solution to that is not going to be helpful to people with (pre-2020) ME/CFS, as they can't be infected with that particular virus. And so we should keep studying ME/CFS. Perhaps it's mostly that she wants to keep funds coming in for ME/CFS research and to keep her team studying it, and not completely jump over to Long Covid as the NIH seems to have done, leaving people with ME/CFS feeling abandoned. Maybe it's about not putting all the eggs in one basket.
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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.
 
Ravn said:
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.
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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 ?
 
Hutan said:
It looks like quite an honour, and perhaps creates opportunities for Maureen to push ME/CFS and Long Covid forward as issues that need attention. I think Maureen is a deserving recipient of the honour - her team's research work is always sensible and solid, as is her advocacy.
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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.
 
Hutan said:
(edit - Mango has just posted about Jonas Bergquist also saying he doesn't think ME/CFS and Long Covid are the same, although there are common mechanisms.
Long Covid in the media and social media 2022.
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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.
 
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