Open Medicine Foundation (OMF)

I have mixed feeling on the OMF. I have so many questions - where is the metabolomics replication, why has the nanoneedle not been tested in other diseases, what progress has been made to uncover (something in the blood). I understand good science takes times, but many of the questions are going on half a decade funded by well over 10 million dollars.

I think we have gaslight ourselves to just be grateful for whatever we get, as long as it's not BPS. That's a terrible attitude for a community to have. I think the most recent Berquist paper funded by the OMF was of a very low quality, and I don't want to not say these things anymore. I think the metabolomics replication being obfuscated or whatever happened is very strange. I think 5 years you should be able to test 10 non-me/cfs sick people or narrow in what's in the blood. If it's nothing that's fine. But we need to know. What's taking the Harvard OMF 4 years to do anything?

But to solely blame the OMF is wrong. What on earth has Griffith University being doing with millions of dollars? Really, wtf. The NIH study was a scandal and they got away with just wishing it away to go study long covid. 5 years! Nothing substantial published. I think other countries have been even worse. Nath's 3-year cutoff was based of a weak from Columbia that was never replicated showing "immune exhaustion". How's Nath got away with that. Numerous other cytokine studies didn't replicate it.

We need to expect better from our me/cfs researchers, not just the OMF. I don't know how to do this in a healthy way, I don't want to feed the narrative of ungrateful me/cfs patients, but I'm actually considering taking a break from s4me because so much research (which is what I mostly read) isn't very interesting or good, or it takes too long. I read it and am desolated.

I'm sorry if me/cfs researchers read this and feel angry. Maybe I'm being unfair. I desperately want to believe. But has any progress been made in the last 5-7 years with tens of millions? idk
 
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New OMF video published on YouTube: "What is ME/CFS?" (1 min 19 sec)



(I can't help wondering how many healthies know what orthostatic intolerance and environmental factors mean in this context.)
 
Announcement from OMF Feb 2022:
https://www.omf.ngo/new-changes-announced-for-omf/

Continuing the Research:

New Changes for OMF Announced

In an effort to continue the tremendous legacy of OMF’s Late Chief Medical Officer, Ronald G. Tompkins, MD, ScD, we would like to share new developments with the community.

We are honored to announce that Jonas Bergquist, MD, PhD, has accepted the role of OMF Chief Medical Officer along with expanding his efforts in his role as Director of the OMF funded ME/CFS Collaboration at Uppsala University.

Additionally, we are excited to announce that David Systrom, MD will join Wenzhong Xiao, PhD, as a Co-Director of the newly named Ronald G. Tompkins Harvard ME/CFS Collaboration at the Harvard Affiliated Hospitals. Dr. Xiao will gratefully continue as the Director of the OMF Computational Research Center for Complex Diseases as well. We also welcome Dr. Systrom to our Scientific Advisory Board.​

About Jonas Bergquist, MD, PhD:

Dr. Jonas Bergquist is a Full Chair Professor in Analytical Chemistry and Neurochemistry in the Department of Chemistry at Uppsala University, Sweden, Adjunct Professor in Pathology at the University of Utah School of Medicine, and Distinguished Professor in Precision Medicine at Binzhou Medical University in Yantai, China.​

Dr. Bergquist has studied numerous conditions, including neurodegenerative disorders. His research into ME/CS is focused on characterizing the neuroimmunological aspects of the disease using proteomics and metabolomics, with a special interest in cerebrospinal fluid studies and autoantibodies.

In 2017, Jonas Bergquist joined OMF’s Scientific Advisory Board, and subsequently launched the OMF funded ME/CFS Collaboration at Uppsala University in 2019.

******

It's disappointing therefore to see this recent paper from Dr Bergquist, which references very poor research as it speculates about the causes of ME/CFS. We need our research leaders to think more critically than Bergquist appears to do in this paper.
Perspective: Drawing on Findings From Critical Illness to Explain ME/CFS, 2022, Stanculescu, Bergquist
 
from email
May Momentum Launches Next Week
With New Research Updates!

Dear friends,
Our annual May Momentum campaign begins next week on May 1, 2022!
In recognition of May ME/CFS Awareness month, this campaign is a special effort by OMF to increase awareness of multi-system chronic complex diseases (msCCD) and energize fundraising efforts so we can continue our urgent research.

Announcing New Webcast Series!

This year we are excited to announce a new webcast series, "May Momentum Tuesdays," to update you on the progress of the OMF Collaborative Research Network!
Every Tuesday during May, we will be sharing new video interviews with Directors of the OMF Collaborative Research Centers (CRC)s, who will update the community on their most recent research projects and progress. Don't miss out! Videos will be uploaded to YouTube, our website, and social media every Tuesday starting May 3rd, 2022 and available to watch at your convenience.

In addition to sharing updates from OMF researchers, we'll share stories from our OMF community, news about worldwide events, and more.
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Merged thread
A history of neglect
Myalgic encephalomyelitis and its relationship with medicine

By Christian Godbout

Only forty years ago, the name “chronic fatigue syndrome” did not even exist. The thing, however, existed nonetheless and plagued the lives of countless people under the name, among others, of myalgic encephalomyelitis – ME. It plagued lives then and still plagues lives today. Unaltered. Always coming with the same sufferings.

This text would like to address the medical field entirely, from medical and research students to policy makers.

It is also written for anyone affected by this condition, which is too often confronted with harmful ignorance. I will discuss a few examples.

But first, let’s consider this scenario. A scenario that makes no sense. Imagine a world-renowned biomedical researcher with fifty years of experience in the field, having received numerous prizes and Lifetime Achievement Awards, and whose son falls so seriously ill that he becomes permanently bedridden.

Now imagine that, despite all his knowledge and impressive background, this researcher has virtually no clue of what is really going on in his son’s body.

That was the situation of biochemist and geneticist Ronald W. Davis in the early 2010s when his son fell into severe ME.

Consider this aberration: a disease capable of ending the professional and social life and all leisures of those it afflicts, who leaves them homebound if not bedbound indefinitely, a disease whose most severe forms have been compared to late stage AIDS, – but whose very existence is hardly taught in medicine. How crazy is that?

A disease hidden from sight

This inhuman scenario of a disease that is both terrible, yet neglected, surely has several causes, including government decisions to favour certain areas of health and turn a blind eye to others. But I will focus here on another cause, which comes from the very nature of this disease. Understanding why medicine fails to place ME under its radar also means in some way understanding a little about ME itself.

ME is often associated with so-called “invisible” diseases, but it could be said differently: ME is not so much an invisible disease as an unwitnessed disease. The most affected patients are too disabled to go to clinics or to sustain any social interaction, and therefore hardly anyone sees them. But one quick look at them and anyone would see they are visibly very sick.

And the less severely affected do not seem so sick at first sight, their relatives can see them, lying on a couch, sometimes seated, they can talk, laugh, their life seems almost normal. And yet these relatives are in presence of something seriously abnormal, but which remains latent: if the patient got up and walked to the corner of the street a few hundred yards away, his or her physical condition would then deteriorate, for days. Or worse: the conversation the patient is having with you couldn’t take place while simply standing without the patient suffering the same consequences.

One can see these patients, but without seeing all they are not doing, all they cannot do. Nor the price they pay if ever they risk it.

Ditto for their appointment with doctors: the latter are never there to witness the subsequent impact of these appointments on their health. These doctors, like all the others, will only have seen a person on temporary adrenaline.

The thing at the heart of this disease that so to speak dooms it to go unnoticed is called “post-exertional malaise.” The name itself already hints at this other cause of underestimation of ME: it manifests itself at its worst “post”, it peaks during an “after”, there is always a lag between the exertion “x” of patients and the time their health worsens. A worsening clearly visible but which almost no one will witness.
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full article
https://www.omf.ngo/christian-godbout-a-person-with-me-speaks-out-on-the-history-of-me-cfs/
 
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This is from 2021 but we don't seem to have anything on it yet.

"You might remember last year OMF announced that we are working on an exciting new project to streamline the arduous diagnostic process for people living with chronic complex diseases.

The “Personalized Automated Symptom Summary – Computer Adaptive Test” (PASS/CAT) is a machine learning tool that will help patients more accurately and efficiently convey their symptoms to their treating physician.

....

What is the vision for how the PASS/CAT will be used by patients and doctors?

Since the assessment is computer-based, the physician can send a link to the patient for completion prior to their visit. The PASS/CAT physician report will quantify the level of the patient’s symptoms and summarize it in a symptom profile. Alternatively, a person with symptoms of chronic, complex diseases like ME/CFS will be able to go to Open Medicine Foundation’s website, complete the assessment and bring the report to their physician to review and discuss the results as a clinical test."

https://www.omf.ngo/transforming-the-diagnosis-of-complex-diseases/
 
Basically a way to turn the symptoms list patients bring into a format that will be accepted, rather than glanced then ignored?

Interesting. Could be very useful. Obviously one of the main obstacles to achieving any progress is that over 90% of the illness is simply ignored, information thrown out right at the first input as if of no relevance. I am convinced that not only would a symptoms-based approach to medicine be far more effective at making progress for ME, it could actually make progress in the biology of symptoms, which has almost seen zero actual progress.

I hope this is what I'm thinking it's describing. This could be transformative by sheer usefulness, if used properly anyway. But it's a big project.
 
Systrom said:
And what we found was evidence that with Mestinon, the right atrial pressures were higher. During the second test, the cardiac output was higher at peak exercise. The VO2 peak was higher at peak exercise.

That was the primary endpoint. And interestingly, if they received placebo, all those things were worse. So we think this was just a single acute dose of 60 milligrams of Mestinon.

And we don’t clinically, most patients who respond to Mestinon with ME/CFS do so over weeks to months, even at higher doses. But the biological signal was there and it was statistically significant.

So we think we had a window into the pathophysiology of the disease and that kind of overriding abnormally low sympathetic tone by enhancing the sympathetic tone through what’s known to be a cholinergic center, sympathetic ganglia We think that what we did was tighten up the venoconstriction, improved preload, and therefore VO2 peak with a single dose. So it’s a proof of concept. The effect size was not great, but again, it was a single acute dose of Mestinon. So I’m not aware of anything quite like that in the field.
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I'm glad this distinction has been recognised - it certainly took larger, regular doses of Mestinon to improve my condition in a way I could readily observe.

Curious to see what comes next. Is there funding/interest to build upon these results, remove that acute dose limitation, show the efficacy in a larger RCT and hopefully get simple Mestinon into the hands of more patients? Or it more likely only going to potentially lead to a more targeted, novel drug test that promises very significant improvements?
 
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Ryan31337 said:
I'm glad this distinction has been recognised - it certainly took larger, regular doses of Mestinon to improve my condition in a way I could readily observe.

Curious to see what comes next. Is there funding/interest to build upon these results, remove that acute dose limitation, show the efficacy in a larger RCT and hopefully get simple Mestinon into the hands of more patients? Or it more likely only going to potentially lead to a more targeted, novel drug test that promises very significant improvements?
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How much better are you with Medtinon?
 
Transcript for Systrom https://www.omf.ngo/may-momentum-tuesdays-2022-interview-transcript-with-david-systrom-md/

The 8 million dollar trial


The other perspective, randomized, placebo-controlled clinical trial we have ongoing is an $8 million study of mitochondrial dysfunction at the Brigham of single site study funded by a Pharma company named Astellas from Japan. It is ME/CFS, but PASC was not excluded. We have already included some patients in the study who have long COVID. And it involves two very difficult to get needle muscle biopsies of the thigh frozen and sent appropriately to Baylor for evaluation of mitochondrial function. And I would emphasize that we take that approach in ME and PASC is very important again, because most of these patients don’t have genetic forms of mitochondrial myopathy. And the study is ongoing. It was powered by 40 patients. We enrolled 27 of the 40 over about six months, and we’re looking to complete this and run our stats on it. It involves two invasive cPETS at baseline and then at the end of six weeks of treatment with PPARD Delta modifier. It’s proprietary, but it’s thought to act favorably on fat metabolism by the Mitochondria. So we don’t know what patients have gotten yet, but stay tuned.
 
PASC is post-acute sequelae of COVID-19, according to a search. (Maybe it's well-known, but I'm somewhat dopy/thick at the moment!)
 
MeSci said:
PASC is post-acute sequelae of COVID-19, according to a search. (Maybe it's well-known, but I'm somewhat dopy/thick at the moment!)
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It's used in quite a few of the research papers we have threads on here, but I think most people suffering from symptoms prefer the term Long Covid.
 
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