Open Medicine Foundation (OMF)

[Hutan]

It therefore begs the question why OMF feels compelled to defend the use of the term at this time.
From the news item:

I understand that this is a complicated and sometimes controversial topic, so before I get into it, let me acknowledge that complexity and say that we do our best to reflect the voices and experiences of the people we are trying to serve.

While the term multi-system chronic complex disease is perhaps overwhelming at first, each component is relatively straightforward when you break it down.

OMF seems to be acknowledging that they have received push-back, that the term is controversial. But, they seem to be doubling down on the term. The word 'complex' is in bold on the OMF home page. Doctors who are members of the forum have confirmed how the word 'complex' is received by many doctors, it plays into the way ME/CFS is seen by BPS proponents. We've told OMF researchers about the impact of that on people with ME/CFS. OMF doesn't just seem to be ignoring that, they seem to be suggesting that people who disagree with them are just overwhelmed and need things explained in very simple terms.

Complex diseases require open collaboration

ME/CFS and Long COVID disrupt many body systems. Traditional research looks at one system at a time. That approach doesn’t work.

That’s where Open Medicine Foundation (OMF) comes in. OMF brings world-renowned scientists together to study, diagnose, treat, and cure complex diseases.

It’s a bold dream. It’s the path that will get you back to a fulfilling life.

OMF believes multisystem disease should not be a life sentence but a solvable puzzle.

What will happen if research remains focused on one system at a time?
How will your life shrink? How many graduations, birthday parties, or everyday activities will you miss? What will happen with your career?
Something has to change.

OMF also makes a big deal about how they see ME/CFS as a multi-system disease, and suggests that funding researchers to look at a range of body systems is some ground-breaking approach. The suggestion that ME/CFS research outside of OMF is 'remaining focussed on one system at a time' and that they are the only organisation looking wider, is just not supported by reality. Researchers, some good and some bad, some within the OMF stable and some not, are looking at a wide range of 'systems' and clearly talk to each other, in conferences and elsewhere.

That OMF home page does not work for me, and does not seem to me to be grounded in truth. But, clearly it is what OMF has chosen, and perhaps it is working for them. So I guess each to their own.

 

[Jonathan Edwards]

Science and marketing never did mix very well.

 

[Sean]

Truth and power are usually not friends.

 

[Caroline Struthers]

Hello! I have been away from S4ME for a while. I have tried unsuccessfully to get funding in the UK to pursue my Trialblazers idea (2 pager and 4 pager attached) which is about how to get patients en masse involved in designing clinical trials. I want to use designing a trial of one or more repurposed drugs for ME as a case-study/proof of concept. I would love to collaborate with OMF/CTN Lite if possible to get this idea off the ground. Funnily enough I was already considering travelling to California this summer to visit my daughter who will be doing an internship at Caltech in Pasadena. Not far from where OMF is based?? Is anyone from OMF/CTN Lite on here and interested in talking to me? If not, should I just write to OMF info@omf.ngo? Any advice gratefully received

I emailed OMF and Linda Tannenbaum said she would discuss my ideas with Danielle Meadows. They are not around when I'm in California - Danielle is based elsewhere in the US anyway. I'm not sure they are taking me too seriously as they were in Cambridge UK a week or so ago, and I would have loved to meet them if they'd let me know they were coming. I think probably they didn't twig I was based in the UK, and I don't think they necessarily need my help or input with CTN Lite anyway.

I think my next move is to try and work on the technical side of developing a citizen science platform to enable crowd-sourcing of trial design by potential trial participants from any patient group (trial setting, choosing outcomes, objective outcome measures, setting the minimally important effect size, ways to minimize participant burden etc.) - I won't focus specifically on ME. I think this approach would lend itself to large trials of repurposed drugs (found to be safe in other contexts) for ME and other long-term conditions where trials are few and/or small and/or badly designed. The issue will be how to get funding to conduct these patient-led trials. At the moment, the funders seem to need to have an academic researcher to lead a funding bid to do a trial. Finding a researcher willing to hand over control of trial design before applying for funding is a challenge. This seems to be what CTN Lite will do for ME trials. But it would be great to develop a standard way to allow other patient groups to do the same.

 

[Andy]

A general question on OMF. Does anybody know if it will fund projects that don't include collaboration with any of their existing teams? I see no mention on their website of how to apply for funding, although I could well have missed it, so I am currently assuming not.

 

[forestglip]

May 20, 2026: Full-Scale Testing Is Underway

"We’re excited to share that testing on all 1000+ BioQuest samples has officially begun at Nightingale Health, where they are conducting NMR metabolomics and Olink proteomics analyses. But that’s just the beginning. Additional testing will take place at OMF’s collaborative research centers:

Montreal Center
Our Montreal center will perform a cytokine panel, haptoglobin phenotyping, and immunoassays targeting specific molecules identified through previous research— including SMPDL3B, GDF-15, FGF-21, and BDNF. These tests will reveal critical immune system patterns and inflammatory markers, and validate existing findings.

Uppsala Center
Our Uppsala center will carry out mass spectrometry-based proteomics and metabolomics, along with additional immunoassays—adding even deeper layers of biological insight."

Link

 

[Chandelier]

MELOPIS: Multimodal Brain Imaging in ME/CFS, Long COVID & POTS (Melbourne Study Update)

00:00 Welcome and Overview
00:44 What Is MELOPIS
01:42 Multimodal Scans and Setup
02:46 Early Neuroinflammation Signals
04:30 Default Mode Network Findings
05:31 Brain Effort During Tasks
06:25 Patient Experience and Support
07:11 Recruitment and Travel Logistics
08:12 Why This Matters Next Steps

YouTube Description:

In this End of Financial Year episode, Dr Chris Armstrong and PhD student Jamie Elliott discuss MELOPIS, an ambitious multimodal imaging study of ME, long COVID and POTS led through the Global Open Medicine Foundation Network at the Melbourne ME/CFS Collaboration, supported by OMF Australia. Based at the Melbourne Brain Centre Imaging Unit, the project combines 7T MRI with multiple PET tracers across two visits (with a second PET about four weeks later) to examine neuroinflammation, brain blood flow, brain metabolism and hypothalamus-related hormone impacts in the same patients.

Preliminary findings using a PET tracer targeting activated astrocytes suggest a potentially revealing neuroinflammatory profile in ME/CFS, with effects concentrated in the default mode network and possible difficulty switching out of resting networks. Task fMRI also indicates patients recruit broader brain areas and expend more energy for similar performance. The team highlights patient-friendly, low-stimulation scanning conditions and calls for final-stage recruitment in Melbourne (or for those able to travel) ahead of sharing further results.

 

[Casterofspells]

OMF just shared this preliminary insight into their MELOPIS multimodal brain imaging study out of Melbourne.

Most interesting findings seem to converge with other fMRI studies finding abnormalities in the Default Mode Network. This time an astrocyte activation marker seems to suggest some kind of chronic inflammation might be causing these issues according to the researchers.

 

[wigglethemouse]

A general question on OMF. Does anybody know if it will fund projects that don't include collaboration with any of their existing teams? I see no mention on their website of how to apply for funding, although I could well have missed it, so I am currently assuming not.

I don't think they are setup for this. When I've looked at financial reports they don't usually fund projects not associated with collaborators at the centers they support. The exception is for their medical education collaboration with Bateman Horne.

However, major donors to OMF also support ME/CFS projects outside of OMF but I don't think there is any public info on who those are.

I see DecodeME has support from the Schmidt foundation. Perhaps you can approach them to see if they are willing to share any contact info for other major funders?

 

[wigglethemouse]

But it would be great to develop a standard way to allow other patient groups to do the same.

Have you tried contacting the people doing the work - that is usually a good way to guage if there is any interest. From the link posted

That knowledge is not just valuable. It is irreplaceable. To help us tap into this knowledge, we’ve been working with a few collaborators—Tess Falor and Isabel Burnett from Renegade Research and Julia Moore Vogel from Scripps Research—to develop this survey and discuss the way forward[\QUOTE]

 

[voner]

A general question on OMF. Does anybody know if it will fund projects that don't include collaboration with any of their existing teams? I see no mention on their website of how to apply for funding, although I could well have missed it, so I am currently assuming not.

for a direct OMF contact, I would just contact Linda Tannenbaum directly. Her email is publicly available. You can contact me if you can’t find it.

best of luck to you…

 

[Andy]

I see DecodeME has support from the Schmidt foundation. Perhaps you can approach them to see if they are willing to share any contact info for other major funders?

SequenceME & LC has, yes. We remain in dialogue with all of our funders so other opportunities may present themselves that way.

 

[Hutan]

Regarding the video on MELOPIS:
The finding that people with ME/CFS are recruiting more brain regions to get a task done does match with what a team at the Melbourne Royal Children's found in young people with ME/CFS.

They (Chris Armstrong and Jamie Elliot) are suggesting that they are finding evidence of activated astrocytes, and therefore evidence of brain inflammation. That's not really what Qiang and the Shan team found. Nor does it tie in with the whole body imaging that the Stanford researcher did, where she did not find evidence of brain inflammation (but did find evidence of something happening in muscles.)

2.46 mins
'There's been a lot of work on neuroinflammation, a lot of interest in neuroinflammation in all sorts of regards. Often it's done with things like looking at bloods or metabolites. We're using a PET tracer that targets astrocytes, particularly astrocytes that are in an active state. And it's something that has only really been used up to this point in Alzheimers disease and dementias. And we are seeing a few potentially revealing things about the neuroinflammatory profile of ME/CFS in particular. The Long Covid stuff we haven't looked into at this point.

But for ME/CFS we are seeing some really potentially targetable and treatable options that are related to the way that astrocytes are being activated in a chronic way in these conditions.'


At the end, the voice over of the OMF Australia Research Manager says
'What stays with me from this conversation is the start of a real mechanistic story. ME/CFS patients using wider brain areas, expending more energy for the same task as healthy people isn't just description, it's explanation! That's the field moving from observation toward treatment.'

Hmm.

 

[neophyte32]

I thought it was now established that there was no neuroinflammation in the MECFS...

 

[Peter T]

I thought it was now established that there was no neuroinflammation in the MECFS...

I just did a quick search and we have lots of threads with the word ‘Neuroinflammation’ in the title, but I don’t know if I am just being stupid in saying I don’t have a good handle on what it means. Inflammation of the skin say is visible and/or palpable, but what does it mean to say that the brain’s immune system is activated?

A very cursory web search gave the following:

Neuroinflammation is defined as an inflammatory response within the brain or spinal cord. This inflammation is mediated by the production of cytokines, chemokines, reactive oxygen species, and secondary messengers. These mediators are produced by resident CNS glia (microglia and astrocytes), endothelial cells, and peripherally derived immune cells. There are immune, physiological, biochemical, and psychological consequences of these neuroinflammatory responses. Moreover, the degree of neuroinflammation depends on the context, duration, and course of the primary stimulus or insult. For instance, inflammation can lead to recruitment of immune cells, edema, tissue damage and potentially cell death. The term neuroinflammation, however, is not universally equivalent.

See Neuroinflammation: the devil is in the detail

Though the consensus here seems to be that we do not have good evidence for neuroinflammation acting as part of the aetiology of ME/CFS there are obviously researchers who would disagree, so would it be worth having a specific thread asking the question does it play a role in the development or course of ME/CFS?

 

[Hutan]

There's some good discussion about the vagueness of the word 'neuroinflammation' on this thread:
Neuroinflammation - an unfortunate term to describe schizophrenia, 2026, Ilorca et al


And there's @ME/CFS Science Blog's excellent discussion

Thread 'ME/CFS Science Blog article - Immune findings in ME/CFS'

Mar 21, 2026

In this article, we have made a comprehensive overview of research findings on the immune system in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In contrast to what is frequently claimed, current data do not suggest that (low-grade) inflammation is a key driver of ME/CFS symptoms. There have been major studies into viral persistence, antibodies, and cytokines, but with mostly null results. The most consistent findings in the ME/CFS literature on the immune system over the past 40 years are reduced natural killer cell cytotoxicity and increased levels of...

• ME/CFS Science Blog
• autoantibodies immune system inflammation me/cfs science blog nk cells viral persistence
• Replies: 75
• Forum: ME/CFS research

• 

 

[Jonathan Edwards]

I just did a quick search and we have lots of threads with the word ‘Neuroinflammation’ in the title, but I don’t know if I am just being stupid in saying I don’t have a good handle on what it means.

I think we had a thread about how we don't know what it means and that a conference of eminent neurologists agreed that they didn't know either.

The cited definition evades the main point - what actually occurs qua 'inflammation'. Cytokines are mediators but that means they are by definition not inflammation themselves but what is supposed to cause (or maybe result from) the inflammation. Their presence without inflammation does not consitute inflammation.

It is standard in biomedical research for the majority of researchers to go on flogging ideas that have died decades before. People assume there is neuroinfammation because of the word ecncephalomyelitis, but, as we have discussed, that term was never relevant to ME/CFS, only to a doubtful acute illness that seemed to precede ME/CFS in some epidemics. Confusion of this sort is routine in the study of pathophysiology. Until we actually have some data on inflammation being there I think we should continue to assume that since we have pretty sensitive tools that do not show inflammation there likely isn't any. The Quiang study is weird because it seems to show the opposite of what was supposed to indicate inflammation.

 

[Mij]

Can we assume that neuroinflammation only applies to a subgroup of pwME/CFS?

 

[Jonathan Edwards]

Can we assume that neuroinflammation only applies to a subgroup of pwME/CFS?

No, we have no good evidence for it applying at all. The one study that might have shown a limited form of 'inflammation' in the sense of glial activation (Nakatomi) was not replicated.

 

[neophyte32]

No, we have no good evidence for it applying at all. The one study that might have shown a limited form of 'inflammation' in the sense of glial activation (Nakatomi) was not replicated.

So the MELOPIS brain imaging study is not interesting?