International Declaration in Support of Research and Drug Development for ME/CFS and Long COVID Berlin, 1 September 2025

[Oliver3]

I think @Wishful 's comment about each person having different thresholds for accepting claims is very on-target.

But I also think that the declaration we are discussing is a "nothing burger". A bunch of ME/CFS researchers and people interested in ME/CFS research published a statement saying there should be more ME/CFS research. What could be more trite?

There is one piece of meat in the declaration: they want more cure/treatment focused research (and presumably less mechanistic research, although they are very careful not to say that!) There are two ways to interpret this statement.

One is, we want more money for cure/treatment research and the same amount for mechanism research. That is just we want more money and is trite. Everyone knows you want more money.

The second is, we want to shift the focus of research (and the money) from mechanism to cure/treatment. That is policy, and is not trite, but I agree with @Wishful again that this is premature. Not because there are no mechanistic studies done to date, but because there are too many different mechanistic ideas out there, all of which are lightly and poorly supported by the evidence. In my opinion, we are too early for a policy statement saying it is time to shift research targets.

Wishful contradicts himself saying he think a cure will come from leftfield and yet we shouldn't test known ideas because there's not strong enough evidence to ' waste money'.
Which mechanism icon ideas are you talking about that are lightly and poorly supported by the evidence?

 

[Oliver3]

https://pubmed.ncbi.nlm.nih.gov/38650940/

Study on whitney last year.
So many reproducible things happening in this case study. Mast cells, cytokines, inflammation, eds. Th2 autoimmunity etc..read it. There's plenty of findings elsewhere mirroring this.
We can already help to treat some of these issues, with mast cell stabilisers abd anti inflammatory meds

 

[Wishful]

He's admitted previously he doesn't even read the literature out there.

I do read some of it. Some of it is beyond my technical knowledge, so I can't interpret the numbers meaningfully. Other papers I skim, and decide whether or not it's worth more effort. I read a lot more papers in more detail earlier in my ME, but the lack of anything coming from those papers has discouraged me from making that much effort. Again, why is it important that I'm not waving a banner in support of whichever paper or theory you feel encouraged about? I'm not making any financial decisions for drug companies or research funding. I recently received an email from OMF? asking for funding for trying to find a biomarker in blood. Well, they haven't convinced me that there is a biomarker to be found in blood.

I've seen papers that I did consider encouraging. I haven't seen any followup for them, so I'm not going to waste time waving a flag about them.

To say that's not existing is disingenuous

Joshualevy and Brightcandle have already answered that for me: that what does exist is unreplicated and debatable in value. It may be valid work, but it's not enough to convince moneyholders to invest in it at this point.

I admit I'm strongly skeptical in personality. I'm not going to change that without suitable feedback. I can be convinced by appropriate arguments or evidence. I'm just still waiting for it.

 

[Wishful]

Study on whitney last year.

"Results: Longitudinal cytokine profiling revealed the significance of Th2-type cytokines and highlighted synergistic activities between mast cells and eosinophils, skewing Th1 toward Th2 immune responses in ME/CFS pathogenesis, particularly in cognitive impairment and sensorial intolerance."

A study on a single patient. Are the abnormalities due to ME, or is the severe ME due to pre-existing abnormalities? I know that there have been plenty of studies of cytokine in ME, with conflicting results. Maybe this is the only study that measured Th1/Th2 ratios and it's a valid finding, or maybe it has been done in other studies with no clear results. I don't know. I haven't seen ScienceDaily with a headline claiming that Th1/2 ratio is a proven biomarker for ME. I'll add that study to all the others in the "hasn't been verified to be an important aspect of ME" pile and wait for something to be properly verified.

I can easily imagine that when ME's mechanism is discovered, they'll look back on previous studies and conclude that none of them were looking for the right things in the right places. I expect that some good knowledge will result from those studies, to improve knowledge of how the body works (and fails).

That brings up an interesting question: what is the typical size of the pile of published papers which don't really help in understanding a mystery vs the ones that do? Probably a pointless question, along the lines of "what music is good" (depends on the listener).

 

[Oliver3]

You read barely anything. It's obvious from what you say.
You literally say nothing every time...
A study on a single patient that's easily repeatable. It's called a case study.
You and the other guys haven't answered anything.
You have to seen it in science daily.ergo..it doesn't exist. You absokute joker!!!!
Almost definite mechanisms include.
Hyperactive glial, th2 dominance, eds, energy disruption , metabolising of amino acids. Specific cytokines. Endothelium dysfunction, mitochondrial dysfunction, sympathetic overdrive. Etc etc.
All seen in many papers but condensed here.
We've seen the large study identifying genetic markers.
You on the other hand openly admit you can't be bothered to read the papers so how can you have an opinion.

You can easily imagine theories been discounted later....welcone to the world of science wishful. It happens in all areas of science since copernicus.
but they are most likley bang on . Imagine that wishful. They could be right!!!.
this is the scientific method. If you dont like it, go take your ' ideas' to some ....oh sorry you literally have no ideas.
Apart from the famous it's a couple of brain cells. Not one study to show your idea mind!!!

The science is converging around all the stuff in this case study.
The omf stripped everything back and worked to try and understand this from the floorboards up.
They've fielded different ideas from many different areas of science and nutrition.
They are also proper sciebtists wishful, interhered by pharmaceutical s abd they are some of the best out there. Show some resoect and know what youre talking about.
You talk absolute garbage mate.
It's the insistence on posting when you have nothing but hot air. Anyone can be as dismissive as you. It's such a false position

 

[joshualevy]

https://pubmed.ncbi.nlm.nih.gov/38650940/

Study on whitney last year.
So many reproducible things happening in this case study. Mast cells, cytokines, inflammation, eds. Th2 autoimmunity etc..read it. There's plenty of findings elsewhere mirroring this.
We can already help to treat some of these issues, with mast cell stabilisers abd anti inflammatory meds

All I can say Oliver3, is that if you wanted to sabotage your own position, you could not have done any better than this. An N=1 study, and you want to rush into cure focused clinical trials? I mean, if that is your threshold for focusing on a cure, then go for it, but I don't agree and I don't think you are going to find anyone with any experience in research who is going to think this is a good idea.

Which mechanism icon ideas are you talking about that are lightly and poorly supported by the evidence?

You listed 5 areas in your post #14: "We know there's an inflammatory issue in m.e., we know there are tissue issues, we know about the propensity towards th2 autoimmunity, we know there's problems I'm the endothelium, we know mitochindria are affected etc etc."

I would say that three of those: th2 autoimmunity, the endothelium, and mitochindria are exactly the sort of lightly and poorly supported theories I was referring to. I think "tissue issues" are too vague to be evaluated, and "inflammatory issue" is the best supported but hardest to follow up on in a useful way because inflammation might be a cause or a symptom and is associated with dozens if not hundreds of diseases, and so on.

Let me ground this by saying that for me personally, I want to see 80% / 80% data for some mechanism before I start to research a cure based on it. That means 80% of the people who have the disease have the mechanism that I'm researching, and 80% of the people who don't have the disease, do not have the mechanism. Do you think any of the mechanisms you listed are 80%/80%? (Obviously, when we fully understand the mechanism and the disease, these percentages will be much higher, but 80/80 is my cut off to be interested. What is yours? And for me, an N=1 study doesn't even weigh in on the scales.)

 

[joshualevy]

That brings up an interesting question: what is the typical size of the pile of published papers which don't really help in understanding a mystery vs the ones that do? Probably a pointless question, along the lines of "what music is good" (depends on the listener).

Not in science, but in science fiction writing, there is Sturgeon's Law, which is roughly "90% of everything is crap". I suspect it is true of early scientific research as well. Once you move into clinical trials, things get better because there are common standards, but prior to that, Sturgeon's Law rules.

 

[Rufous McKinney]

I've gotten considerable help from chinese herbs, via TCM and an expert who studied for years.

The protocols were developed without knowing the causes or the mechanisms. The Yin deficiency (dryness, imbalances, inflammatory, the autoimmune crap); the blood stagnation (lymph and blood not flowing properly....)the spleen this and liver that. TCM probably added ten years of being able to still work despite THIS.

Via careful observation over immense time, they observe improvements and make adjustments that result in more improvements and sometimes full on cures.

It's logical using the scientific method, to want to prove the mechanism or cause. But we should be able to get somewhere on treatment, despite.

There is also an immense amount of information in the world, with us only have a few hours per day.

My GP has written several books on the endothelium, and inflammation and how to correct it. I don't even have his books, let alone I have not read them. He said he'd been nominated for a Nobel Prize. His first book was on Anti-Aging, a thing he is into because he married a forty year old ex Miss Universe. He is 72.

 

[Oliver3]

Not in science, but in science fiction writing, there is Sturgeon's Law, which is roughly "90% of everything is crap". I suspect it is true of early scientific research as well. Once you move into clinical trials, things get better because there are common standards, but prior to that, Sturgeon's Law rules.

I didn't once say that I wanted to rush ANYTHING into trial.
So if you gleaned that from what om saying, I'd say your position is not so steady.

I clearly said I took exception to wishful continually denigrating work done at every opportunity when he doesbt even read any of the literature!.

That's quite clear!

Regarding sturgeons law where everything is crap until trials.
Well, hate to Break it to you, but everything can still be crap and misunderstood even when we have ' effective treatments'.
The mechanism may not be understood, the trials could be concentrating on a part of the pathology that turns out to not be important.

Good example is anti depressants. Their efficacy and how they ' work' has been called into question after 40 years or more of use and ' certainty'.
So is that now crap, or not.

Science is not perfect.

Tissue issues. Absolutely not too vague.
Eds is shown clearly in various studies to be involved in long covid, m.e. and fibromyalgia.
Ron Davies states the same thing here. Suggesting it may be a core element. So not vague.

Mitochondrial fragmentation. Not poorly supported at all. Reproducible studies looking at mitochindria. Naviauxs cell danger response being one classic example.

Endothelial dysfunction is clearly shown across studies to be an issue as hypoxia ( in part contributed to by the connective tissue issue).

Etc etc.

As with everytging in life there Is yin and yang and opposite truths existing at once. So the scientific method is the major tool but intuition often I forms researchers work. It's the human element.

My position , as you call it, is to call out wishful s endless denigrating if literally every idea. I mean literally every idea, even when the sciebtists involved are top notch.
What sort of position Is that.
I didn't once sat I wabted things to go to trial, I maintained there are commonalities consistently shown.
Enough of a signal to investigate and expand on.
Wishful is a troll. That's my ' position'

 

[Oliver3]

Not in science, but in science fiction writing, there is Sturgeon's Law, which is roughly "90% of everything is crap". I suspect it is true of early scientific research as well. Once you move into clinical trials, things get better because there are common standards, but prior to that, Sturgeon's Law rules.

https://www.ehlers-danlos.com/study...ypermobility-may-be-more-prone-to-long-covid/

https://www.sciencedirect.com/science/article/pii/S0022347699701733

https://pmc.ncbi.nlm.nih.gov/articles/PMC10965591/

There's plenty more of these kind of studies.
I say they warrant further investigation.
Wishful just dismissed that as rubbish and guess work. That's ridiculous. You shouldn't be ignoring such a signal.
These studies also have been taken into account in the case study. It's a sensitive , layered attempt to profile a severe severe patient. Done by very good scientists whose only skin in the game is to find a cure. These are important notions to consider. It's not like they decided to profile whitney without a hell of a lot of background knowledge and that they knew core elements of what they considered to be m.e.

The calibre of the scientists involved here is noteworthy. I never once said anything about ergo we go to trial.
I was again explaining to wishful that just dismissing everything out of hand is ridiculous, particularly when ' vague' correlations such as connective tissue disorders are obviously part of the picture.

The assertions by other posters that there's no clear direction is just untrue.
We are not at the point where trials are warranted but I don't think we can describe them as ' dead ends' as wishful said. Such a downright stupid assessment and likely trolling.

As Dr Davies pointed out in this study of whitbey. They used one subject because of contradictory results often seen in larger studies.
Its their very considered opinion that the relapse remission aspect of the disease is given false readings about autoimmunity etc.
So tgis study is a detailed account of variations within one individual to try and capture any signals in this very complicated disease.

Throwing the baby out with the bath water here Is shooting yourself in the foot.

Scientists with good pedigree, much background knowledge of commonalities , decided to capture whitneys experience because it likely describes the condition of many with severe m.e.

It's obviously very expensive to do this type of study at scale and because there is little money. They went down this road to establish a detailed picture from which studies can be built around.

That's where we are. At the detailed description stage of the illness.
All the the things I mentioned are not vague but shown to be part of the disease process that we've been able to elicit so far.

My irritation is directed at wishful. He openly admits he doesn't read studies. Great! How scientific! He literally thinks ' it's a few cells in the brain'.
That's his theory...a completely unsupported theory. Meaningless.
Yet he still comes on here and disses findings that keep cropping up. He's not ill like many of us here. He can exercise. I think he shows little respect for those of us suffering more.
That's my position

 

[Wishful]

He literally thinks ' it's a few cells in the brain'.
That's his theory...a completely unsupported theory.

You're doing the same thing you're claiming irritates you. "Just a few brain cells" is not my theory for ME; it's one theory for why we can feel such severe symptoms without any clear marker in the blood or other tissues. Just a few brain cells malfunctioning could possibly explain the symptoms in response to normal levels of signals. If you don't like that theory, point out its flaws. Not that there's no evidence supporting it, since if that was the mechanism, we don't have the technology yet to find it.

My other theory is that there's a complex feedback loop involved, including the brain and possibly the gut and other organs. No single factor (that's readily measurable) in that loop would stand out as abnormal, but they'd work together so that it has a positive overall value, locking it into an abnormal state. It't possible to have such a loop with an easily measurable abnormal factor, such as a cytokine in the blood, but it's also possible for that abnormal factor to be hiding in a place not easy to measure. Again, feel free to point out specifically why that theory is false.

They went down this road to establish a detailed picture from which studies can be built around.

So now it's just "a detailed picture" for future work, rather than a significant discovery? It's certainly possible for the data to be helpful for future studies. If nothing else, it rules out a lot of theories by what wasn't found. However, if you do a detailed study of one person's blood, how likely is it that you wouldn't find some deviations from the statistical average for a factor? If another group does a similar study, how valid is a comparison between then due to differences in measuring methods? I consider it worthwhile work done in the hope of finding a clear abnormality, but unfortunately, it didn't. What value the deviations from "normal" that were found is yet to be determined.

 

[Oliver3]

Where did I once say significant discovery.
I said it's a detailed picture of likely core mechanisms . Coming from scientists who know all the research inside out.
Unlike you who knows nothing.

You claim its not about a few brain cells , then go on to say it's about a few brain cells.

Your second ' theory' was a result of Mr and others forcing you to consider the idea of different loops in the body.
I remember the conversation.!!! Until that point it was a few brain cells.

I dint mind you having theories . But your denigrating of patterns and known signals is both laughable and deeply stupid. No decency in coning on here and slagging everything off without even reading around, reading specific papers, yet having the arrogance to wade in like you're a genius on the subject.

You obviously didn't read the paper about why Ron Davies chose one patient.
Do you think he chose whitney just for the fun of it. Or that during his research he's nit encountered these signals thousands of times.
He's an expert wishful he's extremely well versed. YoU know nothing.
He specifically says what looks like errors are what he believes to be actually differences in the ebb and flow of the disease and that's why studies are hard to replicate. Not because, he believes, with his expansive knowledge on tgis subject, that the theories are wrong.

You are a troll. You know it. You know you enjoy this kind of crap.
You know virtually nothing Bout m.e. stick to your theory tho

 

[Wishful]

Bout m.e. stick to your theory tho

I'm waiting for your points on why my theories are false. They're valid until falsified. They may not be helpful in pointing to an easy way to find the cause of ME, but ME has no responsibility to have an easy answer.

 

[Oliver3]

You've provided ZERO evidence. Zero. It's just a thought that popped into your rather simple mind
Just so we're clear on this, I've never not said that brain cells might be involved.
But i also dont ignore the plethora of other signals that this is a multisystemic disease.
When you see other clear signals. You trash them. Eds is a clear signal that needs investigation to pull apart.
Why not say m.e. is created by mind control yogis from a basement in panama?

I call your behaviour scummy and deliberate trolling.
You don't read papers.
You carp on about one idea I'm a simplistic top down fashion.
You don't even have normal m.e and are clearly a one off ( yes I went there)
Science doesn't work in the way you think.
If you have an idea that it's a couple of cells in the brain, then show evidence. That's the scientific method.
Why come on here when you disparage everything everytine.
Show some respect for those of us severely affected

 

[Wishful]

You've provided ZERO evidence.

I don't have to provide supporting evidence. The theory remains a possibility until someone proves it false. If I wanted funding for a given theory, I'd need to provide supporting evidence. As an explanation for why we haven't found a clear biomarker yet, it's a valid theory until proven false.

Your second ' theory' was a result of Mr and others forcing you to consider the idea of different loops in the body.
I remember the conversation.!!!

Can you find that conversation? I'm pretty sure I was talking about feedback loops long ago. To me, the rapid switching of state practically screams "positive feedback loop", something I'm familiar with in electronics. I don't have a problem with the loop being long and complex.

 

[Oliver3]

No wishful I'm not wasting time on you. But we' were talking about parkinsonism. I pointed out it may actually start in the kidneys as you were harping on that it's the brain that causes everything.

No wishful. You have delusions of grandeur if you think you have a theory.
You have your own personal intuition based on your symptoms that are very very atypical of m.e.
It's totally great to have that intuition.
It's not cool to come on here boasting of your ignorance by not reading papers and ignoring clear signals because it doesn't fit your very atypical m.e.
My theory of your m.e. could be you don't have m.e. prove it! See how stupid your stance is?

Most of us on here have read a lot. Yes we may have started with our own intuition but we've also followed the science as it stands.
These researchers are , on many cases, very very very astute thinkers.
I'd love to see you disparage their work to them and tell them it's a couple of cells in the brain.
It's so vague as a theory that it's useless.

Like I say, I'm not saying you're necessarily wrong for believing the brain is part of the picture. Glial cells, inflamation in the brain. Low 02 are all there, qeK blood brain barrier etc.
But that doesn't mean it's a disease of the brain primarily.
But again, great to have debate. But you don't do that. You don't post science to support your intuition and you Diss any other real evidence others provude with no comeback.
That's a dishonest, ignorant stance.
I'm afraid if you're going to have a theory. You have to provide evidence . Otherwise it's just an intuition. Again intuition fine but we know your stance. It hasn't developed or got more interesting
Intuitions don't need scientific validation.
I suggest , if that's your belief, then you read around the subject and come back with some solid ideas.
Otherwise you're just shamelessly trolling. Perhaps there are other things going on...

 

[SWAlexander]

May I offer my observations?

The root of the problem lies in a shared lack of knowledge — spanning science, medical interpretation, and the patient's limited understanding. This absence leaves many questions unresolved.

Take, for example, the term “brain fog.” It was coined out of uncertainty and now serves as a pacifier, temporary comfort for those in pain, while simultaneously functioning as a vague, and often lazy, medical placeholder. Instead of identifying potential underlying causes — such as brain inflammation — the term brain fog tends to divert attention from necessary investigation.

As a patient, I would ask:

• Do I have brain inflammation? If so, which part of the brain is affected? Can this be confirmed through MRI or other diagnostic tools?
• What causes brain inflammation? Has there been sufficient investigation into current scientific evidence and documented cases?

In many cases, brain fog presents with symptoms such as irritability, lack of concentration, and cognitive decline. A common, lazy, and uninformed response is to prescribe antidepressants — often without further inquiry. When these medications fail to bring relief, patients are left feeling dismissed. In desperation, they may turn to unproven or alternative sources for help, simply to avoid being labeled rather than genuinely understood, treated, or cured.

Example:
Limited knowledge or a lack of understanding is a key factor behind self-harm.

Observation:

In 2022, a woman contacted me, saying she was in the hospital with shingles and severe headaches. She claimed to have ME/CFS, but said the doctors didn’t believe her.

She sent me a photo of her blood test results, taken with her cell phone. The lab report showed a positive result for Borreliosis. She never understood that her symptoms weren’t caused by shingles, but rather by a Borreliosis-related skin reaction and headaches—symptoms that can occur early on, along with flu-like signs.

She also told me the doctors were insisting she stop taking Effexor.

Fast forward to 2025: she still hasn’t researched or asked any questions about Borreliosis, yet continues to insist she has ME/CFS.

Regarding Effexor, she wrote to me saying that tapering off would take years, based on information she received from a Facebook group. Since then, she has been following their advice and taking all kinds of supplements recommended by the group. They had also sent her a link to a scientific paper, which she forwarded to me.

After reading the paper—which discussed "Antipsychotic Withdrawal Syndrome in Cases of Schizophrenia"—I asked her, “Have you been diagnosed with schizophrenia?”

“Of course not,” she replied. “I have musculoskeletal pain, memory problems, tinnitus, can’t sleep, and have very little energy.”

In a follow-up email, I asked if she knew the difference between antidepressants and antipsychotics. Her answer was no—but she still believes that tapering off Effexor would worsen her ME/CFS.

It appears she is actively reaching out to people across various social media platforms to seek validation for her self-diagnosis of ME/CFS and her belief that Effexor is an effective treatment.

 

[Oliver3]

A very perceptive post sw Alexander

 

[SWAlexander]

to: Oliver3​

There comes a point when helping others must end.

A childhood memory has stayed with me—my godmother’s simple words, reacting to my belligerent father.

She said, "You can cook and serve the food, but you can't make them eat."
Then she added, "And if they don’t like what you serve, lock the door."

Her message was clear: offer what you can, don’t insist if they refuse it, and know when to walk away.
Protect yourself.

 

[Oliver3]

Again wise words. I appreciate them. And heeded. Thank you