Community Symposium on the Molecular Basis of ME/CFS Sept 11 2026 (Stanford/Ron Davis)

[Chandelier]

And it’s not like it’s harmless, it can even be fatal in rare cases.

From the summary:

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It's ME(Jaime) @exceedhergrasp1.bsky.social​

Horner Syndrome should show up after a successful SGB, Luke says. Patients get ptosis (drooping eyelid), flush, sweating, other signs ANS has been messed with. Complications of incorrectly-performed SGB include seizure and cardiac arrythmia, along with nerve injury. Not something to take lightly.​

5/16​

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Luke is saying that SGB doesn't work for everyone, though he hoped it would be-- there seem to be responders and non-responders. Moreover, some people relapse even when they improve at first.​

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[Jonathan Edwards]

Thanks. Are they still going on about that? If it really was that good, why have we not seen any positive controlled trials yet?

I find it astonishing that anyone takes stellate ganglion block seriously. It has been an unproven treatment for all sorts of odd things with no treatments since at least the 1980s - judging by the Liu presentation for 100 years. It is inconceivable to me that it would have any long lasting benefit in anything without causing major harm. All I can see so far is that it can cause major harm.

 

[Jonathan Edwards]

Luke is saying that SGB doesn't work for everyone, though he hoped it would be-- there seem to be responders and non-responders. Moreover, some people relapse even when they improve at first.

In other words there is no real evidence that it works at all.

 

[Chandelier]

In other words there is no real evidence that it works at all.

Apparently, he mentioned one (1) hyperhidrosis case as a successful example:

Liu discussed a case of hyperhydrosis (excessive sweating) where treatments of SGB still showed long-lasting change years later.​

 

[Jonathan Edwards]

Liu discussed a case of hyperhydrosis (excessive sweating) where treatments of SGB still showed long-lasting change years later.

Oh yeah? So what was the objective evidence?
I cannot see why blocking a stellate ganglion should have much effect on sweating.
I despair that a group of scientists should have such little clinical input that they bother with stuff like this.

 

[Chandelier]

So what was the objective evidence?

From

https://www.mayoclinic.org/diseases-conditions/hyperhidrosis/diagnosis-treatment/drc-20367173

There seem to be objective tests like:

Two such tests are an iodine-starch test and a sweat test.​

​

I cannot see why blocking a stellate ganglion should have much effect on sweating.

They also mention surgical procedures with potentially horrendous outcomes:

Nerve surgery (sympathectomy).​

During this procedure, the surgeon removes a small section of the spinal nerves that control sweating in your hands. A possible side effect is permanent heavy sweating in other areas of your body (compensatory sweating).​

 

[MrMagoo]

Is this symposium just “vanity projects vaguely related to something that may be science” it sounds messy.

 

[Nightsong]

rs115186419: 3-186075329-T-C (LocusZoom)
rs73175505: 8-5338479-C-T (LocusZoom)
rs261902: 12-32323793-A-G (LocusZoom)
rs117553493: 13-99911262-C-T (LocusZoom)
rs72741654: 15-61322139-C-T (LocusZoom)
rs74963073: 16-10008215-C-T (LocusZoom)
rs76847656

Haven't been able to listen to the presentation but briefly looking at that list of rsIDs - GRIN2A came up in Zhang, as I recall. And a number of associated genes have relatively high expression in cerebellum,

 

[DHagen]

General consensus in the discussion is that there is no common cure and treatments targeted at subgroups is the only way forward (and the reason why all the clinical trials have failed). Phair being the sole dissenting voice with a comparison to diabetes and the discovery of insulin.

 

[DHagen]

The anemic, inane, barely coherent closing discussion that Rob Phair just dragged the few remaining participants through seemed an apt close.

While I should state first up that I am in a very poor mood to begin with, having thought I was over a really rough period and found myself on very shaky ground today (and quite probably having now set myself back by following along with this conference despite the itchy, desperate-to-stop-the-flow-of-information-brain I have been enduring all day), and so am primed for a negative response... but god damn has this conference made me want to scream. Or spit. Or just weep.

I have no hope. It's not just what was presented today, which seemed the same empty nothing, it's the tone, the attitude, the profound, utter lack of... anything.

 

[SugarSquared]

General consensus in the discussion is that there is no common cure and treatments targeted at subgroups is the only way forward (and the reason why all the clinical trials have failed). Phair being the sole dissenting voice with a comparison to diabetes and the discovery of insulin.

That reminds me of the many threads we have about subtypes and subgroups in ME/CFS research. Here's just a couple:

• Has there been any ME/CFS treatment trials that adequately explored the "it works for a subset" concept?
• Why are patient pleas about subtyping and stratifying in studies seemingly falling on deaf ears?

I personally only believe that this argument will hold weight once subgroups are adequately identified through positive clinical trials or robust biological evidence (ex.: a genetic mutation). I'm interested to see if Fluge and Mella's identification of a high baseline NK-cell count being positively correlated with a clinical response to daratumumab will turn out to be true in their phase 2 trial. That would be a real subgroup.

Until then, the arguement of subgroups being the reason the clinical trials fail sounds like an excuse for not accepting null results. These people need to accept that perhaps their ideas don't work and they need to think beyond them. Maybe if we had more people looking at neurology new avenues could be opened.

 

[SugarSquared]

The anemic, inane, barely coherent closing discussion that Rob Phair just dragged the few remaining participants through seemed an apt close.

While I should state first up that I am in a very poor mood to begin with, having thought I was over a really rough period and found myself on very shaky ground today (and quite probably having now set myself back by following along with this conference despite the itchy, desperate-to-stop-the-flow-of-information-brain I have been enduring all day), and so am primed for a negative response... but god damn has this conference made me want to scream. Or spit. Or just weep.

I have no hope. It's not just what was presented today, which seemed the same empty nothing, it's the tone, the attitude, the profound, utter lack of... anything.

I'm so sorry @DHagen. Thank you for keeping us up to date on what happened today in the conference. Please take care of yourself and don't feel pressured to do it tomorrow.

 

[wigglethemouse]

These are the seven variants from that slide with links to gnomAD, and locuszoom for DecodeME data:

rs115186419: 3-186075329-T-C (LocusZoom)
rs73175505: 8-5338479-C-T (LocusZoom)
rs261902: 12-32323793-A-G (LocusZoom)
rs117553493: 13-99911262-C-T (LocusZoom)
rs72741654: 15-61322139-C-T (LocusZoom)
rs74963073: 16-10008215-C-T (LocusZoom)
rs76847656: 16-28261692-T-C (LocusZoom)

In the Q&A log on Zoom Beentjes answered a question that the preprint has been submitted and should show up in the next week.

 

[Jonathan Edwards]

I have no hope. It's not just what was presented today, which seemed the same empty nothing, it's the tone, the attitude, the profound, utter lack of... anything.

These people need to accept that perhaps their ideas don't work and they need to think beyond them. Maybe if we had more people looking at neurology new avenues could be opened.

I am beginning to think we may be able to make that a reality. The new avenues are in fact wide open, stretching out like vistas before us. We need the neurologists. And to be fair, Rob Phair made sensible suggestions based on what we knew 5 years ago. We now know more.

I thought I might get in touch with Peter Goadsby, the migraine man. I get the feeling that he is someone with a first rate creative brain. Between UCL and King's we have over 2,000 neuroscientists. It must be possible to raise some interest.

 

[Dude]

From Scheibenbogen's presentation(bsky):

Now they're initiating trials using anti-CD38 and anti-CD14 antibodies, with some promising results.

This one was unfortunately quite a lot, referenced a large number of publications — sorry I could not hunt them down fast enough! Remember the recording will be out there in a week or so, likely.

Interesting. I didn't know the trials had already started. I vaguely remember hearing that they would take about a year, so hopefully we should have the results relatively soon.

 

[Jonathan Edwards]

From Scheibenbogen's presentation(bsky):

Do they mean CD14? Maybe CD19? I cannot see a reason to go for CD14.

 

[Dude]

Do they mean CD14? Maybe CD19? I cannot see a reason to go for CD14.

Yea, i think its cd19:

TAME – CD19-Targeted B-Cell Therapy for Post-Infectious Autoimmune ME/CFS Using the Monoclonal Antibody Tafasitamab: Open-Label Follow-up Study to a Randomized, Placebo-Controlled Phase II Trial of the CD19 Antibody Inebilizumab

TAME – CD19-Targeted B-Cell Therapy for Post-Infectious Autoimmune ME/CFS – ME/CFS Research Foundation

Growing scientific evidence suggests that autoantibodies and dysregulated B cells play a significant role in a subset of ME/CFS patients. In…

projects.mecfs-research.org

Edit:
The other study involving CD38 is probably the one using isatuximab.

 

[V.R.T.]

I personally only believe that this argument will hold weight once subgroups are adequately identified through positive clinical trials or robust biological evidence (ex.: a genetic mutation). I'm interested to see if Fluge and Mella's identification of a high baseline NK-cell count being positively correlated with a clinical response to daratumumab will turn out to be true in their phase 2 trial. That would be a real subgroup.

Until then, the arguement of subgroups being the reason the clinical trials fail sounds like an excuse for not accepting null results. These people need to accept that perhaps their ideas don't work and they need to think beyond them

I completely agree. I don't know if there are subgroups but the idea of an infinitely heterogeneous response to treatments meaning every treatment used off label by the community and every failed trial treatment works in a proportion of pwME is a very frustrating argument- it's impossible to disprove without wasting years and years and millions of pounds of research money, and it doesn't seem likely on the face of it.

 

[neophyte32]

I don't think one should worry. We already know that there are potential problems with these UKB-based cohorts. They are small and the selection is almost certainly suboptimal. It is interesting that variants have replicated across these smaller groups. I wonder if they may be telling us about confounding genetic factors relating to selection bias. That had been a worry right from the start.

I didn't see what genes were implicated, or whether it is premature to try to pin that down?

Hello Professor,

Are you sure that Beentjes’ results are not actually bad news for us in light of DecodeME?
It was one of the few things that seemed potentially interesting for us, and, as usual with ME/CFS research, there seems to be another surprise and another disappointment...

Are you sure neurologists — at least British neurologists — are really going to help us despite the disastrous state of ME/CFS research? In France, I saw two neurologists at a well-known hospital, and neither of them even believed in the disease: “There is nothing wrong with your brain.”

If I understood correctly, @DHagen presentation — and perhaps yours as well — was once again rather underwhelming.

But when these researchers talk to one another, do they not realise that something is seriously wrong with the overall direction and results of their work?

Apart from Scheibenbogen and her anti-CD19 trial — perhaps that will finally settle the question of her long-standing focus on anti-GPCR antibodies and the idea of a specific subgroup.

What a mess!

 

[V.R.T.]

Are you sure neurologists — at least British neurologists — are really going to help us despite the disastrous state of ME/CFS research? In France, I saw two neurologists at a well-known hospital, and neither of them even believed in the disease: “There is nothing wrong with your brain.”

The last neurologist I saw repeatedly hit my knee with a reflex hammer whilst asking if I was seeing a psychiatrist on a very pointed way and then said 'I don't know what you want me to do'.

The one before that seemed lovely until MS was ruled out then tried to tell me to do essentially GET.

I would love for neurologists to see the light and get involved but currently they are the last doctors I would ask for help (except psychiatrists I suppose).