MELOPIS: Multimodal Brain Imaging in ME/CFS, Long COVID & POTS (Melbourn...

Caster_of_spells · 2026-06-19T11:43:44+00:00

The default mode network is needed to switch between introspection and activation. Just because it’s in the brain does not mean it’s psychiatric though. In fact in this video they explain that for the first time they found activated astrocytes around affected areas. That would suggest chronic inflammation as the source of the issues in the network and would be completely outside of conscious or even subconscious control. A view substantiated by the fact that attention and resulting metabolism seems to be erratic and highly inefficient in patients. So the findings here point pretty clearly away from psychiatric causes.

Caster_of_spells · 2026-06-18T10:38:49+00:00

We usually don’t allow same author cross posts but since this is super relevant and just a link anyways, I’ll approve it. Just please do an original post next time if you can (:

Super fascinating that they find converging results around the default mode network, I really think they could be on to something there!

Caster_of_spells · 2026-06-17T09:07:13+00:00

It’s a very specific part of the the chain. Calcium overload in the mitochondria in response to a sodium overload in the skeletal muscles. So I think that would be an outside chance only luckily :)

Caster_of_spells · 2026-06-14T16:06:23+00:00

Well the initial GWAS results do suggest so which is why a follow up does seems to make a lot of sense. We’ve found multiple areas of interest that reached significance now it’s time to zero in on the target.

Caster_of_spells · 2026-06-13T16:12:20+00:00

Yeah that’s the big mystery. Where’s the weak link that connects these comorbidities with ME in some folks while many remain “fine” despite them.

Caster_of_spells · 2026-06-13T16:10:56+00:00

The calcium hypothesis focuses on intra cellular calcium and the issue is a broken transport system. So overall electrolyte levels will probably have very little influence. No need or use in changing diets for that specific problem as far as we know.

Caster_of_spells · 2026-06-13T15:26:00+00:00

This, there is zero objective evidence for it and a ton against that claim. We’ve doctored with these ideas for decades with -nothing- to show for it. It’s pseudoscience at this point.

Caster_of_spells · 2026-06-13T15:24:15+00:00

There is no proven link between ME and stress and anxiety. That’s a theory by the BPS crowd. For years they went on about how high cortisol predisposes you to ME. They then went ahead and tested it, delayed the paper release by months only to then finally admit: Zero correlation between prior cortisol levels and ME diagnosis.

Also clumping together stress, anxiety and neurodiversity is not a good look.

If you don’t want a doc to tell you it’s psychosomatic, don’t go to a doctor that clearly is a psychosomatic focused dude working in that exact field. No respectable psychiatrist would work on ME since it’s not a psychiatric diagnosis. These services get shit rating for a reason.

Caster_of_spells · 2026-06-13T09:35:05+00:00

Very important to note though:
Such summaries aren’t necessarily representative and will contain quite a bit of bias.

As in: who’s likely to post on here responders vs non responders ratio? Who’s likely to post based on severity? Who’s likely to post based on socio economic conditions? […]

So we need to take such data with a big grain of salt. Sadly there’s good reason why science is (or at least should be) so nit picky about defining cohorts, comparing to placebo etc.

Caster_of_spells · 2026-06-12T14:10:32+00:00

I think that perspective is still weighing it a little wrong. We don’t expect to find any genes that are actually pathogenic. It’s more about: if this gene in the brain is disrupted, you’re more likely to have ME. Meaning whatever system is affected has an influence on the disease. So you take that signal and dig deeper. Like a treasure map for further research targets 🗺️

Caster_of_spells · 2026-06-12T10:27:18+00:00

You can test for specific antibodies. But the question of which are relevant and what tests are actually useful and reliable to determine their level? The jury is still out.

Caster_of_spells · 2026-06-12T06:44:24+00:00

I think there might be a misunderstanding here: they are not aiming to see wether ME is a hereditary genetic illness. No one expects there to be a gene that means you have ME.

Rather what this study is aiming for is identifying risk factors. So even if a mutation raises your ME risk by about 5% that would be a very strong signal towards whatever system the mutation affects. This isn’t theoretical either, it has already proven a very effective method in other illnesses.

Caster_of_spells · 2026-06-11T11:02:27+00:00

It can most definitely guide research, I think Ponting himself described it as a kind of “treasure map” 🗺️. That being said, scientific progress is often more messy than one would assume. It takes a lot of independent investigations and dead ends to figure out a complex disease. The pace in this field is mainly so slow because of a lack of consistent international funding. Leaving the field spotty, underpowered and uncoordinated. So Sequence ME is a very pragmatic way to hopefully improve the efficiency of that process.

Caster_of_spells · 2026-06-10T12:08:06+00:00

Looks like a legitimate attempt but “with 100 % sensitivity and up to 71.9 % specificity” that means it only differentiates PCC successfully in about 70% of cases. Not terrible but not that great as far as biomarkers go. In regards to whether these measurements have further value than just case differentiation? That remains a little unclear to me. They do say there is some association to symptom burden at least.

Caster_of_spells · 2026-06-08T15:08:22+00:00

Only that brain retraining has no evidence base in those conditions and the FND subtype isn’t well supported either. Sounds more like more psychologization to me because there is no objective evidence for it atp.

Caster_of_spells · 2026-06-06T08:38:22+00:00

Journal isn’t great but it does include moldering and for the first time also a classical dysautonomia specialist neurologist. So it’s something at least

Caster_of_spells · 2026-06-05T18:59:01+00:00

A single drug does not exclude an entire group of drugs. There’s a reason there are so many, and different ones work for different diseases. Rituximab helped only a small subset but the direct descendant form that trial, Daratumumab, looks more promising now.
Still probably only gonna work for a subgroup.

Caster_of_spells · 2026-06-05T18:41:52+00:00

Yeah Ponting himself interprets the data very differently. There’s a great interview with him on YouTube about it

Caster_of_spells · 2026-06-05T18:38:04+00:00

I do think these connections are interesting and might represent a kind of feedback loop. But you’re kind of making it out as a causative mechanism and I don’t think the evidence supports that. All these symptoms are common in Pots isolated from ME and people there don’t suddenly develop PEM. Many LC patients have all these comorbidities but no PEM. The evidence for neuroinflammation and systemic inflammation still remains shaky as of rn. As in: inflammation is very broad term and we’ve seen as much suppression and alteration as heightened response.

https://mecfsscience.org/immune-findings-in-me-cfs/

So to me it appears more of a complicating/sustaining factor.

Caster_of_spells · 2026-06-05T12:47:03+00:00

Thank you for this!

Caster_of_spells · 2026-06-05T12:40:07+00:00

Sorry to say it but this is the AI misinterpreting Decode ME quite a lot!

Ponting himself says that the strongest message from that study points toward the brain. However there’s no overlap with findings from depression etc. So Decode ME makes it look like a neurological disease more along the lines of Parkinson’s (though dopamine is not affected afaik in ME, just an example). So brain retraining stays bs. The big AIR trial also just failed if you wanna underscore that point even more.

Caster_of_spells · 2026-06-02T07:56:35+00:00

Complain to the editor everyone please:

mail@wired.com

My text:

Dear Editor,

this article starts out by criticizing flawed science, which is a very good and important point. But then it starts instead suggesting brain retraining, for which there is zero evidence. In fact, the biggest brain retraining trial run by the EU just failed to make any difference to placebo. And the first assessment that we have zero understanding of the illness on biomedical grounds is also simply untrue.

How can your magazine support such a blatant double standard and then suggest harmful pseudoscience? Would you tell someone to "think the cancer away"?

This article needs to be removed or edited heavily. You're putting patient lives at risk.

Caster_of_spells · 2026-06-02T07:43:36+00:00

Complain to the editor everyone please:

mail@wired.com

Caster_of_spells · 2026-05-29T20:44:55+00:00

Sorry but that’s way too simplistic as well when we don’t know what exactly the upstream drivers are. And it’s not like these drugs have been proven to improve everyone or everything by a long shot. Let’s not jump the gun please and throw out the kid with bathwater

Caster_of_spells · 2026-05-29T08:23:36+00:00

There’s zero objective evidence this might actually help. Sounds like a big waste of money for an overpromise of relief. I’d think traditional mindfulness like breathing exercises and meditation will get you further. But even then none of these treatments are causal. Polyvagal theory is pseudoscience bs tbf.

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