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The paper writes: But on X someone commented: "There is already a known autoimmune disease of the CNS, where autoantibodies directed against AQP4 its named Neuro Myelitis Optica (NMO) The autoantibodies were discovered in 2006/07." "The AQP4 autoantibodies causes extensive and severe...

Yes, so these are probably too important to be defective in ME/CFS; otherwise, we would see other abnormalities in patients. So it should likely be something more specific to this pathway that is defective in ME/CFS, and if DecodeME results are to be believed, might be more on the brain than...

Yes, that's also the explanation I was thinking of: that the sickness behavior pathway involves proteins that are too important elsewhere in the body, so that mutations aren't viable. But that begs the question of why we don't see clear immune dysfunction elsewhere in ME/CFS and why DecodeME...

These seem like the main results: Self-reported activity was the strongest predictor but there was no relationship between objectively measured activity and fatigue changes: Some also suspect that the effect can be explained by people with depression improving with CBT, but not LC. This also...

Yes, feeling terribly awful so that nobody in such condition would be able to ride a Tour stage. The more similar to ME/CFS the better. Which immune responses cause sickness behavior and which don't is interesting, but a different question from the one I wanted to ask. Namely, if there are...

Thanks for the responses. I was mainly thinking about an antiviral immune response that makes most people very sick and fatigued, but in some exceptions, don't cause any symptoms at all. So localised immune activation in the gut or eczema wouldn't count. The main idea is: if sickness...

Was wondering if there is any medical condition where the immune response works normally (for example, in response to an infection) but where patients don't feel ill with fatigue and malaise. In other words, an immune response without sickness behavior. It could be like the opposite of ME/CFS.

Thanks @Ferry, that quote is really clear.

Looks like it was very well done, professionally organized, nice turnout, moving speeches, and lots of national press coverage. Kudos to the organizers and everyone who participated. EDIT: screenshot from the livestream:

Thanks @Dolphin

Did White say this? Thought this mainly came from the CBT psychiatrists like Sharpe and Van Houdenhove.

Looks like this is from Vincent Lombardi's NIH grant with more info here: https://reporter.nih.gov/search/ngGdmGN8a0u3XJm2ZsBoow/project-details/11085301

This seems to be the main idea but not seems highly doubtful if this will work

Incredible, the story is heartbreaking.

Ah, so the h^2 pedigree in the Wainschtein et al. (2025) paper already used the lower heritability estimates using those algorithms, not the high estimates from twin and kin studies?

Counterpoint is this recent paper in Nature, which suggests that we simply need bigger sample sizes and more detailed measurements of all SNPs, including rare ones. Estimation and mapping of the missing heritability of human phenotypes | Nature

I thought they compared identical with non-identical twins, so that environmental confounders are substracted (as they are present in both pairs of twins).

Some weird sentences:

Another increasing issue is AI-created summaries on social media. Researchers often oversell their findings in the paper, and it seems that AI then inflates this even further. Don't have an issue with using AI per se (it can be useful in many situations), but the LLMs people use don't think...

Researchers from the University of Vienna are developing a new PEM questionnaire. https://www.soscisurvey.de/V-PEM-AQ_english/ Shared by Rob Wust on Twitter: