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I noticed that the HLA-region also got a significant finding (HLA-DQA1*05:01 at p = 1.4 x 10-10 but that it somehow reported separately form the other 8 hits. It seems to be a different SNP than what the Norwegians found but perhaps this is due to HLA being difficult to sequence?

The failed replications are disappointing but I suspect that next too broad case definitions for ME/CFS in the other databases, the sample size might also have been too small. In the supplementary material it says that the Lifelines cohort only had 3,440 cases and 17,080 controls (compared to...

Made a brief summary of the results here (EDIT: added full text and Bluesky link) Link to Bluesky: 1) The DecodeME study compared DNA of ca. 15,000 ME/CFS patients and 250,000 controls and found significant differences in 8 regions of our genome. The Manhattan plot below shows the genes and...

I think this is normal for GWAS, they provide clues or pointers to what's going wrong rather than the gene being the culprit behind ME/CFS.

To get a feel of the effect size, I've made an overview of the prevalence of these SNPs in patients versus controls. I couldn't find this in the paper or supplementary material so I've tried to calculate them using R (trying out different guesses until the combined prevalence and odds ratio...

No email yet but seeing some articles being published: Key genetic differences found in people with chronic fatigue syndrome | New Scientist

Thanks for posting Dolphin. The post shows Jaime Seltzer writing:

This is mentioned here in this documentary (38:20): Scheibenbogen later commented on this: https://www.healthrising.org/blog/2021/09/16/autoimmune-options-chronic-fatigue-syndrome-scheibenbogen/

Yes I think so. Perhaps others can double-check.

I heard people suggest that the dosage might be different (and that the Norwegian trial couldn't provide the dosage because of lack of funding). Not sure if this is true. Here's what I could find online: Fluge et al. 2011 (pilot RCT, n=30) Rituximab 500 mg/m2 given twice two weeks apart, with...

There's some more info about this trial in the presentation by Dr Sato during the Berlin conference: Here are some slides:

I also wonder how this relates to the study by @chillier which found no difference in oxygen consumption rate when ME/CFS serum was added to myoblasts. Do these studies contradict each other?

Yes it looks interesting but it seems that this is not for LC in general but for a relatively rare complication called 'Multisystem inflammatory syndrome in children (MIS-C)' This page says: https://www.mayoclinic.org/diseases-conditions/mis-c-in-kids-covid-19/symptoms-causes/syc-20502550

The first sentence is: This also looks strange, perhaps written by an AI? The first author Martin Toby published a case series on chronic symptoms following EBV in 1982 in the Lancet. https://pubmed.ncbi.nlm.nih.gov/6119490/

The link to sickness behaviour is interesting, thanks for highlighting this! If I understand correctly this was only significant in the female-only comparison which had only 34 ME/CFS patients and 27 controls. I think it means that most common allele (C, which is present in 62% of the...

Interesting but wouldn't a decline in neurotransmission result in muscles or cognitive abilities no longer functioning? In ME/CFS the end results always seems to be feeling awful. So instead of normal functions shutting down, it suspect it involves some feedback signal that is turned on too...

It's a bit unclear but it seems that they used this model to see how these factors influence SMPDL3B but that they didn't use it for group comparisons.

Interesting thanks. I wonder if they split the control group in group A and group B and do the same analysis on these groups (rather than ME/CFS versus healthy controls), how high the predictive power and AUC would be.

What do you mean by predictive power > 0.8?

The research team of Unutmaz at Jackson Laboratory has made all of their data public following the BioMapAI publication: https://github.com/ohlab/BioMapAI/tree/main