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Wouldn't this also work for ME/CFS? Except that the T cell attack is either more subtle and not visibile on imaging, or that instead of an attack, there is a persistent danger signal that makes cells exposed to it dysfunctional. That dysfunction then maybe somehow feeds back to the immune system...

I don't see how the polymorphic nature of DQ would lead to spurious associations. What may be happening is a DQ variant that's not contributing to disease being in linkage equilibrium with another variant that is contributing to disease, and of which we don't yet have knowledge. Since DQ was...

I'm sure the data will be used eventually. The prevalence of CFS in the dataset is 3.65% which suggests potential issues with overdiagnosis.

It's that GWAS of somatic symptom disorder, which also assessed FND https://www.medrxiv.org/content/10.1101/2025.07.16.25331639v1.full.pdf

The FND GWAs had 22000 participants and had 3 hits across 2 different conditions. DecodeME had 15000 and 8 hits. DecodeME gives the impression of being more on target. In the FND study, two of the hits seemed potentially relevant to neurological illness. It's a shame that the research is...

That strikes me as unintuitive. ME/CFS is triggered by a variety of pathogens and my intuition tells me that while specific genetic vulnerabilities for ME/CFS would certainly exist for each of these pathogens, they wouldn't be among the top hits in a GWAS. Variants related to disease process...

The genetic findings and the lack of autoantibodies seem to say that roughly the following might be occurring: An immune response against pathogens leads to the side effect of a non-antibody mediated immune attack against the brain. Presumably parts of the brain that are especially involved in...

You want to know if it would make sense to study ME/CFS in certain geographic regions? My understanding is that it would not make sense. ME/CFS is not a disease caused by mutations in a single gene. The variants identified in DecodeME are very common in the population and their effect on the...

I have mixed feelings about the results. I'm happy that a big step forward has occurred, but the results are merely a hint where to look more in detail. We're still far away from a diagnostic test, understanding the disease and treatment. At least we can call it disease now, and the results seem...

Can mildly excessive mitophagy promote metabolic inflexibility by removing mitochondria that might perform a little worse under optimal conditions but better in certain specific situations?

FBXL4 regulates mitophagy, which is a process where surplus, aged or damaged mitochondria are degraded. When FBXL4 is absent, the levels of BNIP3 and NIX raise and hyperactive mitophagy results. Loss-of-function mutations in FBXL4 are known to cause mitochondrial DNA depletion syndrome 13. In...

I have 3 of the 8 SNPs, in RABGAP1L, CCPG1, CA10. I'm not sure what this means. I can't find information on how common these SNPs are to get an idea of whether I have more of these SNPs than expected by chance or not. Presumably these are fairly common ones. I'm going to try and look the...

It's not available for people accessing it from outside a specific geographical region.

I'm not sure if I should be preparing for a little celebration or disappointment.

Why is the narrative of somatization (or similar concepts) necessary to shift the focus away from unnecessary testing and procedures towards rehabilitative care therapies and providing support to patients? Why can't we just say that we don't know what illness the patient has and how to treat it...

@Andy can you say if there are any hits that are statistically significant?

I agree that it's really annoying that so many people have negative attitudes towards ME/CFS patients, but I don't think we should be trying to change their views. They will use anything against us, and if there's nothing, they will just make something up... because they simply don't want to...

Thank you for the discussion and explanations.

It has been suggested that ME/CFS involves genes responsible for neurodevelopment (shared genetic risk factors with autism). It has also been reported that age of onset of ME/CFS has a peak around 15 years. I'm curious about the relationship between this onset peak and the genetic risk factors...

From what I remember, there were many papers on this. There was a small reduction in risk in some studies, in others there was no difference.