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We should probably keep in mind that this is a preprint, and it's already surprising how much press it's getting for a preprint. It might be much more widespread when it's published.

The websites are similar too. I assume they're all owned by the same company, or at least affiliated.

Looking for articles in any major US news like CNN or New York Times, but still not seeing anything. Here's a bunch of smaller newspapers around the world publishing about it using the same wire story: Google Search Edit: Direct link to one: Sacramento Sun

Python. I just copied the manhattan plot code from an example I found.

Oh yeah, I should have read the readme file first. It's got all the info that confirms that. @ME/CFS Science Blog you were wondering which SNPs were imputed. The imputed.info.gz file might have that. Also, I noted the issue with the reported frequencies not making sense. The readme says not...

The preprint is now also on medRxiv: Link

It looks like what we want is in the qced.var.gz file. It just has a list of SNPs, which I assume are those that passed QC. When I filter the main summary stats file (gwas_1.regenie.gz) to only include the SNPs in this list, then it looks like it matches the reported data:

Interesting, thanks! This seems like it could be important. They thought preventing the shingles infection was helping prevent dementia, but this is pointing to a specific ingredient found in multiple vaccines instead.

I was the opposite, barely getting sick, but I also can't tie my ME/CFS to an infection.

Kara Jane's Father interviewed live on Channel 5 [Recorded on Severe ME Day 2025] Kara's new album "In Limbo" was released today. Listen at these places: iTunes/Apple Music Amazon Music Spotify YouTube Or purchase on CD

Exactly. CA10 being the protein that is changed and causing issues in ME/CFS due to these mutations is an educated guess based on the things we know, which you said, but we can't be positive about that yet. So looking at the manhattan plot they gave: Every dot is a location on the DNA. The...

To be clear, this variant/location isn't within the CA10 gene. It's just nearby in DNA that doesn't code for any proteins. Just trying to make sure we know to be cautious in that we don't know that CA10 is for sure what this variant is mainly affecting in ME/CFS. I think you got it, but in...

Replicated blood-based biomarkers for Myalgic Encephalomyelitis not explicable by inactivity, 2024, Beentjes, Ponting et al In that study, both of these were significant in the BMI adjusted results for the combined cohort (from Dataset EV13). IGF-1 was decreased in ME/CFS. SHBG was increased in...

Good chance you know this since your first sentence where you posted figure 4 above was right, but I wanted to correct the wording here. The variant isn't overexpressed anywhere. The variant is just a different letter at a particular point in the DNA, and all cells in the body have the same...

That seems pretty much right, but I'm no expert, so I wanted to find a more reputable source to back it up (these correspond to ChatGPT's points 1 and 2): Prioritization of causal genes from genome-wide association studies by Bayesian data integration across loci (2025, PLOS Computational Biology)

The database (and figure 4 above) are about how the DecodeME's (and other) specific mutations affect the amount of CA10 produced, not how much CA10 there is in general. So it's saying that having this ME/CFS mutation leads to more CA10 in the prostate. Maybe it's possible the effect in other...

My understanding is that it's based on a project (GTEx) that tested expression of all genes in 54 different tissues to see where mutations affect expression. So I think they would have looked at CA10 in all tissues. Paper about GTEx

That's my view. Just a slight bias in how many infections people with ME/CFS get versus healthy people that isn't large enough to be obvious, but might become apparent in the genes in an enormous sample like we have here. With ME/CFS often following an infection being one of the few things we...

So the study found significant locations in the DNA, not necessarily significant specific genes. The trouble is figuring out which gene associated with a given location is the troublemaker in ME/CFS. For some of these locations, there are many possible genes. For example, for the chr1q25.1...

Sorry, my brain is too mushy to follow this very well. If they didn't confirm it's not the same cells, then how can you know it's EBV-infected cells reacting to EBV? And for the "strategy EBV uses" part, it sounds like you're saying it's settled then that they can make EBV antibodies?