Preprint Charting the Circulating Proteome in ME/CFS: Cross System Profiling and Mechanistic insights, 2025, Hoel, Fluge, Mella+

[forestglip]

I'll do a linear model tomorrow.

R^2 of .019

 

[Chestnut tree]

Another group is showing that GDF15 is normal in ME/CFS, @Jonathan Edwards. The testing I was part of showed that the most severe patients had the lowest GDF15. Explaining how this could be would go a long way, in my opinion.

I still think it's plausible that, due to poor microvascular diffusion and reduced gradients, blood values might not reflect tissue values. Something similar is seen in mitochondrial diseases, where lactate levels in the blood can be normal.

There could be many other reasons, of course.

Hi Butter,

Interesting that you were tested for that. Was that as part of a study or something available to the public?

 

[Chestnut tree]

Complement C3 has come up in a couple of studies before, for example this one:
Complement Component C1q as a Potential Diagnostic Tool for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Subtyping - PubMed

If you do not mind me asking, you seem to have a vast knowledge of all these studies. How do you keep track and organize these studies?

I struggle to keep track so was interested in how you do it.

 

[ME/CFS Skeptic]

If you do not mind me asking, you seem to have a vast knowledge of all these studies. How do you keep track and organize these studies?

I try to follow ME/CFS research as closely as I can and sometimes write blogs about them. For example, at the end of the year I write an overview of the most interesting studies of the year, which helps to keep track of the most important ones.
https://mecfsskeptic.com/2024-looking-back-on-a-year-of-me-cfs-research/

I also notice that I tend to ignore the less quality studies more and more. Many papers just aren't worth the time and effort.

 

[Hutan]

Peroxidasin is intersting to me, it might help explain POTS

Mammalian Peroxidasin (PXDN): From Physiology to Pathology

PXDN expresses in the endothelial cells and secretes into blood. PXDN exhibits with much higher concentration in plasma than MPO [20]. Therefore, it is reasonable to speculate that PXDN also plays an important role in vascular tone under physiological and pathological conditions.


According to that review it also seems to be involved in extracellular matrix and fibronectin. i don't know too much about extracellular matrix and fibronectin but I do know that these are bits of biology that keep coming up! Collagen-associated functions suggest a possible link to Ehlers Danlos or similar connective tissue issues.

I find PXDN very interesting too.

Here's a link to a post I made about earlier findings:
Myopathy as a cause of fatigue in long-term post-COVID-19 symptoms: Evidence of skeletal muscle histopathology, 2022, Hejbøl et al

 

[Sean]

I also notice that I tend to ignore the less quality studies more and more. Many papers just aren't worth the time and effort.

Was told once by a senior researcher in materials science that when he gets a paper to read he goes straight to the methodology section, and doesn't read the full paper until he knows it is worth reading. Said it saved him a lot of time.

 

[forestglip]

HLA-C has the 39th highest fold change out of the 7326 aptamers they tested (logFC = 0.35). Not significant though (p=.19, q=.45).

Here are all the ones they tested that mentioned HLA:

Rank | EntrezGeneSymbol | logFC | adj.P.Val
39 | HLA-C | 0.35 | 0.45
1662 | CD74 | 0.05 | 0.11
2047 | HLA-G | 0.04 | 0.64
2255 | HLA-E | 0.03 | 0.78
3243 | CD74 | 0.01 | 0.83
4309 | HLA-DRB3 | -0.01 | 0.94
5759 | HLA-DQA2 | -0.06 | 0.06

Edit: Mistyped the q-value.

 

[wastwater]

Homozygous Mutations in PXDN
Cause Congenital Cataract, Corneal Opacity,
and Developmental Glaucoma

https://www.cell.com/ajhg/pdf/S0002-9297(11)00355-7.pdf