Post

1) A new paper on ME/CFS is getting media attention: it's about how the chromosomes containing our DNA are folded. These 3D structures can influence the expression of genes. Unfortunately, I don't think this study warrants all the attention...

2) I suspect the media attention is mostly driven by commercial interests, rather than the significance of the scientific findings. The paper comes from the company Oxford BioDynamics (OBD) that developed a new test called EpiSwitch which they applied to ME/CFS.

3) Their previous paper used 200 parameters (based on 3D folding of chromosomes) but they tested it in small samples of less than 100 ME/CFS patients. The controls were not properly matched for age, sex and other factors. That paper already raised some eyebrows...

4) In this new study, they compare results for ME/CFS to other fatiguing diseases such as MS, rheumatoid arthritis, PTSD and Long Covid. They report various connections but there's no clear null model to test if these or more than what one would expect based on chance alone.

5) Another issue is that these 3D-folding structures differ per cell type, which the paper didn't fully take into account: they used data from peripheral blood cells which may not be the relevant ones for many of the diseases tested.

6) More critical comments, including from ME/CFS experts such as Prof Chris Ponting and Dr Sjoerd Beentjes can be found below. They say e.g. that it's difficult to evaluate the methods in details because the computational methods used are proprietary. www.sciencemediacent...

7) Ponting writes: "The 2026 study’s claims are impossible to evaluate because the computational methods they used are proprietary, locked within black boxes they term EpiSwitch® Analytical [...] Researchers are thus disallowed from reproducing this study independently."

9) There's a lot of (justified) enthusiasm about genetic findings in ME/CFS but I wouldn't include this study on the same level. It needs more data, openness and above all more persuasive evidence. The direct overlap between diseaseassociated genes was limited.