By David Tuller, DrPH
Along with several colleagues, Professor Chris Ponting, a geneticist at the University of Edinburgh and a leading ME/CFS researcher, recently posted a pre-print called “Replicated blood-based biomarkers for Myalgic Encephalomyelitis not explicable by inactivity.” (A pre-print is a paper that has not yet been formally peer-reviewed.) For this analysis, the investigators examined data for more than 3,000 molecular and cellular traits in samples from the UK Biobank, including from 1,455 ME cases and 131,303 controls. They found 116 traits that were significant among both female and male ME patients.
Earlier today, I spoke about the study with Professor Ponting, who is also the lead investigator for DecodeME, a major genome-wide association study of ME/CFS.
Thanks to both of you for the interview, I think I understand the study a lot better now. It’s important groundwork, and the lack of difference between sexes is especially interesting given the female predominance. Hopefully it’ll provide a focus for future work on identifying biomarker panels.
I don’t think it would be all that surprising if people who had chronic inflammation in the body, with reduced liver function or whatever, felt chronically fatigued. I wonder then – could this study be picking up on a group of people who could possibly be a different group from those who have post-viral chronic fatigue? To my mind, the diagnosis of ME/CFS has been so lazily and liberally applied by doctors that just going by patients reporting that they have a CFS diagnosis probably doesn’t mean all that much. However, it sounds to me like a distinct group has been identified here and if that leads to some sort of biomarker panel that can pick out that group, then that has to be a good thing. The question then would be, what happens to all those patients with ME/CFS diagnoses whose results don’t come back positive with that panel of tests? I’m sure there will be a very large number of them. This marks a good start I think but, from my own experience, it’s extremely easy to get diagnosed with ME/CFS when your symptoms are completely different – and I mean miles apart – from others who have the diagnosis. It’s a massive mess that needs sorting but this does seem to me to be a good step in the right direction (and it’s nice to know that no link was found to inactivity/deconditioning).
Thank you for doing this interview, I hadn’t previously heard about this study.
Chris Ponting’s work on ME is fabulous.
I always feel very hopeful when I hear his genuine passion and care regarding the ME community and finding a solution.
Good to see this is being done. I’m a tad disappointed the biobank didn’t screen for a strict ME/CFS criteria. Preferably the Canadian Consensus Criteria. As those that have self diagnosed or been incorrectly diagnosed do create unnecessary noise in studies. That’s been the ongoing problem. Having people without ME/CFS in ME/CFS studies. So I do feel for this researcher as he’s had to use what he’s been given. I just wonder how we know how many people who didn’t have ME/CFS were in that biobank?. Is that the reason the researchers still can’t say if someone has ME/CFS or not? That was confusing?
As they still found 116 different molecules in the ME/CFS patients. So I would have thought that is showing a patient has ME/CFS. Or is he meaning any ‘one’ of those 116 on their own won’t distinguish if it’s ME/CFS?
I guess it’s too expensive to test for 116 via a lab. But maybe they could find the most common ones of them, maybe just 10 or 20 and then screen for them?
I presume some of these markers will have very expensive methods to analyse them? So maybe it would come down to the most affordable tests of the least amount of markers that are still distinct from healthy controls. And that would mean a lot of work trying to shorten that list, or maybe all 116 are needed?
Lots of questions.
I see Professor Warren Tate from The University of Otago New Zealand found DNA methylation profiles and protein profiles that were distinctly different from healthy controls. But he used mass spectrometry to analyse the samples, which again is restrictive as is so expensive to use this method. But that in my opinion is still a biomarker. Unfortunately it was a very small sample size due to cost. so that needs replicated on a much larger scale.
Because If there was a large insurance claim being denied, then in that case the insurance company should foot the bill for tests even if they are expensive, especially if they are so adamant a patient doesn’t have ME/CFS. Because I bet once they know such a test exists they’d soon backdown in denying claims. After the first few cases. They’d start accepting a doctor diagnosis. Meaning expensive tests still could be helpful.
Side note: Interestingly Professor Tate found the ME/CFS patients matched the Long Covid patients. ( those findings have been published)
Excellent David. I feel like I would never have understood the nature or significance of the this study without hearing this interview. Thank you for the interview and thank you Chris for your work and enthusiasm.
I thought the explanation of why the traits cannot be used to distinguish whether a single person has ME or not, at the 11 min mark, was quite clear.
Does the fact that there were so many markers found relate to the illness being systemic?
Thank you to the researchers for doing such a big and robust study. Exciting!
Were antibodies or cytokines amongst the 3,000 molecules examined?