A nanoelectronics-blood-based diagnostic biomarker for ME/CFS (2019) Esfandyarpour, Davis et al

At the risk of getting no likes, am I alone in thinking that SW comments were surprisingly sensible and even quite helpful? I sincerely hope that this test may be able to differentiate between ME or CFS patients and patients with other sorts of fatiguing illnesses or incapacities but, as far as I can see, we have no evidence to suggest that it can – and it feels appropriate and necessary to make that point loud and clear, lest people start to get carried away.

I also thought his other points were valid and relevant. I wonder to what extent this may be a sign of his changing perceptions of ME/CFS amid the shifting landscape, and whether it may be part and an attempt to try to row back from some of his flawed and unethical ideas and actions. Sadly, I doubt that he has the humility to ever admit that he was wrong or to apologise, but I would love to proved wrong.

I note that on the SMC page, under “declared interests” it states:

What it doesn’t say is that if – very, very big IF imo – this turned out to be useable as a diagnostic test for ME/CFS, it would, or at least should, completely destroy Sir Simon’s credibility as a doctor and a scientist. Although he may claim otherwise, his entire 30 year career in the field of ME/CFS seems to have been predicated on the unhelpful belief that no such test could ever be developed. Unfortunately, this study, while encouraging, would appear to be a very long way from achieving that objective.

 

It wouldn't actually surprise me at all if the nanoneedle test would also respond to other diseases on the same spectrum as ME/CFS. Robert Naviaux for example has looked at suramin use for both ME/CFS and autism and the other drug that made ME/CFS cells behave normal, copaxone, was a drug originally developed for MS. I think it would be incredible news if this test was specific to only ME/CFS patients, but the skeptic in me reckons it won't be. Having said that, this test could still be used to identify that the patient is sick and perhaps whether certain drugs would work or not, regardless if the patient is classified as suffering from ME/CFS or some other condition.

SW's arguments are for some parts sensible to me, for some parts not. The argument about what is a cause and consequence seems like an excuse that could be pulled off every time, even if a valid biomarker was found.

 

Moderator note: This post and those responding to it have been merged with this thread to avoid two separate threads discussing the same research and responses to it.

I am not on Twitter (it makes me way too angry) so could someone tweet this to as many of the BPS cabal as possible? I would put all their handles on one tweet so they can all see they got the same one. Tag Tuller on it so they can see he can see. lol

Blood test for chronic fatigue syndrome could speed diagnosis, study says

https://www.independent.co.uk/news/...lgic-encephalomyelitis-stanford-a8891906.html

Use #mecfs so we can all see it!

You might also want to include PLoS One, The Lancet, and James Coyne.

 

Personally, I think that it's worth doing all we can to avoid linking this finding to criticism of their work. If this finding ends up not working out then that doesn't show that PACE was a decent piece of work, but we've saw how with XMRV that negative result has been used to try to undermine criticism of work like PACE (even though many of us were sceptical of XMRV at the time).

[edit: I'm clearly too tired to write - this post made no sense until I edited it.]

 

I think this is a ways off yet. It's too soon to be getting excited about it.

 

LOTS of coverage. I hope it pans out.

https://news.google.com/stories/CAA...FNFpKekZ6YWJLQUFQAQ?hl=en-US&gl=US&ceid=US:en

 

How different is this to bioimpedance
I had a go of that in York and it reported systemic inflammation and something else,I just saw it as a novelty

 

I think that we should be glad about the progress, but we must remember that much remains to be done: the results must be repeated in different cohorts (preferrably by other research groups), the specificity and sensitivity of the effect must be evaluated, and the researchers must eventually try to understand the underlying process. I think that we should be careful to claim that this is definite proof of an underlying pathology, as there still is much that could go wrong. But the results definitely show that abscence of sensitive and specific physiological abnormalities is not proof of psychogenesis. New technology makes it possible to see things we couldn't see before—although that probably is obvious to everyone except BPS proponents.

 

Whenever I've tried to use #mecfs on my Twitter account, it has not worked. I believe you have to be "someone" one Twitter first (I presume you have to have enough followers) before you can use that hashtag.

 

It does seem to me that every year or so we get the possibility of a clinically useful biomarker prematurely hyped.

This is very interesting research and I do very much hope it leads to a usable everyday clinical tool, but we are not there yet.

Personally I have been excited and then disappoint a number of times already so am more muted in my response than I would previously have been. I also agree that the BPS cult over hype their results and we criticise them for that, so we should not rush to do the same.

As @Esther12 points out, the BPSers are quick to make use of the failure of any one line of biomedical research to dismiss entirely a biomedical approach to ME (even though they theoretically subsume a biomedical approach within their own paradigm). This claiming that the failure of one line of enquiry means the failure of all biogenic models of ME may be a logical falacy (going from the specific to the general), but that will not worry them. Give them opportunity to repeat it often enough and it will become an entrenched belief for the parts of the medical profession that listen and to the general public.

 

Re is this measuring the cause or consequence of ME: we don't know the causes of a great many diseases, and yet we have biomarkers for them. ME may be no different once we get a biomarker. To say we don't know if this study's result indicates a cause or a consequence is no different than many other diseases.

 

There’s still the need to compare results with other sickness groups and larger studies generally? UK reporting has been as simplistic as ever. i’m not sure if this is premature in all the press if it’s in Pilot stage? All UK press coverage is implying that is is the only evidence ME isn’t imaginary, which isnt helpful. In telegraph a non expert and wessely piss on the parade so no need to tweet wessely. It’s true it’s pilot stages but I also think there is clear resistance to moving the illness away from vague psychological syndrome status.
I understand Davis wanting his work known of and funding for it but imo as far as “evidence” goes the recent nih conference or the IOM evaluation was far more solid. I think that the daily mail has a “first evidence not all in the mind” template it’s using for all CFS research news.

It seems what we have long known of has become news because a PNAS paper has been published yesterday. It’s good to put in people’s minds the possibilities of physical abnormality and tests and serious science but the reporting of it has been entirelywithout context of other research or serious depiction of the illness and is still in the uncertain physical evidence “versus psychological” vein.

 

"You don't need a blood test to prove an illness exists..." It's my understanding that this has been one of the long-standing lacks in the minds of the BPS group - no biomarker? "Then it's ours, and not yours."

 

http://www.sciencemediacentre.org/e...al-biomarker-for-chronic-fatigue-syndrome-me/

SMC have four expert responses.

 

In the discussion, the authors say


"According to our experimental results, ME/CFS blood cells display a unique characteristic in the impedance pattern…"


Yes, as they go on to say, it is significantly different from healthy controls. But no one has a problem distinguishing ME patients from healthy controls, it is the comparison with other diseases that is so important.


What they could've said is that they have achieved clear blue water between healthy controls and patients, with the pilot results achieving 100% specificity and 100% sensitivity. This is a remarkable result and does give hope of finding differences with other illnesses.


So the most important step now is to demonstrate its ability to discriminate from other illnesses — at least it is the priority if this is ever to become a biomarker. There I am hardly the first person to say that.

 

Simon Wessely, a psychiatrist at King’s College London’s Institute of Psychiatry,
said
"The (first) issue is, can any biomarker distinguish CFS patients from those with other fatiguing illnesses? And second, is it measuring the cause, and not the consequence, of illness?”

First of all. British psychiatrists should keep their nose out of CFS they've done enough damage.

Second. We test the consequence of 100s of diseases without knowing the cause. Crohns, Alzheimers, cancer, MS. etc

I agree with their first point though, does it identity CFS only.

Either way, it's pretty conclusive that the psychiatrists are wrong. No surprise their backs are up.

 

You can use this link if you don't want SMC to get the hits: http://web.archive.org/web/http://w...al-biomarker-for-chronic-fatigue-syndrome-me/

 

I think we need to read this with caution but at least something has been published now even if it doesn’t quite reveal enough in the abstract etc.

The replication with a larger cohort and being able to distinguish from othe diseases (or align with some) will be the test of this.

These findings have sort of been reproduced already (not the nano needle but in principle) so there is a bit more hope ...but we don’t know whether this is a downstream effect or central to the ‘disease’. I’m being cautiously optimistic that this is at least distinguishable from other more mainstream causes of fatigue. Even if it overlaps with other serious biomedical chronic conditions, it at least shows that it’s something to take seriously (although it’s success will depend on it being reasonably exclusive). If partially distinguishable it still also validates it as a model test for further bench research.

the worst result would be that it doesn’t distinguish healthy people that have run about a bit or have a cold etc.

SW is clearly backpedaling...ready to throw his BPS colleagues under the bus at the right time, hoping that the MUS will still be a done deal regardless.