I do worry that more pathogens or 'triggers' appear to be contributing to a diagnosis of CFS all the time. I know we could look at it the other way round and suggest that more of the triggers are being discovered and that it's a good thing. But I am concerned that when it comes to research and treatments the 'pool' is increasingly being muddied.
There was an article I posted yesterday about a Signalman winning compensation for personal injury. Chemical fumes - toxins - had triggered his diagnosis of CFS. Whilst the award was obviously welcomed and I don't doubt his diagnosis - as let's face it we are all diagnosed based on symptomology - it just gave me pause.
If a research project was underway and they were gathering patients for the cohort - to what extent could the 'trigger' for the diagnosis affect/influence the results? I mean if you are studying viral causes then surely you would exclude all those patients for whom there has been no confirmed viral trigger/pathogen, right? But this isn't what happens in so far as I can tell.
Patients are gathered and their diagnosis reconfirmed based wholly on symptomology and the criteria selected. They don't specifically ensure that only, e.g. EBV patients are enrolled for an EBV study, do they? No they seem to gather a CFS cohort and then go digging for EBV.
And what about treatments? Say you are running a clinical trial for Rituximab - the approach appears to be the same: gather a cohort of CFS patients and give them the medicine en-masse. There's no 'Let's check to see if they have actually had a confirmed viral-infection or have an immune profile consistent with viral infection.
We have the ability to separate into little 'pots' many of those with a shared diagnosis and I can't help but be concerned that this is not adequately being done and is negatively impacting both on treatment and research results. What if a diagnostic marker is being missed because in a large multi-trigger cohort it simply isn't applicable to a significant proportion? What if there is something unique about Giardia or, say, bacterial triggers that doesn't apply to, say, Coxsackie B or Parva-virus or EBV?
I think the larger the 'pot' becomes the more work is needed potentially at the screening stage prior to recruitment for research. Else results might be determined as statistically insignificant.
Layman speaking of course
n.b. do you think you could link to the relevant research in your article please? Although I think it was this one from Norway?
http://www.meassociation.org.uk/?p=10317