IVI's comment:
'24. In Vitro Infidelium Says:
January 13th, 2012 at 12:46 pm
VR wrote: Hoever, there is plausible evidence for an infectious etiology, including observations that the disease is known to occur in outbreaks. Furthermore, in many cases the onset of symptoms appears to begin with a flu-like illness.
There is a double dose of a priori reasoning being applied here. There is no secure epidemiology that can reliably demonstrate commonality of illnes either within reported outbreak cohorts, or between outbreak cohorts; in addition the linkage of symptom onset is a feature wholly of patient report, not of any validated assessment. That is not to say that outbreaks are not representative of occurences of highly localised epidemilogical features of M.E/CFS, nor that M.E/CFS is not characterised by an acute onset, but at this stage these remain speculative features, not definitive descriptions.
While an event characterised by multiple individuals displaying symptoms of a communicable infection which is followed by a chronicity of symptoms that are typical of M.E/CFS is clearly suggestive of an involvement of infection within the aetiology of M.E/CFS, there are simply too many confounding factors to allow a conclusion that M.E/CFS is unequivocally explained by an infection mediated aetiology. It must be asked that if the assumed infectious agent is active in a given population, then what proportion of that population will becom infected, what proportion of those infected will display acute symptoms and what proportion of those who are a) infected and asymptomatic b) infected and display an accute symptomology go to develop a chronic condition that is describable as M.E/CFS ? If we were talking about HIV, the answer to the third part of the question is would be something close to 100% for both a) and b), yet we have no such evidence in the M.E/CFS that infection necessarily equates to chronic disease. In the case of M.E/CFS infection appears only to be associative, not directly causative, something which is echoed in one of the few epidemiologically consistent observations of M.E/CFS patients, that is, there is a strong imbalance in gender representation women being diagnosed at a much higher rate than men. Unless a very unusual exposure process is in play, then the gender imbalance issue is a major stumbling block for any hypothesis of M.E/CFS that is founded on a purely infectious causation.
The patient reported association with acute onset coincident with a viral infection is also problematic. It is of course axiomatically impossibe to have planned a prospective test of a patients health prior to their reporting illness, and the patients observations may well be important evidence. However it can not be discounted that there may have been low level symptomology present prior to an acute infection, with that symptomology being entirely independent of any infection, or alternatively that an infection may be a trigger for an underlying but asymtomatic condition. Given the level of disbelief which has histerically met M.E/CFS patients encountering medical services, there may be very strng predisposition for patients to locate the commencement of chronic illness at point that is coincident with an accepted state of illness in the very natural attempt to provide validity for their very real chronic illhealth.
M.E/CFS is a complex illness that demands significant commitment of research effort, that effort can not be short cut by poorly stated hypotheses, and only through research which is conducted in relation to the known characteristics of the illness can real progress be made. M.E/CFS most certainly is not like HIV, it is nevertheless a debilitating illness and the lack of progress in understanding it undoubtedly raises questions about the perspectives of the medical profession, the research fraternity and polititions.'
I have added another reply, in response to a comment by in vitro infidelum:
35. Alex Young aka alex3619 Says:
January 14th, 2012 at 8:46 am
I am the other Alex, there are two on this page.
I am in partial agreement with in vitro in post 33. There is still insufficient evidence to equate post viral fatigue with ME. They may not be the same thing. This is one of the problems we face. Are we talking about one or several discrete but similar diseases? Are we talking about one disease with a spectrum of manifestations? Are we talking about as subset of post viral fatigue becoming ME? (I think this latter case is the most likely at this point.) Without reliable biomarkers the research can never really address these questions.
Confusion between PVFS and ME may also be responsible for much of the uncertainty over prognosis. For example, most cases of PVFS resolve themselves in a few months to five years at the outside. Looking at data over the five year mark, most long term ME patients never recover. If the under five year data is a combination of ME and PVFS this would explain the discrepancy. Since most people see those with PVFS recover, it would also explain why they do not understand why those with ME do not. But is this explanation correct? We need biomarkers to proceed.
Bye, Alex
The article has certainly led to an interesting exchange of comments I think. Kinda cuts to the chase in many respects, doesn't it?
Personally, I still feel that 'CFS/ME' is too big a 'pot' and that research will only progress if that 'pot' can become smaller 'pots' whose patients fit more relevant and testable criteria.
Even the ICCME doesn't go far enough - even if it does progress to testing. If we are considering 'viral causation' then we need to consider better testing at the point of diagnosis.
This idea of leaving it until it develops - which can be six months or more from the point of acute infection (assuming there is such a point of course) - seems to me to be too late.
But, if you don't test and find what that infection is in the first place.... what's the point of moving the diagnosis point forward e.g. from 6 months to 1 month if indeed this is even prudent for a condition that at present depends on our inability to 'recover' post-infection?
So you could - in theory - be looking at a total reorganisation of the way in which people are investigated and treated when reporting symptoms of viral infection. That each and every person is thoroughly tested to find what that virus is - not as at present when one is diagnosed generally with 'a viral infection'.
And what do you do with folk whose diagnosis is 'a viral infection' but whose virus cannot be found? This is assuming of course that a virus is responsible and I don't personally believe it is.
So define 'it' and how 'it' might infect and cause CFS/ME (whatever) in such a seemingly random (but more female orientated) group people. I don't think you ever will.
Indeed, I would rather (as I have said countless times before) they look at our immune systems - and although you still run into the same problems as above and in the article - I do believe that it is predominantly 'immune dysfunction' (even perhaps some autoimmune thing) that is preventing me from 'recovering' and indeed 'relapsing' when a(nother) virus takes hold - as has happened in my case.
As far as I am concerned there is no 'one virus' responsible and that includes retroviruses. It just doesn't make sense. But I remain open-minded when it comes to published research of any description of course - I just don't 'buy' into the speculation or indeed vaccine causation either by the way and just for the record.