Hi Ember. First, Leonard Jason has made a few studies on patient cohorts using various definitions. I don't recall all the details, I would have to go back and read them, but they are worth reading.
Second, each definition has its own sets of criteria. Some are mandatory, some are optional. CFS, ME etc. are syndromes. That is they are sets of symptoms. While we currently think of them a group as distinct unitary entities, we have no idea if that is correct or not. The Light's data on exercise recovery indicates there are two different groups in strictly defined CFS. The Pacific Fatigue Lab research show that, contrary to regular fatigue, strictly defined CFS has a decline in energy production and work effeciency for a period following activity. Its not just fatigue. Then we have a host of secondary data on immune states, cytokines etc.Some of our mitochondrial issues may be unique too, and of course now we have things like possibly unique EBV antibodies in a distinct subset. This requires further investigation. Even data like that of Chia's findings on enteriviral presence in the gut, or response rates to rituximab, or even 37kd RNase L, have results in about a two third to three quarter split versus the rest. One of the things I really want to know is if any of these findings cluster in the same patients.
One thing that is not clear to me now is that OI in general can separate post viral fatigue and ME. There is at least one study (I posted a link a day or two ago) that shows that post viral fatigue patients have OI at around the same rate as CFS.
Take all these data points, and plot them on a multidimensional graph. Are they all the same syndrome ... highly unlikely, a point I will argue from another perspective in a few paragraphs. The only perspective that makes sense is to look for clusters. That is what definitions like CCC and ICP are based on ... clusters arising from clinical experience. Those clusters will have symptom overlap, but not total overlap. They are overlapping sets.
Then we have the trigger/cause problem. There are many different triggers. Do these lead to a single common path, or multiple paths representing multiple disease states? We do not know. For that we have to look at the physiology, and we need to understand how triggers initiate the syndrome. We just don't know yet. The hypothesis I am currently investigating is that ME is all viral induced. What we call a trigger is the tipping point, not the cause.
Something that has been said very many times, and I agree with, is this. Fatigue is the single most common symptom there is, with the possible exception of pain. Both are warning signals. Historically the process of medical discovery has been to take the huge pool of medically unexplained syndromes and remove disease from that pool, one at a time, and to continue this process inside individual diseases. Once upon a time we had cancer. Then we had breast cancer. Now we have specific breast cancer subsets due to genetic issues. This is a process of continual differentiation, leading to more specific diagnoses and more specific treatments. I think ME and CFS will go the same way, but I can't predict just how many subgroups there will eventually be.
Another way to think of it is this. Run the process in reverse. Suppose that we had yet to discover a whole host of diseases that are now known and hence not medically unexplained. Since they are not discovered, and since they probably cause fatigue, they fit in unexplained fatigue syndromes. Now take this mixed group. Try to find a common biomarker ... no chance. Try to find a common cause ... no chance. Try to find a single treatment that works on everyone ... no chance. Yet we want to call this group Chronic Fatigue Syndrome (Oxford)? Its a nonsense. To assert its all one thing is to assert that every possible disease that will be known in the future is known now. (chortle)
In the time I have been aware of the research there have been quite a number of disease, many genetic, that have been differentiated from CFS. I was in a study to examine cortisol binding globulin mutations. I don't have them, but some do. Prior to the genetic research of an extended family with "CFS", these patients were often diagnosed with CFS ... its a great big wastebasket of too hard cases.
We now have post SARS syndrome too, which would have been called CFS prior to SARS. We don't know if its really CFS or something different. I suspect that a lot of post pathogen fatigue syndromes are the same, but this requires more research to demonstrate this.
One next to final point. I have said overlapping sets are the best way to think of it, but I have not addressed the issue of how much overlap there is. In each case it could be a little or a lot. The problem is that some research simply presumes its either a lot or total overlap. It is not good enough to make this presumption, it should be a priority in research.
My final point is about the Oxford definition and the view that our illness is perpetuated by dysfunctional beliefs. The only thing that holds Oxford together so far as I am concerned is the dysfunctional belief model or its variants. It that model is correct, and there is NO objective evidence it is, and it applies to the vast majority of Oxford CFS patients, then the Oxford CFS definition might make sense. If its wrong, then the Oxford definition will implode under its logical inconsistencies. Given that all the psychosomatic explanations rely on that wastebasket diagnosis idea (over generalization), and further irrationally assert that anything left in the basket is a psychogenic illness (the psychogenic fallacy), I predict the whole thing will implode horribly at some point, though die hards will be claiming its has to be right long after the world moves on. I would also like to add that something that is logically consistent only under one intrepretation, but illogical under others, fits the fallacy of begging the question.
Bye, Alex