I fear @TiredSam might be right; I carefully thought this after reading Baker's answer to the liME letter, too. This thought deepened after the discussion what would happen with the ME/CFS centers. I could imagine they substitute ME by any other psychological diagnosis in future (they are so...
And who knows? Maybe they'll stop diagnosing CFS and instead diagnose MUPS/BDD/somatoform disorder? Nobody forbids them to do so. And maybe the reason why they diagnosed CFS (or "chronic fatigue") at all was because they could say it's psychological and prescribe CBT/GET. Maybe they don't care...
How come they never come along anyone with ME that does some low-level exercise (which obviously doesn't help)? One reason might be they don't exercise themselves or ignore all those who exercise? Is it maybe them with the exercise phobia?
Really... :rolleyes:
There are certain genes that play a role in substance metabolism (and detoxification); this can be checked.
Also, the expression of certain genes can be checked, which can tell if one is a normal, slow or fast "metabolizer".
In my case it explained why I had problems with certain drugs, and...
So, I was able to talk about this with my GP. He doesn't know either what it is (might be an eplipetic seizure, but who knows) and suggests to have it checked by a neurologist. So that will be a new "project".
Ahh, I wish I knew it NOW. :whistle:
That's why I agree with @large donner and others that ME is not a subset of Oxford-CFS.
If I understood correctly, PEM is excluded in Oxford-CFS, but it's an ICC symptom. So, ICC-ME is no subset.
The more I think about that - and having in mind Mr. Bakers words - the more I think that is...
Would you be willing to explain this?
Also, I get confused. Didn't I understand you correctly that from a scientifc view it is correct to use Oxford criteria and transport the results to ME? I.e. didn't you mean that Oxford-CFS is a superset of ME? If so, I realize I didn't understand why that...
Today a psychologist said to my husband (both in acadamia), that they pick data so as to give "good results" (I guess p < 0.05), and if they published raw data (as required for data archiving) people would see that they manipulated. That's why they cannot publish their raw data.
Strictly, one counter-example is enough to falsify a hypothesis.
Hypothesis: Exercise is beneficial in people with fatigue => it is beneficial in ME.
There exists at least on person with ME for whom exercise is not beneficial. I.e. hypothesis is false.
(The reason why the falsification of a...
I think here the discussion could go on and on... :) meaning, in my opinion, your arguments are valid, as the others' are, too.
I think, strictly scientifically, you cannot apply statements/results about joint pain to RA without further steps. Even if it seems logical, obvious or even trivial...
Some doctors seem to forget that this is BIG help. My GP can't do anything substantial to improve my state, too, but he is contributing substantially by supporting me whenever needed. For me, that's major.
I am not an expert on this, but I have some thoughts on it. And although I understand your way of reasoning and what you say - and although, in principle, I could agree to that reasoning - I am not sure you are 100% correct.
It is scientifically relevant how you choose your cohort for your...
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