That was the Kerr study, it later failed to prove these subtypes in the statistical analysis following on from the study because they could not predict the subtype of an individual based on the data and the derived signatures.
My comment was really a rhetorical way of saying we cannot proceed until we have sorted this issue out. If Stanford have found a way to screen their subjects then this needs to be discussed in any write up so we can learn from any criteria they used to get consistency.
For the field as a whole we need a molecular standard for distinguishing subtypes and not get ahead of ourselves because all that will happen is team A will say we found a thing and team B will say we tested our CFS group and found diddley, especially if team B are looking for govt or insurance funding.
My comment was really a rhetorical way of saying we cannot proceed until we have sorted this issue out. If Stanford have found a way to screen their subjects then this needs to be discussed in any write up so we can learn from any criteria they used to get consistency.
For the field as a whole we need a molecular standard for distinguishing subtypes and not get ahead of ourselves because all that will happen is team A will say we found a thing and team B will say we tested our CFS group and found diddley, especially if team B are looking for govt or insurance funding.
BTW - I think that's why some ppl are helped by treating leaky gut... they've caught the illness at a different (earlier?) stage + have the genes to support a recovery by healing leaky gut; other ppl are helped by mold avoidance; etc.. At some point we'll understand why, but tell the ppl who have helped themselves via leaky gut protocols and mold avoidance that they should have done nothing and waited for perfect understanding.... doesn't make any sense.. there's interplay between research + clinical, and you can't have a perfect research hypothesis when you're addressing a broad, complex problem... The nature of testing is very, very iterative...
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