The Problem(s) with "Inflammation"

[Jonathan Edwards]

You could have 10 different pathogenic/inflammatory triggers causing the same downstream causal pathway patholgy in people prone for ME/CFS, but finding 'the missing link' via just one of these triggers (and if it's by accident) might illuminate the whole thing?

Of course. Nobody is disputing that.

To think of perhaps EBV and its potential implications for MS as a permissive step would be more useful in terms of ME/CFS?

It still isn't part of the concept of MS. One day someone may provide a case report of MS in someone who has never encountered EBV. Otherwise, the concept of MS might shift to include the presumption of EBV infection being a step in the common process but it has not so far. Similarly, for ME/CFS the concept does not include any specific inflammatory step as of now.

How can there be any evidence for the relevance of the acute stage if we only study patients at the six-month cutoff, Dr. Edwards?

That isn't what my comment was referring to but I agree that only studying people after 6 months is a problem. But I don't think it is particularly relevant to this discussion. The references to inflammation that I have complained about are universally about inflammation being the result of ME/CFS processes - they all say "and that leads to inflammation". And yet there isn't any at that point (which as you say will be 6 months down the line).

 

[butter.]

Of course. Nobody is disputing that.


It still isn't part of the concept of MS. One day someone may provide a case report of MS in someone who has never encountered EBV. Otherwise, the concept of MS might shift to include the presumption of EBV infection being a step in the common process but it has not so far. Similarly, for ME/CFS the concept does not include any specific inflammatory step as of now.


That isn't what my comment was referring to but I agree that only studying people after 6 months is a problem. But I don't think it is particularly relevant to this discussion. The references to inflammation that I have complained about are universally about inflammation being the result of ME/CFS processes - they all say "and that leads to inflammation". And yet there isn't any at that point (which as you say will be 6 months down the line).

I definitely agree with you that there is no evidence—apart from a slight increase in CRP in the DecodeME dataset—for ‘classical inflammation’ in ME/CFS as it is currently defined.

I think there might be evidence for micoglial activation (to use your preferred term) with as of yet unclear consequences.