The buspirone challenge test clearly distinguishes ME/CFS patients from healthy controls: why is it not being developed and deployed?

Could an imbalance of the short and long forms of prolactin receptors mean that some cells are going into apoptosis or be otherwise misbehaving in some way? Perhaps they’re responding badly to perfectly normal signals?

Could the increase that we see in response to Buspirone be a result of the body over compensating to this and trying to get a signal to somewhere and it's just not being heard so it shouts louder? Maybe some subset of cells up or down regulating in response to this imbalance of receptors elsewhere?
 
Flow chart from @forestglip paper from chat GPT. Does this look ok? Please edit if not OK. Thanks @forestglip

If it looks OK, I may send to OMF along with the review.

p.s. I have no idea how to edit these things.


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I think now that it’s been all finalized a git repo would serve well, that way you can see revisions to the document, push major revisions as a release. This flow chart could be a mermaid .md diagram that is easily edited
 
Flow chart derived from @forestglip paper from chat GPT. Does this look ok? Please edit if not OK. Thanks @forestglip

If it looks OK, I may send to OMF along with the review.

p.s. I have no idea how to edit these things.


View attachment 33887
I'm not quite sure this is the right approach, unless the review is the focus and this is just suggested as draft of possible next steps. @forestglip has written a detailed summary of the problem and possible next steps that are worthwhile and what explorations could follow and how.

I don't think competent investigators should be told what to do next, they should bring in competence to do exactly that, otherwise it's not going to lead anywhere to begin with. They have to understand what the question is and then figure out how to answer it.
 
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