It is very simple. inflammation is a physiological change based on local blood vessel function that involves a change in calibre, permeability to water and solutes and cell diapedesis. It has been known since Roman times through the signs of: dolor, calor, rubor, tumor (and loss of function). In ME/CFS we can see from looking at the body and, most precisely, analysing tissue fluid content with MRI, that this occurs nowhere.
There is no inflammation.
As pointed out in our paper, there may be production of some cytokines that are often seen in inflammation but there is no production of others, and inflammation itself does not occur.
So the need is to construct a model that includes the mediators we think are involved but does not invoke some rag-bag concept of a package deal of events that people like to use as a buzz word but is not relevant.
My credentials are that I did an Experimental Pathology doctorate under Wally Spector and Derek Willoughby at Barts in the 1980s. The department at that time was the premier UK academic centre for inflammation research. I later collaborated with Salvador Moncada's group at the Wellcome Foundation (Moncada had worked with John Vane on the discovery of the action of prostaglandins and the mechanism of action of aspirin, for which John received the Nobel.) I was a founder committee member of the British Inflammation Research Association.
I learned early on that consensus in biomedical science is nearly always wrong. People just don't understand enough detail, so go for the explanation that superficially makes sense despite the fact that after ten minutes analysis you can see it falls apart. The consensus on relevant 'facts' is always heavily skewed by this popular dogma.
