I would just say that I agree with what Woolie has written. fMRI is psychology. One thing that we psychologists bump up against all the time is this widespread misunderstanding among laypeople that psychology is some unscientific claptrap where people sit around all day in a 1960s-style cafe talking about emotions and the id.
Granted, listening to the likes of White one would be excused for dismissing the entire discipline as worthless but even the BPS school has moved on from the brutal stupidity of the 1980s and 1990s level of analysis to a more modern couching of these 'false illness beliefs' in the language of 2000s cognitive neuroscience, hence all the buzzwords about interoceptive networks, insula, basal ganglia etc. which is why you have people like Harrison getting grant money now and people like White are retiring. But it's still false illness beliefs in the sense that the brain thinks the body is sick because its activity in certain areas is altered. You can describe the same phenomenon using different language.
Modern psychology is not Freud, ok? It attempts to understand mental phenomena at all levels of analysis, like peeling the layers of an onion, ranging from basic physiology and all the way through to social phenomena. In my time we had to learn brain anatomy, physiology, neuropsychopharmacology, neuropsychology, neuroimaging techniques etc. in addition to all the woollier bits that the man on the street thinks is 'psychology' like personality, intelligence, emotions, psychopathology etc.
I have a doctorate in the general area that Harrison has been researching so I think this entitles me to an opinion. I had a look at some of his publications last year when we were discussing this. There is nothing of value to be learned from this work. We have known for 30 years that people with 'emotional disorders' like depression have an abnormal reactivity to bacterial endotoxin and that there are immunological alterations of unknown aetiology or significance in these patients. More recently we have found out that immune modulating drugs can improve neurovegetative symptoms of depression. Countless groups have previously demonstrated, using neuroimaging techniques, that areas like the basal ganglia, insula, the DLPFC and anterior cingulate show altered patterns of blood flow / activation and neuropsychological tests tapping into areas underpinning frontal-executive function show decrements in performance compared to controls.
Again, all of this is psychology.
He thinks ME/CFS can be understood at this level of analysis, that altered brain activation is responsible for the symptoms, not that altered brain activity is the result of say an antibody somewhere in the periphery or some sort of generalised metabolic dysfunction. He is entitled to his opinion, for which he has no evidence, and we are entitled to dismiss it. IF there is an antibody, then why waste money studying how the brain responds to being sick? In neuropsychiatric lupus people show altered brain activity but no sane person would argue that this causes the disease.