Yes - this is how he tries to justify himself.
"Before I became involved patients were treated with contempt and nothing of any use was ever done for them.... so what I did may look terrible, but it was probably still an improvement!"
Unfortunanately, long-term patients seem to argue that they started being treated much, much worse once Simon's theories came into fashinon.
It simply isn't true that SW walked in to a vacuum of ignorance at the National ( as opposed to a willful ignorance)
There are a couple of documents by Margaret Williams which are snippets as she says but are a good starting timeline of what was happening in the late 80's and 90's in the UK.
As an example (and I've split it up for readability)
"1988: At a meeting on ME held at The Royal Free Hospital on 16th May 1988, Professor Tim Peters from Northwick Park Hospital said his team had found abnormalities of Type II muscle fibres (anaerobic) in ME patients, which were atrophied, with hypertrophy of Type I muscle fibres; he had measured total RNA in muscle cells and found it to be significantly reduced in ME patients (if there is a decline in RNA, there is a decline in the ability to make muscle protein – infusion of tag-leucine showed overall metabolism is clearly reduced and the rate at which muscle is being formed is reduced).
1989: Professor Peters (then Professor of Clinical Biochemistry and Consultant Chemical Pathologist at Kings College Hospital, London) wrote on page 24 of the magazine InterAction No: 3 of the charity ME Action, now AfME: “Exciting studies have recently been reported of persistent viral RNA in biopsies from patients with ME….
Based on these observations we have started to investigate muscle protein synthesis; that is, the ability of muscle to repair itself…in patients with ME. Measurements of muscle RNA, the machinery for protein synthesis, showed consistently reduced amounts in their biopsies. Studies of whole body and, specifically, thigh muscle protein synthesis rate in these patients show reduced values and thus a pattern is beginning to emerge of persistent viral infection, and possibly re-infection, interfering with the machinery for making tissue protein and thus impairing protein synthesis”.
Discussing the view of those who claim that changes in mitochondrial function and impaired muscle synthesis are merely secondary events due to lack of use of the muscles, Professor Peters continued: “It is hard to see how (this) can explain the persistence of enteroviral RNA in muscle fibres….immobility leads to a selective loss of Type I fibres, a feature not seen in patients with ME”.
The same issue of InterAction reported on page 22 the neurological abnormalities found by Carolyn Warner and her team from Buffalo, NY (elevated IgG synthesis, elevated CSF cell count, prolonged visual evoked response latency, abnormal EEG and MRI lesions, and neuromuscular abnormalities including over 20% polyphasic motor units on quantitative EMG, inflammatory infiltrates and Type II fibre atrophy, these being reported in Neurology 1989:39:Suppl 1: 420).
Commenting on these abnormalities, Dr Goran Jamal, Consultant in Clinical Neurophysiology at The Institute of Neurological Sciences, Glasgow, affirmed that those results are consistent with disturbed immune function and persistent infection, and that it proves once again that one can find neurological abnormalities if one looks."
http://www.meactionuk.org.uk/Grey-Information-on-ME-CFS.htm
http://www.meactionuk.org.uk/Grey-Information-Part-2.htm