MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME

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health problem. There is no desire to change the current status quo. Where do we at King’s stand on this issue? The
answer is simple. We are perfectly happy with the status quo. There is no pressure from here or anywhere else to alter
the current definitions. As practitioners we are aware that CFS/ME is an umbrella term, under which we see a wide
range of disability” (What’s in a name? December 10, 2003: http://tinyurl.com/l8zktz).
This must be compared with the PACE Trial information, which clearly states: “Medical authorities (meaning
the Wessely School) have decided to treat CFS and ME as if they are one illness”.
Despite Wessely’s public assertion that he and his group are “perfectly happy with the status quo” (the status
quo is that ME/CFS is formally classified as a neurological disorder), in October 2008, Cambridge
University Press published the fourth edition of “Essential Psychiatry” co‐edited by Simon Wessely. Chapter
23 (“General Hospital Psychiatry”) is co‐authored by Professors Matthew Hotopf and Simon Wessely and
includes a section on “medically unexplained symptoms”. It is replete with self‐references.
Despite the large body of scientific evidence about ME/CFS, Wessely remains intransigent, asserting
categorically that chronic fatigue syndrome is a functional somatic syndrome (ie. a mental disorder) and that
the aim of CBT is “to help change beliefs about the illness as well as associated behaviours” and that “social factors
which may be important in maintaining unexplained symptoms include systems of state benefit or private
insurance in which the sufferer is forced to maintain a sick role to continue to receive compensation”. He
says: “Cognitive‐behavioural formulations of unexplained syndromes such as chronic fatigue syndrome suggest that
(deconditioning) is one factor that maintains disability, perhaps by a vicious circle of avoidance, deconditioning,
catastrophic interpretations of symptomatology and hence further avoidance”.
Wessely seemingly refuses to accept the documented biological abnormalities known to exist in ME/CFS
as causal, preferring to believe that: “such changes are as a result of behavioural changes related to the
disorder, such as reduced activity and sleep disturbance, rather than a primary cause”.
No matter what pathology is demonstrated in ME/CFS, Wessely often seems to rush to replicate it but
almost invariably fails to do so, thus allegedly substantiating his own belief about the nature of the disorder.
The most recent example is the paper he co‐authored with Otto Erlwein and Professor Myra McClure et al
(Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome. PloS One, 6 th January
2010:5:1:e8519), in which he declared no competing interests. The paper concluded: “Based on our molecular
data, we do not share the conviction that XMRV may be a contributory factor in the pathogenesis of CFS, at least in the
UK”.
However, as the CFIDS Association of America pointed out: “The new report…failed to detect XMRV in CFS,
but should not be considered a valid attempt to replicate the findings described by Lombardi et al in the October 8 th
2009 Science article” (Co‐Cure Res: 5 th January 2010).
Not only did the Wessely et al study not use the same entry criteria as Lombardi and Mikovits et al (who
used both the 1994 Fukuda CDC definition and the Canadian case definition – which the Wessely School
reject), but the scientific director of the CFIDS Association, Dr Suzanne Vernon, provided evidence why the
Wessely et al study should not be considered a valid attempt to replicate the Lombardi and Mikovits study:
“Both studies included CFS patients defined by the 1994 (Fukuda CDC) case definition criteria, but this is where the
comparability ends. Here are some of the ways the PloS ONE and Science methods differ:
• The blood was collected from CFS patients in different types of blood collection tubes
• The genomic DNA was extracted and purified using different techniques
• The amount of genomic DNA included in the amplification assay was different
• Different primer sequences were used that amplified different regions of the XMRV proviral DNA
• The conditions of the PCR amplification assay were different – from the numbers of cycles, to the type of
polymerase used.