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

SECTION 2: COUNTER‐EVIDENCE: THE BIOMEDICAL BASIS OF ME/CFS
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This section is included because it is essential to inform readers of the extensive evidence of the
biomedical basis of ME/CFS that the MRC PACE Trial Investigators choose to ignore and / or dismiss.
Despite the absence of a definitive test, ME/CFS is clinically recognisable: “Once one is familiar with the concept
of (ME/CFS), such patients are in practice not too difficult to differentiate from those with true psychiatric
illnesses…The physical symptoms should be an aid to diagnosis, although they may be wrongly attributed to primary
psychiatric illness unless care is taken in eliciting them” (Professor Rachel Jenkins; BMB 1991:47:4:241‐246).
Fifteen years later, Professor Nancy Klimas said: “There are diagnostic criteria that enable clinicians to
diagnose (ME)CFS in the primary care setting” (CDC Press Conference to launch the (ME)CFS Toolkit,
November 2006) which enable all conscientious clinicians to feel confident in making the diagnosis.
Although there is as yet no definitive test, there are numerous accredited biomarkers of pathology in
ME/CFS (see below), all of which lend support to the diagnosis.
As stated by Dr Suzanne Vernon (see Section 1 above), there are now over 5,000 worldwide peer‐reviewed
scientific papers (and numerous textbooks) showing that ME/CFS is a complex multi‐system disorder
involving demonstrable pathology not only of the central and autonomic nervous systems but also of the
immune, cardiovascular and endocrine systems, and that on‐going inflammation is a significant feature,
with damage to skeletal and cardiac muscle as well as to other end organs including the pancreas and liver.
In his presentation at the Royal Society of Medicine meeting on ME and CFS held on 11 th July 2009,
consultant neurologist Dr Abhijit Chaudhuri demonstrated evidence from three autopsies of people who
had died from ME/CFS, all of which showed inflammatory changes in the dorsal root of the spinal cord.
His abstract states that all three autopsies provide “evidence of neuroinflammation in the dorsal root
ganglia, which are the gatekeepers of peripheral sensory information travelling to the brain. This finding
may help explain the high level of fatigue and pain”.
For many years research has shown evidence of enterovirus (Coxsackie B) in the tissues of people with
ME/CFS, which was roundly dismissed by Wessely School psychiatrists. More recent work of Douche‐
Aourik F et al (Journal of Medical Virology 2003:71:540‐547) confirmed earlier work: “Enterovirus RNA has
been found previously in specimens of muscle biopsy from patients with…(ME)CFS. These results suggest that
skeletal muscle may host persistent enteroviral infection. The presence of viral RNA…is in favour of a persistent
infection involving defective viral replication”.
Research has continued to provide evidence of long‐term enteroviral persistence in the face of the adaptive
immune response: “This previously unknown and unsuspected aspect of enterovirus replication provides an
explanation for previous reports of enteroviral RNA detected in diseased tissue in the apparent absence of
infectious viral particles” (Human Enterovirus and Chronic Infectious Disease. Steven Tracy and Nora M
Chapman. Journal of IiME 2009: 3:1).
A recent paper reported that biopsy of muscle fibres in ME/CFS showed that fibre‐type proportion was
“significantly altered in (ME)CFS samples” and concluded: “Taken together, these results support the view
that muscle tissue is directly involved in the pathogenesis of (ME)CFS” (Int J Immunopathol Pharmacol
2009:22(2):427‐436).
Another recent paper demonstrated that a large percentage (95%) of patients clinically diagnosed with
(ME)CFS have elevated levels of the IgM isotope to CL (cardiolipin), suggesting that acute phase lipids may
be part of disease pathogenesis in patients with (ME)CFS. These lipids may be analogous to acute phase
proteins triggered by cytokines involved in the inflammatory processes in the liver, such as C‐reactive