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

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Information on other abnormalities that have been demonstrated in ME/CFS patients, including abnormal
brain perfusion, more evidence of inflammation, mitochondrial dysfunction, immune system disruption,
and vascular problems that was presented at the Florida research conference can be found at
http://www.meactionuk.org.uk/Facts_from_Florida.htm.
Using neuroimaging techniques, several groups have identified neuro‐anatomical abnormalities in ME/CFS
patients. These include reduced regional blood flow, anatomical abnormalities in cortical and sub‐cortical
regions and reduced glucose metabolism (Marie Thomas and Andrew Smith. The Open Neurology Journal
2009:3:13‐23).
It is impossible to summarise over 5,000 papers in one document, but the evidence of organic pathology in
ME/CFS is extensive. For example, the wealth of scientific biomarkers that distinguish ME/CFS from
“chronic fatigue” (a term used interchangeably with “CFS/ME” by the Wessely School) include the
following:
• abnormal brain scans (SPECT & PET scans) and MRI scans that are consistent with organic brain
syndrome, showing focal demyelination and/or oedema in the sub‐cortical area
• a dysregulated HPA axis
• a dysregulated antiviral pathway (RNase‐L)
• cardiac abnormalities
• abnormal capillary flow
• low circulating blood volume
• abnormal ergometry test (indicating immediate anaerobic threshold)
• haemodynamic instability
• abnormal immune profile
• gene profiling – there are more abnormal genes in ME/CFS than there are in cancer. In the US,
Sorensen et al demonstrated that expression of several complement genes remains at a higher level
in ME/CFS subjects before and post‐exercise, which may lead to uncontrollable inflammation‐
mediated tissue damage. In the UK, Kerr demonstrated differential expression in 88 genes [85 up‐
regulated and 3 down‐regulated] indicating haematological disease and function, immunological
disease and function, cancer, cell death, and infection [J Infect Dis 2008:197(8):1171‐1184], all of
which are seen in ME/CFS but not in states of psychiatric fatigue, ie. “CFS/ME”.
Possible biomarkers discussed at the Reno conference mentioned above include the following:
• ATP profiling of ion channel receptors
• Mitochondrial Energy Score
• Cytokine and chemokine analysis
• Near infrared
• EEG profiles
• Low molecular weight RNaseL
• HLA haplotype 4‐3‐53, VIP, C4a
• Antigliadin and anticardiolipin antibodies.
Professor Lapp’s Reno summary (http://www.drlapp.net/news.htm) records that:
• the sympathetic nervous system is more active than the parasympathetic system in ME/CFS
• the metabolic, adrenergic and immune ion channel receptors were up‐regulated for days after
exercise in people with ME/CFS, with virtually no up‐regulation in healthy controls ‐‐ metabolic,
adrenergic and immune ion channel receptor mRNA markedly increases in people with ME/CFS
or FM but not in healthy controls