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

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vascular inflammatory process” – a process that would affect not only the brain or the heart or the muscles, but
potentially every organ and system in the body.
Dr Park found not only capillary inflammation and perivascular cuffing (the accumulation of immune cells
that surround injured blood vessels), but that all the ME/CFS patients in his study demonstrated remarkably
reduced renal blood flow. He pointed out that diabetics with renal vascular disease also complain of
profound fatigue.
The remarkable similarity in the brain images of patients with ME/CFS and multiple sclerosis was also
noted.
Studies by Professor Kenny De Meirleir et al (Belgium) found that the majority of ME/CFS patients had
increased rates of RNase‐L activity (83%), RNase‐L fragmentation (88%) and a massive 95% had increased
elastase levels. These abnormalities could contribute to the muscle symptoms seen in ME/CFS.
Dr James Baraniuk from Georgetown University, Washington DC described the (quote) “unbelievable”
finding of unique markers in the cerebrospinal fluid of ME/CFS patients that are completely absent from the
control group. The proteomic biosignature of ME/CFS in the cerebrospinal fluid shows:
1. a protease / antiprotease imbalance is present: alpha 2 macroglobulin (anti‐protease) and
orosomucoid 2 (anti‐protease); this implicates increased elastase production
2. several proteins suggest that amyloid deposition in the blood vessels of the brain is
causing micro‐haemorrhaging (amyloidosis is the deposition in the tissues of a starchy,
waxy protein substance; the organs most affected are the liver, kidneys, spleen and heart;
it occurs in conditions of chronic inflammation)
3. one protein present suggests altered (increased) rates of apoptosis (ie. programmed cell
death, a well‐documented finding in ME/CFS)
4. another protein present suggests free radical production is occurring
5. another protein suggests problems with vasoconstriction and endothelial damage
(pigment epithelial derived factor and endothelial proliferation associated with vascular
dysregulation)
6. another protein is associated with inflammation.
One protein that was found – keratin – is of particular interest: it is associated with inflammation of the
leptomeningeal cells in the membranes covering the brain and spinal cord. This proteome is not found in
healthy controls.
Dr Jonathan Kerr from London stated that his gene expression studies are finding three main abnormalities
in ME/CFS patients: these involve the immune system, mitochondrial function and G‐protein signalling.
As noted in Section 2 above, various genes are upregulated in ME/CFS – those associated with apoptosis,
pesticides, mitochondrial function, demyelination and viral binding sites. Kerr mentioned three genes in
particular: gelsolin, which is involved in apoptosis and amyloidosis; one that is upregulated by
organophosphates, and a mitochondrial gene involved in the demyelination of nerves.
The importance of sub‐typing “CFS” was recognised and emphasised.