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

2001
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“There is considerable evidence already that the immune system is in a state of chronic activation in many patients
with (ME)CFS” (Anthony Komaroff, Assistant Professor of Medicine, Harvard Medical School: American
Medical Association Statement, Co‐Cure, 17 July 2001).
2002
“The present review examines the cytokine response to acute exercise stress. The magnitude of this response bears a
relationship to the intensity of effort but many environmental factors also modulate cytokine release. The main source
of exercised‐induced IL‐6 production appears to be the exercising muscle. Cytokine concentrations are
increased in (ME)CFS. Exercise‐induced modulations in cytokine secretion may contribute to allergies (and)
bronchospasm” (Shepherd RJ. Crit Rev Immunol 2002:22(3):165‐182).
2003
A study was carried out by Belgian researchers to determine whether bronchial hyper‐responsiveness (BHR)
in patients with (ME)CFS is caused by immune system abnormalities. Measurements included pulmonary
function testing, histamine bronchoprovocation test, immunophenotyping and ribonuclease (RNase) latent
determination. There were 137 (ME)CFS participants. “Seventy three of the 137 patients presented with
bronchial hyper‐responsiveness. The group of patients in whom BHR was present differed most
significantly from the control group, with eight differences in the immunophenotype profile in the cell count
analysis, and seven differences in the percentage distribution profile. We observed a significant increase in
cytotoxic T‐cell count and in the percentage of BHR+ patients. Immunophenotyping of our sample
confirmed earlier reports on chronic immune activation in patients with (ME)CFS compared to healthy
controls, (with) BHR+ patients having more evidence of immune activation” (Nijs J, De Meirleir K,
McGregor N et al. Chest 2003:123(4):998‐1007).
2003
Japanese researchers focused on immunological abnormalities against neurotransmitter receptors in
(ME)CFS using a sensitive radioligand assay. They examined serum autoantibodies to recombinant human
muscarinic cholinergic receptor 1 (CHRM1) and other receptors in patients with (ME)CFS and the results
were compared with those in patients with autoimmune disease and with healthy controls. The mean anti‐
CHRM1 antibody index was significantly higher in patients with (ME)CFS and with autoimmune disease
than in controls. Anti‐nuclear antibodies were found in 56.7% of patients with (ME)CFS. The patients
with positive autoantibodies to CHRM1 had a significantly higher score of ‘feeling muscle weakness’
than negative patients among (ME)CFS patients. The authors conclude: “Autoantibodies to CHRM1 were
detected in a large number of (ME)CFS patients and were related to (ME)CFS symptoms. Our findings
suggest that subgroups of (ME)CFS are associated with autoimmune abnormalities of CHRM1” (Tanaka S,
Kuratsune H et al. Int J Mol Med 2003:12(2):225‐230).
2003
Looking at complement activation in (ME)CFS in the light of the need to identify biological markers in
(ME)CFS, US researchers used an exercise challenge to induce symptoms of (ME)CFS and to identify a
marker that correlated with those symptoms. “Exercise challenge induced significant increases of the
complement split product C4a at six hours after exercise only in the (ME)CFS group” (Sorensen B et al. J All
Clin Immunol 2003:112(2):397‐403).