ME, CFS support and research

Chronic Fatigue Syndrome is an Acquired Neurological Channelopathy. A Chaudhuri, P Behan. Hum Psychopharmacol Clin Exp 1999:14:7-17
Chronic Fatigue Syndrome: is total body potassium important? Burnett RB et al Medical Journal of Australia 1996:164:6:384
Whistler T, Jones JF, Unger ER, Vernon SD. Exercise responsive genes measured in peripheral blood of women with chronic fatigue syndrome and matched control subjects. BMC Physiol ( 2005 ) 5 : 5. doi: 10.1186/1472 - 6793 - 5 - 5.

Broderick G, Craddock RC, Whistler T, Taylor R, Klimas N, Unger ER. Identifying illness parameters in fatiguing syndromes using classical projection methods. Pharmacogenomics ( 2006 ) 7 : 407 - 419. doi: 10.2217/14622416.7.3.407.

Watson WS, McCreath GT, Chaudhuri A, Behan PO. Possible cell membrane transport defect in chro nic fatigue syndrome? J Chronic Fatigue Syndr ( 1997 ) 3 : 1 - 13. doi: 10.1300/J092v03n03_01.

Cameron B, Galbraith S, Zhang Y, Davenport T, Vollmer - Conna U, Wakefield D, et al. Gene expression correlates of postinfective fatigue syndrome after infectious monon ucleosis. J Infect Dis ( 2007 ) 196 : 56 - 66. doi: 10.1086/518614.

CHRONIC FATIGUE SYNDROME: ACQUIRED NEUROLOGICAL CHANNELOPATHY
Professor Peter O Behan & Dr Abhijit Chaudhuri
Fatigue 2000: International Conference, 23-24 April 1999
Arguments for a role of abnormal ionophore function in Chronic Fatigue Syndrome. A Chaudhuri, WS Watson, PO Behan. Chronic Fatigue Syndrome. ed: Yehuda & Mostofsky pub: Plenum Press, New York, 1997
"Kenny de Meirleir (Brussels, Belgium) gave an overview of the possible immunological pathways that are disrupted in illnesses such as CFS. He presented data suggesting improper activation of 2-5OAS in monocytes in both CFS and chronic MS. (not however in relapsing/remitting MS) This results in inappropriate activation of RNaseL This process ultimately leads to blockade of RNaseL-mediated apoptosis. A complex series of biochemical/immunological events then follows. Resultant RNA fragments are then capable of either activating or down regulating PKR. A subsequent release of NO at high (CFS) rates or low (MS) rates by lymphocytes leads to effects on ion channel, NK cell function, COX2 activation and glutamine release by activated T cells in the brain. The Belgian results suggest that CFS and chronic MS are extremes of an array of dysfunctions in the 2-5A/RNaseL/PKR pathways"
Research paper presented by Kenny de Meirleir (Brussels, Belgium) to The Sydney ME Clinical and Scientific Conference, December 2001

"Much of the Belgian research focused on the abnormal enzyme pathways and 88% of patients tested positive to RnaseL, (as found by Suhadolnik). The 37Kda is produced by calpain cleavage, and the whole process affects the calcium and potassium channel mechanisms. RnaseL is a likely marker for CFS, and correlates with severity. (It is negative in AIDS). The ALT and the haematocrit are adversely affected by the abnormal RnaseL ratio and when the ratio is higher the serum calcium is low, which is consistent with a channelopathy. The channelopathy will lead to low body potassium because of loss, metabolic alkalosis and hyperventilation syndrome. Symptoms relating to CVS, abnormal hormone levels and abnormal exercise response follow. There is a secondary hypomagnesia, abnormal sodium retention and changed tryptophan uptake. The latter leads to depression. The CD4/CD8 ratio correlates with VO2 max. A very complex model was proposed, the mechanism leading to a Th1/Th2 shift with viral reactivation and intracellular opportunistic infections. 68.7% patients were infected with mycoplasma in Belgian studies with a predominance of M.hominis. Mycoplasma can lead to calpain cleavage. Mycoplasma can invade all tissues such as monocytes, muscle cells etc. "
K de Meirleir (Brussels), S Shetzline (Brussels), P Englebienne (Brussels), P de Becker (Brussels), research papers submitted to the AACFS 5th International Research, Clinical and Patient Conference, 2001

"Pathophysiological mechanisms and CFS were discussed by Kenny de Meirleir (Brussels, Belgium). He described this condition as having no single aetiologic agent, but there are a number of predisposing factors leading to abnormalities in the immune system. Viral reactivation and opportunistic infections increase. Resultant ankyrin fragments from pathologically cleaved RNaseL interact with ABC transporters, which become dysfunctional, leading to many of the symptoms of CFS. This is described as an acquired channelopathy. 206 CFS patients were studied and 70% were found to be Mycoplasma positive, and these patients had significantly more cleavage fragments of RNaseL.
He also mentioned the Bijlmer incident, when following this plane crash, 67% were found to be infected with Mycoplasma, and suffered CFS-like symptoms."
Research findings presented by Professor Kenny de Meirleir (Belgium) to The Sydney ME Clinical and Scientific Conference, December 2001