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

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protein and serum amyloid A (which have been reported in ME/CFS and other diseases attributed to toxic
chemicals). The authors note that a survey of the literature reports ACAs (anticardiolipin antibodies) as
common serological markers in many diseases, including diseases resulting from viruses and chemical
exposure, as well as autoimmune diseases such as multiple sclerosis and lupus erythematosus. The authors
conclude that (ME)CFS may be an autoimmune disease, and that classification of it as such may serve to
increase the availability options for patients suffering from the disease. They confirm that experiments are
under way to elucidate why ACAs are produced in (ME)CFS, and that these studies are investigating the
effects of specific chemical agents on mitochondrial metabolic pathways that are indicative of blocked
energy production as occurs in (ME)CFS (Yoshitsugi Hokama et al. J Clin Lab Anal 2009:23:210‐212).
Yet more research has shown that (ME)CFS is an autoimmune disorder: Ortega‐Hernandez et al looked at
the influence of autoantibodies, polymorphisms in the serotonin pathway, and HLA Class II genes in
relation to (ME)CFS, and tested autoantibodies to different components of the central nervous system. They
conclude: “Our results reveal that in (ME)CFS, like other autoimmune diseases, different genetic features are
related to age at onset and symptoms” (Ann N Y Acad Sci 2009:1173:589‐599).
Blaney et al looked at a number of chronic and autoimmune conditions (including multiple sclerosis, lupus,
fibromyalgia and (ME)CFS) and demonstrated the use of 1,25‐D (1,25‐dihydroxyvitamin D3) as a clinical
marker in autoimmune conditions, with results that “showed a strong positive association between these
autoimmune conditions and levels of 1,25‐ D greater than 110 pmol/L”, noting that high levels of 1,25‐D may
result when dysregulation of the vitamin D receptor prevents it from expressing enzymes necessary to keep
1,25‐D in a normal range (Ann N Y Acad Sci 2009: 1173:384‐390).
It has long been known that the resting energy expenditure (REE) in ME/CFS patients is abnormally high
(see, for example: J Neurol Sci 1997:150:S225; JCFS 1998:4:4:3‐14; Medical Hypotheses 2000:54: (1):59‐63).
When individual resting energy expenditure (REE) was predicted on the basis of total body potassium
values, 45.5% of the (ME)CFS patients tested had resting energy expenditure above the upper limit of
normal, suggesting that there is upregulation of the sodium‐potassium pump in (ME)CFS. There was no
evidence that the results were due to lack of activity (which would have affected total body water
estimates).
Given that the energy expended at rest by the ME/CFS patient is significantly elevated when compared with
controls, it is not difficult to understand what may be the result when the ME/CFS patient is subjected to
even minimal exercise.
ME/CFS is not “medically unexplained”
The seminal work of Martin Pall, Professor Emeritus of Biochemistry and Basic Medical Sciences,
Washington State University, is thought to have unravelled the mechanisms that underlie what the Wessely
School regard as “functional somatic syndromes”, including ME/CFS, fibromyalgia, irritable bowel
syndrome and multiple chemical sensitivity (MCS).
Professor Pall’s work is quoted with his specific permission (from his paper “Multiple Chemical Sensitivity:
Toxicological and Sensitivity Mechanisms” on his new website http://www.thetenthparadigm.org ); see also
his book “Explaining ‘Unexplained Illnesses’: Disease Paradigm for Chronic Fatigue Syndrome, Multiple
Chemical Sensitivity, Fibromyalgia, Post‐Traumatic Stress Disorder, Gulf War Syndrome and Others”.
Harrington Park (Haworth) Press, New York, 2007 and “The NO/ONOO‐Cycle as the Cause of Fibromyalgia
and Related Illnesses”; In: New Research in Fibromyalgia, Ed. John A. Pederson, pp 39‐61; Nova Science
Publishers, Inc 2006.