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

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their cortisol response, in that ME/CFS patients’ cortisol level fails to rise but stays the same (or even
drops) after exercise.
It is known that HPA axis dysfunction occurs not only in ME/CFS but also in other NO/ONOO‐cycle
diseases including fibromyalgia and multiple chemical sensitivity, as well as in many other chronic
inflammatory diseases, so changes in cortisol control are not specific to ME/CFS.
However, there is published evidence that ME/CFS patients may have a specific change in cortisol
regulation (Demitrack MA, Crofford LJ. Ann N Y Acad Sci 1998:840:684‐697; Crofford LJ et al. Brain Behav
Immun 2004:18:314‐325; Adler GK et al. The Endocrinologist 2002:12:513‐522), indicating that the post‐
exertional increase in symptoms may be explained by the hypocortisol responses.
Significantly, Jammes et al reported that markers of oxidative stress increased more in ME/CFS patients after
exercise (J Intern Med 2005:257:299‐310), a finding that is entirely consistent with a NO/ONOO‐cycle
elevation.
Pall notes that there is evidence that lowered cortisol levels can produce cardiac dysfunction, a common
finding in ME/CFS (http://www.meactionuk.org.uk/Cardiovascular.htm), and that the need for cortisol
may be particularly important during and immediately following exercise due to the stress placed on the
heart by exercise, suggesting that the cardiac dysfunction seen in many ME/CFS patients may be caused
by their lowered cortisol production during and following exercise.
For the avoidance of doubt, the MRC PACE Trial Principal Investigators did not consider it necessary to
measure participants’ cortisol levels; furthermore, Baschetti et al noted that many people diagnosed on
the Wessely School’s Oxford criteria do not have the hypocortisol response to exercise and therefore may
not have true ME/CFS (J Intern Med 2005:258:292‐292).
Pall provides evidence supporting each of the following in ME/CFS and related multi‐system disorders:
• excessive NMDA activity
• elevated levels of nitric oxide
• elevated peroxynitrite
• oxidative stress
• breakdown of the blood/brain barrier
• inflammatory biochemistry
• elevated levels of inflammatory cytokines
• elevated TRPV1 activity (the vanilloid receptor opens calcium channels, allowing too much calcium
into cells, resulting in cellular dysfunction in a whole range of cells, for example, muscle cells
contract, causing spasm, and there is increased secretion from secretory cells, ie. it is a multi‐system
stimulus)
• mitochondrial / energy metabolism dysfunction
• neural sensitisation
• neurogenic inflammation.
The Wessely School’s claims that ME/CFS and related multi‐system disorders are psychogenic are clearly
flawed because none of the psychogenic advocates has considered how chemicals can act as toxicants in the
body, yet they have dismissed this model as a “belief” without providing any evidence to support their own
beliefs.
As Pall says: “Clearly one cannot claim to be doing science whilst simultaneously ignoring most of the
relevant scientific literature. Wherever data exists clearly contradicting their views, they simply pretend it
does not exist”.