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

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• neuropeptide Y (NPY), a neurotransmitter that is concentrated in sympathetic nerve endings is
elevated in people with ME/CFS in relation to stress much more than in normal controls
• numerous cytokines were significantly different in subject and controls
• IL8 and IL15 were decreased in patients with ME/CFS, while the pro‐inflammatory cytokines
(TNFβ, IL1α, IL1β and IL6) and Type 2 cytokines (IL4, IL5) were increased in ME/CFS, and the
anti‐inflammatory cytokine IL13 was reduced: this is consistent with the Th2 or up‐regulated
immune pattern usually seen in ME/CFS
• bowel dysfunction (dysbiosis, leaky gut, viral infections of the gastric mucosa) is frequently seen in
ME/CFS and there is also a Th1/Th2 immune imbalance. Th1 (normal immunity) is antagonistic to
the Th17 immune axis. Th17 cells are crucial regulators of inflammation and autoimmunity, and
alterations of the Th17 pathway are frequently associated with intestinal disorders such as
irritable bowel syndrome. Th17 cells produce IL17F protein and a variant known as His161Arg,
which confers protection against inflammation. His161Arg was found in only 6% of people with
ME/CFS. This suggests that the Th17 axis and intestinal dysfunction are involved in causing
inflammation and possibly in the pathogenesis of ME/CFS
• ATP is markedly reduced in ME/CFS, which can explain many of the symptoms seen in the
disorder – in fact, the severity of illness is directly related to the level of intracellular ATP
• changes on the brain MRI correlated with symptoms – using regression analysis, significant
correlations could be made between MRI changes and illness severity: cerebellar changes
correlated with coordination and motor function; frontal changes correlated with fatigue and
impaired motor function, and this study correlates known ME/CFS symptoms with specific areas
of the brain, affording further validity to the disorder
• 61% of cases seen in one study had an elevated antigliadin antibody (wheat intolerance) and
anticardiolipid antibody, MMP9, and TGFβ‐1 were also abnormal in many cases
• a greater proportion of female patients with ME/CFS had chronic pelvic pain.
The conference confirmed that multiple bodily systems are involved in ME/CFS.
There is also published evidence that recovery rates for oxygen saturation are 60% lower than those in
normal controls; evidence that the average oxygen uptake is only 15.2 ml/kg/min, whilst for controls it is
66.6 ml/kg/min; evidence of reduced lung function in all parameters tested, and conclusive evidence of
delayed recovery of muscles after exercise.
In light of the above, for the PACE Trial Investigators to assess a participant’s physical capability (and
thus their alleged ability to work) on a six minute walking test would seem to be highly questionable.
However, in his letter in response to an article that was critical of the use of exercise in ME/CFS that resulted
in exacerbations (J Rehabil Med 2008:40:241‐247), Peter White wrote: “A central concept of GET is that patients
maintain their level of exercise as much as possible even after a CFS/ME setback. This is to reduce the many negative
consequences of rest and allow the body to habituate to the increased in activity” (J Rehabil Med
2008:doi:10.2340/16501977‐0261).
This goes beyond even what he said in the GET Manual for therapists, namely: “A central concept of GET is to
maintain exercise as much as possible during a CFS/ME setback”.