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

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subjects, findings which confirm previous suggestions that alterations in all parts of the HPA axis may
mediate and sustain symptoms of (ME)CFS (The Journal of Pain 2009: doi:10.1016/j.pain.2009.06.003).
In 2009, a team led by Professor Myra Nimmo (an internationally renowned metabolic physiologist from the
Strathclyde Institute of Pharmacy and Biomedical Sciences in Glasgow) found that during an incremental
exercise test, the power output at the lactate threshold was 28% lower in ME/CFS patients than in matched
controls and in addition, F2‐isoprostanes (indicators of oxidative stress) were higher in patients than in
controls at rest, as well as after exercise and after 24 hours. These results confirm the earlier work of
Kennedy et al from Dundee which showed raised levels of isoprostanes in ME/CFS patients at rest. Not
only do Nimmo’s results show that the levels remain high during exercise and in the recovery period, but
that the level of isoprostanes in “rested” ME/CFS patients was as great as that reached by the healthy
controls after exercise (Scandinavian Journal of Medicine and Science in Sports 2009: doi:10.1111/j.1600‐
0838.2009.00895.x ).
In 2009, Pietrangelo T and Fulle S et al published a transcription profile analysis of the vastus lateralis
muscle in male and female (ME)CFS patients. They used global transcriptome analysis to identify genes that
were differently expressed in the vastus lateralis, and their results are significant. They found that the
expression of genes that play key roles in mitochondrial function and oxidative balance (including
superoxide dismutase) were altered in (ME)CFS patients. Other genes that were altered in these patients
include the genes involved in energy production, muscular trophism and fibre phenotype determination.
Importantly, the expression of a gene encoding a component of the nicotinic cholinergic receptor binding
site was reduced, suggesting impaired neuromuscular transmission. The authors argue that these major
biological processes could be involved in and/or responsible for the muscle symptoms of (ME)CFS (Int J
Immunopathol Pharmacol 2009:22(3):795‐807).
There is a significant literature suggestive of mitochondrial defects (both structural and functional) in
ME/CFS from 1984 to date.
Mitochondria are the powerhouses of the cells. They are responsible for generating energy as adenosine
triphosphate (ATP) and are involved in the apoptosis signalling pathway (apoptosis being programmed
cell death).
Despite the irrefutable evidence of mitochondrial dysfunction and damage in patients with ME/CFS, the
NICE Guideline on “CFS/ME” proscribes mitochondrial testing and recommends only behavioural
modification in the form of cognitive behavioural therapy, together with incremental aerobic exercise, and
refers to “perceived exertion” (52 page version, page 30). It claims that it “offers the best practice advice on
the care of people with CFS/ME” (52 page version, page 6) and that its advice is “evidence‐based”. It is
notable that the alleged evidence‐base upon which the Guideline Development Group relied specifically
states: “If patients complained of increased fatigue, they were advised to continue at the same level of
exercise” (Fulcher and White, BMJ 1997:314:1647‐1652).
Given the evidence of mitochondrial damage, such advice cannot conceivably qualify as “best practice
advice”.
Medications documented to induce mitochondrial damage include analgesics; anti‐inflammatories;
anaesthetics; angina medications; antibiotics; antidepressants; anxiolytics; barbiturates; cholesterol‐lowering
medications (statins); chemotherapy; and the mood‐stabiliser lithium, amongst others, including
medications for Parkinson’s Disease, diabetes, cancer and HIV/AIDS (Mol Nutr Food Res 2008:52:780‐788).
It is a matter of record that Professor Wessely advises the prescription of lithium for patients with ME/CFS:
“There is no doubt that at least half of CFS patients have a disorder of mood. The management of affective disorders is
an essential part of the treatment of CFS/ME. Numerous trials attest to the efficacy of tricyclic antidepressants in the
treatment of fatigue states. Patients who fail to respond should be treated along similar lines to those