MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME
MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME
MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME
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100<br />
Pall’s <strong>ME</strong>/CFS Review, a requested paper on <strong>ME</strong>/CFS <strong>in</strong> a Nova Biomedical volume on <strong>ME</strong>/CFS was due to<br />
be published towards the end of 2009, and chapter XX <strong>in</strong> the prestigious toxicology reference book “General<br />
and Applied Toxicology”, 3 rd Edition, Eds. Ballantyne, Marrs and Syversen was published by John Wiley &<br />
Sons on 23 rd October 2009. The press release for this book says: “1. MCS is a stunn<strong>in</strong>gly common disease, even<br />
more common than diabetes. 2. MCS is caused by toxic chemical exposure. 3. The role of chemicals act<strong>in</strong>g as toxicants<br />
<strong>in</strong> MCS has been confirmed by genetic studies. 4. We have a detailed and generally well supported mechanism for<br />
MCS. 5. For over 20 years, some have falsely argued that MCS is a psychogenic disease. This view is<br />
completely <strong>in</strong>compatible with all the evidence. It is clear now that MCS is a physiological disease <strong>in</strong>itiated<br />
by toxic chemical exposure”.<br />
Given that MCS <strong>in</strong> the form of <strong>in</strong>tolerance to everyday household chemicals and foods, and to medic<strong>in</strong>al<br />
drugs ‐‐ especially those act<strong>in</strong>g on the central nervous system ‐‐ is a well‐documented feature of <strong>ME</strong>/CFS (a<br />
feature that <strong>in</strong> May 1994 at the Dubl<strong>in</strong> International Symposium on the disorder held under the auspices of<br />
The Ramsay Society and The World Federation of Neurology, the <strong>in</strong>ternationally renowned neurologist<br />
Professor Charles Poser of Harvard described as pathognomonic of the disorder), Pall’s work cannot be<br />
separated from the body of knowledge that now exists about <strong>ME</strong>/CFS.<br />
For a resume of Pall’s significant paper “Exquisite Chemical Sensitivity Mechanisms <strong>in</strong> MCS” (FASEB<br />
2002:16:1407‐1417), see http://www.meactionuk.org.uk/Resume_of_Pall_MCS_paper_‐_August_2002.htm<br />
Pall provides compell<strong>in</strong>g evidence that none of these overlapp<strong>in</strong>g disorders is a somatoform disorder and<br />
that the Wessely School paradigm is deeply flawed.<br />
Pall posits that these multi‐system chronic disorders are <strong>in</strong>itiated and ma<strong>in</strong>ta<strong>in</strong>ed by chemicals that produce<br />
a toxic response <strong>in</strong> the body, characterised by NMDA activity.<br />
NMDA is N‐methyl‐D‐aspartate, an am<strong>in</strong>o acid derivative act<strong>in</strong>g at the NMDA receptor, mimick<strong>in</strong>g the<br />
actions of the neurotransmitter glutamate on that receptor. Glutamate is the most important excitatory<br />
transmitter <strong>in</strong> the bra<strong>in</strong>. Activation of NMDA receptors results <strong>in</strong> the open<strong>in</strong>g of an ion channel. A unique<br />
property of the NMDA receptor is that it allows changes <strong>in</strong> the flow of sodium, calcium and potassium <strong>in</strong>to<br />
and out of the cell.<br />
The ma<strong>in</strong> classes of chemicals that <strong>in</strong>itiate multi‐system disorders such as <strong>ME</strong>/CFS are the very large<br />
class of organic solvents and related compounds, and three classes of pesticides: (i) organophosphorus<br />
and carbamate pesticides, (ii) the organochlor<strong>in</strong>e pesticides and (iii) the pyrethroid pesticides, all of<br />
which are known to produce a common toxic response <strong>in</strong> the body (ie. <strong>in</strong>creased activity of the NMDA<br />
receptors).<br />
Increased NMDA activity is known to produce <strong>in</strong>creased calcium <strong>in</strong>flux <strong>in</strong>to cells, lead<strong>in</strong>g to <strong>in</strong>creased<br />
activity of two calcium‐dependent nitric oxide synthases, nNOS and eNOS, which <strong>in</strong> turn produce <strong>in</strong>creased<br />
nitric oxide. Nitric oxide reacts with superoxide to form peroxynitrite, a potent oxidant. Peroxynitrite leads<br />
to a partial breakdown of the blood‐bra<strong>in</strong> barrier, lead<strong>in</strong>g to <strong>in</strong>creased chemical access to the bra<strong>in</strong>. This<br />
cycle is known as the NO/ONOO‐ cycle.<br />
Cases of <strong>ME</strong>/CFS are also commonly <strong>in</strong>itiated by viral or bacterial <strong>in</strong>fection, <strong>in</strong>clud<strong>in</strong>g Coxsackie, Epste<strong>in</strong>‐<br />
Barr, rubella, varicella, parvovirus, Borna and Ross River viruses; such viral <strong>in</strong>itiat<strong>in</strong>g stressors also act to<br />
<strong>in</strong>crease nitric oxide levels, which is the common feature. Physical trauma also <strong>in</strong>creases nitric oxide levels.<br />
Once the cycle is <strong>in</strong>itiated, it becomes the cause of the chronic illness, with the <strong>in</strong>itiat<strong>in</strong>g chemical, viral<br />
or traumatic stressor often long gone.<br />
Pall notes that the most characteristic symptom <strong>in</strong> <strong>ME</strong>/CFS is the <strong>in</strong>ability to deal effectively with<br />
exercise, and that it has been observed that the difference <strong>in</strong> <strong>ME</strong>/CFS patients <strong>in</strong> response to exercise is