01.12.2012 Views

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

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

177<br />

analysed the gene expression <strong>in</strong> peripheral blood of patients with CFS/<strong>ME</strong> and <strong>in</strong> all of these, genes of immunity<br />

and defence are prom<strong>in</strong>ent….Progress is be<strong>in</strong>g made towards an understand<strong>in</strong>g of the pathogenesis of this<br />

<strong>in</strong>trigu<strong>in</strong>g and devastat<strong>in</strong>g disease” (Jonathan Kerr. Current Rheumatology Reports 2008:10:482‐491).<br />

2008<br />

“…expression of several complement genes rema<strong>in</strong>ed at higher level <strong>in</strong> CFS subjects before and post‐exercise,<br />

<strong>in</strong>dicat<strong>in</strong>g a lack of acute phase transcriptional response by these genes which may lead to localised and<br />

uncontrollable <strong>in</strong>flammation mediated tissue damage” (Sorensen B et al. Mol Med 2008: Nov 16: Epub<br />

ahead of pr<strong>in</strong>t).<br />

2009<br />

“We used global transcriptome analysis to identify genes that were differentially expressed <strong>in</strong> the vastus lateralis<br />

muscle of female and male CFS patients. We found that the expression of genes that play key roles <strong>in</strong><br />

mitochondrial function and oxidative imbalance…were altered, as were genes <strong>in</strong>volved <strong>in</strong> energy<br />

production, muscular trophism and fibre phenotype determ<strong>in</strong>ation. Importantly, the expression of a gene<br />

encod<strong>in</strong>g a component of the nicot<strong>in</strong>ic chol<strong>in</strong>ergic receptor b<strong>in</strong>d<strong>in</strong>g site was reduced, suggest<strong>in</strong>g impaired<br />

neuromuscular transmission. We argue that these major biological processes could be <strong>in</strong>volved <strong>in</strong> and/or<br />

responsible for the muscle symptoms of CFS” (Pietrangelo T, Fulle S et al. Int J Immunpathol Pharmacol<br />

2009:22(3)795‐807).<br />

2009<br />

Referr<strong>in</strong>g to earlier work that demonstrated 88 abnormal genes, the authors state: “We set out to determ<strong>in</strong>e<br />

whether these f<strong>in</strong>d<strong>in</strong>gs were reproducible <strong>in</strong> fresh subjects (and) whether the previously‐reported dysregulation of these<br />

genes also occurred <strong>in</strong> drug‐free patients with endogenous depression…Results show that these f<strong>in</strong>d<strong>in</strong>gs are<br />

reproducible, and that gene expression <strong>in</strong> endogenous depression patients was markedly different to that <strong>in</strong><br />

CFS/<strong>ME</strong> patients and was similar to that <strong>in</strong> normal controls <strong>in</strong> terms of these 88 human genes…In the<br />

present study, we have confirmed this differential expression <strong>in</strong> 62 additional and previously untested CFS/<strong>ME</strong><br />

patients…We have addressed the question of the specificity of these 88 genes to CFS/<strong>ME</strong> by test<strong>in</strong>g drug‐free<br />

patients with endogenous depression. The fact that only 5 of these genes were abnormally expressed <strong>in</strong><br />

endogenous depression patients as compared with normals supports the view that CFS/<strong>ME</strong> and endogenous<br />

depression are biologically dist<strong>in</strong>ct, and that the psychological features of CFS/<strong>ME</strong> are <strong>in</strong> fact secondary to<br />

the pathogenesis” (Lihan Zang, Jonathn Kerr et al. J Cl<strong>in</strong> Pathol 2009: doi 10.1136/jcp2009.072561).<br />

Documented ocular abnormalities <strong>in</strong> <strong>ME</strong>/CFS<br />

1988<br />

David J Brown<strong>in</strong>g found that the most common ocular symptoms <strong>in</strong> <strong>ME</strong>/CFS (CFIDS) are floaters, transient<br />

blurr<strong>in</strong>g of vision, transient double vision, extreme light sensitivity, burn<strong>in</strong>g and pa<strong>in</strong> <strong>in</strong> the eyes (CFIDS<br />

Chronicle October 1988:6‐7).<br />

1992<br />

Nystagmus at a rate 230 times normal, poor fixation stability, and ratchet vision were reported (Meet<strong>in</strong>g‐<br />

Place 1992: 38:38‐40).

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!