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

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symptoms not currently in the CDC case definition were added, these being respiratory infections,
palpitations, dizziness, dyspepsia, dryness of mouth / eyes, allergies, nausea, paraesthesia, loss of hair, skin
alterations, dyscoordination (sic), chest pain, personality changes, eczema, general infections, twitches and
urogenital infections. A significant correlation between the criteria score and immunological parameters
could be evaluated in 472 of the 505 patients. The data confirm that a reduced or unstable immune control
or delayed immune reaction to persisting viruses or bacterial intracellular pathogens, possibly triggered
by common infections or other environmental factors, can lead to a chronic neuroimmune activation state
and autoimmune disorders (JCFS 1996:2: (4):35‐47).
1997
“The level of bioactive transforming growth factor β was measured in serum from patients with (ME)CFS and
compared with normal controls, patients with major depression, patients with systemic lupus erythematosus and
patients with multiple sclerosis. Patients with (ME)CFS had significantly higher levels of bioactive TGFβ than
the healthy controls, patients with major depression, patients with systemic lupus erythematosus and
patients with multiple sclerosis. Of greatest relevance to (ME)CFS are the effects of TGF β on cells of the
immune and central nervous systems. There is accumulating evidence that TGFβ may play a role in
autoimmune and inflammatory diseases” (AL Bennet, AL Komaroff et al. J Clin Virol 1997:17:2:160‐166).
1997
“(ME)CFS is associated with dysregulation of both humoral and cellular immunity, including mitogen
response, reactivation of viruses, abnormal cytokine production, diminished natural killer (NK) cell
function, and changes in intermediary metabolites. The biochemical and immunologic data presented here
identified a subgroup of individuals with (ME)CFS with an RNase L enzyme dysfunction that is more profound than
previously observed (and) is consistent with the possibility that the absence of the 80‐kDa and 40‐kDa RNase L and
presence of the LMW RNase L correlate with the severity of (ME)CFS clinical presentation” (Robert Suhadolnik,
Daniel Peterson, Paul Cheney et al. Journal of Interferon and Cytokine Research 1997:17:377‐385).
Professor Suhadolnik explained in lay terms the significance of this paper (reported by Patti Schmidt in
CFIDS Chronicle, Summer 1997, page 17): “He has found a particular place in the immune system, the 2‐5 RNase L
antiviral pathway, where something is wrong. ‘The whole antiviral pathway heats up out of control’ explained
Suhadolnik. ‘You’re really sick physiologically. Your body just keeps going and going like the Energiser
bunny, making ATP and breaking it down. No wonder you’re tired’. He’s found a novel protein in CFIDS
patients in that viral pathway. ‘In most cases, the human body is able to resist infection thanks to a cascade of
biochemical events triggered by the body’s immune system. If these antiviral defence pathways are functioning
correctly, the spread of the virus is prevented’. Suhadolnik believes that (ME)CFS patients’ bodies are responding to a
central nervous system virus that interferes with their viral pathways’ ability to fight off infection ”.
1997
A highly‐respected paper by Vojdani and Lapp et al stressed the importance of cell apoptosis (and the
pivotal role of protein kinase RNA in this) in ME/CFS: “A prominent feature of (ME)CFS is a disordered
immune system. Recent evidence indicates that induction of apoptosis might be mediated in a dysregulated immune
system by the up‐regulation of growth inhibitory cytokines. The purpose of this study was to evaluate the apoptotic cell
population, interferon‐α and the IFN‐induced protein kinase RNA (PKR) gene transcripts in the peripheral blood
lymphocytes of (ME)CFS individuals, as compared to healthy controls. One of the distinguishing manifestations
of (ME)CFS is abnormal immune function, characterised by a decreased NK cell‐mediated cytotoxic
activity, reduced mitogenic response to lymphocytes, altered cytokine production, elevated titres of
antibodies to a number of viruses, and abnormal production of interferon (IFN). The induction of apoptosis
through immune defence mechanisms is an important mechanism for elimination of cancer cells as well as virus‐
infected cells. In the present study, the up‐regulation of IFN‐α and the IFN‐induced PRK in (ME)CFS individuals is
accompanied by the induction of apoptosis. In addition, dysregulation of cell cycle progression is associated with the