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

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149<br />

produc<strong>in</strong>g any evidence of damage but effect<strong>in</strong>g a profound disturbance of hormones and neurotransmitters”<br />

(AMO Bakheit et al. Acta Neurol Scand 1993:87:234‐238).<br />

1994<br />

“One of the characteristic compla<strong>in</strong>ts of patients with (<strong>ME</strong>)CFS is the skeletal muscle‐related symptom.<br />

We show that patients had a deficiency of serum acylcarnit<strong>in</strong>e. This deficiency might <strong>in</strong>duce an energy<br />

deficit and/or abnormality of the <strong>in</strong>tramitochondrial condition <strong>in</strong> the skeletal muscle, result<strong>in</strong>g <strong>in</strong> general<br />

fatigue, myalgia, muscle weakness and postexertional malaise <strong>in</strong> patients with (<strong>ME</strong>)CFS. The measurement<br />

of acylcarnit<strong>in</strong>e would be a useful tool for the diagnosis and assessment of (<strong>ME</strong>)CFS” (H Kuratsune et al.<br />

Cl<strong>in</strong> Inf Dis 1994:18: (Suppl 1):S62‐S67).<br />

1995<br />

“The role of steroids <strong>in</strong> growth hormone production was determ<strong>in</strong>ed <strong>in</strong> patients with (<strong>ME</strong>)CFS. There were<br />

abnormal responses of growth hormone production to adm<strong>in</strong>istered steroids <strong>in</strong> patients with (<strong>ME</strong>)CFS.<br />

These data suggest an abnormality <strong>in</strong> the glucocorticoid receptor bear<strong>in</strong>g neurones that control growth<br />

hormone responses <strong>in</strong> affected patients. These data clearly po<strong>in</strong>ted to an abnormality <strong>in</strong> neuroendocr<strong>in</strong>e<br />

control. Another condition that bears strik<strong>in</strong>g similarities to (<strong>ME</strong>)CFS is post‐polio syndrome” (T Majeed<br />

et al. Journal of the Irish Colleges of Physicians and Surgeons 1995:24:1:20‐24).<br />

1996<br />

In a study exam<strong>in</strong><strong>in</strong>g abnormality of adrenal function, Japanese researchers found that “these abnormalities<br />

are quite different from those found <strong>in</strong> patients with mental or physical diseases reported previously”<br />

(Yamaguti K et al. JCFS 1996:2:2/3:124‐125).<br />

1996<br />

“In review<strong>in</strong>g stress‐response systems, it is important to keep <strong>in</strong> m<strong>in</strong>d that activity of stress‐response systems is<br />

determ<strong>in</strong>ed by genetic and environmental factors. In (<strong>ME</strong>)CFS we have demonstrated a significant <strong>in</strong>crease <strong>in</strong><br />

plasma levels of the seroton<strong>in</strong> metabolite 5‐hydroxy<strong>in</strong>doleacetic acid. Patients with a longer duration of<br />

disease do tend to have more severe basal abnormalities <strong>in</strong> cortisol levels” (LJ Crofford et al. Rheum Dis<br />

Cl<strong>in</strong> N Am 1996:22:2:267‐284).<br />

1996<br />

“There is an <strong>in</strong>creas<strong>in</strong>g volume of evidence to support the view that patients with (<strong>ME</strong>)CFS have unique<br />

endocr<strong>in</strong>ology patterns. The card<strong>in</strong>al f<strong>in</strong>d<strong>in</strong>gs <strong>in</strong>clude attenuated ACTH responses to CRH and low 24‐hour<br />

ur<strong>in</strong>ary cortisol. These are compatible with a mild central adrenal <strong>in</strong>sufficiency. It is well‐documented that<br />

<strong>in</strong>fectious diseases are often accompanied by various forms of neuroendocr<strong>in</strong>e disturbances with acute viral<br />

<strong>in</strong>fections activat<strong>in</strong>g the HPA axis. An <strong>in</strong>crease <strong>in</strong> peripheral turnover of 5‐HT may expla<strong>in</strong> the heightened<br />

allergic responsiveness as well as the musculoskeletal pa<strong>in</strong> seen <strong>in</strong> (<strong>ME</strong>)CFS” (LV Scott TG D<strong>in</strong>an. JCFS<br />

1996:2:4:49‐59).<br />

1997<br />

“It is notable that the pattern of alteration <strong>in</strong> the stress response suggests a susta<strong>in</strong>ed <strong>in</strong>activation of central nervous<br />

system components of this system. It has not escaped the view of cl<strong>in</strong>ical authors that (<strong>ME</strong>)CFS and its<br />

historical antecedents shares many of the characteristics with endocr<strong>in</strong>e disease states (<strong>in</strong> which there is)<br />

functional <strong>in</strong>terdependence of the endocr<strong>in</strong>e system and the nervous system. It is only recently that cl<strong>in</strong>ical<br />

researchers have clearly documented that neuroendocr<strong>in</strong>e disturbances are evident <strong>in</strong> patients with (<strong>ME</strong>)CFS (which)<br />

have brought <strong>in</strong>to view a broader understand<strong>in</strong>g of the variety of physiologic accompaniments of this condition.

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