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

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150<br />

(<strong>ME</strong>)CFS appears to wax and wane with periods of <strong>in</strong>creased stress. Results of this work provide confirmatory<br />

support for an impairment (of) the HPA axis (and) is consistent with the view that adrenocortical function<br />

is impaired” (MA Demitrack. J psychiat Res 1997:31:1:69‐82).<br />

1998<br />

“Our group has established that impaired activation of the HPA axis is an essential neuroendocr<strong>in</strong>e feature<br />

of (<strong>ME</strong>)CFS. It is now recognised that (<strong>ME</strong>)CFS leads to significant physical and psychological debility <strong>in</strong> a large<br />

segment of the population. We have suggested that the f<strong>in</strong>d<strong>in</strong>gs of reduced adrenal glucocorticoid function <strong>in</strong> (<strong>ME</strong>)CFS<br />

are most consistent with a central nervous system defect <strong>in</strong> the activation of this axis. (We found) a basal<br />

hypocortisolism. On its own, this observation is a strik<strong>in</strong>g f<strong>in</strong>d<strong>in</strong>g. These observations provide an<br />

important clue to the development of more effective treatment for this disabl<strong>in</strong>g condition” (MA Demitrack,<br />

LJ Crofford. Ann N.Y. Acad Sci 1998:840:684‐697).<br />

1999<br />

“The right and left adrenal gland bodies were reduced by over 50% <strong>in</strong> the (<strong>ME</strong>)CFS subjects, <strong>in</strong>dicative of<br />

significant adrenal atrophy <strong>in</strong> a group of (<strong>ME</strong>)CFS with abnormal endocr<strong>in</strong>e parameters” (Scott LV et al.<br />

Psychoneuroendocr<strong>in</strong>ology 1999:24:7:759‐768).<br />

2000<br />

“Basel<strong>in</strong>e adrenal<strong>in</strong>e levels were significantly higher <strong>in</strong> (<strong>ME</strong>)CFS patients. We conclude that (<strong>ME</strong>)CFS is<br />

accompanied by a resistance of the immune system to regulation by the neuroendocr<strong>in</strong>e system. Based on<br />

these data, we suggest (<strong>ME</strong>)CFS should be viewed as a disease of deficient neuroendocr<strong>in</strong>e‐immune<br />

communication” (Kavelaars A et al. J Cl<strong>in</strong> Endocr<strong>in</strong>ol Metab 2000:85:2:692‐696).<br />

2001<br />

“In the <strong>in</strong>vestigation of (<strong>ME</strong>)CFS, f<strong>in</strong>e needle aspiration (FNA) cytology has been tested <strong>in</strong> addition to conventional<br />

biochemical thyroid function tests. Of 219 patients, 40% were diagnosed with def<strong>in</strong>ite cytological lymphocytic<br />

thyroiditis. We strongly advocate FNA cytologic assessment of the thyroid <strong>in</strong> patients with (<strong>ME</strong>)CFS” (B<br />

Wikland et al. Lancet 2001:357:956‐957).<br />

In a subsequent letter, Wikland stated: “In a letter published <strong>in</strong> The Lancet (24 th March 2001) we report on f<strong>in</strong>e<br />

needle aspiration cytology of the thyroid <strong>in</strong> (<strong>ME</strong>)CFS. No less than 40% of our patients showed def<strong>in</strong>ite autoimmune<br />

thyroiditis. Less than half of these patients fulfilled conventional biochemical criteria of hypothyroidism. In our<br />

op<strong>in</strong>ion, this aspect merits wider recognition” (Bo Wikland. eBMJ 9 January 2002).<br />

2001<br />

“One of the most consistent f<strong>in</strong>d<strong>in</strong>gs <strong>in</strong> (<strong>ME</strong>)CFS is a decrease <strong>in</strong> Th1‐mediated immune responses. (<strong>ME</strong>)CFS patients<br />

have been shown to display a disturbed HPA axis and have low levels of cortisol. We speculate that <strong>in</strong> these patients<br />

IL‐10 and IL‐12 are differently affected by glucocorticoids. The present study shows that, <strong>in</strong> particular, IL‐10<br />

secretion (and its sensitivity to GC) differs from that <strong>in</strong> healthy controls” (J Visser et al. Journal of<br />

Neuroimmunology 2001:119:2:343‐349).<br />

2003<br />

“Endocr<strong>in</strong>ologists were not <strong>in</strong>cluded <strong>in</strong> the work<strong>in</strong>g groups that prepared two recent reports on (<strong>ME</strong>)CFS,<br />

despite its cl<strong>in</strong>ical overlap with Addison’s disease, which is a classic endocr<strong>in</strong>e disease. The failure to<br />

<strong>in</strong>clude at least one endocr<strong>in</strong>ologist <strong>in</strong> those panels may expla<strong>in</strong> why <strong>in</strong> their reports there is not a s<strong>in</strong>gle<br />

word about the 42 cl<strong>in</strong>ical features that (<strong>ME</strong>)CFS shares with Addison’s disease. The failure of both the

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