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

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English and Australian reports to mention other important endocrine abnormalities of (ME)CFS represents a serious
omission. Cognitive behaviour therapy may have benefited depressed subjects (but) not patients with (ME)CFS.
(ME)CFS and Addison’s disease also share reduced cardiac dimensions, increased heart rate, postural
hypotension, orthostatic tachycardia, dizziness upon standing, dehydration, anorexia, nausea (and)
diarrhoea. Moreover (they) also share leucocytosis, lymphocytosis, elevations of transaminase values,
enhanced TSH secretion, respiratory muscle dysfunction, reduction in exercise capacity and increased
sensitivity to chemical exposures. Reason suggests that the clinical overlap of (ME)CFS with Addison’s disease
reflects the endocrine and adrenal abnormalities found in (both disorders) and omitted unjustifiably in both the English
and Australian reports, namely hypocortisolism, impaired adrenal cortical function, reduced adrenal gland size,
antibodies against the adrenal gland, and impaired production of DHEA. Richard Horton, editor of The Lancet,
has recently written (JAMA 2002:287:2843‐2847): ‘Failure to recognise the critical footprint of primary
research weakens the validity of guidelines and distorts clinical knowledge’ ” (R Baschetti. Eur J Clin Invest
2003:33:1029‐1031).
(Baschetti was referring to the 2002 UK Report of the CMO’s Working Group and the Australian Report in
the Medical Journal of Australia 2002:176:S17‐S56).
2003
“Patients with (ME)CFS typically present a normal thyroid function. From (our) observations, we raise the hypothesis
that molecular mechanisms could explain the development of a clinical hypothyroid state in the presence of a normal
thyroid function. Whilst biochemically euthyroid, (ME)CFS patients are clinically hypothyroid. Signal transduction
mechanisms could account for a peripheral T3 resistance syndrome leading to a clinically hypothyroid but
biochemically euthyroid state, as observed in diseases characterised by dysregulations in the antiviral pathway or
during the therapeutic use of INF α / β” (P Englebienne et al. Med Hypotheses 2003:60:2:175‐180).
2003
The following article is in Serbian and comes from the Institute of Endocrinology, Belgrade; no author is
listed:
“Similarities between the signs and symptoms of (ME)CFS and adrenal insufficiency prompted the research of the
HPA axis derangement in the pathogenesis of (ME)CFS. We compared cortisol response in the (ME)CFS subjects
with the response in control subjects and in those with secondary adrenal insufficiency. We have shown
that cortisol increment at 15 and 30 minutes is significantly lower in the (ME)CFS group than in controls.
However, there was no difference between the (ME)CFS group and those with secondary adrenal
insufficiency in any of the parameters. Consequently, reduced adrenal responsiveness to ACTH exists in
(ME)CFS” (Srp Arh Celok Lek 2003:131:9‐10:370374).
It should be noted that Wessely School psychiatrists have carried out several endocrinological studies on
“CFS” patients and have had varying results, possibly because of their chosen case definition. Despite the
compelling evidence of international researchers, the Wessely School psychiatrists found no evidence of
endocrine abnormality in some of their studies, whilst in others they did find evidence of such abnormalities
but concluded that even though a distinct abnormality was found (low cortisol), it was likely to be “an
epiphenomenon caused by the behavioural changes typical of CFS” (GJ Rubin, M Hotopf, A Cleare et al.
Psychosom Med 2005:67:3:490‐499).
Documented evidence of inflammation in ME/CFS
A few illustrations of published evidence of inflammation of the central nervous system of ME/CFS patients
include the following: