Psychiatrists have filled the major UK journals with articles postulating that ME/CFS and FMS have a psychiatric basis. In one recent report (Lancet, 1999; 354: 936-9), the authors suggest that the problems seen in conditions such as irritable bowel syndrome, premenstrual syndrome, multiple chemical sensitivity (MCS), CFS and FMS are all in the head.
Such a mindset ignores the established research showing that abnormalities in ME/CFS patients may be due to thyroid, adrenal and other hormonal dysfunction. E.G. Dowsett, an eminent researcher in CFS, found that 5 per cent of female ME patients suffer from thyroiditis (Hyde BM et al., The Clinical and Scientific Basis of ME/CFS, Ottawa: Nightingale Research Foundation, 1992: 285-91). Byron Hyde, the leading Canadian researcher in this field, reports that glucose and TSH tests reveal that up to half of ME patients develop thyroid problems (Proceedings of the Second World Congress on CFS and Related Disorders, Brussels, September 1999, p 60).
At the same conference, Belgian researchers showed that TSH levels, among others, were elevated in CFS patients (Proceedings, p 62). In Why ME? (Crafton Books, 1989), author Dr Belinda Dawes acknowledges that, in ME and other environmental and allergic disorders, thyroid function is disturbed, and low-dose thyroid hormone supplementation, along with other supplements, is often appropriate.
Other eminent international researchers have found that the endocrine system in ME/CFS sufferers is disrupted (Rheum Dis Clin North Am, 1996; 22: 267-84; J Psychiatr Res, 1997; 31: 69-82; Horm Metab Res, 1999; 1: 18-21). A key feature is a defect in the hypothalamic-pituitary-adrenal (HPA) axis (J Clin Endocrinol Metab, 1991; 73: 1224-34; J CFS, 1995; 1: 59-66). In one study, computed tomography (CT) of ME patients showed that both adrenal glands were reduced by as much as 50 per cent compared with the controls (Radiology, 1998; 209P [Suppl]: 411-2).
One reason why this thyroid abnormality is often overlooked in ME patients is that it doesn’t show up in the usual neuroendocrine tests. In one large study, the researchers concluded that these tests are inadequate for ME/CFS patients (Scott LV, The role of the HPA axis in chronic fatigue syndrome [PhD thesis], British Library, 1997).
The evidence suggests that these patients may not have a truly normal thyroid function (‘euthyroid’), but may have what is known as ‘euthyroid sick syndrome’ (J Clin Endocrinol Metab, 1997; 82: 329-34). There may be a problem in conversion from T4 to T3, a process which takes place in the liver and is facilitated by several enzymes, and requires specific micronutrients to proceed smoothly (Medicine Endocrinology 23-24-98 html, Thyroid, Lecturer Dr Blum).
Possibly the most comprehensive list of common symptoms due to hypothyroidism seen in ME/CFS/FMS/MCS can be found on the website of the American Association of Clinical Endocrinologists, Merck Manual, Thyroid Foundation of America (http://thyroid.miningco.com/blchklst.htm?pid=2750&cob=home).
Professor Timothy Dinan, University College in Cork, Ireland, has observed an increased prevalence of subclinical hypothyroidism in CFS patients. At a conference at the Royal Society of Medicine last October, he announced his discovery that, in CFS, as in other stress-related conditions, regulation of the HPA axis is abnormal and associated with diminished organ function.
In a recent randomised, double-blind, placebo-controlled study, a well-known American team treated 72 FMS patients for subclinical thyroid, gonadal and/or adrenal insufficiency, disordered sleep, suspected neurally mediated hypotension, opportunistic infections and suspected nutritional deficiencies.