What Doctors Don't Tell YouA scandalous lack of knowledge by doctors and an epidemic of undiagnosed thyroid problems may be behind the other growing epidemic of our times: ME
Successfully treating thyroid disorders is a tall order for any doctor. It’s vital that he not only knows about the gland itself, but also that he understands the entire endocrine system, including the complex workings of the various biochemical pathways.
Unfortunately, most medical students receive, at most, half a day’s worth of schooling in the complexities of the endocrine system. Small wonder that knowledgeable and expert practitioners able to meet the varying needs of thousands of patients are exceptionally thin on the ground.
The result is an epidemic of people walking around with undiagnosed thyroid disorders. The latest information indicates that thyroid problems may play a significant role in many of the 21st century’s most puzzling illnesses, such as myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) or fibromyalgia syndrome (FMS). This is all the more serious as, in some circumstances, untreated or poorly treated thyroid problems can lead to death (Neal JM, Basic Endocrinology: An Integrated Approach, Oxford: Blackwell Science, 2000).
There is much controversy in medical circles over states of hypothyroidism, in particular where patients have normal blood tests, but show the clinical signs and symptoms of hypothyroidism. These conditions are described as ‘biochemically normal but clinically hypothyroid’.
Subclinical hypothyroidism is common, especially in elderly women. The presence of this condition or of thyroid antibodies increases the risk of developing overt hypothyroidism. The risk is even greater if both are present (BMJ, 1997; 314: 1175-8).
Screening for hypothyroidism is particularly important during pregnancy since undiagnosed hypothyroidism in pregnant women may adversely affect their fetus (N Engl J Med, 1999; 341: 549-55).
One reason that hypothyroidism so often goes undetected is the common misconception that a diagnosis of clinical hypothyroidism can be made from blood tests alone. But many conditions can change the amount of circulating thyroid hormones in the blood – everything from pregnancy, dieting and kidney problems to prescription drugs and even illness.
In such patients, thyroid function tests are virtually useless (BMJ, 2000; 320: 1332-4). Especially in elderly patients, some of whom may have pituitary tumours or hypopituitarism, testing only for TSH may be inappropriate. Unless a doctor diagnoses hypothyroidism through careful clinical examination and history-taking, the diagnosis is likely to be missed (BMJ, 2000: 321: 1275-7)
In addition, when patients are taking thyroid replacement therapy, other drugs can affect the amount needed or absorbed. A study in hypothyroid women treated with thyroxine showed that when they take oestrogen therapy at the same time, the usual doses of thyroxine may be inadequate (N Engl J Med, 2001; 344: 1743-9).
ME: the link with thyroid
Thyroid problems may be a culprit behind unexplained diseases such as ME/CFS and FMS. In most cases, the health problems experienced by these patients are part of a more basic and profound dysfunction, such as primary damage to the hypothalamus or pituitary gland through infection and/or some other insult. In Basic Endocrinology: An Integrative Approach, author J.M. Neal says that these different manifestations of thyroid dysfunction, especially those seen in hypothyroidism, require their own special treatment.
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.
The treated group enjoyed significant improvement compared with the placebo group. Of 38 treated patients, 33 received thyroid replacement therapy, demonstrating that hypothyroidism plays an important role in FMS and CFS (J CFS, 2001; 8: 3-28). An earlier study by the same team reported similar results (Am J Med Sci, 2000; 320: 1-8). One researcher has even postulated that CFS, FMS and Persian Gulf syndrome share a common underlying cause: a magnesium deficiency plus a toxic excess of fluoride (J CFS, 1999; 5: 67-127).
Certain practitioners and researchers have treated patients with thyroid replacement therapy using either conventional synthetic thyroxine (T4) or natural thyroid hormones, such as Armour Thyroid, which contains the full complement of thyroid hormones, including the far more powerful T3. In the UK, Dr Gordon Skinner, perhaps the best known of these practitioners, proposes treating biochemically normal but clinically hypothyroid patients with low-dose thyroxine (BMJ, 1997; 314: 1764).
Skinner’s treatment has received publicity through the publication of Diana Holmes’ book Tears Behind Closed Doors (Avon Books, 1998), in which she tells of her years of being misdiagnosed before being correctly diagnosed and treated by Dr Skinner. Skinner and his team later published the results of their trials with patients like Holmes (J Nutr Environ Med, 2000; 10: 115-24).
Dr Barry Durrant-Peatfield used a similar treatment regime (J Nutr Environ Med, 1996; 6: 371-8). Until recently, he prescribed thyroid replacement therapy to all patients with clinical hypothyroidism (not just patients with CFS/ ME/FMS), with low-dose adrenal support for those who needed it. He gained a solid reputation for successfully treating many patients with CFS/ ME/FMS as well as other thyroid and adrenal dysfunctions.
As Peatfield writes in his own information booklet, ‘With the pituitary-thyroid-adrenal axis damaged, the body’s immune system cannot recover, and the sufferer is frequently ill with apparent relapses of virus illness, other general illnesses, and indeed low-grade parasitic infections.’ (Durrant-Peatfield BJ, Diagnosis and Treatment of ME).
Nevertheless, Skinner’s approach has met with considerable opposition from medical practitioners in endocrinology and clinical biochemistry. Even the medical director of the ME Association, one of two major ME/CFS charities in the UK, opposed Skinner’s treatment on the grounds that its benefits were unproven and potentially dangerous (BMJ, 1997; 315: 813-4). Dr Peatfield recently had his medical licence suspended, the latest victim of the General Medical Council’s witch hunt on doctors using unorthodox procedures (WDDTY, vol 12 no 5).
Despite the wealth of evidence of disturbed thyroid functioning and other abnormalities of the HPA axis (notably adrenal deficiencies) in ME, the medical director of the ME Association recently co-authored a booklet stating: ‘There is no evidence of disturbed thyroid gland function in ME/CFS, and the use of thyroxine supplementation in people who have normal thyroid function tests is a controversial form of treatment which carries a number of risks, including the potential complication of precipitating an Addisonian crisis in patients with hypocortisolaemia [diminished production of cortisol by the adrenals]’.
Fibromyalgia and thyroid
Much of the research on FMS patients also points to thyroid problems as a hidden cause. A recent study reported that almost all of the hormonal feedback mechanisms controlled by the hypothalamus are altered in this condition. This includes elevated levels of ACTH, follicle-stimulating hormone (FSH) and cortisol (hydrocortisone) as well as lowered levels of insulin-like growth factor (IGF)-1, somatomedin C, free triiodothyronine (FT3) and oestrogen (Scand J Rheumatol Suppl, 2000; 11: 8-12).
Studies have shown that thyroid disorders, notably hypothyroidism, and altered reactivity of the HPA axis are a common feature in FMS patients (J Rheumatol, 1992; 19: 12120-2; J Rheumatol, 1993; 20: 469-74).
Dr John Lowe has documented his experiences with FMS patients and his study of fibromyalgia in a 1260-page publication The Metabolic Treatment of Fibromyalgia (McDowell Publishing, 2000). This book effectively argues that fibromyalgia is largely caused by inadequate thryroid hormone regulation of tissue functions.
The medical regulatory bodies have produced four ‘mandates’ to serve as guidelines for the diagnosis and treatment of hypothyroidism:
1. A deficiency of thyroid hormone is the only cause of symptoms and signs characteristic of hypothyroidism
2. Clinicians should not permit patients with ‘normal’ thyroid test results to use thyroid hormone
3. Hypothyroid patients should use thyroid hormones only in ‘replacement dosages’ (dosages that keep TSH within its reference range)
4. Hypothyroid patients should only use thyroxine (T4).
To help the thousands of thyroid patients who fall outside this strict definition, Dr Peatfield and other practitioners have had to resort to violating accepted medical practice, knowing their risk of suspension or revocation of their licences. Indeed, one doctor goes so far as to argue that adherence to these ‘mandates’ is itself contributory to the sudden rise of new diseases.
FMS, CFS, ME and other such syndromes may not be all in the sufferers’ heads so much as in their necks, largely the result of a low thyroid problem not properly treated.
Doris Jones
Maryon Stewart
Dr Jacob Teitelbaum MD
Daniel Redwood DC
Tom Ferguson MD