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Thyroid Canada Newsletter
- Issue 2
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FEBRUARY 2001 Wilson’s Syndrome Merrill Edmonds, MD, FRCPC, FACP My first introduction to “Wilson’s syndrome” was by a track coach who had arranged a referral for one of his elite runners. She suffered from a low body temperature which he felt held back her progress. She would often have to sit in a bath or Jacuzzi just to warm up. He had seen this once before in another athlete in whom all the tests, including thyroid tests, were normal but she started treatment for “Wilson’s syndrome” and (according to him) made an amazing recovery. The present athlete had many of the same symptoms and her temperature would drop as low as 96F and only reached normal when she had a fever which was typical of “Wilson’s syndrome”. She had a couple of big races coming up and he was anxious to get her started on treatment to optimize her performance. “Wilson’s syndrome” refers to the presence of common and non-specific symptoms, relatively low body temperature, and normal levels of thyroid hormones in blood. The syndrome is named after Dr. E. Denis Wilson, whose Florida medical license, according to Quackwatch (http://www.quackwatch.com) was suspended in 1991. Dr. Wilson contends it represents a form of thyroid hormone deficiency responsive to treatment with a special preparation of triiodothyronine (T3) described in his “Doctor’s Manual for Wilson’s Syndrome”. The syndrome and its treatment are extensively described on Dr. Wilson’s website which can be found at “http://www.wilsonssyndrome.com”. Dr. Wilson named this “syndrome” after himself “because it had not been previously described”. The same set of symptoms, however, has been given different names and attributed to a variety of causes by others, including the syndromes of neurasthenia, chronic fatigue, fibromyalgia, multiple chemical sensitivity, chronic Epstein-Barr disease, chronic candidiasis, reactive hypoglycemia, and others. “Wilson’s syndrome” attributes these symptoms to a biochemical abnormality, which is unsupported by laboratory or clinical research and does not acknowledge that such symptoms may be due to a number of different medical or psychological conditions, or that they may simply be a part of modern-day life. The American Thyroid Association (ATA) has reviewed the material presented on the “Wilson’s syndrome” website, considered the relevant studies from the medical literature, and offered advice which can be found on the ATA’s website at “http://www.thyroid.org”. The sole clinical evidence supporting T3 therapy offered by the “Wilson’s syndrome” website is in the form of testimonials from people who feel better after taking T3. As expected, the ATA’s review of the biomedical literature found no scientific evidence supporting the existence of “Wilson’s syndrome”. The proposed basis for this syndrome is inconsistent with well-known and widely-accepted facts about thyroid hormone production, metabolism, and action. The conversion of T4 to T3 occurs in a highly regulated manner and is one reason that T3 is not currently recommended for thyroid hormone treatment in most patients with thyroid hormone deficiency. The diagnostic criteria for “Wilson’s syndrome”, non-specific symptoms and body temperature measurement, are imprecise. At any time, more than 20% of adults report significant fatigue and 30% have current musculoskeletal symptoms1. A typical adult has one of these symptoms every 4 to 6 days, and more than 80% of the general population has one of these symptoms during any 2 to 4 week period. Many normal individuals have body temperatures below 37C at different times of the day2. There is no scientific evidence that T3 therapy is better than a placebo for management of these non-specific symptoms, that have been described as part of “Wilson’s syndrome”, in individuals with normal thyroid hormone concentrations. T4 therapy allows T3 to be produced, as it is naturally, by the regulated metabolism of the administered T4 medication to T3. T3 therapy results in wide fluctuations in T3 concentrations in blood and body tissues which may produce symptoms and cardiovascular and skeletal complications in some patients, and is potentially dangerous. It is easy to understand why the general public is attracted to anyone claiming to have a cure for these common and sometimes very debilitating symptoms. The explosion in the number of available alternative therapies is testimony to the frequency and severity of these symptoms in the general public. The increasing availability of many of these alternative therapies in pharmacies has also given them the appearance of legitimacy, and the tremendous lobbying of groups supporting alternative therapies makes it very difficult for physicians to discourage their use and remind patient of their potential side effects3. The idea that some as yet unidentified abnormality in thyroid hormone action might account for even a small subset of these symptoms does need to be pursued in properly designed clinical trials. Unsupported claims, however, such as those made for “Wilson’s syndrome”, do nothing to further these aims. My attempts to assure the elite runner that she did not need T3 were probably unsuccessful and she likely found someone prepared to treat her problem. Hopefully, she and the many others taking alternative therapies, won’t do themselves harm in the process and waste too many resources that could otherwise be directed to proven therapies or legitimate research.
References:
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EDITORIAL COMMENT I certainly agree with the opinion expressed by Dr.
Edmonds about “Wilson’s Syndrome”. Unfortunately,
several articles have appeared from non-experts in the field which
have supported Wilson. Many of these articles have emanated from
the Broda Barnes Foundation, which supports the notion that a low
basal body temperature reflects hypothyroidism (which it does not),
and that T3 is the appropriate treatment, even when tests of thyroid
function are normal. Of course there is no scientific evidence for
this whatsoever. In addition, there have been some recent articles
in mainline journals suggesting that the further addition of T3
to T4 enhances the response, and this has engendered a tremendous
interest amongst patients in the wish to add T3 to their regimen.
However, in such instances, the total T3 is normal to begin with
when patients take Thyroxine alone, and there is concern that increasing
the total T3 by adding more T3 to the regimen may prove to be risky. **********
Upcoming Events:
********** If you would like to see an upcoming thyroid event published in the next issue of Thyroid Canada, please fax the information to Theramed Corporation at (905) 564-4776 as soon as possible. Published with a grant from Theramed Corporation.
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