American Thyroid Association Statement on "Wilson's Syndrome"

By May 24, 2005 August 7th, 2016 Public Health Statements

Updated May 24, 2005

The American Thyroid Association (ATA) has developed the following response to requests from patients and physicians for information about “Wilson’s syndrome”. The ATA Public Health Committee and Council have reviewed the material presented on the “Wilson’s syndrome” website, considered relevant studies from the medical literature, and offer the following advice.


“Wilson’s syndrome” refers to the presence of common and nonspecific symptoms, relatively low body temperature, and normal levels of thyroid hormones in blood. Dr. E. Denis Wilson, who named the syndrome after himself, contends that it represents a form of thyroid hormone deficiency responsive to treatment with a special preparation of triiodothyronine (T3).

The ATA’s thorough review of the biomedical literature has found no scientific evidence supporting the existence of “Wilson’s syndrome.” The ATA also has specific concerns about the following issues.

First, the proposed basis for this syndrome is inconsistent with well-known and widely-accepted facts about thyroid hormone production, metabolism, and action. T3 is one of the two natural thyroid hormones. Normally, it is mainly produced in target tissues outside of the thyroid gland from metabolism of thyroxine (T4). This production of T3 from T4 occurs in a highly regulated manner. This is one reason that T3 is not currently recommended for thyroid hormone treatment in most patients with thyroid hormone deficiency. T4 therapy allows T3 to be produced, as it is naturally, by the regulated metabolism of the administered T4 medication to T3.

Second, the diagnostic criteria for “Wilson’s syndrome”–nonspecific symptoms and body temperature measurement–are imprecise.

Third, there is no scientific evidence that T3 therapy is better than a placebo would be for management of nonspecific symptoms, such as those that have been described as part of “Wilson’s syndrome,” in individuals with and normal thyroid hormone concentrations.

Fourth, T3 therapy results in wide fluctuations in T3 concentrations in blood and body tissues. This produces symptoms and cardiovascular complications in some patients, and is potentially dangerous.

Complete Review

The “Wilson’s syndrome” website lists 37 symptoms as well as “others” that can occur as part of the condition. All of these symptoms do cause suffering, distress, and functional disability in millions of people. Some of these symptoms can, in fact, be due to true hypothyroidism. In hypothyroid patients, they are typically responsive to thyroid hormone therapy. Other problems, such as asthma, are not associated with thyroid hormone deficiency. Many of these symptoms are present from time to time in virtually everyone. In addition to hypothyroidism, they may be due to a variety of illnesses or life circumstances. In other words, they are nonspecific.

The “Wilson’s syndrome” website states that Dr. Wilson named this concept after himself “because it had not been previously described.” In fact, for more than a century, the same set of symptoms 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 Ebstein Barr disease, and chronic candidiasis.

The frequency of complaints attributed to “Wilson’s syndrome” has been recently reviewed (Barsky AJ, Borus JF. Functional somatic syndromes. Ann Intern Med 1999;130:910-21) At any time, more than 20% of adults report significant fatigue and 30% have current musculoskeletal symptoms. Furthermore, the typical adult has one of the 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.

The advocates of “Wilson’s syndrome” view the cause, diagnostic evaluation, and treatment of these symptoms very narrowly. Their viewpoint does not acknowledge that when these symptoms are persistent, they may be due to a number of different subacute and chronic medical conditions, psychological or social stress, or mood disorders, including depression and anxiety. Some of these symptoms may also simply be a part of life. “Wilson’s syndrome” attributes them all to a biochemical theory, which is unsupported by laboratory or clinical research. It does not consider the impact of other potential illnesses and psychosocial factors on how we feel. In doing so, attributing one or more of these symptoms to “Wilson’s syndrome” may delay recognition of treatable medical illnesses and potentially addressable life stresses.

The ATA has the following specific concerns about “Wilson’s syndrome” and its recommended treatment.

  1. The diagnosis of “Wilson’s syndrome” is based on an incorrect definition of normal body temperature: that it is 98.6ºF. (Mackowiak, et al. JAMA 1992;268:1578-1580) measured oral temperature in 148 healthy persons. Average temperature varied throughout the day. At 8 AM, the average temperature was 97.6ºF with more than 50% of all the measurements less than 98.6ºF, and many less than 98.0ºF. This study concluded that “thirty-seven degrees centigrade (98.6ºF) should be abandoned as a concept relevant to clinical thermometry.”
  2. The prescription of T3 for “Wilson’s syndrome” is inconsistent with normal physiology and represents a potential hazard. There is no question that T3 is an active, effective thyroid hormone. However, in most vital organs, much of the T3 is produced by removal of an iodine atom from T4 delivered by the blood to sites of thyroid hormone action. The extent of T4-to-T3 conversion varies from one organ to the other, but in some organs, like the brain and pituitary, this process provides most of the T3. Treatment with T3 produces an unnaturally large amount of T3 in some organs. This may be inappropriate, especially in times of illness or nutritional deficiency. Long-term T3 treatment may cause harm. Excessive T3 treatment can affect the heart and skeleton. These effects can be serious and even life-threatening.
  3. 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. Evidence of this kind, based on anecdotal reports of an unblinded intervention is potentially erroneous. Such reports fail to take into account two well established facts. First, many people who suffer these symptoms, even for months, get better without any treatment. Second, as many as one-third of people with nonspecific symptoms have a so-called placebo response, i.e., they get better when they are given any treatment, even an inactive capsule or sugar pill. The appropriate way to assess a new treatment is to perform a clinical trial in which patients are randomly assigned to receive either the test drug or placebo. Furthermore, the response to treatment should be assessed in a double blind manner, keeping track of what gets better, what does not change, and what gets worse, with neither the patient nor the doctor knowing which treatment the patient is taking. The ATA has been unable to find any such studies of any treatment, including T3, for “Wilson’s syndrome.” The Wilson syndrome website reports only success stories. Responsible medical research into a new treatment keeps track of, and reports, not only successes, but also success rates, and how often there are inconclusive responses, failures, and side effects.
  4. The term Wilson’s syndrome should not be confused with Wilson’s Disease. Wilson’s Disease is a well established and carefully studied rare metabolic disorder caused by excess accumulation of copper in the body.


The American Thyroid Association has found no scientific evidence supporting the existence of “Wilson’s syndrome.” The theory proposed to explain this condition is at odds with established facts about thyroid hormone. Diagnostic criteria for “Wilson’s syndrome” are imprecise and could lead to misdiagnosis of many other conditions. The T3 therapy advocated for “Wilson’s syndrome” has never been evaluated objectively in a properly designed scientific study. Furthermore, administration of T3 can produce abnormally high concentrations of T3 in the blood, subjecting patients to new symptoms and potentially harmful effects on the heart and bones.

The ATA supports efforts to learn more about the causes of somatic symptoms that affect many individuals, to test rigorously the idea that some as yet unidentified abnormality in thyroid hormone action might account for even a small subset of these symptoms, and to pursue properly designed clinical trials to assess the effectiveness of lifestyle, dietary, and pharmacological treatments for these common ailments. However, unsupported claims, such as those made for “Wilson’s syndrome,” do nothing to further these aims.