Wilson’s Temperature Syndrome was first identified and defined by Dr Denis Wilson. Essentially subclinical hypothyroidism, this is defined by all the symptoms of hypothyroidism, including chronically low body temperatures (below 97.8 orally). Other symptoms include a slower metabolism, hair loss, constipation, fatigue, weight gain, and sometimes depression and heavy periods for women.


Quick rundown of thyroid physiology: TSH is the hormone produced in your pituitary gland, which tells your thyroid to produce T4 (it produces about 80% this, and 20% T3). The rest of the T4 then goes to your peripheral tissues and gets converted into T3, which is active thyroid hormone.

In times of high stress (emotional, physical, or trauma), high cortisol slows down the enzyme that converts T4 to T3. It also encourages conversion of T4 into reverse T3, instead of T3. Reverse T3 will sit on the receptors but won’t stimulate them, effectively acting as a competitive inhibitor to the real T3. The goal is, your body wants to slow down your metabolism so that it can conserve its energy to deal with the stressor. In theory, once the stressor is over, rT3 should decrease and T3 should increase back to normal again.

However, for some, rT3 never goes back to normal—at least not in the peripheral tissues. According to Dr Wilson, this can’t be diagnosed on a blood test, because blood levels only tell you what’s happening in the blood, not in the tissue itself. My assumption here is that rT3 will only show up high on a blood test during the acute stressor, and not after the fact.


Since you can’t tell on a blood test whether or not you have Wilson’s Syndrome, it’s considered a diagnosis of exclusion, primarily implied by hypothyroid symptoms in the absence of a clear cause on labs, and of any other apparent cause. It’s also suggested, and treatment is monitored, by temperatures. Specifically, temps should be measured orally, three hours after waking and then every three hours after that, three times per day.


Treatment of Wilson’s Syndrome involves very carefully timed (every 12 hours, not three minutes off) administration of sustained release T3.

The idea behind it is this: since the presumed problem is due to an excess of both T4 (that hasn’t yet converted into T3) and rT3 in the peripheral tissues, and since the body always wants to create balance, giving T3 will result in feedback inhibition of the body’s production of T4. This will have the effect of “clearing out” the tissues: T4, and therefore rT3 levels, will gradually fall off. How much T3 this takes, and how many cycles, depends on the level of excess there to begin with.

Does it work? This paper certainly suggests that it does!