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T4 Or T3?

T4 Or T3?

Let us consider the case of a perfectly healthy (no symptoms of any kind), 35-year-old woman who suddenly develops classic signs and symptoms of DTSF due to hypothyroidism (low thyroid gland function), demonstrated with blood tests showing T4 levels below the lower limits of normal and TSH levels being above the upper limits of normal. The patient is started on T4 therapy (the treatment of choice for decreased gland function) with many of her symptoms improving and many of the symptoms resolving completely. The T4 therapy is used to return the blood test levels to their normal ranges in the hopes of eliminating all of her symptoms completely. Unfortunately, even upon normalization of the blood test levels, and even after months and years of T4 therapy, the symptoms of DTSF, which first appeared with the development of her hypothyroidism, are still not resolved completely and the patient’s function still remains quite unsatisfactory. The symptoms persist, even after T4 therapy has been used to correct the T4 and TSH blood test levels to within normal limits. So the T4 therapy might replace the T4 that the body is not producing in sufficient levels to bring the T4 level on the blood test back up within the normal range, and satisfy the pituitary gland resulting in normalization of TSH test levels, but the patient may still have symptoms of DTSF. So blood tests aren’t always extremely predictive in how well a patient is going to feel with treatment and how well the thyroid system will be returned back to normal. The reason for this is obvious, because, again, where the “rubber meets the road” in the thyroid system, is not in the pituitary gland, nor the thyroid gland, nor the blood stream, but at the level of the thyroid hormone/ thyroid hormone receptor interaction at the level of the nuclear membrane of the body’s cells.

Therefore, just because circulating raw material (T4) levels have been changed through the use of T4 supplementation to the satisfying of the pituitary and thyroid hormone blood tests does not necessarily mean that adequate levels of T3 are being provided to the active site of the thyroid system. To think so is a little like thinking that one can tell how fast a car is traveling based on how far down the gas pedal is pressed. The pedal may be pressed down, but whether a car is traveling 55 MPH depends also on how well the engine is combusting the fuel, what gear the car is in, and whether it is going up or down hill. Some cars cannot travel 55 MPH no matter how far down the gas pedal is pushed. So a patient can have normal blood tests all day long and still have classic signs and symptoms of Wilson’s Temperature Syndrome or DTSF.

This explains some blood test abnormalities and responses to treatment which many people apparently think are not possible. For example, it is commonly thought that elevated T4 levels and low TSH levels necessarily indicate excessive thyroid system function. Most people think that such blood test findings should correlate well with symptoms of hyperthyroidism (excessive thyroid gland function). However, I have seen patients with elevated T4 levels and low TSH levels who showed the classic signs, symptoms, and presentation of Wilson’s Temperature Syndrome, and whose symptoms of Wilson’s Temperature Syndrome or DTSF resolved quickly and easily with the WT3 protocol. This situation can be seen in both patients who are on no thyroid medication and, especially in patients who are being treated with T4 therapy prior to presentation. In fact, many times patients will come to my office being treated with T4 medicine with T4 levels being above normal in the 15 to 18 range, when the normal range is between 4 to 12. They also sometimes have exceptionally low TSH levels (thyroid stimulating hormone) indicating almost complete suppression of their pituitary gland and, therefore, their own thyroid gland function by the T4 medication they are being given by mouth. Such blood test findings would usually lead a doctor to conclude that if the patient is having any complaints that they necessarily would be due to hyperthyroidism. But sometimes these patients have classic signs and symptoms of decreased thyroid system function and respond very well to weaning the patient’s excessively high T4 supplementation and to the administration of the WT3 protocol. So even though the patients have more than enough T4 floating around in their blood stream according to their blood test levels, they may still lack sufficient levels of the active thyroid hormone at the level of the nuclear membrane of the cells due to impaired T4 to T3 conversion.

Actually, impaired T4 to T3 conversion can be made worse with T4 therapy. If a patient cannot convert the T4 produced by their own body very well, then it is likely that they will not be able to convert effectively T4 given by mouth. In such cases, T4 can actually feed the vicious cycle which leads to Wilson’s Syndrome. That is, if more T4 is given to the body and that T4 cannot be properly converted to T3 either, then more T4 will be shunted towards RT3 which may result in further competitive inhibition of the enzyme 5′-deiodinase, leading to further T4 to T3 conversion impairment. In fact, some of the most severe derangements of the thyroid system that I have seen are in patients who seem to have been pushed too far in the wrong direction with the wrong thyroid hormone medicine, namely T4. The RT3 levels are frequently more elevated in these cases than in other cases of Wilson’s Temperature Syndrome. Frequently, these patients will also have the highest RT3/T3 ratio. So non-judicious use of thyroid hormone supplementation may feed the vicious cycle of Wilson’s Temperature Syndrome rather than reverse it.

I’m not saying that T4 medication is not sometimes a preferable and excellent method of treatment. I’m just saying that it is not always the treatment of choice. And, in every case the choice of thyroid hormone medication, how it is started, how it is adjusted, how it is monitored, and whether or not it should be changed, depends on the underlying cause of the patient’s DTSF.