Why Thyroid Hormone Replacement is inadequate in many patients with  hypothyroidism? This is why. The usual treatment approach for hypothyroidism recommends treating every hypothyroid patient with one approach: Give T4 (Levothyroxine, brand names Synthroid, Levoxyl, Unithroid, Levothroid). We can call it the T4-only hypothesis.

There are a lot of  problems with this T4-only hypothesis. Often, it does not truly take care of symptoms, because the approach itself is suboptimal and unscientific. Why?

1. There are various Causes of hypothyroidism:

There are various causes of hypothyroidism.. Therefore, one-size-fits-all is obviously an unscientific approach. Like other medical conditions, every person with hypothyroidism needs a individualized and not a monolithic, computerized approach.

2. T3 – and not T4 – is the Active thyroid Hormone:

T4-alone hypothesis aims to replenish low T4-state, while hypothyroidism is caused by low T3-state. The scientific fact: T4, even Free T4, does not carry out thyroid function inside the cell. It is simply a substrate for the formation of T3 in the tissues. Then, T3 binds to the Thyroid Hormone Receptor (THR), located inside the nucleus of the cells, and carries out the thyroid hormone action. In the nucleus, all you see is T3 and no That’s why T3 and not T4 is the true Active Thyroid hormone.

3. Presumption That T4 will Convert to T3 is Unscientific:

T4-alone hypothesis makes a big presumption that T4 to T3 conversion proceeds normally in the peripheral tissues, in every individual, without even checking if it really is the case. Very unscientific, isn’t it?!

4. T4 to T3 Conversion Varies from Person to Person:

The scientific fact is that T4 to T3 conversion in the peripheral tissues depends on the normal functioning of an enzyme called Type 1 Deiodinase. It may function normally is a young healthy person. But it often does not function normally in most individuals who have hypothyroidism. Most hypothyroid patients are overweight/obese, which is a condition of elevated Cytokines – substances produced by the immune cells. These cytokines interfere with Type 1 Deiodinase. Hence, T4 to t3 conversion does not take place properly. A  variety of other common conditions, such as stress, aging, diabetes, nutritional issues and certain medications including beta-blockers and steroids can impair Type 1 Deiodinase. Subsequently T4 to t3 conversion goes down.

5.  Normal Thyroid Gland Produces T3:

In normal individuals, about 20% of the daily production of T3 comes from the Thyroid gland itself and about 80% from the peripheral conversion of T4 to T3. Obviously, the T4-only hypothesis does not take into account this very basic scientific fact.

6. TSH can be Incorrect as a Monitoring Test of Thyroid Hormone Replacement:

T4-alone hypothesis recommends simply following serum TSH as the gold standard for the adequacy of thyroid hormone replacement, which can be an incorrect and misleading approach in a lot of individuals. Why? The scientific fact is that TSH production in the pituitary gland depends upon normal functioning of the pituitary gland as well as normal functioning of an enzyme called Type 2 Deiodinase, which is responsible for the T4 to T3 conversion inside the pituitary gland. It is this T3 production inside the pituitary that is the main regulator of TSH production. In a lot of hypothyroid individuals, peripheral conversion of T4 to T3 is low due to sub-optimally functioning Type 1 Deiodinase. But their Type 2 Deiodinase functions normally, producing adequate amounts of T3 from T4 inside the Pituitary. Subsequently, TSH production is normal in these individuals, while their peripheral tissues are hypothyroid. In other words, your pituitary is normal, but your peripheral tissues are actually hypothyroid. In this way, the current T4-only therapy treats the pituitary test (TSH) and not the patient and their hypothyroidism in the peripheral tissues.

7.  A Low TSH Does Not Always Means Too Much Thyroid Hormone:

Sometimes, even the Pituitary gland is not working normally for a variety of reasons, and does not produce adequate amounts of TSH even when a patient is clearly hypothyroid. This can utterly confuse most physicians who have the mind-set that a low TSH always means too much thyroid hormone. Consequently, the physician may even decrease the dose of the patients’ thyroid hormone, thus making the poor patient even more hypothyroid.

8. T4- Only Therapy May Actually Worsen T3 Level:

Normally, a low Free T4 due to primary hypothyroidism leads to decreased production of intra-thyroidal T3, which causes an increase in TSH production, which, in turn, causes an increase secretion of T3 from the thyroid gland. However, when such a person is given T4-only therapy to normalize their TSH, their TSH-stimulated increase in T3 secretion goes away. Net effect is a decrease in total circulating T3 level and ongoing hypothyroidism. So the patient actually feels worse after they get placed on T4-only therapy, although their physician is satisfied because their TSH is now normal. I have heard so many hypothyroid patients say that their “life has gone downhill” ever since they were placed on Levothyroxine (Synthroid, Levoxyl).

9. Keep Increasing The Dose Of Levothyroxine (T-4) May Be Counterproductive:

In order to treat a patient’s symptoms, physicians usually keep increasing the dose of Levothyroxine (T-4) to the point that the serum T4 level gets close to the upper limit. However, the patient continues to suffer from symptoms of hypothyroidism, which may even get worse. Obviously, this frustrates both the patient and the physician.

Why do your symptoms of hypothyroidism fail to improve or even get worse when you are on a high dose of T4-only treatment?  Because Type 2 Deiodinase not only converts T4 to T3 inside your pituitary, but is also responsible for T4 to T3 conversion in the brain and the hypothalamus. Now consider this. Your appetite center is located inside the hypothalamus. Due to a high level of T3 inside your hypothalamus, your appetite may get into turbo charge, causing you to gain more weight. In addition, a high level of T3 inside your brain can lead to anxiety and insomnia, which leads to day-time fatigue and somnolence.

Well, now you understand “Why The Usual Approach To Treat Hypothyroidism Is Suboptimal” in many patients with Hypothyroidism. You also realize you have to understand hypothyroidism in- depth in order to take care of your hypothyroidism – and your health.

To learn more, please refer to my book, ” Hypothyroidism And Hashimoto’s thyroiditis” available at Amazon.