Renew the paradigm of thyroid therapy

The TSH-centered paradigm is like the old Ptolemaic or Geocentric model of the universe that put Earth at the center.

Science has already corrected that incorrect model of the solar system and universe.

Likewise, science has already given us enough evidence that the TSH-centric model is incorrect in the sense that it excludes so much that’s important and distorts the emphasis.

The correct model puts the T3 thyroid hormone at the center of the patient’s health.

Top 10 Reasons

Because Low T3 is hypothyroidism according to your body’s cells, organs and tissues.  This reason alone is sufficient. One does not need all the reasons below in order to move T3 to the center of the thyroid hormone model. Providing adequate supply of T3 to all cells and tissues should be the #1 priority of any thyroid hormone therapy strategy, no matter how mild or extreme the patient’s hypothyroidism is.

Because TSH is the secretion of a very selfish gland that cares more about T4 than T3. Excess TSH above the reference range is a side effect only when your pituitary gland notices that T4 has dropped far below the supply it needs to convert into sufficient T3 within its own tissues. At that point, most of your organs have been hypothyroid for a while already. In addition, the pituitary gland will not respond to Low T3 in bloodstream as long as T4 is sufficient for its own needs. The pituitary gland can convert T4 to T3 at a higher rate than most other glands, so it can be completely blind to the rest of your body experiencing a T3-specific deficiency.

Because TSH assumes you still have a healthy thyroid to stimulate. Thyroid patients no longer have a healthy gland for Thyroid Stimulating Hormone to stimulate. To the degree that our thyroid gland is absent or does not work anymore, TSH has lost its biological function.

Because thyroid medications distort “normal” TSH-T4-T3 relationships. All sorts of T3:T4 ratios are possible in patients on the full range of thyroid hormone medications, and TSH does not know what to make of these ratios. These aberrations rarely occur in nature, and some are only found in thyroid hormone therapy. See All thyroid therapy is artificial

Because TSH is oversensitive to oral dosing with T3 hormone, including NDT (desiccated thyroid). On these medications, acceptable doses will push TSH lower than is normal, and this often results in doctors keeping the patient very underdosed only to keep TSH “normal.” In some patients, TSH can be completely suppressed even when there is very obviously not enough T3 or T4 in bloodstream and clear signs and symptoms of hypothyroidism. See Rationale: L-T3 dosing effects

Because TSH levels are inappropriately high, low, or normal in many common conditions (the effects of all of these are discussed in Chatzitomaris et al, 2017)

• Fetal life
• Starvation
• Exhausting exercise
• Endurance exercise
• Adaptation to cold
• Depression
• Acute psychosis
• Post-traumatic stress disorder PTSD
• “Non-thyroidal” illness (a state of critical illness in which T3 levels drop very low, low enough to kill a person, but TSH does not rise.)
• Pregnancy
• Obesity

Because a wide variety of common drugs can significantly manipulate TSH levels.  (See a discussion of these in Haugen, 2009.)

• Glucocorticosteroids (such as Prednisone, used as an anti-inflammatory)
• Estrogen-containing drugs (including some birth control pills)
• Dopamine agonists (used to treat ADHD, Parkinson’s Disease, etc. See a list of dopamine agonists),
• Somatostatin analogs (used to treat bleeding and tumours, etc. see a list)
• Rexinoids (drugs based on Vitamin A, and drugs used to treat cancers. See a list.)
• Carbemazepine/Oxcarbemazepine (used to treat neuropathic pain, schizophrenia, bipolar disorder etc. See Wikipedia: Carbemazepine)
• Metformin (for Type 2 Diabetes and Polycystic Ovarian Syndrome PCOS)
• Metyrapone (for Adrenal Insufficiency. See Wikipedia: Metyrapone)

Because of TSH -receptor stimulating antibodies. TSH can be artificially lowered if Graves’ disease antibodies are still present in a patient who is hypothyroid after medical treatment and is now on thyroid therapy.

Because of TSH-receptor blocking antibodies. TSH can be artificially raised and may vary without relationship to thyroid hormone levels if the hypothyroid patient has fluctuating levels of TSH-receptor blocking antibodies. These antibodies are the primary cause of autoimmune Atrophic thyroiditis, a hypothyroid variant of Graves’ disease that is often misdiagnosed as Hashimoto’s thyroiditis. These patients often have an extremely high TSH (>100) before beginning hormone therapy.

Because TSH hormone level is not the “cause” of any diseases. Many population-wide studies have used TSH alone as a convenient variable. These studies then associate TSH levels with disease, showing that TSH is a risk factor. Association is not causation. TSH achieves its indirect relationship to disease by means of its role in the secretion and conversion of T4 and T3.  The association between TSH and diseases can easily break down due to any one of the factors listed above. See Rationale: Low TSH vs. true hyperthyroidism

We urge you…

Doctors and medical associations — give up on the outdated TSH-centric model, already! You should know by now that the T3 hormone is the Queen of all thyroid hormones.

TSH is a selfish, blind and crippled indicator of thyroid status.

Put TSH in its rightful place — it’s an ever-shifting moon, a variable indicator, which rotates around T4, the lesser hormone, as its center-point.

Tania S. Smith