Reverse T3 and Reverse T3 Dominance
The thyroid gland is located in the lower part of the neck near your Adam’s Apple. It secretes two essential thyroid hormones: triiodothyronine (T3) and thyroxine (T4) which are responsible for regulating cell metabolism in every cell in your body. They promote optimal growth, development, function and maintenance of all body tissues. They are also critical for nervous, skeletal and reproductive tissue as well as regulating body temperature, heart rate, body weight and cholesterol.
In a healthy patient a normal thyroid gland secretes all of the circulating T4 (about 90 to 100mcg daily) and about 20% of the circulating T3. The T4 made by the thyroid gland circulates throughout the body and is converted by the 5-deiodinase enzymes Type 1 & 2 into T3 or via the 5-deiodinase Type 3 enzymes into reverse T3 in roughly equal amounts of T3. Most of the biological activity of thyroid hormones is due to T3. It has a higher affinity for thyroid receptors and is approximately 4 times more potent than T4. Because 80% of serum T3 is derived from T4 in tissues such as the liver and kidney, T4 is considered a pro-hormone. No receptors have ever been identified for T4. Normal physiological production ratio of T4 to T3 is 3.3:1.
Reverse T3 (rT3) is virtually inactive having only 1% the activity of T3 and being a T3 antagonist binds to T3 receptors blocking the action of T3 and thus acting as a metabolic break. Normal metabolism of T4 requires the production of the appropriate ratio, or balance, of T3 to rT3. If the proportion of rT3 dominates then it will antagonize T3 thus producing hypothyroid symptoms despite sufficient circulating levels of T4 and T3. Reverse T3 has the same molecular structure as T3 however its three dimensional arrangement (stereochemistry) of atoms is a mirror image of T3 and thus fits into the receptor upside down without causing a thyroid response and thus preventing or antagonizing the active T3 from binding to the receptor acting as a metabolic break.
Reverse T3 dominance, also known as Wilson’s Syndrome, is a condition that exhibits most hypothyroid symptoms although circulating levels of T3 and T4 are within normal test limits. The metabolism of T4 into rT3 is in excess when compared to T3 therefore it is a T4 metabolism malfunction rather than a straight forward thyroid deficiency. Periods of prolonged stress may cause an increase in cortisol levels as the adrenal glands respond to the stress. The high cortisol levels inhibit the 5-deiodinase enzyme Type 1 and thus the conversion of T4 into T3 thus reducing active T3 levels. The conversion of T4 is then shunted towards the production of the inactive rT3 via the 5-deiodinase enzyme Type 3. This rT3 dominance may persist even after the stress passes and cortisol levels have returned to normal as the rT3:T3 imbalance itself may also inhibit the 5-deiodinase enzyme Type 1 thus perpetuating the production of the inactive rT3 isomer. There is some argument to this last point with some research indicating that the elevated rT3 is only temporary and not a permanent condition and in most healthy people this may well be the case. We have however found that in many patients suffering from a range of hypothyroid symptoms do indeed have prolonged elevated rT3 levels which respond favorably to this treatment. Many medical practitioners do not accept rT3 dominance theory and thus many doctors will refuse to treat this condition despite the fact many suffers have been successfully treated. See below for the evidence in the references.
Other causes of reverse T3 dominance include: leptin resistance, inflammation (NF kappa-B), dieting, nutrient difficiencies such as low iron, selenium, zinc, chromium, Vit B6 and B12, Vit D and iodine, Low testosterone, low human growth hormone, Insulin dependent Diabetes, Pain, Stress, environmental toxins, Free radical load, Hemorrhagic shock, Liver disease, Kidney disease, Severe or systemic illness, severe injury, Surgery, Toxic metal exposure.
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