HYPOXIA #27: WHY SEAFOOD AND SUNLIGHT RAISE OXYGEN in tissues

Thyroid function is like a relay race, with hormones passing the baton from the hypothalamus in the brain to the pituitary gland beneath it, then to the thyroid gland, to the liver, and finally to cells throughout the body.

The hypothalamus delivers messages to the pituitary gland via the chemical messenger thyrotropin releasing hormone (TRH). Once TRH delivers its message, the pituitary gland releases thyroid stimulating hormone (TSH).

TSH goes straight to the thyroid gland where it triggers the production of a protein called thyroglobulin. The thyroglobulin joins up with four molecules of iodine to produce the thyroid hormone T4, or thyroxine.

About 94 percent of the hormone made in the thyroid gland is T4. The remaining 6 percent is triiodothyronine (T3), named for its three molecules of iodine.

These thyroid hormones hitch a ride through the bloodstream on thyroid-binding proteins, during which they are referred to as “bound.” When they are dropped off at the cells for active duty, they are called “free” hormones.

Although the thyroid gland secretes only a little T3, it is the most active form the body can use. T4 must be converted to T3 before the body can use it. Most of this conversion happens in the liver, but also take place in cells of the heart, muscle, gut, and nerves. These cells convert T4 to T3 with an enzyme called tetraidothyronine 5’ deiodinase, which removes one molecule of iodine.

In the end, only about 60 percent of T4 is converted into usable T3. Twenty percent becomes reverse T3 (rT3), an inactive form the body cannot use. Levels of rT3 can become too high in times of major trauma, surgery, or severe chronic illness. Another 20 percent of T4 can be converted to T3 by healthy gut bacteria in the digestive tract.

HOW DOES ALTERED T3 LEAD TO HYPOXIA IN ILLNESS?  

A key discovery during the coronavirus H1N1 pandemic of 2009, ... victims’ lungs lacked T3, a thyroid hormone that would normally be detectable. T3 reduces inflammation and coaxes epithelial cells in the lungs to absorb fluids.   Since AM sunlight creates T3 the antiviral link of sunlight should now be apparent.  This can be seen in the pic below.

In non-thyroidal illness (NTI) plasma T3 is often decreased and plasma rT3 increased; plasma FT4 is still in the normal range depending on the severity of the disease. The changes in plasma T3 and rT3 are explained by a diminished conversion of T4 to T3 and of rT3 to 3,3-T2 by D1 in the liver.

Most plasma T3 is derived from the peripheral conversion of T4.  Viral diseases are known to act as mitochondrial toxins that can lower oxidative phosphorylation and subsequent ATP production.  This causes a relative pseudohypoxia to develop in the colony of mitochondria during a viral illness.

T3 increases mitochondrial ATP production in oxidative muscle despite increased expression of UCP2 and -3.  So a lack of T3 would exacerbate mitochondrial hypoxia in illness.  This is what we have seen clinically in C19 patients who became symptomatic.  Those with mitochondrial dysfunction before infection are at the highest risk of C19 sequela.  Their Vitamin D levels have acted as a predictive lab for clinicians because solar exposure is critical in making Vitamin D3 and T3 in humans photosynthetically.

Since H1N1 is an RNA virus that shows homology to SARS_CoV_2 #COVID19 it should be obvious why T3 drugs are now being tested clinically in high latitude cities in the USA where the sun has lost its power.

As solar power is lost what happens in mitochondria?  Oxygen tensions change, and this causes changes in energy production and alterations in ROS because dissolved oxygen in cells increase as ATP drops.  

Recall that ATP production is increased by exposure to red light.  Sunlight is 43% red light.  Here is another link of sunlight to energy production.  

Thyroid hormone is indispensable for the normal development and metabolism of most cells and tissues. Thyroid hormones are metabolized by different pathways: glucuronidation, sulfation, and deiodination, the latter being the most important. Three enzymes catalyzing deiodination have been identified, called type 1 (D1), type 2 (D2), and type 3 (D3) iodothyronine deiodinases. D1 and D2 have outer ring deiodinase activity, converting the prohormone T4 to its bioactive form T3 and degrading rT3 to 3,3’-T2. D3 has inner ring deiodinase activity and degrades T4 to rT3 and T3 to 3,3’-T2.

The most remarkable feature of all three iodothyronine deiodinase is that they are selenoproteins, i.e. they contain a selenocysteine (Sec) residue in the center of the amino acid sequence.  Seafood is loaded with selenoproteins.  It is also loaded with iodine.  This is why seafood is also another antihypoxic C19 strategy because it has a huge supply of selenium and iodine involved in T3 optimization to improve mitochondrial function.

D1 is largely expressed in the liver and kidney. Its main role is clearance of rT3 from the circulation and it also contributes to the production of plasma T3. D2 is importantly expressed in the central nervous system, pituitary, brown adipose tissue, and muscle and, generally, its expression reciprocally responds to changes in thyroid state. D2 serves to adapt cellular thyroid state to changing physiological needs. D3 is importantly expressed in fetal tissues and in adult brain tissue. In addition, D3 can be re-expressed under certain pathological conditions such as critical illness or in specific cancers and infectious diseases.

CITES:

https://www.startribune.com/hormone-boost-could-be-covid-19-key/572944532/

Bianco AC, Salvatore D, Gereben B, Berry MJ, Larsen PR. Biochemistry, cellular and molecular biology, and physiological roles of the iodothyronine selenodeiodinases. Endocr Rev. 2002 Feb;23(1):38-89.

Larsen PR, Zavacki AM. Role of the Iodothyronine Deiodinases in the Physiology and Pathophysiology of Thyroid Hormone Action. Eur Thyroid J. 2012.