Thyroid Function & Selenium

• Thyroid function
The thyroid gland is actually a collection of individual glands (follicles). Here, newly synthesized hormone is secreted into a central lumen prior to release into the bloodstream. In general, thyroid hormones refer to T3 (triiodothyronine) and T4 (thyroxine). Though T4 is the main product, T3 is 3 to 4 times more active. T4 (with 4 atoms of iodine) is converted to T3 (with 3 atoms of iodine) via peripheral tissues, especially the liver and lung. Parafollicular thyroid cells secrete calcitonin, a hormone employed in calcium and phosphate homeostasis. Calcitonin inhibits bone breakdown and accelerates bone calcium and phosphate uptake. Blood
calcium levels control the secretion of calcitonin by a pathway independent of the pituitary gland.
• Thyroid hormones regulate metabolism and energy balance, as well as growth, development and activity of the nervous system (1). Thyroid hormones stimulate carbohydrate and fat breakdown, increase protein synthesis, and increase the basal metabolic rate.
• Several factors, including low metabolic rate, falling blood pressure, and conditions that increase the need for energy such as a cold environment, hypoglycemia, pregnancy or high altitude, stimulate the secretion of thyroid hormones.

Thyroid hormones regulate their production via feedback mechanisms on the hypothalamus/pituitary axis. Thyroxine completes a negative feedback loop by blocking the release of the trophic hormone thyrotropin releasing hormone (TRH). High blood levels of estrogens and androgens decrease TRH production and thus thyroid function. Aging generally decreases glandular processes, including thyroid function.

Thyroid hormone synthesis
An individual consumes up to 500 mcg of iodine per day. Fully one third is absorbed by the thyroid, where the synthesis of thyroid hormone begins, and the remainder is excreted. Iodine is oxidized by the thyroid to organic iodine via iodoperoxidase, an enzyme requiring hydrogen peroxide. The addition of iodine occurs at the 2,5 positions of tyrosine residues of thyroglobulin. Two di-iodotyrosine residues are coupled to form a thyroxine precursor on thyroglobulin. Secretion of thyroid hormones is initiated by the lysosomal degradation of thyroglobulin to release T3 and T4. In the bloodstream, T3 and T4 are carried by thyroxine-binding globulin, thyroxine binding prealbumin and serum albumin. It is the concentration of free (unbound) hormone that is important. T4 is converted to T3 and is taken up by appropriate target cells. Thyroid hormone is transported to the nucleus where it activates transcription. The actual thyroid hormone receptor is a chromosomal protein locked into the nucleus. Hormone binding activates the receptor as a transcription factor, resulting in the synthesis of multiple enzymes affecting metabolism. Thyroid hormone receptors also occur in mitochondria, so that thyroid hormones regulate oxygen consumption and ATP production directly. Brown fat-induced reactions to hypothermia are triggered by thyroid hormones.

Abnormal levels of thyroid hormones
Varying degrees of hypothyroid function are routinely detected by laboratory tests and other measures (2). Hypothyroidism is characterized by obesity, cold, dry skin and fatigue, while hyperthyroidism has opposite effects. Goiter and thyroid hyperplasia are consequences of abnormally low dietary iodine.

Nutritional support for the thyroid

Iodine
The common form of iodine in foods is iodide. This is the reduced form of iodine. In thyroid tissue, follicles normally concentrate iodide 40-fold greater than blood concentrations. At maximal activity, the thyroid can contain up to 300 fold greater concentration of iodide than blood levels. Cells oxidize iodide to organically bound iodine, which is then chemically combined with tyrosine. Kelp is a natural source of iodine.

Tyrosine
This amino acid is a protein building block. In particular, many of the tyrosine residues of thyroglobulin are iodinated. Each molecule of thyroid hormone contains the equivalent of two tyrosine molecules. The uptake of tyrosine decreases with age (3).

Minerals
• Selenium
This trace mineral in the form of selenocysteine is required by a family of antioxidant enzymes, the glutathione peroxidases. These enzymes reduce peroxidized fatty acids in membranes to safe by products. On the other hand, selenium is also required for iodothyronine de-iodinase, the enzyme located in peripheral tissues that is required to convert T4 to T3. Selenium deficiency decreases the iodothyronine de-iodinase activity. High iodine intake when selenium intake is low can lead to thyroid damage, because thyroid glutathione peroxidase
activity is reduced (4).

• Magnesium
Thyroid hormone is intimately associated with regulation of energy production and mitochondrial function. Indeed, mitochondria possess thyroid hormone receptors. Enzyme utilization of ATP generated by mitochondria requires complex formation with magnesium, generally in a 1:1 ratio. Magnesium is essential for protein synthesis, cell replication and activation of the sodium-potassium pump, as well as regulation of calcitonin and parathyroid hormone.

• Copper
Copper is a cofactor for the antioxidant enzyme, superoxide dismutase, and it is implicated in thyroid gland metabolism. Animal studies suggest that copper deficiency decreased hepatic mono-deiodinase (5), and that condition is associated with a reduction in T4 levels. Hormone reduction could be due to decreased T4 synthesis or to impaired T4 release (6).

• Manganese
This trace element can be considered an antioxidant because it is a cofactor for mitochondrial superoxide dismutase. Manganese complexes with ATP in certain energy requiring steps associated with carbohydrate metabolism. Very low manganese intake in lab animals retarded growth and thyroid hormone metabolism (7).
• Rubidium
A variety of anecdotal reports and case studies suggest that rubidium promotes thyroid metabolism. The mechanism is unknown.
• Tyrosinase
This is a copper-containing enzyme and belongs to the family of monophenol oxidases. Tyrosinase is implicated in tyrosine pathways.
• Vitamin A
Vitamin A is required for the normal development and maintenance of epithelial tissues. Both Vitamin A and thyroid hormone regulate gene expression, depending upon the organ (8). Furthermore, vitamin A supports the expression of receptors for thyroid and other hormones (9).

References
1. Surks MI, Fevert R. Drugs and Thyroid Function. New Engl J Med 1995; 333: 1688-1694.
2. Lindsay RS. Hypothyroidism. Lancet 1997; 346: 413-417.
3. Chen TS et al. Intestinal transport during the life span of the mouse. J. Gerantol 1990 45: B129- B133.
4. Hotz CS et al. Dietary iodine and selenium interact to affect thyroid hormone metabolism of rats. J Nutr 1997; 127: 1214-1218.
5. Kralik A et al. Concentrations of thyroid hormone in serum and activity of hepatic 5-monodeiodinase in copper-deficient rats. Z. Ernahrung Swiss 1996; 35: 288-291.
6. Allen DK et al. Function of pituitary-thyroid axis in copper-deficient rats. J Nutr 1982; 112: 2043-2046.
7. Eder K et al. The effect of manganese supply on thyroid hormone metabolism on the off span of manganese depleted dams. Biol Trace Elem Res 1996; 55: 137-145.
8. Shull JD et al. Cell-type specific interaction between retinoic acid and thyroid hormone in the regulation of expressing of the gene encoding ornithine amino transferase. Endocrinology 1995; 136: 2120-2126.
9. Coustaut M et al. The influence of dietary vitamin A in triiodothyronine, retinoic and glucocorticoid receptor in liver of hypothyroid rats. Br J Nutr 1996; 176: 295-306.
10. Christensen F. Glandulars: comparison of sources. Am Chiropractor 1985; September.

 

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