Part 11 of 11
This is part 11 of the series and continues the explanation of why we have a major “Iodine Crisis.”
Vit A (retinoic acid) is involved in several Iodine related functions. VAD (vitamin A deficiency) and Iodine deficiency often coexist, the effects are more pronounced than if just Iodine is deficient. Concurrent deficiencies of these two nutrients is estimated to affect over 30% of the global population. VAD alone has multiple negative effects on the pituitary-thyroid axis as Vitamin A status modulates thyroid gland metabolism, peripheral metabolism of thyroid hormone, and production of Thyrotropin (aka TSH) by the pituitary.
Concurrent VAD & Iodine deficiency produce more severe primary hypothyroidism than Iodine deficiency alone.
Selenium: Selenium is needed for the metabolism of thyroid hormone including for the enzyme that deiodinizes T4 to T3 (the relatively inactive form of thyroid hormone to the active form). Combined selenium and iodine deficiency leads to myxedematous cretinism. (Myxedematous cretinism is considered to result from iodine deficiency and hypothyroidism in the fetus during late pregnancy or in the neonatal period, resulting in mental retardation, short stature, goiter, and hypothyroidism.)
The normal thyroid gland retains high selenium concentrations even under conditions of inadequate selenium supply and is therefore able to continue expressing many of the known selenocysteine-containing proteins (including glutathione peroxidase, deiodinase, and thioredoxine reductase families of enzymes). Obviously, for the thyroid to be able to maintain adequate levels of selenium in spite of inadequate overall intake, it must ‘rob Peter to pay Paul,’ i.e., it has to take it from other tissues that also need it.
Adequate selenium supports efficient thyroid hormone synthesis and metabolism while protecting the thyroid gland from damage by excessive iodide exposure (this latter part is rarely needed as the vast majority of the planet’s people have iodine deficiency). It has been shown that in regions of combined severe iodine and selenium deficiency, normalization of iodine supply is mandatory before initiation of selenium supplementation to prevent hypothyroidism. Both deficiencies appear to be quite common in both developing and industrialized societies.
Iron: Iron deficiency impairs thyroid hormone synthesis by reducing activity of the heme-dependent thyroid peroxidase enzyme. Iron-deficiency anemia blunts and iron supplementation improves the efficacy of iodine supplementation. There are complex relationships between the relative amounts of iron and iodine that are still not well understood. Much more research is needed to gain a better grasp of this complex interaction.
Zinc: Zinc is second only to magnesium in the number of enzymes it plays a key role in. Estimates of the number of enzymatic reactions that involve zinc are between 200-300 different reactions. With all of those processes, it is easy to see how zinc status can impact virtually any and every cell and tissue in the body.
It is well established that zinc plays several roles in relation to iodine and the thyroid gland. Here are a few of those interactions: 1. Adequate zinc levels are positively correlated with free T3 levels (the active form of thyroid hormone). 2. Low zinc is correlated with increased TSH (thyroid stimulating hormone), increased thyroid volume (goiter), and decreased thyroid function (hypothyroidism). 3. Thyroid hormones are essential for the absorption of zinc, therefore, hypothyroidism can result in acquired zinc deficiency (thus a vicious cycle). 4. Zinc replenishment is required to reverse the hair loss associated with hypothyroidism.
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