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HYPOTHYROIDISM THEORY

Hypothyroidism is usually the result of either too little thyroid hormone, T4, being produced or from inadequate conversion of T4 to T3, which is the hormone the cells use. For most people, hypothyroidism is the result of an inadequate supply of nutrients needed to make the thyroid hormone. However, hypothyroidism can also result from damage to the thyroid from radiation (RAI treatment for hyperthyroidism) or surgical removal of part of the thyroid gland. 

Most people who think that they have no thyroid actually have some of their thyroid left. Here is one way to judge approximately how much of your thyroid function you have left. An intact thyroid produces about 300 mcg of thyroid hormone. If you are taking 100 mcg of Synthroid then your thyroid gland is producing two thirds of the hormone you need. If you are taking 200 mcg, then it's producing only one third. If you are taking 300 mcg, then your thyroid function is at or close to zero.

If your thyroid has some function, then by providing the proper nutrients you should be able to increase the amount of T3 that it can produce. Shortages of iodine, iron, zinc, manganese, cobalt, chromium, copper, and other nutrients may cause your thyroid production to be low. If most of your thyroid has been removed, you might have only one third of its normal capacity but you may be able to increase that to half or two thirds through supplementation. Therefore if you are taking supplements, you have to be aware that your thyroid may increase production and you may have to decrease the amount of replacement hormone you are taking.

The next factor to consider is how much of your total T4 (what your thyroid produces plus the replacement hormone you are taking) is converted to T3, which is the cellularly active hormone. This conversion depends upon a selenium enzyme and there may be other minerals, like zinc, involved in this process.

Also you need to consider the effect of the T3 on the cells. This is apparently increased by the calcium/magnesium ratio (more calcium: more effect), and perhaps by potassium and other minerals.

Lastly you need to look at how fast the T3 is deactivated by either deamination or conversion to T2. Selenium may be involved in this process, but copper seems to be the critical mineral in this stage. Copper is necessary to form the monoamine and diamine oxidases that break down T3 after use. If copper is in short supply, T3 can stay in circulation longer than normal resulting in hyperthyroidism.