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Abraham
The safe and effective implementation of orthoiodosupplementation in medical practice.Abraham GE The Original Internist, 11:17-36, 2004
"We have incorporated a total nutritional program with orthoiodosupplementation, emphasizing magnesium instead of calcium (discussed further in Section VII). The effect of this nutritional program with orthoiodosupplementation on thyroid function tests in a 40-years-old female patient with severe hyperthyroidism is displayed in Table 3.
"She was a classic case of Graves' disease with exophthalmia. After researching the medical literature, she refused treatment with radioiodides, goitrogens and surgery. She was placed on the nutritional program, including 1,200 mg of magnesium/day for one month prior to iodine supplementation, followed by the same program with the addition of 12.5 mg elemental iodine (1 tablet Iodoral®) daily afterward...."
"We would like to propose a mechanism for the oxidative damage caused by low levels of iodide supply to the thyroid gland, aggravated by goitrogens, activates the thyroid peroxydase (TPO) system through elevated TSH, low levels of iodinated lipids, and high cytosolic free calcium, resulting in excess production of H2O2 production is evidenced by the fact that antioxidants used in Bagchi's experiments did not interfere with the oxidation and organification of iodide and therefore neutralized only the excess oxidant. This H2O2 production is above normal due to a deficient feed back system caused by high cytosolic calcium resulting from magnesium deficiency and low levels of iodinated lipids which requires for their synthesis iodide levels two orders of magnitude greater than the RDA for iodine. Once the low iodide supply is depleted, TPO in the presence of H2O2 and organic substrate reverts to its peroxydase function which is the primary function of haloperoxydases, causing oxidative damage to molecules nearest to the site of action: TPO and the substrate thyroglobulin (Tg). Oxydized TPO and Tg elicit an autoimmune reaction with production of antibodies against these altered proteins with subsequent damage to the apical membrane of the thyroid cells, resulting in the lymphocytic infiltration and in the clinical manifestations of Hashimoto's thyroiditis. In laboratory animals prone to autoimmune thyroiditis, the genetic defect may be in the production of H2O2 in excess of what is needed.
"The iodination of thyrosine residues by TPO requires the presence of Tg, H2O2 and iodide. The supply of H2O2 comes from the NADPH oxydase system. This system is inhibited by certain iodinated lipids and is enhanced by cytosolic free calcium Ca++. The equation for organification of iodide by TPO is displayed in Figure 1, together with the feedback system controlling the production of H2O2. The logical deduction from this equation is that increased cytosolic free calcium will cause an excess of H2O2. Increased levels of iodinated lipids, on the other hand, would limit the production of iodinated lipids? In 1976, Rabinovitch, et al reported their results regarding the effect of three levels of iodide supplementation on the production of iodinated lipids in the thyroid glands of dogs: low iodide diet, normal iodide diet, and high iodine diet. The dogs were kept on those diets for six weeks. Iodinated lipids in the plasma membrane and in the cell total lipids were observed only in the dogs receiving the high iodide diet. What about human subjects? In 1994, Dugrillon, et al reported for the first time the presence of 5-hydroxy-6-iodo-8,11,14-eicosatrienoic delta lactone (delta iodolactone) in a human thyroid, following the ingestion of 15 mg iodide/day for 10 days in the host. It was the first time this biologically active iodolipid was isolated from human thyroid glands. The amount of iodide the host received was 100 times the RDA, but it is the amount of iodine/iodide we recommended for orthoiodosupplementation. Dugrillon, et al stated, "These results demonstrate for the first time that delta-iodo-lactone is present in iodide-treated human thyroid."
"Magnesium deficiency, which is prevalent in the US population, results in increased levels of cytosolic free calcium. Intracellular free calcium levels above the normal range are cytotoxic causing calcification of mitochondria and cell death. The cell membrane possesses an ATP-dependant calcium pump that keeps intracellular levels of free ionized calcium within narrow limits. This calcium pump is magnesium-dependent for normal function. Magnesium deficiency results in a defective calcium pump and intracellular accumulation of ionized calcium. Inadequate iodine/iodide intake below orthoiodosupplementation results in decreased levels of delta-iodo-lactone.
"Combined magnesium and iodine/iodide deficiency based on the concept of orthoiodosupplementation are the basic factors involved in the oxidative damage caused by excess H2O2 and reactive oxygen species.
"If this proposed mechanism is valid, orthoiodosupplementation, combined with magnesium intake between 800-1,200 mg/day, a daily amount this author recommended 21 years ago for magnesium sufficiency, should reverse autoimmune thyroiditis. This nutritional approach is also effective in Graves' autoimmune thyroiditis as previously discussed."
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