|
|
The Iodine Group | |
|
Home | Orthoiodosupplementation | Body | Disease | Special | Overviews |
||
|
|
Abraham
The historical background of the iodine project.Abraham GE The Original Internist, 12(2):57-66, 2005
"Another factor involved in the increased demand for iodine is the presence of excessive amounts of goitrogens in the diet and from lifestyle. For example, smoking increases serum thiocyanate levels, interfering with the sodium/iodide symporter function. Sources of goitrogens are available from medical textbooks, although the halides fluoride and bromide are not listed as goitrogens. Fluoride interferes with the uptake of iodide by the thyroid gland symporter system, but it is itself not transported inside the thyrocyte, suggesting that fluoride causes oxidative damage to the halide-binding site of the symporter. The author previously discussed the goitrogenic effect of bromide even at low concentrations. Patients who used water from wells and municipal plants may be exposed to potassium perchlorate, a very powerful goitrogen that behaves like fluoride, binding to the halide-binding site of the symporter without itself being symported. A recent Internet publication by Kirk et al reported the presence of high concentrations of perchlorate in dairy milk sold in grocery stores and in human milk. The mean levels of perchlorate were 5 times higher in breast milk than dairy milk. Perchlorate has a selectivity factor of at least 30 over iodide. To compete effectively against this goitrogen, the peripheral concentration of inorganic iodide must be at least 100 times higher than the concentration of perchlorate. Kirk et al (16) observed that breast and dairy iodide levels were inversely correlated with the levels of perchlorate. Perchlorate and fluoride, due to their high redox potential, may cause oxidative damage to the halide binding site, decreasing its efficiency for iodide transport.
"If the pre-orthoiodosupplementation loading test report shows 90% or more of the ingested iodine in the 24 hr urine collection of patients on a Western diet, serum inorganic iodide levels are indicated to rule out an iodide transport defect or damage not just in the thyroid gland but throughout the whole body. In our experience, this is very rare and was observed in only 2 cases. The intestinal absorption of iodine/iodide involves a different mechanism than the uptake of iodide by target cells via the sodium/iodide symporter. For example, chloride competes with iodide in the intestinal tract but chloride has no detectable effect on the iodide symporter system. This explains why a patient with iodide transport damage is able to absorb iodine/iodide efficiently but unable to transfer peripheral iodine/iodide into the cells. Peripheral iodide is cleared very rapidly by the kidneys, resulting in quantitative recovery of ingested iodine/iodide in the urine in a patient who is very iodine-deficient, if the cellular transport system is defective. In those cases, serum inorganic iodide levels 24 hrs after the loading test will be low, even though the loading test suggests whole body sufficiency for iodine. In two obese female patients with poor clinical response to orthoiodosupplementation, high urinary iodide excretion was associated with serum inorganic iodide levels below 10-6M (0.13 mg/L). The expected serum levels associated with high urinary iodide excretion should be between 5 × 10-6M to 10-5M.
"Although congenital hypothyroidism due to sodium/iodide symporter defect is extremely rare, milder forms of iodine/iodide transport defect/damage throughout the whole body may be more common and undetected. As of 1997, only 38 cases of congenital hypothyroidism due to sodium/iodide symporter defect were reported. Of interest is that in one of these cases, a male Japanese subject, the diagnosis was not made until he was 30 years old. At the time of evaluation, he was euthyroid with a goiter, while on the high iodine Japanese diet. But he became hypothyroidism on a Western diet. Administration of 50 mg iodide restored euthyroidism. An active transport system for iodide by a sodium/iodide symporter has been demonstrated in several organs beside the thyroid gland, capable of concentrating peripheral inorganic iodide 20-40 fold against a gradient. The cellular uptake of iodide in some tissues may involve other mechanisms than the symporter system. Inorganic iodine/iodide has been detected in every organ and tissue examined, with relatively high levels in the thyroid gland, liver, lung, heart and adrenal glands. The highest quantity of iodine was found in fat tissue and muscle. Exposure to fluoride and perchlorate can cause oxidative damage to the halide binding site of the sodium/iodide symport system, due to their high redox potential. In such cases, more than 50 mg iodine/day may be required to overcome the low efficiency of the iodine transport system."
|
|
Home | Orthoiodosupplementation | Body | Disease | Special Topics | OverviewsThe Iodine Group | Books | Disclaimers | Contact Us | Search
|
||
