during pregnancy as cause of developmental delays, reduced IQs, and autism- the
mercury and toxic metal connection.
have documented that mercury causes hypothyroidism (50,84,390,407), damage of
Infants of women with hypothyroxinemia at 12 weeks' gestation had significantly lower scores on the Neonatal Behavioral Assessment Scale orientation index compared with subjects(10b). Regression analysis showed that first-trimester maternal free thyroid hormone T4 was a significant predictor of orientation scores. This study confirmed that maternal hypothyroxinemia constitutes a serious risk factor for neurodevelopmental difficulties that can be identified in neonates as young as 3 weeks of age.
Mercury (especially mercury vapor from dental amalgam or organic mercury) rapidly crosses the blood brain barrier and is stored preferentially in the pituitary gland, thyroid gland, hypothalamus, and occipital cortex in direct proportion to the number and extent of dental amalgam surfaces (14,19,85,99,273,274,407), and likewise rapidly crosses the placenta and accumulates in the fetus including the fetal brain and hormone glands at levels commonly higher than the level in the mother(20,22-27). Milk from mothers with 7 or more mercury amalgam dental fillings was found to have levels of mercury approximately 10 times that of amalgam free mothers(22b). The milk sampled ranged from 0.2 to 57 ug/L. In a population of German women, the concentration of mercury in early breast milk ranged from 0.2 to 20.3 ug/L (26). A Japanese study found that the average mercury level in samples tested increased 60% between 1980 and 1990. The study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening, but more so in the linguistic pathway(25). The level of mercury in umbilical cord blood, meconium, and placenta is usually higher than that in mother's blood[23-25].
The thyroid gland has iodine binding sites where the iodine needed for its function is obtained. For those with chronic mercury exposure the mercury occupies some of the iodine binding sites, blocking full utilization of iodine by the thyroid, in addition to the direct damage to the thyroid since mercury is highly cytotoxic (392,394,etc.).
Alterations of cortical neuronal migration and cerebellar Purkinje cells have been observed in autism. Neuronal migration, via reelin regulation, requires triiodothyronine (T3) produced by deiodination of thyroxine (T4) by fetal brain deiodinases(407). Experimental animal models have shown that transient intrauterine deficits of thyroid hormones (as brief as 3 days) result in permanent alterations of cerebral cortical architecture reminiscent of those observed in brains of patients with autism. Early maternal hypothyroxinemia resulting in low T3 in the fetal brain during the period of neuronal cell migration (weeks 8-12 of pregnancy) may produce morphological brain changes leading to autism. Insufficient dietary iodine intake and a number of environmental antithyroid and goitrogenic agents such as mercury, soy, and peanuts can affect maternal thyroid function during pregnancy. The thyroid gland has iodine binding sites where the iodine needed for its function is obtained. For those with chronic mercury exposure the mercury occupies some of the iodine binding sites, blocking full utilization of iodine by the thyroid, in addition to the direct damage to the thyroid since mercury is highly cytotoxic.
Mercury can have significant effects on thyroid function even though the main hormone levels remain in the normal range, so the usual thyroid tests are not adequate in such cases. Prenatal methylmercury exposure severely affects the activity of selenoenzymes, including glutathione peroxidase (GPx) and 5-iodothyronine deiodinases(5-Di and 5'-DI) in the fetal brain, even though thyroxine(T4) levels are normal(390de). Another mechanism by which mercury exerts such effects is mercury’s effects on selenium levels which are required for conversion of T4 to T3(392,390d). Gpx activity is severely inhibited, while 5-DI levels are decreased and 5'-DI increased in the fetal brain, similar to hypothyroidism. Thus normal thyroid tests will not pick up this condition.
Mercury reduces the bloods ability to transport oxygen to fetus and transport of essential nutrients including amino acids, glucose, magnesium, zinc, selenium and Vit B12 (43,96,198,263,264,338, 339,392,427); depresses enzyme isocitric dehydrogenase (ICD) in fetus, causes reduced iodine uptake, autoimmune thyroiditis, & hypothyroidism. (50,91,212,222,369,382,392,394,407,35). Minerals such as calcium, zinc, and manganese are also necessary for thyroid health and hormone production, and their absorption is blocked by mercury exposure. Because of the evidence of widespread effects on infants, the American Assoc. of Clinical Endocrinologists advises that all women considering becoming pregnant should get a serum thyrotropin test so that hypothyroidism can be diagnosed and treated early(558,7b). Since mercury and toxic metals are common causes of hypothyroidism, another test that should be considered is a hair element test for mercury or toxic metal exposures and essential mineral imbalances.
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