In pregnant women who suffer from hypothyroidism, there is a four-time greater risk for miscarriage during the second trimester than in those who don't. Women with untreated thyroid deficiency are four-times more likely to have a child with a developmental disability and lower I.Q. Mercury blocks thyroid hormone production by occupying iodine-binding sites and inhibiting hormone action even when the measured thyroid levels appears to be in the proper range. There are several aspects of iodine deficiency and hypothyroidism-related effects on fetal and perinatal brain development that can be aggravated or otherwise affected by the presence of mercury. Mercury has the ability to reduce cerebellar brain weight through significant reductions in total cell population of the cerebellum. Reductions of total body weight at birth are related to maternal exposure to mercury. Lead and mercury also have a direct effect on neuronal development leading to learning deficits. These are the same type of birth defects produced by maternal iodine deficiency and hypothyroidism. Mercury can have a negative effect on both iodine and thyroid status. A pregnant woman with a mouthful of mercury amalgam fillings has a much greater chance of experiencing some degree of hypothyroidism and/or iodine deficiency during pregnancy than one without amalgam fillings.

Both the pituitary and the thyroid display an affinity for accumulating mercury. The enzymatic effects of mercury intoxication can be overcome by the administration of the thyroid hormone thyroxine. Through a feedback loop, the pituitary releases thyrotropin-releasing hormone, which in effect tells the thyroid how much thyroxine hormone to release into the blood. Mercury first stimulates and then suppresses the thyroid function. Chronic intake of mercury for more than ninety days results in signs of mercury poisoning, together with decreased uptake of iodine and depression of thyroid hormonal secretion. The thyroid and hypothalamus regulate body temperature and many metabolic processes including enzymatic processes that, when inhibited, result in higher dental decay. Mercury damage thus commonly results in poor body temperature control, in addition to many problems caused by hormonal imbalances such as depression. Such hormonal secretions are affected at levels of mercury exposure much lower than the acute toxicity effects normally tested. Mercury also damages the blood brain barrier and facilitates penetration of the brain by other toxic metals and substances. Hypothyroidism is also a major factor in cardiovascular disease.

The thyroid gland has four binding sites for iodine. When mercury attaches to one of these sites, the hormone activity is altered. There is a relationship between thyroid function and the nutritional status of folate, vitamin B12, and methionine. There is also a strong association between lowered zinc intake, lowered basal metabolic rate, lowered thyroid hormones and lowered protein utilization. Mercury affects the nutritional status of folate, vitamin B12, methionine, and zinc, as well as protein. The thyroid is one of the important glands influencing dental decay.

There is a fluid flow from the pulp chamber, through the dentin, through the enamel and into the mouth in people who have no dental decay. Thyroid is part of the endocrine function that controls the direction of this fluid flow. Low thyroid hormone production allows this fluid flow to run in the opposite direction--from the mouth, into the enamel, dentin, and pulp chamber. This fluid brings bacteria and debris from the mouth with it, leading to dental decay. When the teeth are susceptible to decay, the whole body is susceptible to degenerative disease. The thyroid is involved with maintenance of proper body temperature. Most mercury toxic patients have lower than optimum body temperatures. The most toxic persons may have temperatures as low as 96.2. When the amalgam fillings are removed, there is a trend for the temperature to approach 98.6, sometimes within 24 hours of removing all of the amalgams. The thyroid gland is controlled by the pituitary gland. When the thyroid is influenced by mercury, there is a high incidence of unexplained depression and anxiety. A person may have adequate levels of T3 and T4 hormones, but if the hormones are contaminated, the person is functionally thyroid deficient. Thyroid imbalances cause chronic conditions such as clogged arteries and chronic heart failure. People who test hypothyroid usually have significantly higher homocysteine and cholesterol--documented risk factors in heart disease.

Fifty percent of those also have high levels of homocysteine, and 90% are either hyperhomocystemic or hypercholesterolemic. The major regulator of adrenocortical growth and secretion activity is the pituitary hormone ACTH (adreno-cortico-tropic hormone). ACTH attaches to receptors on the surface of the adrenal cortical cell and activates an enzymatic action that ultimately produces cyclic adenosine monophosphate (cAMP). cAMP, in turn, serves as a co-factor in activating key enzymes in the adrenal cortex. The adrenal cortex is able to synthesize cholesterol and to also take it up from circulation. All steroid hormones produced by the adrenal glands are derived from cholesterol through a series of enzymatic actions, which are all stimulated initially by ACTH. Steroid biosynthesis involves the conversion of cholesterol to pregnenolone, which is then enzymatically transformed into the major biologically active corticosteroids. cAMP is produced from adenosine triphosphate (ATP) by the action of adenylate cyclase. Adenylate cyclase activity in the brain is inhibited by micromolar concentrations of lead, mercury, and cadmium. One of the key biochemical steps in the conversion of adrenal pregnenolone to cortisol and aldosterone involves an enzyme identified as 21-hydroxylase.

Mercury causes a defect in adrenal steroid biosynthesis by inhibiting the activity of 21a-hydroxylase. The consequences of this inhibition include lowered plasma levels of corticosterone and elevated concentrations of progesterone and dehydroepiandrosterone (DHEA). DHEA is an adrenal male hormone. Because patients with 21-hydroxylase deficiencies are incapable of synthesizing cortisol with normal efficiency, there's a compensatory rise in ACTH leading to adrenal hyperplasia and excessive excretion of 17a-hydroxyprogesterone, which, without the enzyme 21-hydroxylase, cannot be converted to cortisol. The inhibition of the 21-hydroxylase system may be the mechanism behind the mercury-induced adrenal hyperplasia. Adrenal hyperplasia can stress the adrenal glands by their accelerated activity to produce steroids to the point that production begins to diminish and the glands will atrophy. The result is a subnormal production of corticosteroids. Both lead and mercury can precipitate pathophysiological changes along the hypothalamus-pituitary-adrenal and gonadal axis that may seriously affect reproductive function, organs, and tissues. Leukocyte production, distribution, and function are markedly altered by glucocorticosteroid administration. In Addison's disease (hypofunction of adrenal glands), neutrophilia occurs 4-6 hours after administration of a single dose of hydrocortisone, prednisone, or dexamethasone. Neutrophilia is an increase in the number of neutrophils in the blood. Neutrophils are also called polymorphonuclear leukocytes (PMNs). Mercury not only causes a suppression of adrenocorticosteroids that would normally have stimulated an increase of PMNs, but at the same time also affect the ability of existing PMNs to perform immunity by inhibiting a reaction that destroys foreign substances.

Small amounts of corticoid sex hormones, both male and female, are also produced by the adrenal cortex. Two primary nutrients for the adrenal glands are pantothenic acid and vitamin C. A deficiency of pantothenic acid can lead to adrenal exhaustion (chronic fatigue) and ultimately to destruction of the adrenal glands. A deficiency of pantothenic acid also causes a progressive fall in the level of adrenal hormones produced. One of the largest tissue stores of vitamin C is the adrenals; it is exceeded only by the level of vitamin C in the pituitary.

Physical and mental stress increase the excretion of adrenocorticotropic hormone (ACTH) from the pituitary, which is the hormone that tells the adrenals to increase their activity. The increased adrenal activity, in turn, depletes both vitamin C and pantothenic acid from the glands. Humans cannot produce vitamin C. They therefore attempt to replenish the needs of the adrenals by taking the vitamin from other storage locations in the body. If your overall ascorbate status is low, there may be an insufficient amount available to satisfy the needs of the adrenals. Under this condition, normal adrenal hormone response may become inadequate, leading to an inadequate immune function.

Mercury builds up in the pituitary gland and depletes the adrenals of both pantothenic acid and vitamin C. Stress and the presence of mercury will have a very negative effect on the adrenal production of critical steroids. The ability of the adrenal gland to produce steroids is called steroidogenesis and is dependent upon reactions mediated by the enzyme cytochrome P-450. Cytochrome P-450 reacts with cholesterol to produce pregnenolone, which is then converted to progesterone. Cytochrome P-450 can then convert progesterone to deoxycorticosterone which is then converted to corticosterone or aldosterone by other enzymes in the adrenals. These adrenal functions are also affected by metal ions. Still today, the ADA and other governmental agencies tell us that the mercury in your mouth, or from vaccinations, is perfectly safe. Scientists say this is a ridiculous statement that is in violation of science and common sense.

Many of the known health effects of PBDEs are thought to stem from their ability to disrupt the body's thyroid hormone balance, by depressing levels of the T3 and T4 hormones important to metabolism. In adults, hypothyroidism can cause fatigue, depression, anxiety, unexplained weight gain, hair loss and low libido. This can lead to more serious problems if left untreated, but the consequences of depressed thyroid hormone levels on developing fetuses and infants can be devastating. One study, for instance, found that women whose levels of T4 measured in the lowest 10 percent of the population during the first trimester of pregnancy were more than 2.5 times as likely to have a child with an IQ of less than 85 (in the lowest 20 percent of the range of IQs) and five times as likely to have a child with an IQ of less than 70, meeting the diagnosis of "mild retardation." Even short-term exposures to commercial PBDE mixes or individual congeners can alter thyroid hormone levels in animals, and the effects are more profound in fetuses and offspring than in adults. These results aren't surprising, but are ominous as data in humans indicate that pregnancy itself stresses the thyroid, and developing fetuses and infants don't have the thyroid hormone reserves adults do to help buffer insults to the system.

Most studies on thyroid hormone disruption by PBDEs have been very short--with exposures of 14 days or less. The real question is how low doses over the long term affect the body's thyroid hormone balance. The answer is important, because the entire U.S. population is exposed daily to low levels of PBDEs, and studies of other thyroid hormone disrupters have found that long-term exposures can cause more serious harm at lower levels of exposure. Although no direct link could be made, one study found higher rates of hypothyroidism among workers exposed to brominated flame retardants on the job.

Similarly, selenium supplementation may be important, as those living in areas of the world where selenium is deficient have a greater incidence of thyroid disease. Of particular significance is the fact that while a selenium deficiency does not decrease the conversion of T4 to T3 in the thyroid or the pituitary, it does result in a great decrease in this conversion in the other cells of the body. People with a deficiency of selenium have elevated levels of T4 and TSH.

Supplementation with selenium results in a decrease in T4 and TSH and normalization of thyroid activity. Selenium is deficient in about 50% of people's diets, which, along with the high incidence of mercury toxicity, may account for the large number of people with low thyroid activity. Research demonstrates that a selenium deficiency results in low thyroid activity in the cells even though hormone levels are normal or even elevated,and provides some support for Barnes' contentions.

The normal range of basal temperature is between 97.8 and 98.2 degrees Fahrenheit, if there is no sinus or throat infection present. A reading below this normal range suggests low thyroid function. If it is above the normal range, one must be suspicious of some infection or an overactive thyroid gland. In women of menstruating years, because temperature can be elevated with ovulation, basal temperature is best measured on the second and third days of the period after flow starts. Before the menarche or after the menopause, the basal temperature may be taken on any day. When symptoms of thyroid deficiency are present, the basal temperature may be one, two, or even three degrees below normal. With thyroid therapy, the temperature will start to rise toward normal.