Mercury-Caused Endocrine Conditions Causing Widespread Adverse Health Effects,                                       Cognitive Effects, and Fertility Effects   B.Windham (Ed.)


I. Introduction.

As will be documented in this paper, the majority of the population receives significant mercury exposures and significant adverse health effects are common.  Mercury has been found to be an endocrine system disrupting chemical in animals and people, disrupting function of the pituitary gland, thyroid gland, parathyroid gland, thymus gland, adrenal gland, pineal gland, enzyme production processes, and affecting many hormonal and enzymatic functions at very low levels of exposure.  The main factors determining whether chronic conditions are induced by metals appear to be exposure and genetic susceptibility, which determines individual’s immune sensitivity and ability to detoxify metals (405).  Very low levels of exposure have been found to seriously affect large groups of individuals who are immune sensitive to toxic metals or have an inability to detoxify metals   due to such as deficient sulfoxidation or metallothionein function or other inhibited enzymatic processes related to detoxification or excretion of metals. Dental amalgam has been found to be the largest source of mercury in most people and includes methyl mercury since oral bacteria methylate mercury to methylmercury.   Toxic metal exposures are common, and they often have additive or synergistic adverse effects. 

        Thyroid conditions are extremely common and adversely affect the health of millions of people, though most cases are undiagnosed (580,581). The thyroid gland secretes hormones which control the body’s metabolic rate, using iodine to create thyroid hormone.  So, iodine deficiency is a common cause of hypothyroid condition (395).  The hypothalamus secretes a hormone which triggers thyroid-stimulating hormone (TSH) from the pituitary gland to cause the thyroid gland to produce thyryroxine (T4) and triiodothyronine (T3) (produces mostly T4). T4 is then converted in the body to the active thyroid hormone T3.  A problem with any of these steps can cause hypothyroidism. As will be seen, toxic metal exposures such as mercury can accumulate and block or inhibit any of these necessary processes, as can other factors. The hypothalamus also controls hormone secretions by the pituitary gland. Mercury has been found to commonly accumulate in the hypothalamus (303), affecting hormone secretions of the pituitary or thyroid gland and many bodily functions.  Calcitonin is another hormone secreted by the thyroid gland that maintains blood calcium levels and prevents hypercalcemia and which can be affected.  

        Effects and Symptoms of Thyroid Deficiency:  fatigue, nervousness, depression, increased allergies, cold sensitivity, skin problems, brittle nails, weight problems, constipation, infertility, memory problems, low immune function, carpal tunnel syndrome.  

Tests for thyroid deficiency (580)): Standard test is blood test for TSH level (concentrations chronically above 2.0 mU/L indicate thyroid problem and cause long term health effects). 

Another sensitive thyroid function test is the TRH stimulation test.  Another test is the Achilles tendon reflex test.  A good home test is the Barnes Basal Temperature Test (put a thermometer in reach of bed, before getting up take temperature under arm shoulder joint (holding tight for at least 3 minutes).  Below 97.8 degrees indicates you are T3 deficient. Repeat several times. 

        Hashimoto’s thyroiditis is chronic inflammation of thyroid caused by an autoimmune reaction to environmental factors such as mercury or toxic metals or gluten sensitivity or milk casein sensitivity (which is commonly caused by toxic metals blocking enzymatic process needed to digest gluten or milk casein). (seelater documentation) Thyroiditis is the most common thyroid condition (369).  Symptoms include weight gain, fatigue, constipation, dry hair, depression, joint and muscle pain, infertility and often increased cholesterol—and research indicates that it’s seven times more common in women than in men (1). It has been found that patients with AT and other autoimmune diseases, such as multiple sclerosis, psoriasis, systemic lupus erythematosus and atopic eczema, show increased lymphocyte reactivity in vitro to inorganic mercury, nickel and other metals compared to healthy controls. The important source of mercury is dental amalgam. Replacement of amalgam in mercury-allergic subjects resulted in improvement of health in about 70% of patients(369).

On the other end of the spectrum is Grave’s disease—marked by dangerously increased thyroid function (hyperthyroidism). Also, an autoimmune disorder, Grave’s disease results when your thyroid-stimulating antibodies begin to mimic thyroid-stimulating hormone—boosting your thyroid hormone production as a result. Thus, many of its symptoms—such as rapid heartbeat, heat intolerance, weight loss and frequent bowel movements—are opposite that of hypothyroidism. But like Hashimoto’s, women are also at significantly higher risk (4). 

        Other common hormone problems are related to the adrenal glands.  The adrenal medulla manufactures epinephrine and norepinephrine (adrenaline and noradrenaline) – the fight or flight hormones. Prolonged stress and anxiety commonly cause imbalances of these hormones, and also can be a factor in causing mercury to accumulate in the endocrine gland. Mercury tends to accumulate in body areas that are stressed or inflamed due to various factors (303).    The adrenal cortex makes steroid hormones (cortisone, hydrocortisone, testosterone, estrogen, DHEA, pregnenolone, aldosterone, androstenedrone, progesterone.  Some of these are also made in other parts of the body. The hormone aldosterone, together with the kidneys, regulates the balance of sodium and potassium in the body, which is commonly out of balance.  Mercury can accumulate in the adrenal gland and inhibit proper function of any of these hormones. Both mercury and stress commonly cause imbalances that result in adrenal fatigue, which is a factor in chronic fatigue (303)

        Besides imbalances of the various adrenal hormones that can cause effects, there are common chronic conditions that have been identified.  Addison’s Disease is chronic adrenal failure, usually related to autoimmune attack on the adrenal glands, commonly caused by toxic exposures such as mercury (see more later).  It usually results in chronic hypocortisolism, resulting in inability to properly deal with stress. This also affects blood pressure, insulin regulation, inflammatory response, and metabolism of proteins, carbohydrates, and fats. (580) Symptoms of Addison’s Disease include: skin changes such as dark tanning on scars, skin folds, toes, lips, elbows, knees, knuckles. 

Cushing’s Syndrome is overproduction of cortisol, usually related to tumor of pituitary or other organs.  It is also common caused by prescription drug effects of steroid hormones, etc. Symptoms include: stomach fat, thin extremities, moon face, buffalo hump, excessive hair growth, irregular menstrual periods, infertility. 

        Adrenal fatigue can be caused by chronic anxiety or stress, poor nutrition, toxic metal accumulation, etc. The adrenals can become depleted leading to fatigue, weakening of immune response, disrupted sugar metabolism, etc. (580) Environmental toxic exposure such as mercury can block or inhibit any of the adrenal hormone processes and contribute to such conditions.   


II. Common Exposures to Significant Levels of Mercury and Distribution in the Body


 Dental amalgam fillings have been documented to be the largest source of mercury in most people who have several amalgam fillings, and most people with several amalgam fillings get daily exposure of mercury at levels well above U.S. government health guidelines (16,19,20,49,199, 211,501) which amount to about 4 to 8 micrograms per day (217).  Mixed metals in the mouth such as amalgam dental fillings, metal crowns, and metal braces have been found to result in galvanic currents in the metals which drive the metals into the saliva and tissues of the oral cavity at high levels as well as systemically, with accumulations in the brain and hormonal glands (14,19,84,85,183,192,348,369, 381,500). Additionally, electric and electromagnetic fields from appliances, computer monitors, power lines, etc. cause electric currents in metals in the mouth which further increase exposures to mercury and other metals (28).   Mercury and nickel, which are highly neurotoxic (19,84,217,372, 500) and immunotoxic (181,91,114ab,380b,369,383ab,405), are often found at high levels in tests of those with mixed metals in the mouth and are known to commonly cause DNA damage(296,458,114), immune reactivity (234,330,331,342,369,375, 383,405,91), and hormonal effects in animals and humans (50,84,104,105,369,382,459), including related reproductive effects.  Government health agencies in other countries such as Health Canada and  amalgam manufacturers have warned against using amalgam near other metals(209,500), but this is still common in the U.S.  and several other countries.   Children typically also get high levels of exposure to highly toxic organic mercury compounds such as ethyl mercury through thimerosal, used as a preservative in vaccines (160,409,476,555), and to methyl mercury from fish(2). Warnings to ban or limit consumption of fish have been issued for over 30 percent of all U.S. lakes, including all Great Lakes, as well as U.S. river miles and bays(2).

A 2009 study found that inorganic mercury levels in women have been increasing rapidly in recent years(515). It used data from the U.S. Centers for Disease Control and Prevention’s National Health Nutrition Examination Survey (NHANES) finding that while inorganic mercury was detected in the blood of 2 percent of women aged 18 to 49 in the 1999-2000 NHANES survey, that level rose to 30 percent of women by 2005-2006.


Studies have documented that mercury causes hypothyroidism (50,84,390,392,407), damage of thyroid RNA(458), autoimmune thyroiditis (369,382,91), and impairment of conversion of thyroid T4 hormone to the active T3 form(369,382,390,392,407,50d). 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 (394,395), in addition to the direct damage to the thyroid since mercury is highly cytotoxic (392,394,500, etc.).  These studies and clinical experience indicate that mercury and toxic metal exposures appear to be the most common cause of hypothyroidism and the majority treated by metals detoxification recover or significantly improve (503,303).  

The estimated prevalence of hypothyroidism from a large federal health survey, NHANES III, was 4.6%, but the incidence was twice as high for women as for men and many with sub clinical hypothyroidism are not aware of their condition(3a).  Another large study(3b) found that 11.7% tested had abnormal thyroid TSH levels with 9.5% being hypothyroid and 2.1% hyperthyroid.  According to survey tests, 8 to 10 % of untreated women were found to have thyroid imbalances so the actual level of hypothyroidism is higher than commonly recognized (508).  Even larger percentages of women had elevated levels of antithyroglobulin(anti-TG) or antithyroid peroxidase antibody(anti-TP). Tests have found approx. 30% of pregnant women to have low free T4 in the first trimester(509b).     

Thyroid hormones are of primary importance for the perinatal development of the central nervous system, and for normal function of the adult brain (10a). Hypothyroidism of the adults causes most frequently dementia and depression.  Nearly all the hyperthyroid patients show minor psychiatric signs, and sometimes psychosis, dementia, confusion state, depression, apathetic thyrotoxicosis, thyrotoxic crisis, seizures, pyramidal signs, or chorea occur(10a). These hormones primarily regulate the transcription of specific target genes. They increase the cortical serotonergic neurotransmission, and play an important role in regulating central noradrenergic and GABA function. 

 Studies indicate that slight thyroid deficiency/imbalance(sub clinical) during the perinatal period can result in delayed neuropsychological development in neonate and child or permanent neuropsychiatric damage in the developing fetus or autism or mental retardation  (10,509,511).    Low first trimester levels of free T4 and positive levels of anti-TP antibodies in the mother during pregnancy have been found to result in significantly reduced IQs (509a-e) and causes psychomotor deficits(509f). Women with the highest levels of thyroid-stimulating-hormone(TSH) and lowest free levels of thyroxin 17 weeks into their pregnancies were significantly more likely to have children who tested at least one standard deviation below normal on an IQ test taken at age 8(509a).  Based on study findings, maternal hypothyroidism appears to play a role in at least 15% of children whose IQs are more than 1 standard deviation below the mean, millions of children. Overt autoimmune thyroiditis is preceded by a rise in levels of thyroid peroxidase antibodies. "Collectively, reports show that 30-60% of women positive for TPO antibodies in pregnancy develop postpartum thyroiditis," the researchers point out (561,8), calling it "a strong association." Without treatment, many of the women with thyroiditis  go on to develop overt clinical hypothyroidism as they age and, eventually, associated complications such as cardiovascular disease. About 7.5% of pregnant women develop thyroiditis after birth(8).  Studies have also established  a connection between maternal thyroid disease and babies born with heart defects(509h).  

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[25].   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].  


        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 (395).


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, 339,347,392,427); depresses enzyme isocitric dehydrogenase (ICD) in fetus, causes reduced iodine uptake, autoimmune thyroiditis,  & hypothyroidism. (50,91,212,222,369,382,394,407,459,35).  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. 



       Studies have also established a “clear association” between the presence of thyroid antibodies and spontaneous abortions(511).  Levels of recurrent abortions in a population with positive levels of thyroid antibodies in one study were 40%, 5 times the normal rate(511).  Hypothyroidism is a well documented risk factor in spontaneous abortions and infertility(9,511).    Another study of pregnant women who suffer from hypothyroidism (underactive thyroid) found a four-times greater  risk for miscarriage during the second trimester than those who don’t(511), and women with untreated thyroid deficiency were four-times more likely to have a child with a developmental disabilities(509f-h).  Mercury through its affects on the endocrine system is also documented to cause other reproductive effects including infertility, low sperm counts, abnormal sperm, endometriosis, PMS, adverse effects on reproductive organs, etc.  (9,50,104,105,390,500,559).  

Mercury blocks thyroid hormone production by occupying iodine binding sites and inhibiting hormone action even when the measured thyroid level appears to be in proper range(390,394,35).   The thyroid and hypothalamus regulate body temperature and many metabolic processes including enzymatic processes that when inhibited result in higher dental decay(35) . Mercury damage thus commonly results in poor bodily 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 (50,390,84), as previously confirmed by hormonal/reproductive problems in animal populations (104,381c,50d).  Mercury also damages the blood brain barrier and facilitates penetration of the brain by other toxic metals and substances(311).   Hypothyroidism is also known to be a major factor in cardiovascular disease(510,509h).                             


 The pituitary gland controls many of the body’s endocrine system functions and secretes hormones that control most bodily processes, including the immune system and reproductive  systems .  One study found mercury levels in the pituitary gland ranged from 6.3 to 77 ppb(85), while another(348) found the mean level to be 30ppb- levels found to be neurotoxic and cytotoxic in animal studies.  Some of the effect on depression is related to mercury’s effect of reducing the level of posterior pituitary hormone(oxytocin).   Low levels of pituitary function are associated with depression and suicidal thoughts, and appear to be a major factor in suicide of teenagers and other vulnerable groups.   The pituitary glands of a group of dentists had 800 times more mercury than controls(99).  This may explain why dentists have much higher levels of emotional problems, depression, suicide, etc(500,Section VIII.). A study by a neuroscience researcher found a connection between the levels of pituitary hormone lutropin and chronic mercury exposure(515). The authors indicated that inorganic mercury binding to luteinizing hormone can impair gonadotrophin regulation affecting fertility and reproductive function ,as well as immune function and has been found to accumulate in the brain and stay there for years, which may help explain mercury’s link to neurodegenerative disease.

 Amalgam fillings, nickel and gold crowns are major factors in reducing pituitary function(35,50,369,etc.).  Supplementary oxytocin extract has been found to alleviate many of these mood problems (35), along with replacement of metals in the mouth(107,500-Section VI.).  The normalization of pituitary function also often normalizes menstrual cycle problems, endometriosis, and increases fertility(35,9,500).

          Mercury accumulates in the adrenal gland and disrupts adrenal gland function(84,369,381).

In general immune activation from toxics such as heavy metals resulting in cytokine release and abnormalities of the hypothalamus-pituitary-adrenal axis can cause changes in the brain, fatigue, and severe psychological symptoms (369,375,379-383,107) such as depression,  profound fatigue, muscoskeletal pain, sleep disturbances, gastrointestinal and neurological problems as are seen in CFS, Fibromyalgia, and autoimmune thyroiditis. Such symptoms usually improve significantly after amalgam removal (503,303).   Such hypersensitivity has been found most common in those with genetic predisposition to heavy metal sensitivity (342,369,375,382) such as found more frequently in patients with HLA-DRA antigens(375,381,383). A significant portion of the population appears to fall in this category and adrenal problems have been increasing significantly in recent years (570).                

Mercury (and other toxic metals) has been found to accumulate in the pineal gland and reduce melatonin levels, which is thought to be a significant factor in mercury’s toxic effects(569). Melatonin has found to have a significant protective action against methyl mercury toxicity, likely from antioxidative effect of melatonin on the MMC induced neurotoxicity(567). 

There is also evidence that mercury affects neurotransmitter levels which has effects on conditions like depression, mood disorders, ADHD, etc.  There is evidence that mercury can block the dopamine-beta-hydroxylase (DBH) enzyme(571).   DBH is used to make the noradrenaline neurotransmitter and low noradrenaline can cause fatigue and depression. Mercury molecules can block all copper catalyzed dithiolane oxidases, such as coproporphyrin oxidase(260)  and DBH.

Thyroid imbalances, which are documented to be commonly caused by mercury (369,382,459,35,50,91,212), have been found to play a major role in chronic heart conditions such as clogged arteries, mycardial infarction, and chronic heart failure (510).  In a recent study, published in the Annals of Internal Medicine, researchers reported that subclinical hypothyroidism is highly prevalent in elderly women and is strongly and independently associated with cardiac atherosclerosis and myocardial infarction(510c).  People who tested hypothyroid usually have significantly higher levels of homocysteine and cholesterol, which are documented factors in heart disease.  50% of those testing hypothyroid, also had high levels of homocysteine (hyperhomocysteinenic) and 90% were either hyperhomocystemic or hypercholesterolemic(510a). These are also known factors in developing arteriosclerotic vascular disease. Homocysteine levels are significantly increased in hypothtyroid patients and normalize with treatment(510efg).



The thymus gland plays a significant part in the establishment of the immune system and lymphatic system from the 12th week of gestation until puberty.   Inhibition of thymus function can thus affect proper development of the immune and lymphatic systems.  Lymphocyte differentiation, maturation and peripheral functions are affected by the thymic protein hormone thymulin. Mercury at very low concentrations has been seen to impair some lymphocytic functions causing subclinical manifestations in exposed workers. Animal studies have shown mercury significantly inhibits thymulin production at very low micromolar levels of exposure(513a).    The metal allergens mercuric chloride and nickel sulfate were found to stimulate DNA synthesis of both immature and mature thymocytes at low levels of exposure, so chronic exposure can have long term effects(513b). Also, micromolar levels of mercuric ions specifically blocked synthesis of ribosomal RNA, causing fibrillarin relocation from the nucleolus to the nucleoplasm in epithelial cells as a consequence of the blockade of ribosomal RNA synthesis.  This appears to be a factor in deregulation of basic cellular events and in autoimmunity caused by mercury.     There were specific immunotoxic and biochemical alterations in lymphoid organs of mice treated at the lower doses of mercury. The immunological defects were consistent with altered T-cell function as evidenced by decreases in both T-cell mitogen and mixed leukocyte responses. Mercury caused increased immunoreactivity for glial fibrillary protein at 1 nanamole (0.2 ppb) concentration, and microglial response at even lower levels(175).  There was a particular association between the T-cell defects and inhibition of thymic pyruvate kinase, the rate-limiting enzyme for glycolysis(513c).    Pyruvate and glycolysis problems are often seen in mercury toxic children being treated for autism(409).       

A direct mechanism involving mercury’s inhibition of hormones and cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino acids appears to be a major part of the connection to allergic/immune reactive/autoimmune conditions such as autism/ADHD(409-411,439,464,468,476,33,160), schizophrenia(409,410), lupus(113,126,234,330,331,33,468), Scleroderma(468),   eczema and psoriasis (323,375,385,419,33), and allergies (271,313,330,331, 369,375,468).  Mercury and other toxic metals also form inorganic compounds with OH, NH2, CL, in addition to the SH radical and thus inhibits many cellular enzyme processes, coenzymes, hormones, and blood cells(405,409,500,555).     For example mercury has been found to strongly inhibit the activity of dipeptyl peptidase (DPP IV) which is required in the digestion of the milk protein casein(411,412) as well as of xanthine oxidase(439). Studies involving a large sample of autistic and schizophrenic patients found that over 90 % of those tested had high levels of the neurotoxic milk protein beta-casomorphine-7 in their blood and urine and defective enzymatic processes for digesting milk protein(410).  Elimination of milk products from the diet has been found to improve the condition. Similar results have been seen in similarly but lesser affected patients with other pervasive developmental conditions such as ADHD.    Such populations have also been found to have many with high levels of mercury who recover after mercury detox (409,413,369,160). As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs. Additional cellular level enzymatic effects of mercury’s binding with proteins include blockage of sulfur oxidation processes (33,114,194,330,331 ,412), enzymatic processes involving vitamins B6 and B12(418), effects on the cytochrome-C energy processes (43,84,338c,35), along with mercury’s adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium (43,96,333,338,160,500).    Thus some of the main mechanisms of toxic effects of metals include cytotoxicity; changes in cellular membrane permeability; inhibition of enzymes, coenzymes, and hormones; and  generation of lipid peroxides or  free radicals- which result in neurotoxicity, immunotoxicity, impaired cellular respiration, gastrointestinal/metabolic effects, hormonal effects,  and immune reactivity or autoimmunity.   


       Mercury has been found to cause hormonal changes which cause hair loss and greying of hair.  In a large German study where 20,000 were tested, allergies and hair-loss were found to be 2-3 times as high in a group with large numbers of amalgam fillings compared to controls(199,9).    Levels of mercury in follicular fluid was significantly higher for those with amalgam fillings (9,146). Based on this finding, a Gynecological Clinic that sees a large number of women suffering from alopecia/hair loss that was not responding to treatment had amalgams replaced in 132 women who had not responded to treatment.     68 % of the women then responded to treatment and alopecia was alleviated(187).  In other studies involving amalgam removal, the majority had significant improvement (40,317,503).  Higher levels of hormone disturbances, immune disturbances, infertility, and recurrent fungal infections were also found in the amalgam group. The results of hormone tests, cell culture studies, and intervention studies agree(9,146).  Other clinics have also found alleviation of hair loss/alopecia after amalgam removal and detox(40,317). Another study in Japan found significantly higher levels of mercury in gray hair than in dark hair(402).  


 III. Treatment of thyroid conditions.  

         As previously documented, for those with amalgam fillings or toxic metal exposure amalgam replacement and detoxification usually bring about significant improvement in thyroid function, including thyroiditis.  

        Conventional treatment of hypothyroidism is Synthroid or Unithroid or Levoxyl (synthetic T4).  Clinical experience has found Armour Thyroid (desiccated thyroid gland of pig) and Cytomel (synthetic T3) and Thyrolar (synthetic T4/T3 mix) to often be more effective than the conventional treatments. (580) 

        Nutrient supplementation found by clinical experience to benefit hypothyroidism include complex vit B, vit C, E, A, CoQ10, L-Carnitine, and minerals magnesium, manganese, selenium, and zinc. The B vitamins riboflavin and niacin act as cofactors in the production of your cellular energy (ATP) and in the conversion of iodide into iodine within your body(418b).  Studies show that supplementation with these B vitamins can reduce thyroid hormones (including T4 and T3) without inducing hypothyroidism or any of its negative symptoms(418b).  The amino acid L-Carnitine is essential to proper energy metabolism, and reduced levels may be behind the muscle weakness seen in patients with both underactive and overactive thyroids. Studies show, however, that once thyroid function is normalized, muscle carnitine levels and carnitine excretion in the urine both normalize in response.(580c).  Clinical research also reveals that L-carnitine supplementation can minimize even severe cases of hyperthyroidism.    Deficiencies of any of these can prevent conversion of T4 to T3 and should be corrected.  (580,581).  

        Iodine is the primary mineral requirement for thyroid function and deficiency can cause hypothyroidism and other problems. It is found in kelp, seaweeds, sea salt, and iodized salt. Statistics show that as our country’s median iodine intake has dropped, our risk of autoimmune disease has steadily risen(395b).  Clinical trials show that daily iodide supplementation can reduce levels of harmful antibodies in patients with Hashimoto’s thyroiditis(395c).  Iodoral is an iodine supplement that commonly cures or improves hypothyroidism. (395ac)   Selenium assists in removing toxins from the body and deficiency has been found to result in some cases of hypothyroidism.  Found in asparagus, grains, garlic, mushrooms- except the soil in some areas is deficient. Tyrosine is a necessary precursor of thyroid hormone and the neurotransmitters dopamine, norepinephrine, epinephrine.  A deficiency can lead to hypothyroidism and low adrenal function as well as mood disorders. DHEA  is a hormone that affects other hormone levels and metabolic function and is commonly found low in hypothyroidism. Levels can be determined  by blood test.  Raw cabbage, cauliflower, or turnips contain low levels of goitrogens, though cooking inactivates them.  (580)


        Natural treatments for adrenal fatigue include vit C (3 gm/day),DHEA (50 gm/day) L-theanine (100-400 mg/day, vit B5 (1500 mg/day), Phosphatidylserine (300 mg/day), Licorice (no more than 1000 mg), Melatonin (300 mcg to 6 mg at bedtime). Limit processed foods, alcohol, smoking.    (580) 

        Natural treatments of Addisons Disease or hypocortisolism  includes DHEA, Licorice, pantothenic acid (B5), and L-Theanine (green tea extract).  A physician should be consulted to test for DHEA levels and high doses of licorice should be used long term only under care of a doctor.   DHEA deficiency is common in the aging population, and chronic conditions like Addisons make this more likely.  Clinical studies found significant benefit in the majority. Licorice helps to break down the amount of hydrocortisone broken down by the liver, reducing the workload of the adrenal glands.  Vit B5 activates the adrenal glands.   L-Theanine works by increasing GABA levels, which helps modulate stress and mood. (580) 

        Natural treatments for Cushings Syndrome that have demonstrated benefits include DHEA, Vit C, Phosphatidylserine (PS), and Melatonin (nightly) (580).  



(1)American Association of Clinical Endocrinologists. Hashimoto’s Thyroiditis. Available at:; & Bindra A, Braunstein GD. Thyroiditis. American Family Physician. 2006;73(10):1769-76


(2) United States  Environmental Protection  Agency,    Office of Water, Novermber 2000, The National Listing of Fish and Wildlife Advisories:, EPA‑823‑F‑00‑20,‑Hg.htm     & The Conference of New England Governors and Eastern Canadian Premiers,  New England Governors/ Eastern Canadian Premiers Mercury Action Plan- 1998; ; &  U.S. EPA, FDA, Advisory on Fish Consumption by Women of Child Bearing Age and Children,  

(3) The Third National Health and Nutrition Examination Survey (NHANES III) 

(4) Grave’s Disease Foundation. Understanding Grave’s Disease. Available at: Accessed on: 4-10-10.

(6) The study of the prevalence of depressive disorders in primary care patients in Poland], Wiad Lek.2007;60(3-4):109-13. Drózdz W, Wojnar M, Araszkiewicz A, Nawacka-Pawlaczyk D, Urbański R, Cwiklińska-Jurkowska M, Rybakowski J

(7) Thyroid malfunction in women; Ginecol Obstet Mex. 2001 May;69:200-5, Zárate A, Basurto L, Hernández M; & (b) Clinical controversies in screening women for thyroid disorders during pregnancy. Wier FA, Farley CL.  J Midwifery Womens Health. 2006 May-Jun;51(3):152-8.

(8) Postpartum thyroiditis.  Best Pract Res Clin Endocrinol Metab. 2004 Jun;18(2):303-16. Stagnaro-Green A; & Recognizing, understanding, and treating postpartum thyroiditis. Endocrinol Metab Clin North Am. 2000 Jun;29(2):417-30, ix. Stagnaro-Green A; & (b) Postpartum depression and thyroid antibody status.  Thyroid. 1999 Jul;9(7):699-703, Harris B.

(9)(a) Dr.I.Gerhard, Dr. E.Roller,et al, Tubingen Univ. Gynecological Clinic,  Heidelberg,1996;   & (b)Gerhard I, Monga B, Waldbrenner A, Runnebaum B  “Heavy Metals and Fertility”, J of Toxicology and Environmental Health,Part A, 54(8):593-611, 1998; & (c) Gerhard I, Waibel S, Daniel V, Runnebaum B   “Impact of heavy metals on hormonal and immunological factors in women with repeated miscarriages”, Hum Reprod Update 1998 May;4(3):301‑309; & (d) Gerhard I, “Ganzheitiche Diagnostik un Therapie bie Infertilitat”,                          Erfahrungsheilkunde,1993, 42(3): 100-106; & (e)“Hormonal conditions affecting women caused by environmental poisons” in Pravention, Diagnose und Therapie von Umwelterkrankungen, JD Kruse-Jarres(Ed.), 1993, p51-68;               &   (f) Gerhard I, Waldbrenner P, Thuro H, Runnebaum B, Diagnosis of heavy metal loading by the oral DMPS and chewing gum tests. Klinisches Labor 1992, 38:404-411.   

(10) Some neurologic and psychiatric complications in endocrine disorders: the thyroid gland, [Article in Hungarian]   Aszalós Z.  Orv Hetil. 2007 Feb 18;148(7):303-10; &(b) Neonatal effects of maternal hypothyroxinemia during early pregnancy.  Pediatrics. 2006 Jan;117(1):161-7.  Kooistra L, Crawford S, van Baar AL, Brouwers EP, Pop VJ; & (c) Hypothyroidism and pregnancy: impact on mother and child health.]  Ann Biol Clin (Paris). 2008 Jan 29;66(1):43-51, [Article in French], Menif O, Omar S, Feki M, Kaabachi N.

(11) Neuropsychiatric aspects of hypothyroidism and treatment reversibility. Minerva Endocrine. 2007 Mar;32(1):49-65, Davis JD, Tremont G; & (b) Subclinical hypothyroidism: psychiatric disorders and symptoms. Rev Bras Psiquiatr. 2007 Jun;29(2):157-9, Almeida C, Brasil MA, Costa AJ et al. 


(14) (a) Mercury accumulation in tissues from dental staff and controls in relation to exposure.  Nylander M, Friberg L, Eggleston D, Björkman L.  Swed Dent J. 1989;13(6):235-43; & (b) Mercury burden of human fetal and infant tissues.  Drasch G, Schupp I, Höfl H, Reinke R, Roider G. Eur J Pediatr. 1994 Aug;153(8):607-10; & (c ) Dental amalgam and mercury levels in autopsy tissues: food for thought.    Guzzi G, Grandi M,  Severi G et al.   Am J Forensic Med Pathol. 2006 Mar;27(1):42-5                              

(16) Lichtenberg H, "Mercury vapor in the oral cavity in relation to number of amalgam surfaces and the classic symptoms of chronic mercury poisoning", J Orthomol Med (1996), v11, n.2, 87-94

(19)(a) Mercury in human brain, blood, muscle and toenails in relation to exposure: an autopsy study. Environ Health. 2007 Oct 11;6:30Björkman L, Lundekvam BF, Vahter M et al, & (b)  Matts Hanson. Dept of  Zoophysiology,   University of Lund, Sweden.  “Amalgam hazards in your teeth”,  J. Orthomolecular Psychiatry 1983; 2(3): 194-201;    

(20)(a) Vimy MJ, Takahashi,Y, Lorscheider FL; Maternal ‑Fetal Distribution of Mercury Released From Dental Amalgam Fillings. Dept of Medicine and Medical  Physiology , faculty of Medicine, Univ. of Calgary, Calgary Alberta Canada,  Amer.J.Physiol.,1990,  258:R939-945; & (b)  Hahn LJ, Kloiber R, Leininger RW, Vimy MJ, Lorscheider FL. Distribution of mercury released from  amalgam fillings into monkey tissues”,    FASEB J.,1990, 4:5536              


(21) R.A.Goyer,”Toxic effects of metals”inCaserett and Doull’s Toxicology- TheBasic Science of Poisons, McGraw-Hill Inc., N.Y., 1993; &(b) Goodman, Gillman, The Pharmacological Basis of Therapeutics, Mac Millan Publishing Company, N.Y. 1985; &(c) Encyclopedia of Occumpational Health and Safety, International Labour Office, Geneva, Vol 2, 3rd Edition.  

                                   22. Oskarsson A, Schultz A, Skerfving S, Hallen IP, Ohlin B, Lagerkvist BJ. Mercury in breast milk in relation to fish consumption  and amalgam.  Arch Environ Health, 1996,51(3):234‑41;&(b)  Drasch G, Aigner S, Roider G, Staiger F, Lipowsky G.   Mercury in human colostrum and early breast milk.  J Trace Elem Med Biol 1998; 12:23‑27; &(c) Paccagnella B, Riolfatti M.  Total mercury levels in human milk from Italian mothers. Ann Ig 1989: 1(3-4):661-71; 

23. Yang J, Jiang Z,Wang Y, Qureshi IA, Wu XD. Maternal‑fetal transfer of  metallic mercury via placenta and milk. Ann Clin Lab Sci 1997; 27(2):135‑141; & (b)  Soong YK, Tseng R, Liu C, Lin PW.  J of Formosa Medical Assoc 1991; 90(1): 59‑65; & (c ) Sundberg J, Ersson B, Lonnerdal B, Oskarsson A.   Protein binding of mercury in milk and                 plasma from mice and man‑‑a comparison between methylmercury and inorganic mercury.            Toxicology 1999 Oct 1;137(3):169‑84.  

24. Kuhnert PM, Kuhnert BR, Erhard P.  Comparison of mercury levels in maternal blood, fetal blood, fetal cord blood, and placental tissues. Am J Obstet Gynecol, 1981, 139(2): 209-13, & Vahter M, Akesson A, Lind B, Bjors U, Schutz A, Berglund M, "Longitudinal study of methylmercury and inorganic mercury in blood and urine of pregnant and lactating women, as well as in umbilical cord blood", Environ Res 2000 Oct;84(2):186-94; &   Kuntz WD, Pitkin RM, Bostrom AW, Hughes MS.  Maternal and chord blood mercury  background levels; a longitudinal surveillance. Am J Obstet and Gynecol 1982; 143(4):                 440‑443.


25. Ramirez GB, Cruz MC, Pagulayan O, Ostrea E, Dalisay C.  The Tagum study I: analysis and clinical correlates of mercury in maternal and cord blood, breast milk, meconium, and infants' hair.   Pediatrics 2000 Oct;106(4):774‑81; & (b) Ramirez GB, Pagulayan O, Akagi H, Francisco Rivera A, Lee LV, Berroya A, Vince Cruz MC, Casintahan D.  Tagum study II: follow-up study at two years of age after prenatal exposure to mercury.  Pediatrics. 2003 Mar;111(3):e289-95; &(c)  Warfvinge K, Berlin M, Logdberg B.  The effect on pregnancy outcome and fetal brain development of prenatal exposure to mercury vapour. Neurotoxicology 1994; 15(4).

26. Drexler H, Schaller KH.  The mercury concentration in breast milk resulting from amalgam fillings and dietary habits.  Environ Res 1998; 77(2): 124-9.

27.  Mottet NK, Shaw CM, Burbacher, TM,  Health Risks from Increases in Methylmercury Exposure, Health Perspect 1985; 63: 133‑140; & (b) P.Grandjean et al, “MeHg and neurotoxicity in children”, Am J Epidemiol, 1999; & Sorensen N, et al; Prenatal mercury exposure raises blood pressure, Epidemiology 1999, 10:370-375; & Grandjean P; Jurgensen

(33) (a)  Markovich et al,  "Heavy   metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat‑1", Toxicol  Appl Pharmacol,    1999,154(2):181‑7; & (b)2S.A.McFadden, “Xenobiotic metabolism and adverse environmental response: sulfur-dependent detox pathways”,Toxicology, 1996, 111(1-3):43-65; &(c)  S.C. Langley-Evans et al, “SO2: a potent glutathion depleting agent”, Comp Biochem Physiol Pharmocol Toxicol Endocrinol, 114(2):89-98; & (d)Alberti A, Pirrone P, Elia M, Waring RH, Romano C.  Sulphation deficit in “low-functioning” autistic children. Biol Psychiatry 1999, 46(3):420-4.

(35)    Huggins HA, Levy,TEUniformed Consent: the hidden dangers in dental care, 1999, Hampton Roads Publishing Company Inc;   &  Hal Huggins, Its All in Your Head, 1997; & Center for Progressive Medicine, 1999,

 (38)   Sensitization to inorganic mercury could be a risk factor for infertility; Podzimek S, Prochazkova J, Bultasova L, Bartova J, Ulcova-Gallova Z, Mrklas L, Stejskal VD.  Neuro Endocrinol Lett. 2005 Aug;26(4):277-82; & S.Ziff and M.Ziff,  Infertility and Birth Defects: Is Mercury from Dental Fillings a Hidden Cause?, Bio-Probe, Inc. ISBN: 0-941011-03-8.1987

(40)   F.Perger, Amalgamtherape, in Kompendiu der Regulationspathologie und Therapie, Sonntag-Verlag, 1990; & “Belastungen durch toxische Schwermetalle”, 1993, 87(2): 157-63;   & K.H.Friese, ”Homoopathische Behandlung der Amalgamvergiftung”, 

          AllgHomoopathische Z, 241(5); 184-187, & Erfahrungsheikunde, 1996, (4): 251-253; & “Amalgamvergiftung_moglicher”Der Naturazt,1995,135(8):13-15; & “Schnupfen-Was tun?”, Therapeutikon, 1994, 8(3): 62-68;

(43) (a)Knapp LT; Klann E.   Superoxide‑induced stimulation of protein kinase C via  

thiol modification and modulation of zinc content. J Biol Chem 2000 May 22; &

(b) B.Rajanna et al, “Modulation of protein kinase C by heavy metals”, Toxicol Lett, 1995, 


(49)    A.Kingman et al, National Institute of Dental Research, “Mercury concentrations in urine and blood associated with amalgam exposure in the U.S. military population”, Dent Res, 1998, 77(3):461-71.

(50)     Sin YM, Teh WF, Wong MK, Reddy PK - "Effect of Mercury on Glutathione and Thyroid Hormones" Bulletin of Environmental Contamination and Toxicology 44(4):616-622 (1990);  & (b) J.Kawada et al, “Effects of inorganic and methyl mercury on thyroidal function”, J Pharmacobiodyn, 1980, 3(3):149-59; & (c) Ghosh N.  Thyrotoxicity of cadmium and  mercury.  Biomed Environ Sci 1992, 5(3): 236-40; &(d) Goldman, Blackburn, The Effect of Mercuric Chloride on  Thyroid Function of the Rat, Toxicol and Applied Pharm 1979, 48: 49-55; &(e)Kabuto M - "Chronic effects of methylmercury on the urinary excretion of catecholamines and their responses to hypoglycemic stress" Arch Toxicol 65(2):164-7 (1991)  ; & Assoc. for Birth Defect Children, Birth Defect News, March 2001;     

 (61)   (a)E.Lutz et al, “Concentrations of mercury in brain and kidney of fetuses and  infants”, Journal of Trace Elements in Medicine and Biology, 1996,10:61-67;  & (b)G.Drasch et al, “Mercury Burden of Human Fetal and Infant Tissues”, Eur J Pediatr 153:607-610,1994;                                     

(84) (a)J.C.Veltman et al, “Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland”, Arch Biochem Biophys, 1986, 248(2):467-78; &(b) A.G.Riedl et al, Neurodegenerative Disease Research Center, King’s College, UK, “P450 and hemeoxygenase enzymes in the basal ganglia and their role’s in Parkinson’s disease”, Adv Neurol, 1999; 80:271-86; &(c) Alfred V. Zamm. Dental Mercury: A Factor that Aggravates and Induces Xenobiotic Intolerance.  J. Orthmol. Med. v6#2 pp67-77 (1991); & (d)

Nishida M, Muraoka K, et al, Differential effects of methylmercuric chloride and mercuric chloride on the histochemistry of rat thyroid peroxidase and the thyroid peroxidase activity of isolated pig thyroid cells. J Histochem Cytochem. 1989 May;37(5):723-7; &  (e)     Khayat A, Dencker L.  Whole body and liver distribution of inhaled mercury vapor in the mouse: influence of ethanol and aminotriazole pretreatment. J Appl Toxicol. 1983 Apr;3(2):66-74;    

(85) Weiner JA, Nylander M;   The relationship between mercury concentration in human organs and different predictor variables.    Sci Total Environ 1993 Sep 30;138(1‑3):101‑15 ;   & (b)Falnoga I, Tusek-Znidaric M, Horvat M, Stegnar P.  Mercury, selenium, and cadmium in human autopsy samples from Idrija residents and mercury mine workers.  Environ Res. 2000 Nov;84(3):211-8

(91)    B.Lindqvist et al, "Effects of removing amalgam fillings from patients with diseases affecting the immune         

system", Med Sci Res 24(5): 355-356, 1996.                                      

(96) A.F.Goldberg et al, “Effect of Amalgam restorations on whole body potassium and bone mineral content in older men”,Gen Dent,   1996, 44(3): 246-8; & (b) K.Schirrmacher,1998, “Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+]I in bone cells”, Calcif Tissue Int 1998 Aug;63(2):134‑9.          

(99)    M. Nylander et al, Mercury accumulation in tissues from dental staff and  controls”, Swedish Dental Journal, 13:235-243, 1989; &     (b) Nylander M,  “Mercury in pituitary glands of dentists”, Lancet,442, Feb 26, 1986.

(104)  (a)C.F.Facemire et al, “Reproductive impairment in the Florida Panther”, Health Perspect,1995, 103 (Supp4):79-86; &(b)Yang JM, Jiang XZ, Chen QY, Li PJ, Zhou YF, Wang YL.  , “The distribution of HgCl2 in rat body and its effect on fetus”, Environ Sci , 1996, 9(4): 437-42; & (c) M.Maretta et al, “Effect of mercury on the epithelium of the fowl testis”, Vet Hung 1995, 43(1):153-6.                            

(105)  (a)T.Colborn(Ed.),Chemically Induced Alterations in Functional Development,    Princeton Scientific Press,1992;     &(b) Colborn T, ” Developmental Effects of Endocrine-Disrupting Chemicals",Environ Heath Perspectives, V 101, No.5, Oct 1993; & (c)B.Windham, "Health, Hormonal, and Reproductive Effects of Endocrine Disrupting Chemicals" (including mercury),   Annotated Bibliography ,2000; &(d) Giwercman A, Carlsen E, Keiding N, Skakkabaek NE, Evidence for increasing incidence of abnormalities of the human testis: a review.   Environ Health Perspect 1993; 101 Suppl(2): 65-71.

(107)  R.L.Siblerud et al,”Psychometric evidence that mercury from dental fillings may be a factor in depression,anger,and anxiety", Psychol Rep,  v74,n1,1994;  & Amer. J. Of Psychotherapy, 1989; 58: 575-87; Poisoning and Toxicology compendium, Leikin & Palouchek, Lexi-Comp,1998, p705.           

(113)  (a)T.A.Glavinskiaia et al, “Complexons in the treatment of  lupus erghematousus”, Dermatol Venerol, 1980, 12: 24-28;               & (b)A.F.Hall, Arch Dermatol 47, 1943, 610-611; & Panasiuk J ,   Peripheral blood lymphocyte transformation test in various skin diseases of allergic origin. (nickel    & lupus)    Przegl Dermatol 1980;67(6):823‑9 [Article in Polish] ; &  S Moore,  Lupus: Alternative Therapies That Work;     www.shirleys‑wellness‑    

(114)  (a)M.Aschner et al, “Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury

                   vapor”, Brain Research, 1997, dec 5, 778(1):222-32; & (b) O’Halloran TV, “Transition metals in control

Of gene expression”, Science, 1993, 261(5122):715-25; & (c)Matts RL, Schatz JR, Hurst R, Kagen R.   Toxic heavy metal ions inhibit reduction of disulfide bonds.  J Biol Chem 1991; 266(19): 12695-702; & (d) Boot JH.  Effects of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes.  Cell Struct Funct 1995; 20(3): 233-8. 

(122)   B.Ono et al, “Reduced tyrosine uptake in strains sensitive to inorganic mercury”, Genet, 1987,11(5):399-

(126)  Noda M, Wataha JC, Lockwood PE, Volkmann KR, Kaga M, Sano H.  Sublethal, 2-week exposures of           dental material components alter TNF-alpha secretion of THP-1 monocytes Dent Mater. 2003;19(2):101-5;  & Kim SH, Johnson VJ, Sharma RP.    Mercury inhibits nitric oxide production but activates proinflammatory cytokine expression in murine macrophage: differential modulation of NF- kappaB and p38 MAPK signaling pathways.    Nitric Oxide. 2002 Aug;7(1):67-74; & Chen L, Nordlind K, Liden S, Sticherling M., Increased expression of keratinocyte interleukin-8 in human contact eczematous reactions to heavy metals.  APMIS.1996 Jul-Aug;104(7-8):509-14; & & Feighery L, Collins C, Feighery C, Mahmud N, Coughlan G, Willoughby R, Jackson J. Anti-transglutaminase antibodies and the serological diagnosis of coeliac disease.  Br J Biomed Sci. 2003;60(1):14-8.

(146) (a) Gerhard I, Runnebaum B,  The limits of hormone substitution in pollutant exposure and fertility disorders  Zentralbl Gynakol, 1992, 114, 593-602: &(b)Gerhard, I.: Fortpflanzungsstörungen durch Umweltgifte? Therapeutikon 7, 478‑491 (1993).;  &(c)Roller, E., Vallon, U. und Clédon, Ph.: Einfluß von Schwermetallen auf die Progesteronsynthese von Leydig‑Zellen. J Fert Reprod 3, 33 (1995).   &(d) Vallon U, Roller E,  und Clédon, Ph.: Schwermetallionen beeinflussen die Progesteronsynthese von humanen Granulosazellen bei IVF‑Patientinnen: Anwendung eines alternativen in‑vitro‑Zytotoxizitätstests. J Fert Reprod 3, 31 (1995).

(160)     B. Windham, Cognitive and Behavioral Effects of Toxic Metals, 2001.   (over 200 medical study references)    

(175) Monnet-Tschudi F, Zurich MG, Honegger P.  Comparison of the developmental effects of two mercury compounds on glial cells and neurons in aggregate cultures of rat telencephalon..  Brain Res. 1996 Nov 25;741(1-2):52-9. 

(181) Mathieson PW, “Mercury: god of TH2 cells”,1995, Clinical Exp Immunol.,102(2):229-30; & Heo Y, Parsons PJ, Lawrence DA, Lead differentially modifies cytokine production in vitro and in vivo.  Toxicol Appl Pharmacol, 196; 138:149-57; & Murdoch RD, Pepys J; Enhancement of antibody and IgE production by mercury and platinum salts. Int Arch Allergy Appl Immunol 1986 80: 405-11.

(183) World Health Organization(WHO),1991, Environmental Health Criteria 118,  Inorganic  Mercury, WHO, Geneva, Switzerland. 

(187)  (a)Klobusch J, Rabe T, Gerhard I,  Runnebaum B, "Alopecia and environmental pollution" Klinisches Labor 1992, 38:469‑ 476; & (b)“Schwermetallbelastungen bei Patientinnen mit Alopezie” Arch Gynecol. Obstet., 1993,254(1-4):278-80;& (c)G. Kunzel et al, “Arch Gynecol. Obstet., 1993, 254:277-8; & Schrallhammer-Benkler K, et al,   Acute  mercury intoxication with lichenoid drug eruption followed by mercury contact allergy and development of antinuclear antibodies. Acta Derm Venereol. 1992 Aug;72(4):294-6.    

(192)  (a)N.Nogi, “Electric current around dental metals as a factor producing allergic metal ions in the oral cavity”, Nippon Hifuka Gakkai Zasshi, 1989, 99(12):1243-54;  & J. Bergdahl, A.J.Certosimo et al, National Naval Dental Center, “Oral Electricity”, Gen Dent, 1996, 44(4):324-6; & B.M.Owens et al, “Localized galvanic shock after insertion of an amalgam restoration”, Compendium, 1993, 14(10),1302,1304,1306-7  & (b)M.D.Rose et al, Eastman Dental Institute, “The tarnished history of a posteria restoration”, Br Dent J 1998;185(9):436;&     & R.D.Meyer et al, “Intraoral galvanic corrosion”,Prosthet Dent, 1993,69(2):141-3  R.H.Ogletree et al, School of Materials Science, GIT, Atlanta,”Effect of mercury on corrosion of eta’ Cu-Sn phase in dental amalgams”, Dent Mater, 1995, 11(5):332-6; &(c) Johansson E, Liliefors T, "Heavy elements in root tips from teeth with  amalgam fillings", Department of Radiation Sciences, Division of Physical Biology, Box 535, 751 21 Uppsala, Sweden

(198) B.R.G.Danielsson et al,”Ferotoxicity of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus”, Biol Res Preg Perinatal. 5(3):102-109,1984; &   Danielsson et al, Neurotoxicol. Teratol.,  18:129-134

(199)  Dr. P.Kraub & M.Deyhle, Universitat Tubingen- Institut fur Organische Chemie, “Field  Study on the Mercury Content of Saliva”, 1997   http://www.uni‑;  

(20,000 people tested for mercury level in saliva and health status/symptoms compiled)

(211)  Mercury from maternal "silver" tooth fillings in sheep and human breast milk. A source of neonatal exposure.  Vimy MJ, Hooper DE, King WW, Lorscheider FL. Biol Trace Elem Res. 1997 Feb;56(2):143-52; & Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Vimy MJ, Takahashi Y, Lorscheider FL.  Am J Physiol. 1990 Apr;258(4 Pt 2):R939-45; & R.Schiele et al, Institute of Occupational Medicine, Univ. Of Erlamgem- Nurnberg, “Studies of organ mercury content related to number of amalgam  fillings”,Symposium paper, March 12, 1984, Cologne, Germany; (in 38);

 (217) Agency for Toxic Substances and Disease Registry, U.S. Public Health   Service, Toxicological Profile for Mercury , 1999; & (b)Apr 19,1999 Media Advisory, New MRLs for toxic substances, MRL:elemental mercury vapor/inhalation/chronic & MRL:   methyl mercury/ oral/acute; &

(234)  P.E. Bigazzi, “Autoimmunity and Heavy Metals”, Lupus, 1994; 3: 449-453;(b) & Pollard KM, Pearson Dl, Hultman P.  Lupus-prone mice as model to study xenobiotic-induced autoimmunity.  Environ Health Perspect 1999; 107(Suppl 5): 729-735; &(c) Nielsen JB; Hultman P.  Experimental studies on genetically determined susceptibility to mercury‑induced autoimmune response.   Ren Fail 1999 May‑Jul;21(3‑4):343‑8; &(d) Hultman P, Enestrom S, Mercury induced antinuclear antibodies in mice,  Clinical and Exper Immunology, 1988, 71(2): 269-274.

(260) J.S. Woods et al,  “Urinary porphyrin profiles as biomarker of mercury exposure: studies on dentists”, J Toxicol Environ Health, 40(2-3):1993, p235-;  & “Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity”, Physiol Pharmocol, 1996,74(2):210-15

(263)     Kumar AR, Kurup PA.  Inhibition of membrane Na+-K+ ATPase activity: a common pathway in central nervous system disorders.  J Assoc Physicians India. 2002 Mar;50:400-6

(264) B.R. Danielsson et al, “ ”Behavioral effects of prenatal metallic mercury inhalation exposure in rats”,        Neurotoxicol Teratol,           1993, 15(6): 391-6;&  A. Fredriksson et al,”Prenatal exposure to metallic mercury         vapor and methyl mercury produce         interactive behavioral changes in adult rats”, Neurotoxicol Teratol,           1996, 18(2): 129-34

(271) B.A.Weber, “The Marburg Amalgam Study”, Arzt und Umwelt, Apr, 1995; (266 cases)  & (b)  “Amalgam and Allergy”, Institute for Naturopathic Medicine, 1994;   

 (40 MS cases),              http://home,t‑"    

(273)  Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS). H V Aposhian ;  Environ Health Perspect. 1998 August; 106(Suppl 4): 1017–1025,;  &(b) R.Schiele et al,  Mercury Mobilization by DMPS in persons with and without amalgam fillings ”,  Zahnarztl. Mitt, 1989, 79(17): 1866-1868;                      

(274)  L.Friberg et al, “Mercury in the brain and CNS in relation to amalgam fillings”, Lakartidningen, 83(7):519-521,1986(Swedish Medical Journal),

(287)  Warvinge K, Mercury distribution in the neonatal and adult cerebellum after mercury vapor exposure of pregnant squirrel monkeys, Environ Res 2000, 83(2): 93-101; 

 (296)   L.Bucio et al, Uptake, cellular distribution and DNA damage produced by mercuric 

          chloride in a human fetal     hepatic cell line.  Mutat Res 1999 Jan 

          25;423(1‑2):65‑72; &  (b) Ho PI, Ortiz D, Rogers E, Shea TB. 

          Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase 

          hyperactivation and DNA damage.   J Neurosci Res. 2002 Dec 1;70(5):694-702; 

          &(c) Snyder RD; Lachmann PJ;  Thiol involvement in 

          the inhibition of DNA repair by metals in mammalian       cells.  Source Mol Toxicol

          1989 Apr‑Jun, 2:2,    117‑28 ; &    L.Verschaeve et al, “Comparative in vitro 

          cytogenetic studies in mercury-exposed human lymphocytes”, Muta Res, 1985, 

          157(2-3):221-6;  &  L.Verschaeve,“Genetic damage induced by low level mercury  

          exposure”, Envir Res,12:306-10,1976.     

(303)   Heavy Metal and Chemical Toxicity,  Dietrich Klinghardt, MD, Ph.D. ; &     Mercury Toxicity and Systemic Elimination Agents, D. Klinghardt & J Mercola(DO), J of Nutritional and Environmental Medicine, 2001, 11:53-62; & Amalgam Detox, Klinghardt Academy of Neurobiology, 2008

(317) S.Zinecker, “Amalgam: inorganic mercury in the brain”, der Kassenarzt, 1992, 32(4):23;        “Praxiproblem Amalgam”, Der Allgermeinarzt, 1995,17(11):1215-1221. (1800 patients)

(323) (a)Dr. Kohdera, Faculty of Dentistry, Osaka Univ., International Congress of Allergology and Clinical Immunology, EAACI, Stockholm, June 1994;  & Heavy  Metal Bulletin, Vol 1, Issue 2, Oct 1994.   (160 cases cured-eczema); (b)  Tsunetoshi Kohdera, MD, dermatology, allergology,  31 Higashitakada‑cho Mibu Nakagyo‑ku Schimazu Clinics    Kyoto 604 Japan   e‑mail:smc‑‑       &(c) P.Dallmann,”Dermatalogical conditions caused by amalgam? PeDa_Eigenverisg, 1995;         & (d)G. Ionescu, Biol Med, 1996, (2): 65-68; & (e) Ionescu G.: Tooth alloys. Electro‑chemical and biological processes.  Materialprueuefung..Komplementaeaermed. , 3, 72-77, 1996; & (f) Ionescu G; Heavy metal load by Dental materials. Experience  with Neurodermitis and Psoriasis patients.. Zeitung f. Umweltmedizin, 3, 163-171, 1997

(327)  Danscher G; Horsted‑Bindslev P; Rungby J.  Traces of mercury in organs from primates with amalgam fillings.  Exp Mol Pathol 1990;52(3):291‑9;                                                                                 

 (330) (a) Wilkinson LJ, Waring RH.  Cysteine dioxygenase: modulation of expression in human cell lines by cytokines and control of sulphate production. Toxicol In Vitro. 2002 Aug;16(4):481-3; & (b) C.M. Tanner et al,“Abnormal Liver Enzyme Metabolism in Parkinson’s”,Neurology,  1991, 41(5): Suppl 2, 89-92; &      M.T.Heafield et al, "Plasma cysteine and sulphate levels in patients with Motor neurone disease, Parkinson's Disease, and Alzheimer’s's Disease", Neurosci Lett, 1990, 110(1‑2), 216,20; &    A.Pean et al, "Pathways of cysteine metabolism in MND/ALS", J neurol Sci, 1994, 124, Suppl:59‑61;  & Steventon GB, et al; Xenobiotic metabolism in motor neuron disease, The Lancet,  Sept 17 1988, p 644-47; & Neurology 1990,   40:1095-98.

(331) C.Gordon et al, “Abnormal sulphur oxidation in systemic lupus erythrmatosus(SLE)”, Lancet,                        1992,339:8784,25-6; & P.Emory et al, “Poor sulphoxidation in patients with rheumatoid arthitis”, Ann Rheum             Dis,  1992,  51:3,318-20; & Bradley H,et al,  Sulfate metabolism is abnormal in patients with rheumatoid arthritis.        Confirmation by in vivo biochemical findings.  J Rheumatol. 1994 Jul;21(7):1192-6; & T.L. Perry et al,                         “Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase defieciency”, Ann Neural, 1985,               18(4):482-489.

(333) (a)A.J.Freitas et al, “Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain”, Brain       Research,        1996, 738(2): 257-64; & (b)P.R.Yallapragoda et al,“Inhibition of calcium transport by Hg salts” in rat cerebellum          and cerebral cortex”, J Appl toxicol, 1996, 164(4): 325-30;     &     (c) E.Chavez et al, “Mitochondrial calcium         release by Hg+2",J Biol Chem, 1988, 263:8, 3582-;&(d)  A. Szucs et al, Cell Mol Neurobiol, 1997,17(3): 273-8; &     (e) D.Busselberg, 1995, “Calcium channels as target sites of heavy metals”,Toxicol Lett, Dec;82‑83:255‑61; &           Cell Mol Neurobiol 1994 Dec;14(6):675‑87;   & (f) Rossi AD, et al, Modifications of Ca2+ signaling by      inorganic mercury in PC12 cells.  FASEB J 1993, 7:1507-14.                    

(337) H.G. Abadin, et al, U.S. ATSDR, “Breast-feeding exposure of infants to mercury, lead, and cadmium: A Public Health   Perspective”, Toxicol Ind Health, 1997, 13(4): 495-517.            

(338) (a)W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, “In vitro effect of          mercury on enzyme activities and its accumulation in the first-trimester human   placenta”,      Environ Res, 1992, 57(1):96-106;& “In vitro exposure to mercury and cadmium alters term human placental      membrane fluidity”, Pharmacol, 1992, 116(1): 17-23;  & (b)J.Urbach et al, Dept. of Obstetrics & Gynecology,              Rambam Medical Center, Haifa, Israel, “Effect of inorganic mercury on in vitro placental nutrient transfer      and      oxygen consumption”, Reprod Toxicol, 1992,6(1):69-75;& ©  Karp W, Gale TF et al, Effect of mercuric           acetate on selected enzymes of maternal and fetal hamsters” Environmental Research, 36:351-358; &  W.B. Karp         et al, “Correlation of human placental enzymatic  activity with trace         metal concentration in placenta”, Environ            Res. 13:470- 477,1977; & (d)  Boot JH.  Effects of SH‑blocking compounds on the energy metabolism and           glucose uptake in isolated rat  hepatocytes.  Cell Struct Funct 1995 Jun;20(3):233‑8; &  Semczuk M,                            Semczuk‑Sikora A.  New data on toxic metal intoxication (Cd, Pb, and Hg in particular)  and Mg status during             pregnancy.  Med Sci Monit 2001 Mar;7(2):332‑340

(342)  Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al. Metal- specific                  memory lymphocytes: biomarkers of sensitivity in man.  Neuroendocrinology Letters, 1999; 20: 289-98.

(348)(a) Kistner A, “Mercury poisoning by amalgam:  Diagnosis and therapy” ZWR, 1995,104(5):412-417;        &(b)       Mass C, Bruck W.  “Study on the significance of mercury accumulation in the brain from dental amalgam fillings           through direct mouth-nose-brain transport”, Zentralbl Hyg Umweltmed 1996; 198(3): 275-91.

(363) J.W.Reinhardt, Univ. Of Iowa College of Dentistry, “Side effects: mercury contribution to

body burden from dental amalgam”, Adv Dent Res, 1992, 6: 110-3.

(366) (a)“Tooth amalgam  and pregnancy”, Geburtshilfe Frauenheikd. 1995, 55(6): M63-M65; &(b) T. Zinke,       “There are new realizations to the Amalgam problem”, in Status Quo and perspectiveves of Amalgam and           Other       Dental Materials, L.F. Friberg(Ed.), Georg=Thieme-Verlag, Stuttgart, New York, 1995, p1-7. 

(367)(a) Gerhard I, “Amalgam from gynacological view”, Der Frauenarzt, 1995,36(6): 627-28; & (b)“Schdstoffe und         Fertillitatsstorungen”, Schwermetalle und Mineralstoffe, Geburtshilfe Frauenheikd, 1992, 52(7):383-396; & (c) Gerhard I, “Reproductive risks of heavy metals and pesticides in women”, in: Reproductive Toxicology,  M.Richardson(ed.), VCH Weinhelm, 1993, 167-83;   & (d)Gerhard I, “Infertility with women by environmental illnesses, JD. Kruse-Jarres(Ed.), 1993, 51-68.

(369) Sterzl I, Prochazkova J, Stejskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity.  Neuroendocrinology Letters 1999; 20:221-228.; & The role of environmental factors in autoimmune thyroiditis. Hybenova M et al: Neuro Endocrinol Lett. 2010;31(3):283-9; & The beneficial effect of amalgam replacement on health in patients with autoimmunity. Prochazkova J, Stejskal VD, et al;Neuro Endocrinol Lett. 2004 Jun;25(3):211-8.


(372) (a)Atchison WD.  Effects of neurotoxicants on synaptic transmission. Neurotoxicol Teratol 1998, 10(5):393-        416; &   Sidransky H, Verney E, Influence of lead acetate and selected metal salts on tryptophan binding to         rat hepatic nuclei. Toxicol Pathol 1999, 27(4):441-7; &(b) Shukla GS, Chandra SV, Effect of interaction of       Mn2+withZn2+, Hg2+, and Cd2+ on some neurochemicals in rats. Toxicol Lett 1982, 10(2-3):163-8;  &(c)Brouwer M et al, Functional changes induced by heavy metal ions.  Biochemistry, 1982, 21(20): 2529-38.

(375) (a) Stejskal VDM, Danersund A, Lindvall A.  Metal-specific memory lymphocytes: biomarkers of sensitivity in   man.  Neuroendocrinology Letters 1999; &(b) Stejskal V, Hudecek R, Mayer W, "Metal-specific lymphocytes: risk factors in CFS and other related diseases", Neuroendocrinology Letters, 20: 289-298, 1999

(379) (a) MacDonald EM, Mann AH, Thomas HC. Interferons as mediators of psychiatric morbidity.  The Lancet         1978; Nov 21, 1175-78; & (b) Hickie I, Lloyd A.  Are cytokines associated with neuropsychiatric syndrome in   humans?  Int J Immunopharm 1995; 4:285-294.

(380) (a) Komaroff AL, Buchwald DS.  Chronic fatigue syndrom: an update.  Ann Rev Med 1998; 49: 1-13; & 


(b) Buchwald DS, Wener MH, Kith P.  Markers of inflamation and immune activation in CFS.  J Rheumatol     1997; 24:372-76.

(381) (a) Demitrack MA, Dale JK.   Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in   patients with chronic fatigue syndrome.  J Clin Endocrinol Metabol 1991; 73:1224-1234; & (b)Turnbull AV, Rivier C.  Regulation of the HPA axis by cytokines.  Brain Behav Immun 1995; 20:253-75; & (c)Ng TB, Liu   WK.  In Vitro Cell Dev Biol 1990 Jan;26(1):24‑8.  Toxic effect of heavy metals on cells isolated from the rat   adrenal and testis.

(382) Sterzl I, Fucikova T, Zamrazil V.  The fatigue syndrome in autoimmune thyroiditis with polyglandular   activation of autoimmunity.  Vnitrni Lekarstvi 1998; 44: 456-60.;   &(b) Sterzl I, Hrda P, Prochazkova J, Bartova J,   Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitr Lek 1999 Sep;45(9):527‑31; &     & (c)Kolenic J, Palcakova D, Benicky L, Kolenicova M - "The frequency of auto-antibody occurrence in occupational risk (mercury)" Prac Lek 45(2):75-77 (1993), &  ; &(c) The beneficial effect of amalgam replacement on health in patients with autoimmunity. Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; Neuro Endocrinol Lett. 2004 Jun;25(3):211-8. ; & (d) Removal of dental amalgam decreases anti-TPO and anti-Tg autoantibodies in patients with autoimmune thyroiditis, Ivan Sterzl , Jarmila P, Pavlina H, Petr M, Jirina B & Vera  D.M. , Neuroendocrinol Lett 2006; 27(Suppl 1):101–000

(383)(a)  Saito K.  Analysis of a genetic factor of metal allergy-polymorphism of HLA-DR-DO gene.  Kokubyo       Gakkai Zasschi 1996; 63: 53-69; &(b) Prochazkova J, Ivaskova E, Bartova J, Stejskal VDM.  Immunogentic findings in patients with altered tolerance to heavy metals.  Eur J Human Genet 1998; 6: 175.

(385)(a) Kohdera T, Koh N, Koh R.  Antigen-specific lymphocyte stimulation test on patients with psoriasis vulgaris. XVI International Congress of Allergology and Clinical Immunology, Oct 1997, Cancoon, Mexico; & (b)Ionescu G,. Heavy metal load with atopic Dermatitis and Psoriasis, Biol Med 1996; 2:65-68; &

(c) A subset of patients with common variable immunodeficiency.  Blood 1993, 82(1): 192-20.   

 (390) (b) Ellingsen DG, Efskind J, Haug E, Thomassen Y, Martinsen I, Gaarder PI - "Effects of low mercury vapour exposure on the thyroid function in chloralkali workers" J Appl Toxicol 20(6):483-9 (2000);  &(c) Barregard L, Lindstedt G, Schutz A, Sallsten G - "Endocrine function in mercury exposed chloralkali workers" Occup Environ Med 51(8):536-40 (1994) 7951778&form=6&db=m&Dopt=r ; & (d) Watanabe C - "Selenium deficiency and brain functions: the significance for methylmercury toxicity" Nippon Eiseigaku Zasshi 55(4):581-9 (2001); & (e) Watanabe C, Yoshida K, Kasanuma Y, Kun Y, Satoh H.   In utero methylmercury exposure differentially affects the activities of selenoenzymes in the fetal mouse brain. Environ Res 1999 Apr;80(3):208-14; &(f) Li MX, Tan ZQ, Qin SZ, Zhong LP, Li FH, Wang HZ,[Three cases of hypothyroidism induced by cosmetics containing mercury], Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2004 Aug;22(4):312-3. Chinese.

(392) Selenium and antioxidant defenses as major mediators in the development of chronic heart failure.  Heart Fail Rev. 2006 Mar;11(1):13-7.  de Lorgeril M, Salen P.

(394) Amalgam Illness Diagnosis and Treatment, Andrew Hall Cutler, PhD, PE,; & Heavy Metals and Halogens Displace and Block Utilization of Essential Minerals- Iodine and Chelation, International Medical Veritas Associatio; & The effect of mercuric chloride on thyroid function in the rat., Goldman M, Blackburn P.  Toxicol Appl Pharmacol. 1979 Mar 30;48; & THE EFFECT OF CERTAIN METALLIC CATIONS ON THE IODIDE UPTAKE IN THE THYROID GLAND OF MICE. Acta Endocrinol (Copenh). 1964 Aug;46:643-52.  ANBAR M, INBAR M.

(395) Iodine: Why You Need It, Why You Can't Live Without It (4th Edition), Dr. David Brownstein, 2008; & Overcoming Thyroid Disorders, Dr. David Brownstein , & (b) 8. Abraham GE. Facts about Iodine and Autoimmune Thyroiditis. The Original Internist. 2008 Jun; 15(2): 75-6; &  Hollowell JG, Staehling NW, Hannon WH, et al. Iodine nutrition in the United States. Trends and public health implications: iodine excretion data from National Health and Nutrition Examination Surveys I and III (1971-1974 and 1988-1994). J Clin Endocrinol Metab. 1998 Oct;83(10):3401-8; &  Abraham GE, Flechas JD, and Hakala JC. Orthoiodosupplementation: Iodine sufficiency of the whole human body. The Original Internist. 2002; 9:30-41; & (c )  Rink T, Schroth HJ, Holle LH, et al. Effect of iodine and thyroid hormones in the induction and therapy of Hashimoto’s thyroiditis. Nuklearmedizin. 1999;38(5):144-9.

(402) Ando T, Wakisaka I, Hatano H.  Mercury concentration in gray hair.  Nippon Eiseigaku Zasshi 1989;  43(6):1063-8. (405)   Jenny Stejskal, Vera Stejskal. The role of metals in autoimmune diseases and the link to neuroendocrinology Neuroendocrinology Letters, 20:345‑358, 1999. 

(407)  Autism: transient in utero hypothyroxinemia related to maternal flavonoid ingestion during pregnancy and to other environmental antithyroid agents. J Neurol Sci. 2007 Nov 15;262(1-2):15-26. Epub 2007 Jul 24..  Román GC.

(409) (a)Autism: a unique form of mercury poisoning.  ; & (b) Yazbak FE(MD,FAAP)  Autism 99: A National Emergency, &


; & (c) Dr. A Holmes, Autism Treatment Center,Baton Rouge, La,; & (c)Jaquelyn McCandless,  M.D., Autism Spectrum Treatment Center,  Woodland Hills, Ca

(410) J.R. Cade et al,  Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion.  Autism,         Mar 1999.

(411) (a) Puschel G, Mentlein R, Heymann E, 'Isolation and characterization of dipeptyl peptidase IV from human placenta', Eur J Biochem 1982 Aug;126(2):359-65; &(b) Kar NC, Pearson CM.  Dipeptyl Peptidases in     human muscle disease.  Clin Chim Acta 1978; 82(1-2): 185-92; &(c) Seroussi K, Autism and Pervasive Developmental Disorders , 1998, p174, etc.


(412) (c) Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V,   Plasma excitatory amino acids in autism.  Invest Clin 1996,37(2): 113-28; & (b)Rolf LH, Haarman FY, Grotemeyer KH, Kehrer H.  Serotonin and amino acid content in platelets of autistic children.  Acta Psychiatr Scand 1993, 87(5): 312-6; & (c)Naruse H,    Hayashi T, Takesada M, Yamazaki K.  Metabolic changes in aromatic amino acids and monoamines in infantile autism and a new related treatment,  No To Hattatsu, 1989, 21(2):181-9; &(d) Carlsson ML. Is infantile autism a hypoglutamatergic disorder?  J Neural Transm 1998, 105(4-5): 525-35.

(413) (a) Edelson SB, Cantor DS.  Autism: xenobiotic influences.  Toxicol Ind Health 1998; 14(4): 553-63;     & (b) Liska, DJ.  The detoxification  enzyme systems. Altern Med Rev 1998. 3(3):187-98;

(418)   Srikantaiah MV; Radhakrishnan AN.   Studies on the metabolism of vitamin B6 in the small intestine.           Purification and properties of monkey  intestinal pyridoxal kinase. Indian J Biochem 1970 Sep;7(3):151‑6; & (b) Abraham GE, Flechas JD. The effect of daily ingestion on 100mg iodine in a tablet form of Lugol solution (Iodoral®) combined with high doses of vitamins B-2 and B3 (ATP Cofactors) on various clinical and laboratory parameters in 5 subjects with Fibromyalgia. The Original Internist. 2008 Mar; 15(1):8-15; &  Shakir KM, Kroll S, Aprill BS, et al. Nicotinic acid decreases serum thyroid hormone levels while maintaining a euthyroid state. Mayo Clin Proc. 1995 Jun;70(6):556-8.

(419)    Lipozencic J; Milavec‑Puretic V; Pasic A.   Contact allergy and psoriasis. Arh Hig Rada Toksikol 1992 Sep;43(3):249‑54; &      Roujeau JC et al,  Acute generalized exanthematous pustulosis. Analysis of 63     cases;  Arch Dermatol 1991 Sep;127(9):1333‑8;   & Yiannias JA; Winkelmann RK; Connolly SM.   Contact  sensitivities in palmar plantar pustulosis   (acropustulosis).Contact Dermatitis 1998 Sep;39(3):108‑11      

(427) Chetty CS, McBride V, Sands S, Rajanna B.   Effects in vitro on rat brain Mg(++)-ATPase.   Arch Int Physiol    Biochem 1990, 98(5):261-7;  & Bara M, Guiet-Bara A, Durlach J. Comparison of the effects of taurine and magnesium on electrical characteristics of artificial and natural membranes. V. Study on the human amnion of the antagonism between magnesium, taurine and polluting metals. [ French] Magnesium. 1985;4(5-6):325-32. 

(439) (a) Mercuric chloride intoxication. Part 1, Bull Environ Contam Toxicol 1978; 20(6): 729-35; & (b) Mondal MS, Mitra S.  Inhibition      of bovine xanthine oxidase activity by Hg2+ and other metal ions.  J Inorg Biochem          1996; 62(4): 271-9; & (c) Sastry KV, Gupta PK.  In vitro inhibition of digestive enzymes by heavy metals      and their reversal by chelating agents: 

 (458) Dowling AL, Iannacone EA, Zoeller RT.   Maternal Hypothyroidism Selectively Affects the Expression of         Neuroendocrine‑Specific Protein A Messenger Ribonucleic Acid in the Proliferative Zone of the Fetal Rat       Brain Cortex.  Endocrinology 2001 Jan 1;142(1):390‑399

(459) Isny Clinic(South Germany) Kurt Muller , MD,  member of Editorial board for Ganzheitliches Medicine Journal.  Wassertornstrasse 6 , Isny, BRD   fax: 0049 7562 550 52

(464) (a) Walsh, WJ, Health Research Institute, Autism and Metal Metabolism,, Oct 20, 2000; &    (b)  Walsh WJ, Pfeiffer Treatment Center, Metal‑Metabolism and Human Functioning, 2000,

(468) Overzet K, Gensler TJ, Kim SJ, Geiger ME, van Venrooij WJ, Pollard KM, Anderson  P, Utz PJ. Small nucleolar RNP Scleroderma      autoantigens associate with phosphorylated serine/arginine splicing factors during apoptosis.  Arthritis Rheum 2000 Jun;43(6):1327‑36

(476) (a) Dr Thomas Verstraeten, US Centres for Disease  Control and Prevention, Summary Results: Vaccine Safety  Datalink Project ‑ a database of 400,000 children , May 2000; & (b) Halsey, NA. Limiting Infant Exposure to Thimerosal in vaccines.   J. of the Amer. Medical Assoc., 282: 1763-66; & (c) The Center for Biologics Evaluation and Research (CBER), Review of the Use of Thimerosal in Vaccines, The US Food and Drug Administration (FDA), Jul 4, 2000.

(500) B.Windham, Common Exposure Levels and Adverse Health Effects from Mercury/Amalgam Dental Fillings, and Results of Replacement of Amalgam Fillings, Review, 2001.   (over 3000 peer-reviewed studies documenting

common exposures more than Gov’t health guidelines and mechinisms of causality of 40 chronic conditions, and 60,000 clinical cases of recovery or significant improvement after amalgam replacement as followed by doctors)

(501) Review: Documentation of common mercury exposure levels from amalgam by medical labs, Government agency studies, peer-reviewed studies. B Windham (Ed),     &

(502) Effects of prenatal and neonatal mercury exposure on children, B Windham(Ed), over 150 peer-reviewed studies,

(503) Summary of results of treatment of chronic health conditions by amalgam replacement, as reported to the FDA and treatment clinics,  &

 (508)(a) Bonar DB, McColgan B, Smith DR, Darke C, Guttridge MG, Williams HSmyth PPA,   Hypothyroidism  and aging: The Rosses’ Survey.  Thyroid 2000, 10(9):821-827;& (b) Canaris GJ, Manowitz NR, Mayor G, Ridgway EC.   The Colorado thyroid disease prevalence study. Arch Tntern Med 2000, 160(4):526-34; &(c) GS Connection 11(12): Prevelence of Thyroid Imbalance, Thyroid in Pregnancy, GSDL,

(509)(a) Klein RZ, Sargent JD, Larsen PR, Waisbren Se, Haddow JE, Mitchell ML, Relation of severity of maternal hypothyroidism to cognitive development of offspring.  J Med Screen 2001: 8:18-20; &(b) de Escobar DM, Orbregon MF, del Rey FE, Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia?  J Clin Endocrin Metab 2000; 3975-3987; &(c) Thyroid Imbalances in Pregnancy Linked to Poor Child Neurodelopment, Great Smokies Diagnostic Lab,

&(d) J. E. Haddow et al, Babies Born to Mothers with Untreated Hypothyroidism Have Lower I.Q.'s,   New England Journal of Medicine, Aug 19, 1999; & (e) Lavado-Autric et al. Early maternal hypothyroxinemia alters histogenesis and cerebral cortex cytoarchitecture of the progeny. JCI 111:1073-1082 (2003); & (f)Pop VJ, Vader HL et al, Low maternal free thyroxine during early pregnancy is associated with impaired psychomotor development in infancy, Clin Endocrinol(Oxf), 50:149-55, 1999; & Man EB, Brown JF, Serunian SA. Maternal hypothyroxinemia: psychoneurological deficits of progeny. Ann Clin Lab Sci 1991;21(4):227-39; & Pharoah POD, Connolly KJ et al, Maternal thyroid hormone levels in pregnancy and cognitive and motor performance of the children, Clin Endocrinol(Oxf), 1984, 21:265-70; & (g) Pop VJ, de Vries E, et al, Maternal thyroid peroxidase antibodies during pregnancy: and impaired child development, J Clin Endocrinol Metab., 1995, 80:3561-3566 & Connors MH, Styne DM, Neonatal athyreosis resulting from thyrotropin-binding inhibitory immonoglobulins, Pediatrics, 1986, 78:287-290; &  (h) Asami T, Suzuki H, Effects of thyroid hormone deficiency on electrocardiogram findings of congenenitally hypothyroid neonates. Thyroid 11: 765-8, 2001; &  Kumar R, Chaudhuri BN. Altered maternal thyroid function: fetal and neonatal heart cholesterol and phospholipids,  .Indian J Physiol Pharmacol 1993 Jul;37(3):176-82

(510) (a)Morris MS, Bostom AG, Jacques PJ, Selhub J, Rosenberg IH, Hyperhomocysteinemia and       hypercholesterolemia associated with hypothyroidism in the third U.S. National Health and Nutrition Examination      Survey, Artherosclerosis 2001, 155:195-200; & (b) Shanoudy H. Soliman A, Moe S, Hadian D, Veldhuis F, Iranmanesh  A, Russell D, Early manifestations of “sick eythyroid syndrome” in patients with compensated chronic heart failure, J Card Fail 2001, 7(2):146-52; & (c)AE. Hak, HAP. Pols, TJ. Visser, et al., The Rotterdam Study., Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women, Ann Int Med, 2000, vol. 132, pp. 270--278  &(d)Thyroid Dysfunction Linked to Elevated Cardiac Risk, GSDL,; &(e) Biondi B, Palmieri EA, Lombardi G, Fazio S.  Effects of subclinical thyroid dysfunction on the heart.  Ann Intern Med 2002 Dec 3;137(11):904-14; & (f) B.G. Nedreboe, O. Nygard, et al, Plasma Total Homocysteine of hypothyroid patients during 12 months of treatment, Haukeland Univ. Hospital, Bergen, Norway,  (references 7 other studies with similar findings); & (g) Hussein, WI, Green, R, Jacobsen, DW, Faiman, C. Normalization of hyperhomocysteinemia with L-thyroxine in hypothyroidism. Ann Intern Med 1999; 131:348;

(511) (a) Abramson J, Stagnaro-Green A, Thyroid antibodies and fetal loss, Thyroid 2001, 11(1): 57-63; &(b) Thyroid Antibodies May Spur Pregnancy Loss, GSDL, www.gsdl.con/news/connections/vol12/conn20010411.html

& (c)Allan W.(MD), Maternal Hypothyroidism During Pregnancy Linked to Increased Risk for Miscarriage,  Journal of Medical Screening, November 22, 2000; & (d) Abstract # 274: Wolfberg, Adam J. and David      A. Nagey, "Thyroid Disease During Pregnancy and Subsequent Congenital Anomalies."St Johns Univ. ; & Birth Defect News, Jan 2002, p2; & (e)Emerson, C.H. (1996).  Thyroid Disease During and After Pregnancy.  In L.E. Braverman & R.D. Utiger (Eds.), The Thyroid, A Fundamental and Clinical Text (pp. 1021-1031; & (f) Man EB, Jones WS, Thyroid function in human pregnancy: retardation in 8-month old infants, Am J Obstet Gynecol, 1969, 104:898-908; & Brent GA, Maternal hyrothyroidism: recognition and management, Thyroid, 1999, 9:661-5.

(513) (a) Valentino M, Santarelli L, Pieragostini E, Soleo L, Mocchegiani E.  In vitro inhibition of thymulin production in mercury-exposed thymus of young mice. Sci Total Environ 2001 Apr 10;270(1-3):109-112; &

(b)  Nordlind K.     Stimulating effect of mercuric chloride and nickel sulfate on DNA synthesis of thymocytes and peripheral lymphoid cells.  Int Arch Allergy Appl Immunol 1983;72(2):177-179; & Chen M, von Mikecz A.  Specific inhibition of rRNA transcription and dynamic relocation of fibrillarin induced by mercury.  Exp Cell Res 2000 Aug 25;259(1):225‑238; & © Dieter MP, Luster MI, Boorman GA, Jameson CW, Dean JH, Cox JW. Immunological and biochemical responses in mice treated with mercuric chloride. Toxicol Appl Pharmacol 1983 Apr;68(2):218‑228.

(515) Laks, Dan R. Assessment of chronic mercury exposure within the U.S. population, National Health and Nutrition Examination Survey, 1999–2006. Biometals. August 2009; & Laks, D.R. et al, Mercury has an affinity for pituitary hormones, Medical Hypotheses, Dec 2009. 

(555)  Lewis RN; Bowler K.    Rat brain (Na+‑K+)ATPase: modulation of its ouabain‑sensitive K+‑PNPPase activity by thimerosal. Int J Biochem 1983;15(1):5‑7; Bellabarba D, and Tremblay R; Effect of thimerosal on serum binding of thyroid hormones, Can J Physsiol Pharmacol,173, 51:156-159: & Hokkfen B, Kodding R, Hesch RD; Regulation of thyroid hormone metabolism in rat liver fractions, Biochim Biophys Acta 1978, 539:(1): 114-24.          

(558) American Assoc. of Clinical Endocrinologists and American College of Endocrinolog.  AACE clinical practice guidelines for the evaluation and treatment of hyperthyroidism and hypothyroidism.  Endocr Pract., 1995, 1: 54-62.

(559) Choy CM, Lam CW, et al, 2002, Infertility, blood mercury concentrations, and dietary seafood consumption: a case control study, BJOG: An International Journal of Obstetrics and Gynaecology, 109: 1121-1125.

(560) Nath J, Safar R. Late-onset bipolar disorder due to hyperthyroidism. Acta Psychiatr Scand 2001;104:72-75.

(561) Muller AF, Drexhage HA, Berghout A. Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care. Endocrine Reviews 2001;22(5):605-30.

(567) Kim CY, Satoh H, et al, Protective effect of melatonin on methylmercury-Induced mortality in mice.  Tohoku J Exp Med. 2000 Aug;191(4):241-6; & Olivieri G,  Hock C, et al , Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells.  J Neurochem. 2000 Jan;74(1):231-6.

(568) Bemis JC, Seegal RF; 2000, PCBs and methylmercury alter intracellular calcium concentrations in rat cerebellar granule cells. Neurotoxicology, 21(6): 1123-1134. 

(569) Baccarelli A, Pesatori AC, Bertazzi PA. Occupational and environmental agents as endocrine disruptors: experimental and human evidence.   J Endocrinol Invest. 2000 Dec;23(11):771-81

(570) Libe R, Baccarelli A, et al, Long-term follow-up study of patients with adrenal incidentalomas.Eur J Endocrinol. 2002 Oct;147(4):489-94. 

 (571) Manzo L,Candura SM, Costa LG, et al;  Biochemical markers of neurotoxicity. A review of mechanistic studies and applications. Hum Exp Toxicol, 1996 Mar, 15 Suppl 1:, S20-35. 

(580)  Life Extension Foundation (MDs), Disease Prevention and Treatment, Expanded 5th Edition, 20133; &

(b) American Journal of Clinical Nutrition, 2008 & Life Extension Foundation, Life Extension, Jan 2009, ,; & (b) Sinclair C, Gilchrist JM, Hennessey JV, et al. Muscle carnitine in hypo- and hyperthyroidism. Muscle Nerve. 2005 Sep;32(3):357-9; & Maebashi M, Kawamura N, Sato M, et al. Urinary excretion of carnitine in patients with hyperthyroidism and hypothyroidism: augmentation by thyroid hormone. Metabolism. 1977 Apr;26(4):351-6; &  Benvenga S, Amato A, Calvani M, et al. Effects of carnitine on thyroid hormone action. Ann N Y Acad Sci. 2004 Nov;1033:158-67; & Benvenga S, Ruggeri RM, Russo A, et al. Usefulness of L-carnitine, a naturally occurring peripheral antagonist of thyroid hormone action, in iatrogenic hyperthyroidism: a randomized, double-blind, placebo-controlled clinical trial. J Clin Endocrinol Metab. 2001 Aug;86(8):3579-94.

 (581) Vitamin Research News, weekly journal (several editions), 2003-2009,