Neurological Effects of Mercury Exposure

B. Windham (Ed.)

I. Introduction

Toxic metals such as mercury, lead, cadmium, etc. have been documented to be neurotoxic, according to U.S. Government agencies cause adverse health effects and learning disabilities to millions in the U.S. each year, especially children and the elderly(160,105,27d).The health effects of toxic metals are synergistic with other toxic exposures such as pesticides, endocrine disrupting substances like organochlorine compounds and PCBs, etc. There are also synergistic effects with the various types of parasites, bacteria, viruses to which people have common exposures and commonly become infected when the immune system is weakened by toxic exposures (485,469b,470,581). Studies have found considerable genetic variability in susceptibility to toxic metals as well. While there is considerable commonality to the health effects commonly caused by these toxic metals, and effects are cumulative and synergistic in many cases, this paper will concentrate on the health effects of elemental mercury from amalgam fillings.

Mercury amalgam dental fillings have been found to be the largest source of both inorganic and methyl mercury in most who have several amalgam fillings. Those with several amalgam fillings have been found by hundreds of thousands of medical lab tests to have mercury exposure levels approximately 10 times the average level of those without amalgam, and saliva and excretion levels decline 90% after amalgam replacement.

Clinical experience has identified some of the factors that cause mercury to accumulate in various areas of the body(581). These include past physical trauma to an area, inflammation, food allergies, Geopathic Stress, scars and dental trauma, structural abnormalities, biochemical deficiencies such as zinc, environmental toxicity, and unresolved psychological problems.

II. Neurological Effects of Mercury and Toxic Metals

Studies have found that mercury is neurotoxic(kills or damages brain cells and nerve cells) (19,27,34,36,43,69,70,147,148,175,207,211,258,273, 291,295,327,329,301,303,305,395/39,262, 274,303); generates high levels of reactive oxygen species(ROS) and oxidative stress, depletes glutathione and thiols causing increased neurotoxicity from interactions of ROS, glutamate, and dopamine (13,56,98,102, 145,169,170, 184,213,219,250,257,259,286,288,290,291,302,324, 326, 329,416,424, 442, 496,564,565); kills or inhibits production of brain tubulin cells (66,67,161,166, 207,258,300); inhibits production of neurotransmitters by inhibiting: calcium-dependent neurotransmitter release(372,432), dihydroteridine reductase (27,122,257,333), nitric oxide synthase(259), blocking neurotransmitter amino acids (412), causes abnormal migration of neurons in the cerebral cortex(149), and effecting phenylalanine, serotonin, tyrosine and tryptophan transport to neurons (34,122,126,257, 285,288,333,372,374,412/333) Part of the toxic effects of mercury, lead, cadmium, etc. are through their replacing essential minerals such as zinc at their sites in enzymes, disabling the necessary enzymatic processes.

While there have been large increases of most neurological and immune conditions among adults over the last 2 decades(574), the incidence of neurotoxic or immune reactive conditions in infants such as autism, schizophrenia, ADD, dyslexia, learning disabilities, etc. have been increasing especially rapidly in recent years (2,409,441,476). A report by the National Research Council found that 50% of all pregnancies in the U.S. were resulting in prenatal or postnatal mortality, significant birth defects, developmental neurological or immune conditions, or otherwise chronically unhealthy babies(441). Exposure to toxic chemicals or environmental factors appear to be a factor in as much as 28 percent of the 4 million children born each year(441,160), with 1 in 6 having one of the neurological conditions previously listed. EPA estimates that over 3 million of these are related to lead or mercury toxicity (2,125,276,409), with approximately 25% of U.S. infants receiving dangerous levels of mercury exposure(276). A study found that prenatal Hg exposure is correlated with lower scores in neurodevelopmental screening, but more so in the linguistic pathway(32c). A study at the U.S. CDC found "statistically significant associations" between certain neurologic developmental disorders such as attention deficit disorder(ADD) and autism with exposure to mercury from thimerosal‑ containing vaccines before the age of 6 months(476), and a follow on study using federal vaccine data bases confirmed that autism, speaking disorders, and heart arrest have increased exponentially with increasing exposures to mercury thimerosal-containing vaccines(476b). Thimerosal has also been found to cause hormonal effects(555,413). Prenatal exposure to mercury has also been found to predispose animals and infants to seizures and epilepsy (5,52). There is evidence supporting a link between the aluminum hydroxide used in vaccines causing brain inflammation and symptoms associated with Parkinson's, amyotrophic lateral sclerosis (Lou Gehrig's disease), and Alzheimer's(585). Brain inflammation has also been found to be a factor in autism.

A large epidemiological study, NHANES III, by the National Institute for Health has found a significant correlation between several chronic health conditions and having more than average number of dental amalgam surfaces. The conditions in which the number of dental amalgam surfaces were most highly correlated with disease incidence were MS, epilepsy, migraines, mental disorders, diseases of the nervous system, disorders of the thyroid gland, cancer, and infectious diseases (543). Other conditions where incidence was significantly correlated with having more than the average number of amalgam surfaces are: diseases of the male and female genital tracts, Disorders of the peripheral nervous system, Diseases of the respiratory system, and Diseases of the genitourinary system (543).

There has been a huge increase in the incidence of degenerative neurological conditions in virtually all Western countries over the last 2 decades(574,581). The increase in Alzheimer’s has been over 300% while the increase in Parkinson’s and other motor neuron disease has been over 50%. The primary cause appears to be increased exposures to toxic pollutants(574).

Oxidative stress and reactive oxygen species(ROS) have been implicated as major factors in neurological disorders including stroke, PD, MS, Alzheimer’s, ALS, MND,FM,CFS, etc. (13,35c,56,84,98,145,169,207b,258,424,442-444,453,462,496,581). Mercury induced lipid peroxidation has been found to be a major factor in mercury’s neurotoxicity, along with leading to decreased levels of glutathione peroxidation and superoxide dismustase(SOD)(13,254,489,494-496,577). Metalloprotein(MT) is involved in metals transport and detoxification (442,464). Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally bind cuprous ions(477), thus allowing buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD function. Exposure to mercury results in changes in metalloprotein compounds that have genetic effects, having both structural and catalytic effects on gene expression (114,241,296,297,442,464,477,495). Some of the processes affected by such MT control of genes include cellular respiration, metabolism, enzymatic processes, metal-specific homeostasis, and adrenal stress response systems. Significant physiological changes occur when metal ion concentrations exceed threshold levels. Such MT formation also appears to have a relation to autoimmune reactions in significant numbers of people (114,60,313,342,369,442,464). Of a population of over 3000 tested by the immune lymphocyte reactivity test(MELISA,60,275), 22% tested positive for inorganic mercury and 8% for methyl mercury .

Programmed cell death(apoptosis) is documented to be a major factor in degenerative neurological conditions like ALS, Alzheimer’s, MS, Parkinson’s, etc. Some of the factors documented to be involved in apoptosis of neurons and immune cells include inducement of the inflammatory cytokine Tumor Necrosis Factor-alpha(TNFa) (126), reactive oxygen species and oxidative stress(13,43b,56a,296b), reduced glutathione levels(56,126a,111a), inhibition of protein kinase C(43), nitric oxide and peroxynitrite toxicity(43a), excitotoxicity (490,496,521,524), excess free cysteine levels(56d,111a),excess glutamate toxicity(13b, 416e), excess dopamine toxicity (56d,13a), beta-amyloid generation(462), increased calcium influx toxicity (416e,296b,333,432,462c,507)and DNA fragmentation(296,297) and mitochondrial membrane dysfunction (56d,416e,51a).

Mitochondrial DNA mutations or damage are important contributors to aging and degenerative diseases(297b,298), and mercury is common cause of mitochondrial DNA damage and degeneration(296,297a,56d,416e,51a). Pyrroloquinoline Quinone (PPQ), an essential micronutrient many are deficient in, has been found to improve such damage(299).

TNFa(tumor necrosis factor-alpha) is a cytokine that controls a wide range of immune cell response in mammals, including cell death(apoptosis). This process is involved in inflammatory and degenerative neurological conditions like ALS, MS, Parkinson’s, rheumatoid arthritis, etc. Cell signaling mechanisms like sphingolipids are part of the control mechanism for the TNFa apoptosis mechanism(126a). Glutathione is an amino acid that is a normal cellular mechanism for controlling apoptosis. When glutathione is depleted in the brain, reactive oxidative species increased, and CNS and cell signaling mechanisms are disrupted by toxic exposures such as mercury, neuronal cell apoptosis results and neurological damage. Mercury has been shown to induce TNFa and deplete glutathione, causing inflammatory effects and cellular apoptosis in neuronal and immune cells(126b,126c).

Another neurological effect of mercury that occurs at very low levels is inhibition of nerve growth factors, for which deficiencies result in nerve degeneration. Mercury vapor is lipid soluble and has an affinity for red blood cells and CNS cells(21a). Only a few micrograms of mercury severely disturb cellular function and inhibits nerve growth (175,147,226,255,305,149). Prenatal or neonatal exposures have been found to have life long effects on nerve function and susceptibility to toxic effects. Prenatal mercury vapor exposure that results in levels of only 4 parts per billion in newborn rat brains was found to cause decreases in nerve growth factor and other effects(305). This is a level that is common in the population with several amalgam fillings or other exposures(500). Insulin-like-growth factor I (IGF-I) are positively correlated with growth hormone levels and have been found to be the best easily measured marker for levels of growth hormone, but males have been found more responsive to this factor than women(497). IGF-I controls the survival of spinal motor neurons affected in ALS during development as well as later in life(497,498). IGF-I and insulin levels have been found to be reduced in ALS patients with evidence this is a factor in ALS(497,498). Several clinical trials have found IGF-I treatment is effective at reducing the damage and slowing the progression of ALS and Alzheimer’s with no medically important adverse effects(498). It has also been found that in chronically ill patients the levels of pituitary and thyroid hormones that control many bodily processes are low, and that supplementing both thyrotropin-releasing hormone and growth control hormone is more effective at increasing all of these hormone levels in the patient.

Mercury can cause depression and mood disorders through increased neurological problems related to lowered levels of neurotransmitters dopamine, serotonin, noreprenephrine, and acetylcholinesterase (35,38,104,107,125,140,141,175,251,254,275,288,290,296,297,305,365,367, 372,381,432,451,465,412,581,582). In such cases mercury has been found to accumulate in and affect the function of the brain limbic system(581). The reduced neurotransmitter levels in those with amalgam appear to be a factor encouraging smoking since nicotine increases these neurotransmitter levels and a much higher percentage of those with amalgam smoke than in those without amalgam(141).

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(Section VIII.). 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(Section VI.). The normalization of pituitary function also often normalizes menstrual cycle problems, endometriosis, and increases fertility(35,9).

Animal studies of developmental effects of mercury on the brain have found significant effects at extremely low exposure levels, levels commonly seen in those with amalgam fillings or in dental staff working with amalgam. One study(305) found prenatal mercury vapor exposure decreased NGF concentration in newborn rat’s forebrain at 4 parts per billion(ppb) tissue concentration. Another study(175) found general toxicity effects at 1 micromole(uM) levels in immature cell cultures, increased immunoreactivity for glial fibrillary protein at 1 nanamole (0.2 ppb) concentration, and microglial response at even lower levels. Other animal studies on rodents and monkeys have found brain cellular migration disturbances, behavioral changes, along with reduced learning and adaption capacity after low levels of mercury vapor exposure (149,175,210,264,287,305). The exposure levels in these studies are seen in the fetus and newborn babies of mother’s with amalgam fillings or who had work involving amalgam during pregnancy(61). Mercury vapor has been found to primarily affect the central nervous system, while methyl mercury primarily affects the peripheral nervous system(175c).

Long term occupational exposure to low levels of mercury can induce slight cognitive deficits, lability, fatigue, decreased stress tolerance, etc. Higher levels have been found to cause more serious neurological problems (119,128,160,285,457,etc.). Other studies(285bg,395) found that workers exposed at high levels at least 20 years previous(urine peak levels above 600 ug/L demonstrated significantly decreased strength, decreased coordination, increased tremor, paresthesia, decreased sensation, polyneuropathy, etc. Significant correlations between increasing urine mercury concentrations and prolonged motor and sensory distal latencies were established(285g). Elemental mercury can affect both motor and sensory peripheral nerve conduction and the degree of involvement is related to time‑integrated urine mercury concentrations. Thirty percent of dentists with more than average exposure were found to have neuropathies and visuographic dysfunction compared to none in the control group(395d). Other studies have also found a connection between mercury with peripheral neuropathy and paresthesia (190,449,502,71bdef,395,581,582). Chronic mercury exposure has been found to be a significant factor in many neurological conditions including Alzheimer’s, Dementia, Parkinson’s, MS, etc. Neurological problems are among the most common and serious problems caused by mercury and include memory loss, moodiness, depression, anger and sudden bursts of anger/rage/violence

(290,465,480-483,487,534), self-effacement, suicidal thoughts, lack of strength/force to resolve doubts or resist obsessions or compulsions, etc. Many studies of patients with major neurological diseases have found evidence amalgam fillings may play a major role in development of conditions such as depression (94,107,109,212,222,271,294,212,229, 233,285e,317,320,322,372,374,453,581,582), schizophrenia (34,35,295,465,560), bipolar disorder (294), memory problems (212,222,581,582), and other more serious neurological diseases such as MS, ALS, Parkinson’s, and Alzheimer’s. A large U.S. CDC study found that those with more amalgam fillings have significantly more chronic health problems, especially neurological problems and cancer(543).

Some factors that have been documented in depression are low serotonin levels, abnormal glucose tolerance(hypoglycemia), and low folate levels(480-83), which mercury has also been found to be a cause of. Occupational exposure to mercury has been documented to cause depression and anxiety(534). One mechanism by which mercury has been found to be a factor in aggressiveness and violence is its documented inhibition of the brain neurotransmitter acetylcholinesterase (175,251c,305,451,465,254). Low serotonin levels and/or hypoglycemia have also been found in the majority of those with impulsive and violent behavior(481,482).

Numerous studies have found long term chronic low doses of mercury cause neurological, memory, behavior, sleep, hearing loss(566), and mood problems (3,34,60,69,70,71,74,107-109,119,140,141,160,199,212,222, 246,255,257, 282,290,453,581,582). Neurological effects have been documented at very low levels of exposure (urine Hg< 4 ug/L), levels commonly received by those with amalgam fillings(290). One of the studies at a German University(199) assessed 20,000 people. There is also evidence that fetal or infant exposure causes delayed neurotoxicity evidenced in serious effect at middle age(255,306). Organic tin compounds formed from amalgam are even more neurotoxic than mercury (222,262). Studies of groups of patients with amalgam fillings found significantly more neurological, memory, mood, and behavioral problems than the control groups. (3,34,107,108,109,140,141,160,199,212,222,290,453,581,582).

Other studies(285c) found that mercury at levels below the current occupational safety limit causes adverse effects on memory at very low exposure levels. More studies found that long term exposure causes increased micro nuclei in lymphocytes and significantly increased IgE levels at exposures below current safety levels(128), as well as maternal exposure being linked to mental retardation(110). Very high levels of mercury are found in brain memory areas such as the cerebral cortex and hippocampus of patients with diseases with memory related symptoms (158,34,207,etc.} Mercury has been found to cause memory loss by inactivating enzymes necessary for brain cell energy production and proper assembly of the protein tubulin into microtubules(258). DMSO has been found to have some capability to repair such damage(581).

III. Treatment of Toxic Related Neurological Conditions

The mechanisms by which mercury causes neurological conditions have been documented, but it has also been found that people with such conditions commonly recover or have significant improvement after amalgam replacement- from conditions including:

memory disorders (8,35,94,212,222,322,440,453,552,557,581,582), schizophrenia and bipolar disorder(294,295,465,560,581,34,35), depression (62,94,107,163,185,212,222,229,233bcfh,271,294,285e,317,322,376, 386de,453,465,485,523,525c,532,538,551,556,557,581,582,35,40), insomnia (35,62,94,212,222,233ag,271,317,322,376,525c,581,582), anger(212,233,102,557,35,62), anxiety & mental confusion (62,94,212,222,229,233abcfgh,271,317,322,440,453,525c,532,551,557, 581,35,57), neuropathy/paresthesia (8,35,62,94,163,212,222,322,556,557,581,582), MS(62,94,95,102,163,170,212,222,229,271,291,302,322,369,469,485,34, 35c,229,523,532,581), ALS(97,423,405,469,470,485,535,35), Parkinson’s/ muscle tremor (222,248,228a,229,233f, 271,322,469,535,557,581,582, 212,62,94, 98,35), Alzheimer’s(62,204,251c,386e,535,581,35),

headaches/migraines (5,8,34,35,47f,62,95,185,212ab,222,229, 233abdefgh,271,317,322,349, 354,115,376,440,453, 523,525,532,537,538, 552,556,581,582,583), epilepsy (5,35,309,229,386e,557,581), ataxia/balance problems (250c,581,582);

Lipoic acid has been found to have protective effects against cerebral ischemic-reperfusion, excitotoxic amino acid(glutamate) brain injury, mitochondrial dysfunction, diabetic neuropathy(572,550). Other antioxidants such as carnosine (495a), Coenzyme Q10,Vitamins C & E, ginkgo biloba, pycnogenol and selenium have also been found protective against degenerative neurological conditions and ginkgo biloba and 5-HTP for ADHD(176,494,495e, 444,237,550,20). Several doctors have found thiamin(B3), Vit B6, inositol, and folic acid supplementation to alleviate peripheral neuropathies, pain, tinnitus, and other neurological conditions(502). Several studies have documented that lipoic acid(an antioxidant and chelator) resulted in improvement in the majority of diabetes cases it was used for, by improving glucose metabolism, increasing insulin sensitivity, and reducing nerve damage(including in diabetic neuropathy)(501e,550). Properly formulated nutritional treatments have been found to be effective in treating ADHD and depression(522). Hormonal imbalances such as from taking birth control pills can be a factor in causing B vitamin deficiencies such as B6 and Riboflavin which can be a factor in migraine headaches. Supplementation has been found to be helpful in such circumstances (20).

One chelation expert(581) suggests when chelating with DMPS supplementation with a good multivitamin/multimineral plus Vit E(400 IU), selenium(200-400 ug), and Vit C(=>2 grams or Vit C IV) (581). He also finds chlorella beneficial for most. He has found that other factors that reduce detoxification include:

Low sodium, calcium, potassium, or selenium levels

Low protein in diet or low stomach acid

Hormonal problems

Low serum cholesterol (carrier)

Low glutathione or other detox enzymes

Kidney problems or damage from mother’s amalgams

Constipation or Leaky Gut

Electromagnetic influences(scars, Geopathic Stress, EMF, RF waves)

For information and treatment of factors involved in neurological conditions other than toxic metals, see the treatment section of the individual condition review paper of interest, linked above.

References:

(2)U.S. Environmental Protection Agency(EPA), 1999, "Integrated Risk Information System, National Center for Environmental Assessment, Cincinnati, Ohio, http://www.epa.gov/ncea/iris.htm

(3) Marlowe M et al, “Main and interactive effects of metallic toxins on classroom behavior”, J Abnormal Child Psychol, 1985, 13(2):185-98; & Moon C et al, “Main and Interactive Effect of Metallic Pollutants on Cognitive Functioning”, Journal of Learning Disabilities, April, 1985; & Pihl RO et al, “Hair element content in Learning Disabled Children”, Science, Vol 198, 1977, 204-6; & Gowdy JM et al, “Whole blood mercury in mental hospital patients”, Am J Psychiatry, 1978, 135(1):115-7.

(5) D.Klinghardt(MD), “Migraines, Seizures, and Mercury Toxicity”, Future Medicine Publishing,1997;& Migraines, Seizures, and Mercury Toxicity; Klinghardt D. Alternative Medicine Magazine ,Issue21 Dec,1997/Jan,1998. www.healingartscenter.com/Library/articles/art10.htm & (b) Klinghardt D; A series of fibromyalgia cases treated for heavy metal toxicity: case report and hypothesis; Journal of Orthopaedic Medicine 2001 23 58-59

(8) Redhe,O. Sick From Amalgam R-Dental Ab, Frejavagen 33, S-79133 Falun, Sweden(100 cases).Olle Redhe ; [olle.redhe@telia.com]

(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.

(13)(a) S.Hussain et al, “Mercuric chloride‑induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain”,J Environ Sci Health B 1997 May;32(3):395‑409; & P.Bulat, “Activity of Gpx and SOD in workers occupationally exposed to mercury”, Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995; 18(2): 321-36 ; & D.Jay, “Glutathione inhibits SOD activity of Hg”, Arch Inst cardiol Mex, 1998,68(6):457-61 &(b) S.Tan et al, “Oxidative stress induces programmed cell death in neuronal cells”, J Neurochem, 1998, 71(1):95-105; & Matsuda T, Takuma K, Lee E, et al. Apoptosis of astroglial cells [Article in Japanese] Nippon Yakurigaku Zasshi. 1998 Oct;112 Suppl 1:24P-; & Lee YW, Ha MS, Kim YK.. Role of reactive oxygen species and glutathione in inorganic mercury-induced injury in human glioma cells. Neurochem Res. 2001 Nov;26(11):1187-93. & (c)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; & (d) Pizzichini M et al, Influence of amalgam fillings on Hg levels and total antioxidant activity in plasma of healthy donars. Sci Total Environ 2003, 301(1-3):43-50; & (e) Metals, toxicity and oxidative stress. Valko M, Morris H, Cronin MT. Curr Med Chem. 2005;12(10):1161-208.

(19) Matts Hanson. Dept of Zoophysiology, University of Lund, Sweden. “Amalgam hazards in your teeth”, J. Orthomolecular Psychiatry 1983; 2(3): 194-201; & F.L.Lorscheider et al, “Evaluation of the safety issue of mercury release from amalgam fillings”, 1993, FASEB J, 7:1432-33; & b Momoi Y, et al; Measurement of galvanic current and electrical potential in extracted human teeth”, J Dent Res, 65(12): 1441-1444; & Holland RI, Galvanic currents between gold and amalgam. Scand J Dent Res, 1980,88:269-72; & Wang Chen CP and Greener EH, A galvanic study of different amalgams, Journal of Oral Rehabilitation, 1977, 4:23-7; & Lemons JE et al, intraoral corrosion resulting from coupling dental implants and restorative metallic systems, Implant Dent, 1992, 1(2):107-112

(20) The 24 Hour Pharmacist, S. Cohen, Rodale Books, 2007.

(21) R.A.Goyer,”Toxic effects of metals”in: Caserett 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.;&(d) Arena, Drew, Poisoning. Fifth Edition. Toxicology-Symptoms-Treatment, Charles C. Thomas-Publisher, Springfield, Il 1986.

(27) Matts Hanson.” Why is Mercury toxic?: Basic chemical and biochemical properties of Mercury/amalgam in relation to biological effects”. ICBM conference Colorado Springs, Co,1988, Proceedings; &(b) Hartman DE. Missed diagnoses and misdiagnoses of environmental toxicant exposure, MCS. Psychiatr Clin North Am 1998, 21(3):659-70. & (c) Merritt’s Textbook of Neurology, 9th Ed., Williams and Wilkins, Baltimore, 1995, p668-, & Clinical Management of Poisoning, 3rd Ed.,(p753) Haddad, Shannon, and Winchester, W.B. Saunders and Company, Philadelphia, 1998; &(d) National Human Adipose Tissue Survey FY82, EPA-560/5-86-039, Dec.1986; *EPA Report: 100% Of Human Adipose Fat Samples Studied Are Laced With Chlorinated Solvents and Heavy Metals www.health‑doc.com/healtharticles/bftoxicityreport.html

(32) T.A.Cook et al, “Fatal mercury intoxication in a dental surgery assistant”, British Dent Journal, 1969, 127:533-555.

(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.

(34) PatrickStörtebecker,Associate Professor of Neurology, Karolinska Institute, Stockholm. Mercury Poisoning from Dental amalgam-A Hazard to the Human Brains, ISBN: 0-941011001-1 & Dental Caries as a Cause of Nervous Disorders, Bioprobe.Inc.,http://www.bioprobe.com; & Neurology for Barefoot Doctors, Stortebecker Foundation for Research, 1988: & J Canadian Dental Assoc, 33(6): 300-;& (b) Henriksson J, Tjalve H. Uptake of inorganic mercury in the olfactory bulbs via olfactory pathways in rats. Environ Res. 1998 May;77(2):130-40..

(35) (a)Huggins HA, Levy,TE, Uniformed Consent: the hidden dangers in dental care, 1999, Hampton Roads Publishing Company Inc; & (b) Hal Huggins, Its All in Your Head, 1997; & (c) Huggins, HA, Solving the MS Mystery: Help, hope and recovery, 2002; &(d) Toxic Elements Research Foundation, Colorado Springs Colorado, “Survery of 1320 patients being treated for heavy metal toxicity”, 2001. 800-331-2303; &

(e)Center for Progressive Medicine, 1999, http://www.hugnet.com

(36) Sam Queen; Chronic Mercury Toxicity- New Hope Against an Endemic Disease. http://www.bioprobe.com; & F.L.Lorscheider et al, "Mercury exposure from silver tooth fillings: emerging evidence questions a paradigm", FASEB J 9:504-508,1995.

(38) 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

(39)M.Inouye et al, Behavioral and neuropathological effects of prenatal methyl mercury exposure in mice”. Neurobehav.Toxicol Teratol., 1985:7;227‑232; &(b) Z.Annau et al, Johns Hopkins Univ., School of Public Health, “Mechanisms of neurotoxicity and their relationships to behavioral changes”, Toxicology, 1988, 49(2): 219-25; &(c) Vinay SD, Sood PP. Inability of thiol compounds to restore CNS arylsulfatases inhibited by methyl mercury. Pharmacol Toxicol 1991 Jul;69(1):71-4;&(d) P.Grandjean et al, “MeHg and neurotoxicity in children”, Am J Epidemiol, 1999, 150(3):301-5: &(e) Budtz-Jorgensen E, Grandjean P, Keiding N, White RF, Weihe P. Benchmark dose calculations of methylmercury-associated neurobehavioral deficits. Toxicol Lett 2000 Mar 15;112-113:193- ; & (f) Crump KS, Kjellstrom T, Shipp AM, Silvers A, Stewart A. Influence of prenatal mercury exposure upon scholastic and psychological test performance: benchmark analysis of a New Zealand cohort. Risk Anal 1998 Dec;18(6):701-13; &(g) Grandjean P, Weihe P, Murata K, Sorensen N, Dahl R, Jorgensen PJ. Cognitive deficit in 7-year-old children with prenatal exposure to methylmercury. Neurotoxicol Teratol 1997 Nov-Dec;19(6):417-28; & (h) More evidence of mercury effects in children; Environ Health Perspect. 1999 Nov;107(11):A554-5; & Epidemiology July 1999;10:370-375; & (i) [Environmental epidemiology research leads to a decrease of the exposure limit for mercury] [Article in Danish] Weihe P, Debes F, White RF, Sorensen N, Budtz-Jorgensen E, Keiding N, Grandjean P. Ugeskr Laeger. 2003 Jan 6;165(2):107-11.

(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”, Allg. Homoopathische 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;& Homoopathische Behandlung de Amalgamvergiftung & “Polemik und Wirklichkeit”, Allgemeine Homoopathische zeitschrift, 1994, 239(6): 225-233 ; & “Amalgamtherapie fur Arzte und Zahnarzte”, Panta 3, 1992, Haug-Verlag.; & Natura Med 1992, 7(4): 295-306; & M.Strassburg et al, “Generalized allergic reaction from silver amalgam fillings”, Dtsche Zahnarztliche Zeit, 22:3-9, 1967.(total:over 1200 cases)

(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; & P.Jenner,“Oxidative mechanisms in PD”, Mov Disord, 1998; 13(Supp1):24-34; & Offen D, et al;. Antibodies from ALS patients inhibit dopamine release mediated by L-type calcium channels. Neurology 1998 Oct;51(4):1100-3. &(b) B.Rajanna et al, “Modulation of protein kinase C by heavy metals”, Toxicol Lett, 1995, 81(2-3):197-203: & A.Badou et al, “HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels”J Biol Chem. 1997 Dec 19;272(51):32411-8., & D.B.Veprintsev, 1996, Institute for Biological Instrumentation, Russian Academy of Sciences, Pb2+ and Hg2+ binding to alpha‑lactalbumin”.Biochem Mol Biol Int 1996 Aug;39(6):1255‑65; & M. J. McCabe, University of Rochester School of Medicine & Dentistry, 2002, Mechanisms of Immunomodulation by Metals, www2.envmed.rochester.edu/envmed/TOX/faculty/mccabe.html;

(48) K.Arvidson,”Corrosion studies of dental gold alloy in contact with amalgam”, Swed. Dent. J 68: 135-139,1984; & Skinner, EW, The Science of Dental Materials, 4th Ed.revised, W.B.Saunders Co., Philadelphia, p284-285,1957; & Schoonover IC, Souder W. Corrosion of dental alloys. JADA, 1941, 28: 1278-91.

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

(50) (a)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;

(51) Heintze et al,“Methylation of Mercury from dental amalgam and mercuric chloride by oral Streptococci”.,Scan. J. Dent. Res. 1983, 91:150‑152: & Rowland, Grasso, Davies “The Methylation of Mercuric Chloride by Human Intestinal Bacteria”. Experientia. Basel 1975 ,31: 1064‑1065; & M.K.Hamdy et al, “Formation of methyl mercury by bacteria”, App Microbiol, 1975, Sept.; & W.Forth, “Toxikologie von Quecksilberverbindungen”, in Quecksilber in der Umwelt-Hearing zur Amalgamprolematik, Niedersachsisches Umweltministerium, 1991; & Brun A, Abdulla M, Ihse I, Samuelsson B. Uptake and localization of mercury in the brain of rats after prolonged oral feeding with mercuric chloride. Histochemistry. 1976 Apr 21;47(1):23-9; & Ludwicki JK Studies on the role of gastrointestinal tract contents in the methylation of inorganic mercury compounds Bull Env Contam Toxicol 42 1989 283-288; & Choi SC, Bartha R.. Cobalamin-mediated mercury methylation by Desulfovibrio desulfuricans LS. Appl Environ Microbiol. 1993 Jan;59(1):290-5; & Wang J, Liu Z; [.In vitro Study of Strepcoccus Mutans in the Plaque on the Surface of Amalgam Fillings on the Convertion of Inorganic Mercury to Organic Mercury][Article in Chinese], Shanghai Kou Qiang Yi Xue. 2000 Jun;9(2):70-2.

(52) Szasz A, Barna B, Gajda Z, Galbacs G, Kirsch-Volders M, Szente M. Effects of continuous low-dose exposure to organic and inorganic mercury during development on epileptogenicity in rats.Neurotoxicology. 2002 Jul;23(2):197-206. szente@bio.u-szeged.hu

(56)(a) A.Nicole et al, “Direct evidence for glutathione as mediator of apoptosis in neuronal cells”, Biomed Pharmacother, 1998; 52(9):349-55; & J.P.Spencer et al, “Cysteine & GSH in PD”, mechanisms involving ROS”, J Neurochem, 1998, 71(5):2112-22: & & J.S. Bains et al, “Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death”, Brain Res Rev, 1997, 25(3):335-58;&

Medina S, Martinez M, Hernanz A, Antioxidants inhibit the human cortical neuron apoptosis induced by hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid peptide 1-42.. Free Radic Res. 2002 Nov;36(11):1179-84. &(b) D. Offen et al, “Use of thiols in treatment of PD”, Exp Neurol, 1996,141(1):32-9; & Pocernich CB, et al. Glutathione elevation and its protective role in acrolein-induced protein damage in synaptosomal membranes: relevance to brain lipid peroxidation in neurodegenerative disease. Neurochem Int 2001 Aug;39(2):141-9; & (c) Pearce RK, Owen A, Daniel S, Jenner P, Marsden CD. Alterations in the distribution of glutathione in the substantia nigra in Parkinson's disease. J Neural Transm. 1997;104(6-7):661-77; & A.D.Owen et al, Ann NY Acad Sci, 1996, 786:217-33; & JJ Heales et al, Neurochem Res, 1996, 21(1):35-39; & & X.M.Shen et al, Neurobehavioral effects of NAC conjugates of dopamine: possible relevance for Parkinson’sDisease”, Chem Res Toxicol, 1996, 9(7):1117-26; & Chem Res Toxicol, 1998, 11(7):824-37; & (d) Li H, Shen XM, Dryhurst G. Brain mitochondria catalyze the oxidation of 7-(2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1,4-benzothiazine-3-carboxyli c acid (DHBT-1) to intermediates that irreversibly inhibit complex I and scavenge glutathione: potential relevance to the pathogenesis of Parkinson's disease. J Neurochem. 1998 Nov;71(5):2049-62; & (e) Araragi S, Sato M. et al, Mercuric chloride induces apoptosis via a mitochondrial-dependent pathway in human leukemia cells. Toxicology. 2003 Feb 14;184(1):1-9.

(57) N.Campbell & M.Godfrey,“Confirmation of Mercury Retention and Toxicity using DMPS provocation” ,J of Advancement in Medicine, 7(1) 1994;(80 cases); & (b)D.Zander et al, “Mercury mobilization by DMPS in subjects with and without amalgams”, Zentralbl Hyg Umweltmed, 1992, 192(5): 447-54(12 cases);

(60) V.D.M.Stejskal, Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden LYMPHOCYTE IMMUNO‑STIMULATION ASSAY ‑MELISA” & VDM Stejskal et al, "MELISA: tool for the study of metal allergy", Toxicology in Vitro, 8(5):991-1000, 1994; & (c) Stejskal V. Immunological effects of amalgam components: MELISA—a new test for the diagnosis of mercury allergy. Proceedings of the International Symposium Status Quo and Perspectives of Amalgam and other Dental Materials; April 29–May 14, 1994; Otzenhausen, Germany. http://www.melisa.org

(61) 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; & G.Drasch et al, “Mercury Burden of Human Fetal and Infant Tissues”, Eur J Pediatr 153:607-610,1994;

(62) Dr. J.E. Hardy, Mercury Free: the wisdom behind the growing consumer moverment to ban silver dental fillings,

1998.

(66) “Regional brain trace‑element studies in Alzheimer’s disease”. C.MThompson,W.R. Markesbery, et al, Univ. Of Kentucky Dept. Of Chemistry, Neurotoxicology (1988 Spring) 9(1):1‑7 & Hock et al, “Increased blood mercury levels in Alzheimer’s patients”, Neural. Transm. 1998, 105:59-68 & Cornett et al, “Imbalances of trace elements related to oxidative damage in Alzheimer’s diseased brain”, Neurotoxicolgy,1998, 19:339-345.

(67) A search for longitudinal variations in trace element levels in nails of Alzheimer’s disease patients. Vance DE Ehmann WD Markesbery WR In: Biol Trace Elem Res (1990 Jul‑Dec)26‑27:461‑70; & Ehmann et al, 1986, Neurotoxicology, 7:195-206; & Thompson et al, 1988, Neurotoxicology, 9:1-7.

(68) K.A.Ritchie et al, Univ. Of Glasgow,"Psychomotor testing of dentists with chronic low level mercury exposure", J Dent Res 74:420, IADR Abstract 160(1995): & Occup Environ Med, 1995, 52(12): 813-7

(69) D Gonzalez-Ramirez et al; "Uninary mercury, porphyrins, and neurobehavioral changes of dental workers in Monterrey, Mexico”, J Pharmocology and Experimental Therapeutics, 272(1): 264-274,1995

(70) D.Echeverria et al, Batelle Center for Public Health Research, Seattle, "Behavioral Effects of Low Level Exposure to Hg vapor Among Dentists", Neurotoxicology & Teratology; 17(2):161-168(1995);

(71) S.C.Foo et al, "Neurobehavioral effects in Occupational Chemical Exposure", Environmental Research, 60(2): 267-273, 1993; &(b) D.G. Mantyla et al, "Mercury toxicity in the dental office: a neglected problem", JADA, 92:1189-1194, 1976; & A case of mercury contamination of a dental suite, JADA, 1976, Vol 92; &(d) Symington D, Mercury poisoning in dentists, J Soc Occup Med, 1980, 30:37-39; & (e) Mercury intoxication resulting from school barometers in three unrelated adolescents, Koyun M, Akman S, Güven AG. Eur J Pediatr. 2004 , Mar;163(3):131-4; & (f) Subclinical inorganic mercury neuropathy: Neurophysiological investigations in 17 occupationally exposed subjects, The Italian Journal of Neurological Sciences. Volume 8, Number 3 / June, 1987, Zampollo A. et al.

(84) 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; & 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; & Alfred V. Zamm. Dental Mercury: A Factor that Aggravates and Induces Xenobiotic Intolerance. J. Orthmol. Med. v6#2 pp67-77 (1991).

(94) F.Berglund, Case reports spanning 150 years on the adverse effects of dental amalgam, Bio-Probe, Inc.,Orlando,Fl,1995;ISBN 0-9410011-14-3(245 cured); & Tuthill JY, "Mercurial neurosis resulting from amalgam fillings", The Brooklyn Medical Journal, December 1898, v.12, n.12, p725-742

(97) Redhe O, Pleva J, "Recovery from ALS and from asthma after removal of dental amalgam fillings", Int J Risk & Safety in Med 1994; 4:229-236, & Adams CR, Ziegler DK, Lin JT., “Mercury intoxication simulating ALS”, JAMA, 1983, 250(5):642-5;

(98) A.Seidler et al, Possible environmental factors for Parkinson's disease",Neurology 46(5): 1275- 1284, 1996; & Vroom FO, Greer M, "Mercury vapor intoxication", 95: 305-318, 1972; & Ohlson et al, “Parkinson’s Disease and Occupational Exposure to Mercury”, Scand J. Of Work Environment Health, Vol7, No.4: 252-256, 1981; L.G. Golota, “Therapeutic properties of Unitihiol” Farm. Zh. 1980, 1: 18-22.

(111) (a) Quig D, Doctors Data Lab,"Cysteine metabolism and metal toxicity", Altern Med Rev, 1998;3:4, p262‑270, & (b) J.de Ceaurriz et al, Role of gamma‑ glutamyltraspeptidase(GGC) and extracellular glutathione in dissipation of inorganic mercury",J Appl Toxicol,1994, 14(3): 201‑; & W.O. Berndt et al,

"Renal glutathione and mercury uptake", Fundam Appl Toxicol, 1985, 5(5):832‑9; & Zalups RK, Barfuss DW. Accumulation and handling of inorganic mercury in the kidney after coadministration with glutathione, J

Toxicol Environ Health, 1995, 44(4): 385-99; & T.W.Clarkson et al, "Billiary secretion of glutathione‑metal complexes", Fundam Appl Toxicol, 1985, 5(5):816‑31;

(114) 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; & Aschner M, Rising L, Mullaney KJ. Differential sensitivity of neonatal rat astrocyte cultures to mercuric chloride (MC) and methylmercury (MeHg): studies on K+ and amino acid transport and metallothionein (MT) induction. Neurotoxicology. 1996 Spring;17(1):107-16. & T.V. O’Halloran, “Transition metals in control of gene expression”, Science, 1993, 261(5122):715-25; & 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; Boot JH. Effects of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes. Cell Struct Funct 1995; 20(3): 233-8; & Baauweegers HG, Troost D. Localization of metallothionein in the mammilian central nervous system.. Biol Signals 1994, 3:181-7.

(119) (a) L.Ronnback et al, "Chronic encephalopaties induced by low doses of mercury or lead", Br J Ind Med 49: 233-240, 1992; &(b) H.Langauer‑Lewowicka,” Changes in the nervous system due to occupational metallic mercury poisoning” Neurol Neurochir Pol 1997 Sep‑Oct;31(5):905‑13; &(c) Langauer-Lewowicka H. [Chronic toxic encephalopathies] [Polish] Med Pr. 1982;33(1-3):113-7; & (d)[Pneuropsychological disorders after occupational exposure to mercury vapors in El Bagre (Antioquia, Colombia)] Rev Neurol. 2000 Oct 16-31;31(8):712-6. Tirado V, Garcia MA et al; & (e) Chronic neurobehavioural effects of mercury poisoning on a group of Zulu chemical workers. Brain Inj. 2000 Sep;14(9):797-814. Powell TJ: & (f) Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol. 1999;6(4):193-200, Haut MW, Morrow LA et al: & (g) Personality traits in miners with past occupational elemental mercury exposure. Environ Health Perspect. 2006 Feb;114(2):290-6; Kobal Grum D, Kobal AB

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

(125) U.S. CDC, National Center for Environmental Health , National Report on Human Exposure to Environmental Chemicals, 2001, www.cdc.gov/nceh/dls/report/Highlights.htm ; & National Research Council, Toxicological Effects of Methyl mercury (2000), pp. 304‑332: Risk Characterization and Public Health Implications, Nat'l Academy Press 2000. & U.S. Centers for Disease Control, Morbidity and Mortality Weekly Report, Mar 2, 2001, www.cdc.gov/mmwr/preview/mmwrhtml/mm5008a2.html; & U.S. CDC,

Second National Report on Human Exposure to Environmental Chemicals, www.cdc.gov/exposurereport/

(126) (a)Singh I, Pahan K, Khan M, Singh AK. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatory cytokine-mediated apoptosis in demyelinating diseases. J Biol Chem. 1998 Aug 7;273(32):20354-62; & Pahan K, Raymond JR, Singh I. Inhibition of phosphatidylinositol 3-kinase induces nitric-oxide synthase in lipopolysaccharide- or cytokine-stimulated C6 glial cells. J. Biol. Chem. 274: 7528-7536, 1999; &Xu J, Yeh CH, et al, Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death. J Biol Chem. 1998 Jun 26;273(26):16521-6; & Dbaibo GS, El-Assaad W, et al, Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death. FEBS Lett. 2001 Aug 10;503(1):7-12; & Liu B, Hannun YA.et al, Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell death.J Biol Chem. 1998 May 1;273(18):11313-20; & (b) Noda M, Wataha JC, et al, Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes. Dent Mater. 2003 Mar;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; & Dastych J, Metcalfe DD et al, Murine mast cells exposed to mercuric chloride release granule-associated N-acetyl-beta-D-hexosaminidase and secrete IL-4 and TNF-alpha. J Allergy Clin Immunol. 1999 Jun;103(6):1108-14. & (c) Tortarolo M, Veglianese P, et al, Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression.. Mol Cell Neurosci. 2003 Jun;23(2):180-92.

(128) M.L.S.Queiroz et al, "Immunoglobulin Levels in Workers Exposed to Inorganic Mercury", Pharmacol Toxicol 74:72-75, 1994; & “Presence of Micronuclei in lymphocytes of mercury exposed workers’, Immunopharmacol Immunotoxicol, 1999, 21(1):141-50; & D.C.Santos, “Immunoglobulin E in mercury exposed workers”, 1997, 19(3):383-92..

(140) R.L.Siblerud, "Health Effects After Dental Amalgam Removal", J Orthomolecular Med 5(2): 95 -106.

(141) RL.Siblerud et al, "Evidence that mercury from dental fillings may be an etiological factor in smoking", Toxicol Lett,v68,n3,1993,p307- & v69(3):305.

(145) Carpenter DO. Effects of metals on the nervous system of humans and animals. Int J Occup Med Environ Health. 2001;14(3):209-18; & J.M.Gorell et al, “Occupational exposure to mercury, manganese, copper, lead, and the risk of Parkinson’s disease”, Neurotoxicology, 1999, 20(2-3):239-47; & J.M. Gorell et al,”Occupational exposures to metals as risk factors for Parkinson's disease”, Neurology, 1997 Mar, 48:3, 650‑8; & Discalzi G, Meliga F et al; Occupational Mn parkinsonism: magnetic resonance imaging and clinical patterns following CaNa2-EDTA chelation. Neurotoxicology. 2000 Oct;21(5):863-6.

(147) .M.Wood,"Mechanisms for the Neurotoxicity of Mercury", in Organotransitional Metal Chemistry, Plenum Publishing Corp, N.Y, N.Y, 1987. & R.P. Sharma et al, “Metals and Neurotoxic Effects”, J of Comp Pathology, Vol 91, 1981.

(148) H.R.Casdorph, Toxic Metal Syndrome, Avery Publishing Group, 1995.

(149) (a)B.Choi et al, "Abnormal neuronal migration of human fetal brain", Journal of Neurophalogy, Vol 37, p719-733, 1978; & (b)L.Larkfors et al,"Methyl mercury induced alterations in the nerve growth factor level in the developing brain ", Res Dev Res,62(2),1991,287- ; & (c)Belletti S, Gatti R. Time course assessment of methylmercury effects on C6 glioma cells: submicromolar concentrations induce oxidative DNA damage and apoptosis. J Neurosci Res. 2002 Dec 1;70(5):703-11;

(158) Wenstrup et al, “Trace element imbalances in the brains of Alzheimer’s patients”, Research, Vol 533,p125-131,1990; & F.L.Lorscheider,B.Haley,et al, “Mercury vapor inhibits tubulin binding ”, FASEB J,9(4):A-3485.,1995 & Vance et al, 1988, Neurotoxicology, 9:197-208; & de Saint-Georges et al, “Inhibition by mercuric chloride of the in vitro polymerization of microtubules”, CR Seances Soc Biol Fil, 1984; 178(5):562-6.

(160) B. Windham, Cognitive and Behavioral Effects of Toxic Metals, 2003. (over 150 medical study references) www.flcv.com/tmlbn.html ; & B.Windham, "Health Effects of Toxic Metals: An Annotated Bibliography",1999; www.flcv.com/tm98.html; &National Human Adipose Tissue Survey FY82, EPA-560/5-86-039, Dec.1986; *EPA Report: 100% Of Human Adipose Fat Samples Studied Are Laced With Chlorinated Solvents and Heavy Metals www.health‑doc.com/healtharticles/bftoxicityreport.html

(161) F.L.Lorscheider et al, “Inorganic mercury and the CNS: genetic linkage of mercury and antibiotic resistance”,Toxicology,1995,97(1): 19-22; & M.C.Roberts, Dept. Of Pathobiology, Univ. Of Washington, “Antibiotic resistance in oral/respiratory bacteria”, Crit Rev Oral biol Med, 1998;9(4):522-

(166) H.Basun et al, J Neural Transm Park Dis Dement Sect, “Metals in plasma and cerebrospinal fluid in normal aging and Alzheimer’s disease”,1991,3(4):231-58

(169) C.H.Ngim et al, Neuroepidemiology,”Epidemiologic study on the association between body burden mercury level and idiopathic Parkinson’s disease”, 1989, 8(3):128-41.

(170) Birgitta Brunes, Adima Bergli, From MS diagnosis to better health ,1996. www.melisa.org; & DAMS, Recoveries from MS after amalgam replacement, www.whale.to/d/ms1.html; & Maile Pouls, Townsend Letter, 1999, www.heall.com/healingnews/may/heavy_metals.html

(175) F. Monnet-Tschudi et al, “Comparison of the developmental effects of 2 mercury compounds on glial cells and neurons in the rat telencephalon”, Brain Research, 1996, 741: 52-59; & Chang LW, Hartmann HA, “Quantitative cytochemical studies of RNA in experimental mercury poisoning”, Acta Neruopathol(Berlin), 1973, 23(1):77-83;.&(c) Sorensen FW, Larsen JO, Eide R, Schionning JD; Neuron loss in cerebellar cortex of rats exposed to mercury vapor: a stereological study. Acta Neuropathol (Berl). 2000 Jul;100(1):95-100.

(176) Niederhofer H. Ginkgo biloba treating patients with attention-deficit disorder. Phytother Res. 2009 May 14.

(184) T.H.Ingalls, Clustering of multiple sclerosis in Galion, Ohio, 1982-1985. Amer J Forensic Med Pathol 1989; 10: 213-5; & “Endemic clustering of multiple sclerosis in time and place”, Am J.Fors Med Path, 1986,7:3-8; & J Forsenic Medicine and Pathology, Vol 4, No 1, 1953; & Epidemiology, etiology and prevention of MS”,Am J Fors Med & Pathology, 1983, 4:55-61; & Craelius W, Comparative epidemiology of multiple sclerosis and dental caries”, J of Epidemiological and Community Health 32:155-65.

(190) P.Urban et al, “Neurological examination on 3 groups of workers exposed to mercury vapor”, Eur J Neurology, 1999, 6(5): 571-7; & B. Polakowska, “Neurological Assessment of Health Status in Dentists”, Med Pr, 1994, 45(3):221-5; & L.Ekenvall et al, “Sensory perception in the hands of dentists” J Work Environ Health, 1990, 16(5):334-9.

(199) Kraub P, Deyhle M, Maier KH, Roller HD, "Field Study on the mercury content of saliva", Heavy Metal Bull, vol.3, issue 1, April '96; & Dr. P.Kraub & M.Deyhle, Universitat Tubingen- Institut fur Organische Chemie, “Field Study on the Mercury Content of Saliva”, 1997 (20,000 people tested for mercury level in saliva and health status/symptoms compiled); http://www.xs4all.nl/~stgvisie/AMALGAM/EN/SCIENCE/tubingen.html

www.bio.net/bionet/mm/toxicol/1999-September/002567.html

(204) Tom Warren, Beating Alzheimer’s, Avery Publishing Group, 1991. www.the7thfire.com/ADApolitics.htm & www.whale.to/m/alzheimer.html

(207) Pendergrass JC, Haley BE, Univ. Of Kentucky Dept. Of Chemistry “ The Toxic Effects of Mercury on CNS Proteins: Similarity to Observations in Alzheimer’s Disease”, IAOMT Symposium paper, March 1997 & “Mercury Vapor Inhalation Inhibits Binding of GTP ...-Similarity to Lesions in Alzheimer’s Diseased Brains”, Neurotoxicology 1997, 18(2)::315-24; & Met Ions Biol Syst, 1997, 34:461-

(210) Mats Berlin, “Is amalgam in dental fillings hazardous to health?”, Lakartidningen, 1992; 89(37):2918-23; & “Mercury in dental filling materials- environmental medicine risk analysis”, in: [Swedish Council for Coordinating and Planning Research, Amalgam and Health, FRN,1999];

& Berlin, M; et al. Prenatal Exposure to Mercury Vapor: Effects on Brain Development. The Toxicologist, 12(1):7(A245), 1992; & "Expert Consulted For Amalgam Study Demands Amalgam Ban", Swedish Dental Materials Study ,"Dagens Nyheter", April 26 2003, www.tv4.se/nyheterna/lopsedel.html www.dn.se/DNet/jsp/polopoly.jsp?d=597&a=134259&previousRenderType=6

(211) M.J.Vimy and F.L. Lorscheider, Faculty of Medicine, Univ. Of Calgary, July 1991. (Study findings) & J. Trace Elem. Exper. Med., 1990,3, 111-123.

(212)(a) Ziff, M.F., “Documented clinical side effects to dental amalgams”, ADV. Dent. Res.,1992; 1(6):131-134; & Ziff, S.,Dentistry without Mercury, 8th Edition, 1996, Bio-Probe, Inc. , ISBN 0-941011-04-6; &

Dental Mercury Detox, Bio-Probe, Inc. http://www.bioprobe.com. (Cases: FDA Patient Adverse Reaction Reports-762, Dr.M.Hanson-Swedish patients-519, Dr. H. Lichtenberg-100 Danish patients , Siblerud, RL. Health effects after dental amalgam removal. J. Orthomol. Med. 5, 1990, 95-106(86 patients); & P. Larose. The effect of amalgam removal on 37 health symptoms in humans. Updated 1992 from study reported in Dental Health & Facts 2(1) 1989. Foundation for Toxic-free Dentistry/Bio-Probe, Orlando(80 patients); & Zamm, AV. Removal of dental mercury: often an effective treatment for the very sensitive patient. J Orthomol. Med. 5, 1990, 138-142(22 patients)

www.flcv.com/hgrecovp.html & (b)Hovmand, O. Oral galvanisme - erfaringer fra praxis. Tandlaegebladet 91, 1987, 473-476. & (c)over 1000 additional cases of significant improvement reported directly to FDA)

(213) Dr. C. Kousmine, Multiple Sclerosis is Curable, 1995.

(219) D.E. Cutright et al, Dept. Of Prosthodontics, Temple Univ.“Systemic mercury levels caused by inhaling mist during high-speed amalgam grinding”, J Oral Med 28(4):100-104,1973 ; & (b) A.Nimmo et al, “Inhalation during removal of amalgam restorations”, J Prosthet Dent, 63(2):1990 Feb, 228-33; &(c) Stonehouse CA, Newman AP. Mercury vapour release from a dental aspirator. Br Dent J 2001 May 26;190(10):558-60 &(d) Taskinen H, Kinnunen E, Riihimaki V. A possible case of mercury-related toxicity resulting from the grinding of old amalgam restorations. Scand J Work Environ Health 1989; 15 (4): 302-4; &

http://atsdr1.atsdr.cdc.gov:8080/97list.html.

(222) M. Daunderer, Handbuch der Amalgamvergiftung, Ecomed Verlag, Landsberg 1998, ISBN 3‑609‑71750‑5 (in German); & “Improvement of Nerve and Immunological Damages after Amalgam Removal”, Amer. J. Of Probiotic Dentistry and Medicine, Jan 1991; & Toxicologische erfahrungen am menchen; Quecksilber in der umwelf-hearing zum amalgamproblem”,Niedersachsiscles Umweltministerium, 1991; & “Amalgam”, Ecomed-Verlag, Landsberg, 1995; & “Amalgamtest”, Forum Prakt.Allgen.Arzt, 1990, 29(8): 213-4; & “Besserung von Nerven- und Immunschaden nach Amalgamsanierung”,Dtsch.Aschr. F. Biologische Zahnmedzin, 1990, 6(4):152-7. ( amalgam removal & DMPS, over 5,000 cases)

(226) (a)B.J. Shenker et al, Dept. Of Pathology, Univ. Of Penn. School of Dental Med.,”Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cell viability” Immunopharmacologicol Immunotoxical, 1992, 14(3):555-77; & M.A.Miller et al, “Mercuric chloride induces apoptosis in human T lymphocytes”, Toxicol Appl Pharmacol, 153(2):250‑7 1998;& Rossi AD,Viviani B, Vahter M. Inorganic mercury modifies Ca2+ signals, triggers apoptosis, and potentiates NMDA toxicity in cerebral granule neurons. Cell Death and Differentiation 1997; 4(4):317-24. & Goering PL, Thomas D, Rojko JL, Lucas AD. Mercuric chloride-induced apoptosis is dependent on protein synthesis. Toxicol Lett 1999; 105(3): 183-95; , &(b) B.J. Shenker et al “Immune suppression of human T-cell activation”, Immunopharmacologicol Immunotoxical, 1992, 14(3):555-77, & 14(3):539-53; & 1993, 15(2-3):273-90;

(228) (a)A.F.Zamm, “Removal of dental mercury: often an effective treatment for very sensitive patients”, J Orthomolecular Med, 1990, 5(53):138-142. (22 patients); & (b)Dr. T. Rau, Paracelsus Alergy Clinic, Lustmuhle, Switzerland, Allergies: Causes, Clarification, Treatment; Explore, 8(4),1996, www.explorepub.com/articles/bio‑therapy.html ; & (c) Dr. B. Shelton, Director, The Allergy Center, Phoenix, Arizona, www.hamptonroadspub.com/main/books/excerpts/elements2.html; & (d) E. Cutler, Winning the War against Asthma & Allergies, Delmar Learning; 1st edition (July 9, 1997)

(229) M.Davis, editor, Defense Against Mystery Syndromes”, Chek Printing Co., &

March, 1994(case histories documented); & Andrew Hall Cutler, PhD, PE; Amalgam Illness:Diagnosis and Treatment; 1996 , www.noamalgam.com/

.(233) F.Berglund,Bjerner/Helm,Klock,Ripa,Lindforss,Mornstad,Ostlin), “Improved Health after Removal of

dental amalgam fillings”, Swedish Assoc. Of Dental Mercury Patients, 1998. (www.tf.nu) ,

(a) Lindforss, H, Marqvardsen, O, Olsson, S, Henningsson, M. Effekter på hälsan efter avlägsnandet av amalgamfyllningar (Effects on health after removal of amalgam fillings). Tandläkartidn. 86(4), 1994, 205-211; (503 patients); & (b)Östlin, L. Amalgamutbyte - en väg mot bättre hälsa? (Amalgam removal - a road to better health?) Försäkringskassan, Stockholms län, 1991(308 patients); &

(c)Olsson, G & Lindh, U. Veränderung des allgemeinen Gesundheitszustand nach Amalgamentfernung. (Changes in general health after amalgam removal) GZM, Ganzheitl. Zahnmed. 2(1), 1997, 22-28(253 patients); &

(d) Strömberg, R, Langworth, S. Förbättras hälsan efter borttagning av amalgam? (Does health improve after removal of amalgam?) Tandläkartidn. 90(9), 1998, 23-29(233 patients); & (e)LEK-studien, Landstinget Dalarna, Bjerner, B & Hjelm, H. dec. 1991, LEK-studien Dalarna. Sammanställning inför hearing med SoS:s "tungmetallgrupp", 90-11-21(207 patients); &(f) Klock, B, Blomgren, J, Ripa, U, Andrup B. Effekt av amalgamavlägsnande på patienter som misstänker att de lider eller har lidit av amalgamförgiftning. (Effect of amalgam removal in patients who suspect amalgam poisoning) Tandläkartidningen 81, 1989, 1297-1302(198 patients); & (g)Sven Langworth et al, Amalgam news and Amalgamkadefonden, 1997.(www.tf.nu)

(234) (a) Cooper GS, Dooley MA., et al, NIEHS, Occupational risk factors for the development of systemic lupus erythematosus, J Rheumatol. 2004 Oct;31(10):1928-33; & (b) P.E. Bigazzi, “Autoimmunity and Heavy Metals”, Lupus, 1994; 3: 449-453; & (c)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; & 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; & Hultman P, Enestrom S, Mercury induced antinuclear antibodies in mice, Clinical and Exper Immunology, 1988, 71(2): 269-274; & (d)Robbins SM, Quintrell NA, Bishop JM. Mercuric chloride activates the Src-family protein tyrosine kinase, Hck in myelomonocytic cells. Eur J Biochem. 2000 Dec;267(24):7201-8; & (e) Via CS, Nguyen P, Silbergeld EK, et al, Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus, Environ Health Perspect. 2003, 111(10):1273-7; & (f) Silbergeld EK, Silva IA, Nyland JF. Mercury and autoimmunity: implications for occupational and environmental health. Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):282-92. .

(241) R.Schoeny, U.S.EPA, “Use of genetic toxicology data in U.S. EPA risk assessment: the mercury study”, Environ Health Perspect, 1996, 104, Supp 3: 663-73; & C.H.Lee et al, “Genotoxicity of phenylHg acetate in humans as compared to other mercury compounds”, 392(3):269-76.

(246) K.Iyer et al, “Mercury Poisoning in a dentist”, Arch Neurol,1976, 33:788-790.

(248) Y.Finkelstein,“The enigma of parkinsonism in chronic borderline mercury intoxication, resolved by challenge with penicillamine. Neurotoxicology, 1996, Spring, 17(1): 291-5: & Hryhorczuk E et al, Treatment of Mercury Intoxication in a Dentist with penicilamine, J Toxicol Clin Toxicol, 1982, 19(4):401-

(249) C.H.Ngim et al, Dept. of Occupational Medicine, Univ. Of Singapore,“Chronic neurobehavioral effects of elemental mercury in dentists”, British Journal of Industrial Medicine, 1992; 49(11):782-790.

(250) B.A.Rybicki et al,”Parkinson's disease mortality and the industrial use of heavy metals in Michigan”, Mov Disord, 1993, 8:1, 87‑92. & Yamanaga H, “Quantitative analysis of tremor in Minamata disease”, Tokhoku J Exp Med, 1983 Sep, 141:1, 13‑22, & Studies documenting mercury causes ataxia/tremor www.flcv.com/ataxiaHG.html

(251) (a) Y.Omura et al, Heart Disease Research Foundation, NY,NY, “Role of mercury in resistant infections and recovery after Hg detox with cilantro”, Acupuncture & Electro-Therapeutics Research, 20(3):195-229, 1995; &(b) “Mercury exposure from silver fillings”, Acupuncture & Electrotherapy Res, 1996, 133- ; &

(c)Omura, Yoshiaki; Abnormal Deposits of Al, Pb, and Hg in the Brain, Particularly in the Hippocampus, as One of the Main Causes of Decreased Cerebral Acetylcholine, Electromagnetic Field Hypersensitivity, Pre-Alzheimer's Disease, and Autism in Children; Acupuncture & Electro-Therapeutics Research, 2000, Vol. 25 Issue 3/4, p230, 3p

(254) al-Saleh I, Shinwari N. Urinary mercury levels in females: influence of dental amalgam fillings. Biometals 1997; 10(4): 315-23; & (b) Mortada WL, Sobh MA, El-Defrawy MM, Farahat SE. Mercury in dental restoration: is there a risk of nephrotoxicity? J Nephrol. 2002 Mar-Apr;15(2):171-6; & (c) Zabinski Z; Dabrowski Z; Moszczynski P; Rutowski J. The activity of erythrocyte enzymes and basic indices of peripheral blood erythrocytes from workers chronically exposed to mercury vapors. Toxicol Ind Health 2000 Feb;16(2):58‑64.

(255) D.C. Rice, “Evidence of delayed neurotoxicity produced by methyl mercury developmental exposure”, Neurotoxicology, Fall 1996, 17(3-4), p583-96; &(b) Weiss B, Clarkson TW, Simon W. Silent latency periods in methylmercury poisoning and in neurodegenerative disease. Environ Health Perspect. 2002 Oct;110 Suppl 5:851-4: &© Residual neurologic deficits 30 years after occupational exposure to elemental mercury. Neurotoxicology. 2000 Aug;21(4):459-74., Letz R, Gerr F, Cragle D, Green RC, Watkins J, Fidler AT.

(257) I. Smith et al, “Pteridines and mono-amines: relevance to neurological damage”, Postgrad Med J, 62(724): 113-123, 1986; & A.D.Kay et al, “Cerebrospinal fluid biopterin is decreased in Alzheimer’s disease”, Arch Neurol, 43(10): 996-9, Oct 1986; & T.Yamiguchi et al, “Effects of tyrosine administration on serum bipterin In patients with Parkinson’s Disease and normal controls”, Science, 219(4580):75-77, Jan 1983; & T.Nagatsu et al, “Catecholoamine-related enzymes and the biopterin cofactor in Parkinson’s”, Neurol, 1984, 40: 467-73.

(258) Ely, J.T.A., Mercury Induced Alzheimer’s Disease: Accelerating Incicdence?, Bull Environ Contam Toxicol,

2001, 67: 800-6.

(262) Chang LW, “The Neurotoxicology and pathology of organomercury, organolead, and organotin” J Toxicol Sci, 1990, 15 Suppl 4: 125-51; & “Latent effects of methyl mercury on the nervous system after prenatal exposure”, Environ Res 1977, 13(2): 171-85.

(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; & “Behavioral effects of neonatal

metallic mercury exposure in rats”, Toxicology, 1992, 74(2-3):151‑160;

(271) B.A.Weber, “The Marburg Amalgam Study”, Arzt und Umwelt, Apr, 1995; (266 cases) & (b) “Amalgam and Allergy”, Institute for Naturopathic Medicine, 1994; www.karlloren.com/ultrasound/p23.htm

& © “Conjunctivitis sicca(dry eye study)”,Institute for Naturopathic Medicine, 1994; & , “Alternative treatment of Multiple Schlerosis, Tumor, or Cancer”, Institute for Naturopathic Medicine 1997 (40 MS cases),

(273) 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; (& 38); & “Quecksilber-Mobiliztion durch DMPS bei Personen mit und ohne Amalgamfullungen”, Zahnarztl. Mitt, 1989, 79(17): 1866-1868; & J.J.Kleber, “Quecksilberverkonzen- tration im Urin nach DMPS” in [Status Quo and Perspectives of Amalgam], L.T. Friberg(ed.), Georg-Thieme Verlag, Stuttgart, New York, 1005, p 61-69.

(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); & T.Suzuki et al, Ind Health,4:69-75,1966.

(275) L.M.Mikhailova et al, “Influence of occupational factors on disease of reproductive organs”, Pediatriya Akusherstvoi Ginekologiya,33(6):56-58,1971; & Elghany NA, Stopford W, Bunn WB, Fleming LE. Occupational exposure to inorganic mercury vapour and reproductive outcomes. Occup Med (Lond). 1997 Aug;47(6):333-6.

(288) (a)Hisatome I, Kurata Y, et al; Block of sodium channels by divalent mercury: role of specific cysteinyl residues in the P-loop region. Biophys J. 2000 Sep;79(3):1336-45; & Bhattacharya S, Sen S et al, Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction. Biometals. 1997 Jul;10(3):157-62; & Anner BM, Moosmayer M, Imesch E. Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism. Am J Physiol. 1992 May;262(5 Pt 2):F830-6. & Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol 1992; 262(5 Pt2):F84308; & Wagner CA, Waldegger S,et al; Heavy metals inhibit Pi-induced currents through human brush-border NaPi-3 cotransporter in Xenopus oocytes.. Am J Physiol. 1996 Oct;271(4 Pt 2):F926-30; & 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

& (b) Rajanna B, Hobson M, Harris L, Ware L, Chetty CS. Effects of cadmium and mercury on Na(+)-K(+) ATPase and uptake of 3H-dopamine in rat brain synaptosomes. Arch Int Physiol Biochem 1990, 98(5):291-6; & M.Hobson, B.Rajanna, “Influence of mercury on uptake of dopamine and norepinephrine”, Toxicol Letters, Dep 1985, 27:2-3:7-14; & & McKay SJ, Reynolds JN, Racz WJ. Effects of mercury compounds on the spontaneous and potassium-evoked release of [3H]dopamine from mouse striatial slices. Can J Physiol Pharmacol 1986, 64(12):1507-14; & Scheuhammer AM; Cherian MG. Effects of heavy metal cations, sulfhydryl reagents and other chemical agents on striatal D2 dopamine receptors. Biochem Pharmacol 1985 Oct 1;34(19):3405‑13 ;& K.R.Hoyt et al, “Mechanisms of dopamine-induced cell death and differences from glutamate Induced cell death”, Exp Neurol 1997, 143(2):269-81; & & (c)Offen D, et al, Antibodies from ALS patients inhibit dopamine release mediated by L-type calcium channels. Neurology 1998 Oct;51(4):1100-3.

(290) D. Echeverria et al, “Neurobehavioral effects from exposure to dental amalgam: new distinctions between recent exposure and Hg body burden” FASEB J, Aug 1998, 12(11):971-980; & (b) Echeverria, Woods JS, Heyer NJ, Rohlman DS, Farin FM, Bittner AC Jr, Li T, Garabedian C. Chronic low-level mercury exposure, BDNF polymorphism, and associations with cognitive and motor function. Neurotoxicol Teratol. 2005 Nov-Dec;27(6):781-96; & The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans. Neurotoxicol Teratol. 2006 Jan-Feb;28(1):39-48. Epub 2005 Dec 15; Echeverria D, Woods JS, et al. & (c)Amalgam and Health, Swedish Council for Planning and Coordination of Research, 1999; p297-307

(291) H.A.Huggins & TE Levy, “Cerebrospinal fluid protein changes in MS after Dental amalgam removal”, Alternative Med Rev, Aug 1998, 3(4):295-300.

(294) Siblerud, Robert L., et al. Psychometric evidence that dental amalgam mercury may be an etiological factor in manic depression. Journal of Orthomolecular Medicine, Vol. 13, No. 1, First Quarter 1998, pp. 31‑ 40 www.yourhealthbase.com/amalgams.html & Bioplar Disorder: A possible dental connection, Dr. G. H. Smith, International Center for Nutritional Research, http://www.icnr.com/articles/bipolardentalconnection.html ; & Lieb J, Hershman D. Isaac Newton: mercury poisoning or manic depression?. Lancet. 1983 Dec 24-31;2(8365-66):1479-80.

(295) Cecil Textbook of Medicine, 20th Ed., Bennett & Plum, W.B. Saunders and Company, Philadelphia, 1996, p 69; & Comprehensive Psychiatry, 18(6), 1977, pp595-598, &Poisoning & Toxicology Compendium, Leikin and Palouchek, Lexi-Comp., Cleveland, 1998; & Harrison’s Principles Of Internal Medicine, 14th Ed., McGraw-Hill, N.y., 1998; & Sunderman FW. Perils of mercury. Ann Clin Lab Sci 1988 Mar‑Apr;18(2):89‑101.

(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 5;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 ; & (d) L.Verschaeve et al, “Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes”, Muta Res, 1985, 157(2-3):221-6; & (e) L. Verschaeve,“Genetic damage induced by low level mercury exposure”, Envir Res,12:306-10,1976.

(297) (a) Mercury (II) alters mitochondrial activity of monocytes at sublethal doses via oxidative stress mechanisms. Messer RL, Lockwood PE, J Biomed Mater Res B Appl Biomater. 2005 Nov;75(2):257-63; & Effect of Methyl Mercury on Phosphorylation, Transport, and Oxidation in Mammalian Mitochondria, Nobuhito SONE, Margareta K. LARSSTUVOLD^* and Yasuo KAGAWA, The Journal of Biochemistry Volume82, Issue3, Pp. 859-868; & mercury-mitochondria citations, www.mitochondrial.net/showcitationlist.php?keyword=mercury ; & (b) Mitochondrial DNA mutations as an important contributor to aging and degenerative …diseases, Linnane AW et al, Lancet, Mar 1989, 1(8639), p642-5;& Mitochondrial dynamics …in cell death and neurodegeneration, Cho DH, et al, Cell Mol Life Sci, June 2010; & …Mitochondrial theory of aging: roles of mtDNA mutation and oxidative stress in human …aging, Zhonghua Yi Xue Za Zhi (Taipai), 2001, 64(5):259-70;& Mitochondrial function, fibre types, and aging, Conley KE et al, Exp Physiol, 2007, 92(2):333-9.

(298) Mitochondria in the diabetic heart, Bugger H et al, Cardiovascular Research, July 2010; & (b)Mitochondrial dysfunction in cardiac desease: ischemia-reperfusin, aging, and heart failure, Lesnefsky EJ, et al, J Mol Cell Cardiol, 2001, 33(6):1065-69; & (c) Mitochondrial dysfunction and Alzheimer’s Disease, Maruszak A et al, Prog Neurophyschopharacol Biol Pyschiatry, Jul 2010; & (d)PPQ prevents oxidative stress- induced neuronal death through changes in oxidative status of DJ-1, Nunome K et al, Biol Pharm Bull, 2008, 31(7): 1321-6. (Parkinson’s); & (e)Mitochondria damage checkpoint, aging, and cancer, Singh KK, Ann NY Acad Sci, 2006, 1067: 182-90

(299) Mitochondria: rejuvenate your cells with Pyrroloquinoline Quinone (PPQ), Life Extension, Special Winter Edition, 2010, www.lef.org. (many peer-review studies cited)

(300) C.Hock et al, “Increased blood mercury levels in patients with Alzheimer’s disease”, J. Neural Transm, 1998, 105(1):59-68.

(301) Chang LW, Neurotoxic effects of mercury, Environ. Res.,1977, 14(3):329-73; & Histochemical study on the localization and distribution of mercury in the nervous system after mercury intoxication, Exp Neurol, 1972, 35(1):122-37; & Ultrastructural studies of the nervous system after mercury intoxication, Acta Neuropathol(Berlin), 1972, 20(2):122-38 and 20(4):316-34.

(302) D, Klinghardt, IAOMT Conference & tape, 1998; “large study by M.Daunderer(Germany) of MS patients after amalgam removal”.

(303)H.V.Aposhian, Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS).Environ Health Perspect. 1998 Aug;106 Suppl 4:1017-25. ; & Toxicology, 1995, 97(1-3): 23-38; & “Urinary Mercury after Administrationof DMPS”, FASEB J., 6: 2472-2476, 1992.

(305) Soderstrom S, Fredriksson A, Dencker L, Ebendal T, “The effect of mercury vapor on cholinergic neurons in the fetal brain, Brain Research & Developmental Brain Res, 1995, 85:96-108; & Toxicol Lett 1995; 75(1-3):133-44.; & E.M. Abdulla et al, “Comparison of neurite outgrowth with neurofilament protein levels In neuroblastoma cells following mercuric oxide exposure”, Clin Exp Pharmocol Physiol, 1995, 22(5): 362-3;

& Leong CC, Syed NI, Lorscheider FL. Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neuroreport 2001 Mar 26;12(4):733-7

(313) V.D.M.Stejskal et al, “Mercury-specific Lymphocytes: an indication of mercury allergy in man”, J. Of Clinical Immunology, 1996, Vol 16(1);31-40.

(317) S.Zinecker, “Amalgam: Quecksilberdamfe bis ins Gehirn”, der Kassenarzt, 1992, 32(4):23; “Praxiproblem Amalgam”, Der Allgermeinarzt, 1995,17(11):1215-1221. (1800 patients)

(320) U.F.Malt et al, “Physical and mental problems attributed to dental amalgam fillings”, Psychosomatic medicine, 1997, 59:32-41.

(322) P.Engel, “Beobachtungen uber die gesundheit vor und nach amalgamentfernug”,Separatdruck aus Schweiz. Monatsschr Zahnm. 1998, vol 108(8).(75 cases amalgam removal) http://soho.globalpoint.ch/paul‑engel (89% significant improvement) www.melisa.org/articles/engel‑e.pdf

(324) D. Bangsi, Ghadirian P et al, “Dental amalgam and multiple sclerosis”, International J of Epidemiology, 1998, Aug, 27(4):667-71; & E. Mauch et al, “umweltgifte und multiple sklerose”, Der Allgremeinarzt, 1996, 20:2226-2220; & (c) McGrother CW, Dugmore C, Phillips MJ, et al: Multiple sclerosis, dental caries and fillings: a case-control study. Br Dent J, 1999 Sep 11;187(5): 261-4.

(326) E.Baasch, “Is multiple sclerosis a mercury allergy?”, Schweiz arch Neurol Neurochir Psichiatr, 1966, 98:1-19; & J. Clausen, “Mercury and MS”, Acta Neurol Scand, 1993;87:461-; & "Sur un cas de mercurialisme chronique simulant la sclerose en plaque",Nord med Ark Stockholm 1880 xii no 17 1‑48 1 pl & P. Le Quesne,“Metal-induced diseases of the nervous system”,1982,Br J Hosp Med,28:534-

(327) (a)G. Danscher et al, Environ Res, “Localization of mercury in the CNS”, 1986, 41:29-43; &(b) 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; & (c) ”Ultrastructural localization of mercury after exposure to mercury vapor”, Prog Histochem Cytochem, 1991, 23:249-255; &(d) Pamphlett R,Coote P , “Entry of low doses of mercury vapor into the nervous system”, Neurotoxicology, 1998, 19(1):39-47; & (e) Pamphlett et al, “Oxidative damage to nucleic acids in motor neurons containing Hg”, J Neurol Sci,1998,159(2):121-6. (rats & primates); & (f) Pamphlett R, Waley P, "Motor Neuron Uptake of Low Dose Inorganic Mercury", J. Neurological Sciences 135: 63‑67 (1996); &(g) Schionning JD, Danscher G, "Autometallographic inorganic mercury correlates with degenerative changes in dorsal root ganglia of rats intoxicated with organic mercury", APMIS 1999 Mar;107(3):303‑10

(329)(a) Arvidson B; Arvidsson J; Johansson K, "Mercury Deposits in Neurons of the Trigeminal Ganglia After Insertion of Dental Amalgam in Rats", Biometals; 7 (3) p261-263 1994; & (b)Arvidson B. Inorganic mercury is transported from muscular nerve terminasl to spinal and brainstem motorneurons. Muscle Nerve 1992, 15:1089-94; & B. Arvidson et al, Acta Neurol Scand, “Retograde axonal transport of mercury in primary sensory neurons” 1990,82:324-237 & Neurosci Letters, 1990, 115:29-32; &Arvidson B, Arvidsson J. Retrograde axonal transport of mercury in primary sensory neurons innervating the tooth pulp in the rat. Neurosci Lett. 1990 Jul 17;115(1):29-32. & (c) S.M. Candura et al, “Effects of mercuryic chloride and methyly mercury on cholinergic neuromusular transmission”, Pharmacol Toxicol 1997; 80(5): 218-24; & Castoldi AF et al, “Interaction of mercury compounds with muscarinic receptor subtypes in the rat brain”, Neurotoxicology 1996; 17(3-4): 735-41;

(333) A.J.Freitas et al, “Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain”, Brain Research, 1996, 738(2): 257-64; & 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; & E.Chavez et al, “Mitochondrial calcium release by Hg+2",J Biol Chem, 1988, 263:8, 3582-; & A. Szucs et al, Effects of inorganic mercury and methylmercury on the ionic currents of cultured rat hippocampal neurons. Cell Mol Neurobiol, 1997,17(3): 273-8; & 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; & Rossi AD, et al, Modifications of Ca2+ signaling by inorganic mercury in PC12 cells. FASEB J 1993, 7:1507-14.

(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.

(365) C. Schulte-Uebbing, “Umweltbedingte Frauenkranheiten”, Sonntag-Verlag, Stuttgart, 1996; &

Umweltmedizin in der Frauenheilkunde, Arztezeitschr. Naturheilkunde, 35(2):9-17.

(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; & Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; The beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuro Endocrinol Lett. 2004 Jun;25(3):211-8. www.melisa.org

& Kosuda LL, Greiner DL, Bigazzi PE. Effects of HgCl2 on the expression of autoimmune responses and disease in diabetes‑prone (DP) BB rats. Autoimmunity 1997;26(3):173‑87.

(372) 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; & 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; &Brouwer M et al, Functional changes induced by heavy metal ions. Biochemistry, 1982, 21(20): 2529-38.

(374) Benkelfat C et al, Mood lowering effect of tryptophan depletion. Arch Gen Psychiatry, 1994, 51(9): 687- 97; & Young SN et al, Tryptophan depletion causes a rapid lowering of mood in normal males. Psychopharmacology, 1985, 87(2):173-77; & Smith KA et al, Relapse of depression after depletion of tryptophan, Lancet 1997, 349(9056):915-19; & Delgado PL et al, Serotonin function, depletion of plasma tryptophan, and the mechanism of antidepressant action. Arch Gen Psychiatry 1990, 47(5):411-18.

(381) 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; & Turnbull AV, Rivier C. Regulation of the HPA axis by cytokines. Brain Behav Immun 1995; 20:253-75; & 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.

(386) Great Smokies Diagnostic Lab, research web pages (by condition) http://www.gsdl.com; & Doctors Data Lab , http://www.doctorsdata.com , inquiries @doctors data.com, www.doctorsdata.com, & MetaMetrix Lab, www.metametrix.com; &(d) Biospectron Lab, LMI, Lennart Månsson International AB, lmi.analyslab@swipnet.se http://home.swipnet.se/misac/research11.html#biospectrons

& (e) Great Plains Laboratory www.greatplainslaboratory.com/test19.html

(395) Baranski B. Environmental Health Perspectives 1993; 101(suppl 2): 85-90; & (b)Baranski B. Effect of mercury on the sexual cycle and prenatal and postnatal development of progeny. Med Pr 1981; 32(4): 271-6; &(c) Hooper A, Mercury poisoning in Dentistry, Wisconsin Medical J, Aug 1980, vol 79; & (d) Shapiro IM, Cornblath DR, Sumner AJ. Neurophysiological and neuropsychological function in mercury-exposed dentists. The Lancet 1982; 1:1147-1150; &(e) Uzzell BP and Oler J. Chronic low-level mercury exposure and neuropsychological functioning. J of Clin and Exper Neuropsych 1986; 8:581-93; & (f) Epidemiological case definitions of peripheral neuropathy, Ger. F, Letz R. Neurotoxicology. 2000 Oct;21(5):761-8. & (g) Residual neurologic deficits 30 years after occupational exposure to elemental mercury, Letz R, Ger F, et al, Neurotoxicology. 2000 Aug;21(4):459-74 ; & (h) Chronic inorganic mercury induced peripheral neuropathy, Chu CC, Wu TL, et al, Acta Neurol Scand. 1998 Dec;98(6):461-5

(405) Stejskal J, Stejskal V. The role of metals in autoimmune diseases and the link to neuroendocrinology Neuroendocrinology Letters, 20:345‑358, 1999. www.melisa.org/knowledge/education14.html

(409) Bernard S, Enayati A, Redwood L, Roger H, Binstock T. Autism: a novel form of mercury poisoning. Med Hypotheses 2001 Apr;56(4):462-71. http://www.autism.com/ari/mercurylong.html : & Yazbak FE(MD,FAAP) Autism 99 : A National Emergency, www.garynull.com/documents/autism_99.htm

& Amy Holmes, MD, Autism Treatment Clinic, Baton Rouge, La, http://www.healing-arts.org/children/holmes.htm#wethink

(412) (a) Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V, Plasma excitatory amino acids in autism. Invest Clin 1996,37(2):113-28;& Carlsson ML. Is infantile autsim a hypoglutamatergic disorer? J Neural Transm 1998, 105(4-5): 525-35. & (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;

(413) Autism-Mercury@egroups.com, web group of parents with autistic kids and autism doctors and researchers;

www.flcv.com/autismc.html & Autism, PDD, and Immune Reactive Conditions; the mercury connection, www.flcv.com/kidshg.html & Edelson SB, Cantor DS. Autism: xenobiotic influences. Toxicol Ind Health 1998; 14(4): 553-63; www.edelsoncenter.com/Autism/autism.htm & Liska, DJ. The detoxification enzyme systems. Altern Med Rev 1998. 3(3):187-98.

(416)(a) Plaitakis A, Constantakakis E. Altered metabolism of excitatory amino acids, N-acetyl-aspartate and – acetyl-aspartyl-glutamate in amyotrophic lateral sclerosis. Brain Res Bull 1993;30(3-4):381-6 &(b)Rothstein JD, Martin LJ, Kuncl RW. Decreased glutamate transport by the brain and spinal cord in ALS. New Engl J Med 1992, 326: 1464-8:& (c) Leigh Pn. Pathologic mechanisms in ALS and other motor neuron diseases. In: Calne DB(Ed.), Neurodegenerative Diseases, WB Saunder Co., 1997, p473-88; & P.Froissard et al, Universite de Caen, “Role of glutathione metabolism in the glutamate-induced programmed cell death of neuronal cells” Eur J Pharmacol, 1997, 236(1): 93-99; & (d) Kim P, Choi BH. “Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes”, Yonsei Med J 1995; 36(3): 299-305; & Brookes N. In vitro evidence for the role of glutatmate in the CNS toxicity of mercury. Toxicology 1992, 76(3):245-56; & Albrecht J, Matyja E. Glutamate: a potential mediator of inorganic mercury toxicity. Metab Brain Dis 1996; 11:175-84; &(e) Tirosh O, Sen CK, Roy S, Packer L. Cellular and mitochondrial changes in glutamate-induced HT4 neuronal cell death Neuroscience. 2000;97(3):531-41;

(423) T.Barber, “Inorganic mercury intoxification similar to ALS”, J of Occup Med, 1978, 20:667-9; & Brown IA. Chronic mercurialism-a cause of the clinical syndrome of ALS. Arch Neurol Psychiatry 1954, 72:674- 9; & Schwarz S, Husstedt I. ALS after accidental injection of mercury. J Neurol Neurosurg Psychiatry 1996, 60:698; & Felmus MT, Patten BM, Swanke L; Antecedent events in amyotrophic lateral sclerosis Neurology 1976 Feb;26(2):167‑72; & Patten BM, Mallette LE. Motor neuron disease: retrospective study of associated abnormalities. Dis Nerv Syst 1976 Jun;37(6):318‑21; & Kantarjian A, "A syndrome clinically resembling amyotrophic lateral sclerosis following chronic mercurialism", Neurology 11:639‑644 (1961)

(424) Munch G; Gerlach M; Sian J; Wong A; Riederer P. Advanced glycation end products in neurodegeneration: more than early markers of oxidative stress? Ann Neurol 1998 Sep;44(3 Suppl 1):S85‑8.

(432) Sutton KG, McRory JE, Guthrie H, Snutch TP. P/Q-type calcium channels mediate the activity-dependent

feedback of syntaxin-1A. Nature 1999, 401(6755):800-4;

(440) Kidd RF. Results of dental amalgam removal and mercury detoxification. Altern Ther Health Med 2000 Jul;6(4):49‑55; & Gary Null, www.garynull.com/Documents/Dental/Amalgam/Amalgam6.htm

(441)(a)National Academy of Sciences, National Research Council, Committee on Developmental Toxicology, Scientific Frontiers in Developmental Toxicology and Risk Assessment, June 1, 2000, 313 pages; & Evaluating Chemical and Other Agent Exposures for Reproductive and Developmental Toxicity Subcommittee on Reproductive and Developmental Toxicity, Committee on Toxicology, Board on Environmental Studies and Toxicology, National Research Council, National Academy Press, 262 pages, 6 x 9, 2001; &(b) National Environmental Trust (NET), Physicians for Social Responsibility and the Learning Disabilities Association of America, "Polluting Our Future: Chemical Pollution in the U.S. that Affects Child Development and Learning" Sept 2000; www.safekidsinfo.org

(442) Olanow CW, Arendash GW. Metals and free radicals in neurodegeneration. Curr Opin Neurol 1994, 7(6):548-58; & Kasarskis EJ(MD), Metallothionein in ALS Motor Neurons(IRB #91-22026), FEDRIP DATABASE, National Technical Information Service(NTIS), ID: FEDRIP/1999/07802766.

(443) Troy CM, Shelanski ML. Down-regulation of copper/zinc superoxide dismustase causes apoptotic death in PC12 neuronal cells. Proc. National Acad Sci, USA, 1994, 91(14):6384-7; & Rothstein JD, Dristol LA, Hosier B, Brown RH, Kunci RW. Chronic inhibition of superoxide dismustase produces apoptotic death of spinal neurons. Proc Nat Acad Sci, USA, 1994, 91(10):4155-9.

(444) (a) Beal MF. Coenzyme Q10 administration and its potential for treatment of neurodegenerative diseases. Biofactors 1999, 9(2-4):262-6; & DiMauro S, Moses LG; CoQ10 Use Leads To Dramatic Improvements In Patients With Muscular Disorder, Neurology, April 2001;& C.Schultz et al, CoQ10 slows progression of Parkinson’s Disease; Archives of Neurology, October 15, 2002 & Matthews RT, Yang L, Browne S, Baik M, Beal MF. Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects. Proc Natl Acad Sci U S A 1998 Jul 21;95(15):8892-7; & Schulz JB, Matthews RT, Henshaw DR, Beal MF. Neuroprotective strategies for treatment of lesions produced by mitochondrial toxins: implications for neurodegenerative diseases. Neuroscience 1996 Apr;71(4):1043-8; & Idebenone - Monograph. A potent antioxidant and stimulator of nerve growth factor. Altern Med Rev 2001 Feb;6(1):83-86; & (b)Nagano S, Ogawa Y, Yanaghara T, Sakoda S. Benefit of a combined treatment with trientine and ascorbate in familial amyotrophic lateral sclerosis model mice. Neurosci Lett 1999, 265(3):159-62; & (c) C. Gooch et al, Eleanor & Lou Gehrig MDA/ALS Center at Columbia-Presbyterian Medical Center in New York; ALS Newsletter Vol. 6, No. 3 June 2001; & (d) Kidd PM., Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors, and prospects for brain rebuilding using integrative management. Altern Med Rev. 2005 Dec;10(4):268-293.

(449) Schaumburg H, Spencer P: Toxic Neuropathies. Neurology 29:431, 1979; & Levine SP; Cavender GD; Langolf GD; Albers JW. Elemental mercury exposure: peripheral neurotoxicity. Br J Ind Med 1982 May;39(2):136‑9

(451) Miszta H; Dabrowski Z. Effect of mercury and combined effect of mercury on the activity of

acetylcholinesterase of rat lymphocytes during in vitro incubation. Folia Haematol Int Mag Klin Morphol Blutforsch 1989;116(1):151‑5; & Bear, David; Rosenbaum, Jerrold; Norman, Robert. Aggression in cat and human precipitated by a cholinesterase inhibitor. The journal Psychosomatics, July 1986, vol. 27, #7, pgs. 535‑536; & Devinsky, Orrin; Kernan, Jennifer: Bear, David. Aggressive Behavior Following Exposure to Cholinesterase Inhibitors. Journal of Neuropsychiatry, vol. 4, #2, Spring 1992, pgs. 189‑199.

(453) Blumer W, "Mercury toxicity and dental amalgam fillings", Journal of Advancement in Medicine, v.11, n.3, Fall 1998, p.219

(457) International Labor Organization, Mental health in the workplace in Finland, Germany, United Kingdom and United States. Oct 2000, www.ilo.org/public/english/bureau/inf/pr/2000/37.htm

(462) Olivieri G; Brack C; Muller‑Spahn F; Stahelin HB; Herrmann M; Renard P; Brockhaus M; Hock C. 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; & (b) Tabner BJ, Turnbull S, El-Agnaf OM, Allsop D. Formation of hydrogen peroxide and hydroxyl radicals from A(beta) and alpha-synuclein as a possible mechanism of cell death in Alzheimer's disease and Parkinson's disease. Free Radic Biol Med. 2002 Jun 1;32(11):1076-83; &(c) Ho PI, Collins SC, et al; Homocysteine potentiates beta-amyloid neurotoxicity: role of oxidative stress. J Neurochem. 2001 Jul;78(2):249-53.

(464) Walsh, WJ, Health Research Institute, Autism and Metal Metabolism, www.hriptc.org/autism.htm, Oct 20, 2000; & Walsh WJ, Pfeiffer Treatment Center, Metal‑Metabolism and Human Functioning, 2000,; http://www.hriptc.org/metal_metabolism.html

(465) Walsh WJ, Health Research Institute, Biochemical Treatment of Mental Illness and Behavior Disorders, Minnesota Brain Bio Assoc, Nov 17, 1997; http://www.hriptc.org/Minnesota.htm; & William J. Walsh, Laura B. Glab, and Mary L. Haakenson; Pfieffer Treatment Center, Biochemical Therapy and Behavior Outcomes; 2000, http://www.hriptc.org/btbres.htm

(469)BrainRecovery.com, the book, by David Perlmutter MD; Perlmutter Health Center, Naples, Florida,

http://www.perlhealth.com/about.htm; &(b) M.M. van Benschoten, ““Acupoint Energetics of Mercury Toxicity and Amalgam Removal with Case Studies,”” American Journal of Acupuncture, Vol. 22, No. 3, 1994, pp. 251-262; & M.M. Van Benschoten and Associates, Reseda, Calif. Clinic; http://www.mmvbs.com/

http://www.fda.gov/ohrms/dockets/dailys/01/Jan01/011201/emc000010.txt

(470) Dr. Garth Nicholson, Institute for Molecular Medicine, Huntington Beach, Calif., www.immed.org

& Michael Guthrie, R.Ph. ImmuneSupport.com 07‑18‑2001 Mycoplasmas – The Missing Link in Fatiguing Illnesses, www.immunesupport.com/library/showarticle.cfm?ID=3066; & New Treatments for Chronic Infections Found in Fibromyalgia Syndrome, Chronic Fatigue Syndrome, Rheumatoid Arthritis, and Gulf War Illnesses, www.immed.org/reports/autoimmune_illness/rep1.html ; & Prof. Garth L. Nicolson, Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Other Fatigue Conditions, www.immed.org/illness/fatigue_illness_research.html; & Dr. G. Nicholson, Institute for Molecular Medicine, New Treatments for Chronic Infections Found in Fibromyalgia Syndrome, Chronic Fatigue Syndrome, Rheumatoid Arthritis, Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and Gulf War Illnesses, www.immed.org/reports/autoimmune_illness/rep1.html & (b) Immunosciences Lab,

www.immuno‑sci‑lab.com/index2.html

(476) Dr Thomas Verstraeten, US Centres for Disease Control and Prevention, Summary Results: Vaccine Safety Datalink Project ‑ a database of 400,000 children , May 2000; & Geier M.R., Geier DA; Timerosal in Childhood Vaccines, Neurodevelopmental Disorders, and Heart Disease in the U.S. ; J of Amer Physicians and Surgeons, Vol 8(1), Spring 2003

(477) Lars Landner and Lennart Lindestrom. Swedish Environmental Research Group(MFG), Copper in society and the Environment, 2nd revised edition. 1999.

(480) Salzer HM, Relative hypoglycemia as a cause of neuropsychiatric illness, J National Med Assoc, 1996,

58(1): 12-17; & Heninger GR et al, Depressive symptoms, glucose tolerance, and insulin tolerance, J Nervous and Mental Dis, 1975; 161(6):421-32; & Winokur A et al, Insulin resistance in patients with major depression, Am J Psychiatry, 1988, 145(3): 325-30.

(481) Virkkunen M, Huttunen MO; Evidence for abnormal glucose tolerance among violent offenders, Neuropsychiobilogy, 1982, 8:30-40; &(b) Markku I, Virkkunen L; Aggression, suicidality, and serotonin, J Clinical Psy 1992, 53(10): 46-51; & (c) Assessment of chronic neuropsychological effects of mercury vapour poisoning in chloral-alkali plant workers. Bosn J Basic Med Sci. 2002 Dec;2(1-2):29-34. Pranjic N, Sinanovic O, et al.
(482) Linnoila M et al, Low serotonin metabolite differentiates impulsive from nonimpulsive violent behavior, Life Sciences, 1983, 33(26): 2609-2614; & Lopez-Ibor JJ , Serotonin and psychiatric disorders,

Int Clinical Psychopharm, 1992, 7(2): 5-11.

(483) Thomas DE et al, Tryptophan and nutritional status in patients with senile dementia, Psychological Med 1986, 16:297-305; & Yaryura-Tobias JA et al, Changes in serum tryptophan and glucose in psychotics and neurotics, Nutrition, No.4557, p1132; Carney MWP, Brit Med J, 1967, 4:512-516.

(485) Dr. Hulda Clark, The Cure for all Diseases, New Century Press,2000, www.drclark.net (amalgam replacement and treatment for parasites/bacteria)(U.S. CDC confirms parasites common in those with chronic immune conditions)

& U.S. Center for Disease Control, Parasites(widespread exposures),

www.dpd.cdc.gov/dpdx/HTML/Para_Health.htm ;www.cdc.gov/ncidod/diseases/list_parasites.htm

http://www.cdc.gov/ncidod/dpd/parasites/ascaris/prevention.htm www.cdc.gov/healthypets/browse_by_diseases.htm ;www.cdc.gov/ncidod/diseases/index.htm

(486) Dr. Hulda Clark, The Cure for All Cancers, 1998, www.drclark.net; & Gerson Clinics, www.gerson.org.

& Charlotte Du Bois and John Lubecki, The End of Cancer, Nelson’s Books, 2003; & The Cancer Homepage www.curezone.com/diseases/cancer/cancer_dental_risk.asp

& Dr. Hulda Clark, The Cure of HIV/AIDS, New Century Press, 1993.

(487) Haut MW; Morrow LA; Pool D; Callahan TS; Haut JS; Franzen MD. Neurobehavioral effects of acute exposure to inorganic mercury vapor. Appl Neuropsychol 1999;6(4):193‑200.

(490) Rojas M, Olivet C . Occupational exposure and health effects of metallic mercury among dentists and dental assistants: a preliminary study. Valencia, Venezuela; Acta Cient Venez 2000;51(1):32‑8; & Nadorfy‑Lopez E, Bello B. Skeletal muscle abnormalities associated with occupational exposure to mercury vapors. Histol Histopathol 2000 Jul;15(3):673‑82.

(495) Kang JH, Eum WS. Enhanced oxidative damage by the familial amyotrophic lateral sclerosis‑associated Cu,Zn‑superoxide dismustase mutants. Biochem Biophys Acta 2000 Dec 15;1524(2‑3):162‑70; & (b) JH, Eum WS. Enhanced oxidative damage by the familial amyotrophic lateral sclerosis‑ associated Cu,Zn‑superoxide dismustase mutants. Biochem Biophys Acta 2000 Dec 15; 1524(2‑3): 162‑70; & © Liu H, Zhu H, Eggers DK, Nersissian AM, Faull KF, Goto JJ, Ai J, Sanders‑Loehr J, Gralla EB, Valentine JS. Copper(2+) binding to the surface residue cysteine 111 of His46Arg human copper‑zinc superoxide dismustase, a familial amyotrophic lateral sclerosis mutant. Biochemistry 2000 Jul 18;39(28):8125‑32; &(d) Wong PC, Gitlin JD; et al, Copper chaperone for superoxide dismustase is essential to activate mammalian Cu/Zn superoxide dismustase. Proc Natl Acad Sci U S A 2000 Mar 14;97(6):2886‑91; & (e)Kruman II, Pedersen WA, Springer JE, Mattson MP. ALS‑linked Cu/Zn‑SOD mutation increases vulnerability of motor neurons to excitotoxicity by a mechanism involving increased oxidative stress and perturbed calcium homeostasis. Exp Neurol 1999 Nov;160(1):28‑39

(496) Doble A. The role of excitotoxicity in neurodegenerative disease: implications for therapy. Pharmacol Ther 1999 Mar;81(3):163‑221; & Urushitani M, Shimohama S. N‑methyl‑D‑aspartate receptor‑mediated mitochondrial Ca(2+) overload in acute excitotoxic motor neuron death: a mechanism distinct from chronic neurotoxicity after Ca(2+) influx. J Neurosci Res 2001 Mar 1;63(5):377‑87; & Cookson MR, Shaw PJ. Oxidative stress and motor neurons disease. Brain Pathol 1999 Jan;9(1):165‑86

(497) Torres‑Aleman I, Barrios V, Berciano J. The peripheral insulin‑like growth factor system in amyotrophic lateral sclerosis and in multiple sclerosis. Neurology 1998 Mar;50(3):772‑6 ; & Dall R, Sonksen PH et al; The effect of four weeks of supraphysiological growth hormone administration on the insulin‑like growth factor axis in women and men. GH‑2000 Study Group. J Clin Endocrinol Metab 2000 Nov;85(11):4193‑200; & Pons S, Torres-Aleman I. Insulin-like growth factor-I stimulates dephosphorylation of ikappa B through the serine phosphatase calcineurin. J Biol Chem 2000 Dec 8;275(49):38620-5;

(498) Lai EC, Rudnicki SA. Effect of recombinant human insulin‑like growth factor‑I on progression of ALS. A placebo‑controlled study. Neurology 1997 Dec;49(6):1621‑30; & Yuen EC, Mobley WC. Therapeutic applications of neurotrophic factors in disorders of motor neurons and peripheral nerves. Mol Med Today 1995 Sep;1(6):278‑86; & Dore S, Kar S, Quirion R. Rediscovering an old friend, IGF‑I: potential use in the treatment of neurodegenerative diseases. Trends Neurosci 1997 Aug;20(8):326‑31; & Couratier P, Vallat JM. Therapeutic effects of neurotrophic factors in ALS; Rev Neurol (Paris). 2000 Dec;156(12):1075‑7. French

(502) Toxic Neuropathy, Jonathan S Rutchik, MD, MPH,

http://emedicine.medscape.com/article/1175276-overview

(521) Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol 2001 Oct;60(4):838-46; & Mahboob M, Shireen KF, Atkinson A, Khan AT. Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury. J Environ Sci Health B. 2001 Sep;36(5):687-97.

(522) Nutrition Supplements Found Effective for Metal Disorders, Dr. Julia Rucklidge, University of Canterbury, Journal of Attention Disorders , January 2010 (EMPowerPlus, TrueHope)

(523) CBS Television Network,” 60 Minutes”, television program narrated by Morley Safer, December 12, 1990

www.vimy‑dentistry.com/tttoc.htm#_Toc499123411

(524)(a) Urushitani M, Shimohama S. The role of nitric oxide in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord 2001 Jun;2(2):71-81; &(b) Torreilles F, Salman-Tabcheh S, Guerin M, Torreilles J. Neurodegenerative disorders: the role of peroxynitrite.Brain Res Brain Res Rev 1999 Aug;30(2):153-63; & (c)Aoyama K, Matsubara K, Kobayashi S. Nitration of manganese superoxide dismutase in cerebrospinal fluids is a marker for peroxynitrite-mediated oxidative stress in neurodegenerative diseases. Ann Neurol 2000 Apr;47(4):524-7; &(d) Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are differentially prevented by antioxidants. Mol Pharmacol 2001 Oct;60(4):838-46