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. 

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(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


(525) Cheshire, William P., Jr. The shocking tooth about trigeminal neuralgia. New England Journal of Medicine, Vol. 342, June 29, 2000, p. 2003, &  Bergman M, Ginstrup O, Nilsson B. Potentials of and currents between dental metallic restorations. Scand J Dent Res 1982;90:404-8; & Hugoson A. Results obtained from patients referred for the investigation of complaints related to oral galvanism. Swed Dent J 1986;10:15-28;(b) &  Muller AW, Van Loon LA, Davidson CL. Electrical potentials of restorations in subjects without oral complaints. J Oral Rehabil 1990;17:419-24;  & (c) Raue H., "Resistance to therapy; Think of tooth fillings", Medical Practice, vol. 32, n.72, p.2303- 2309, 6 Sept 1980(over 1000 cases)  &(d) Johann Lechner, "Dental Materials and Psychoneuroimmunology      Conference". Danderyd Hospital, 14-16 August, 1998;  www.melisa.org/archive/6th_melisa_study_group.html

(532) El-essawy Dental Clinic   www.el-essawy.com  (large number of cases-most chronic conditions improve after amalgam replacement)                      www.wholisticresearch.com/info/artshow.php3?artid=7

(534) Tirado V, Garcia MA, Franco A.,  Pneuropsychological disorders after occupational exposure to mercury vapors,   Rev Neurol 2000 Oct 16-31;31(8):712-6; & Powell TJ.  Chronic neurobehavioural effects of mercury poisoning on a group of  chemical workers. Brain Inj 2000 Sep;14(9):797-814

(535) K. Sullivan, Evidence Implicating Amalgam in Alzheimer’s Disease, www.bhoffcomp.com/coping/amalgam.html

(538) C. Malmstrom, DDS, Medical Research and Development, http://home.swipnet.se/misac/maineng.html

&  http://home.swipnet.se/misac/infpatient.html             (Over 2000 cases, about 90% signif. improvement)

       & Malmstrom detox high fiber diet( http://home.swipnet.se/misac/vararticles8.html)

           &  Health, Teeth, and Mercury Toxicity,      www.earthtym.net/merc‑tox.htm; & Eric Davis Dental                       Center,       www.ericdavisdental.com/the_program.htm

(543) U.S. Centers for Disease Control, National Center for Health Statistics,  NHANES III study(thousands of people’s health monitored), www.flcv.com/nhanes3.html

http://www.mercola.com/article/mercury/no_mercury.htm

(550) Life Enhancement Foundation (MDs), Disease Prevention and Treatment, Expanded Forth Edition, 2003

(551) Dr. Harald Hamre(Norwegian physician treating mercury toxicity) , Amalgam and Illness, 1998.

(552) Lindh U, Hudecek R, Danersund A, Eriksson S, Lindvall A.,  Removal of dental amalgam and other metal alloys supported by antioxidant therapy alleviates symptoms and improves quality of life in patients with amalgam-associated ill health.  Neuroendocrinol Lett 2002 Oct-Dec;23(5-6):459-82.   (750 cases)

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

(556) Aspen Clinic for Preventive and Environ-mental Medicine in Colorado

http://curezone.org/testimonials/003.htm;    & Alpine Holistic Health Clinic, Dr. Lewis Cone, Plano, Texas, www.drlewiscone.com/toxic_metals.htm; & ICNR Case Study #11        www.icnr.com/cs/cs_11.html

(557) Psychiatric Disturbances and Toxic Metals, Townsend Letter for Doctor's & Patients April 2002; &

Alternative & Complementary Therapies (a magazine for doctors), Aug 2002.

(560) Mercury connection to autism and schizophrenia through enzymatic blockages,  B Windham (Ed) ,   www.flcv.com/autismgc.html

(564) Uversky VN, Li J, Fink AL.  Metal-triggered structural transformations, aggregation, and fibrillation of human alpha-synuclein. A possible molecular NK between Parkinson's disease and heavy metal exposure.  J Biol Chem. 2001 Nov 23;276(47):44284-96. Epub 2001 Sep 11

(565) Beuter A, de Geoffroy A, Edwards R.  Quantitative analysis of rapid pointing movements in Cree subjects exposed to mercury and in subjects with neurological deficits. Environ Res. 1999 Jan;80(1):50-63.  

(566) Mercury, dental amalgam, and hearing loss.Cesarani A, Minoia C, Pigatto PD, Guzzi G., Int J Audiol. 2010 Jan;49(1):69-70.

(574) Pritchard C. et al, Pollutants appear to be the cause of the huge rise in degenerative neurological conditions. Public Health, Aug 2004.

(577) Joachim Mutter et al, Alzheimer Disease: Mercury as pathogenetic factor and apolipoprotein E as a moderator,  Neuroendocrinol Lett 2004; 25(5):331–339; & (b) Mutter J, Daschner F, et al, Amalgam risk assessment with coverage of references up to 2005] , Gesundheitswesen. 2005 Mar;67(3):204-16.

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

(582) R.F Kidd, Results of Dental Amalgam Removal and Mercury Detoxification using DMPS and Neural Therapy, Alternative Therapies, July 2000, Vol 6, No 4, p49-55.

(585) Aluminum Hydroxide: Another Poison Pediatricians Inject in Babies; IMVA, http://imva.info/index.php/vaccines/aluminum-hydroxide/ ; & (b) “Vaccines Show Sinister Side” March 23,2006,  www.straight.com/content.cfm?id=16717 ; (c) Blaylock, Russell. The Blaylock Wellness Report Vol 1, Issue 1; & (d) Cave, Stephanie,  Mitchell, Deborah “What Your Doctor May Not Tell You About Children’s Vaccinations”, Warner Books, 01 September, 2001; & (e) Waly, M. et al Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal. Department of Pharmaceutical Sciences, Northeastern University. Molecular Psychiatry (2004) 1-13; & (f)  Haley, Boyd. Mercury and Thimerosal Toxicity: A Factor in Autism; & (g) Dr. Fudenberg’s comments above were from his speech at the NVIC International Vaccine Conference, Arlington VA September, 1997; & (h)  http://www.chinadaily.com.cn/china/2006-03/25/content_552145.htm

References not found here   www.flcv.com/amalg6.html