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Flaxsee Oil Removes Mercury
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Published: 16 years ago

Flaxsee Oil Removes Mercury

And most Yeasts proliferate in the presence of mercury, and altered pH (a great debate!), which accompanies abnormal composition of bacterial flora - and actually drives down the iron levels - because the yeasts have a way of not using iron! Also, I found that historically, flax seed oil has been used to remove mercury from the body, and this is where "you come in."

When I got this far in my little investigation, I did a search for "mercury flaxseed" and the following was at the top of the list! I made all of that text blue, so you can keep track of what it says, and whatever I might add. You can find this web page at

"Daily mercury exposures to those with Amalgam dental fillings commonly exceed the Government health guideline for mercury, due to mercury's negative vapor pressure and galvanic action with other metals in the mouth(500). People also commonly get exposures to mercury and other toxic metals such as lead, arsenic, nickel, and aluminum from food, water, and other sources(501). All of these are highly neurotoxic and are documented to cause neurological damage which can result in chronic neurological conditions over time.

Mercury has been found to accumulate preferentially in the primary motor function related areas involved in ALS- such as the brain stem, cerebellum, rhombencephalon, dorsal root ganglia, and anterior horn motor neurons, which enervate the skeletal muscles(48,291,327,329,442,500). Many studies of patients with major neurological or degenerative diseases have found evidence Amalgam fillings play a major role in development of conditions such as such as ALS (48,92,97,207,229b,325,416,423,442,468,470,35).

Here's what it does! A direct mechanism involving mercury's inhibition of cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino acids appears to be the noticeable effects that pertain to a major part of the connection to allergic/immune reactive conditions such as autism, schizophrenia, eczema, psoriasis, and allergies(500), as well as to autoimmune conditions such as ALS, Lupus, Alzheimer's(AD), Scleroderma, Chronic Fatigue(CFS), and Fibromyalgia(FM), etc . For example the patient has a lot of intestinal distress with all types of milk products, simply because, mercury has been found to strongly inhibit the activity of dipeptyl peptidase (DPP IV) which is required in the digestion of the milk protein casein(411,412) as well as of xanthine oxidase(439) Additional cellular level enzymatic effects of mercury's binding with proteins include blockage of sulfur oxidation processes (33,114,194,412), enzymatic processes involving vitamins B6 and B12(418), effects on the cytochrome-C energy processes (43,84,232,338c,35), along with mercury's adverse effects on cellular mineral levels of calcium, magnesium, copper,zinc, and lithium (43,96,119,198,333, 386,427,432,489,500). And along with these blockages of cellular enzymatic processes, mercury has been found to cause additional neurological and immune system effects in many through immune/autoimmune reactions (60,313,314,375,405) A recent study gives a comprehensive review of studies finding a connection between ALS, toxic metals, and autoimmunity(405).

Oxidative stress and reactive oxygen species(ROS) have been implicated as major factors in neurological disorders including ALS, motor neuron disease(MND), CFS, FM, Parkinson's(PD), Multiple Schlerosis(MS), and Alzheimer's(AD) (13,56,84,98,145,169,207b,424,442-444,453, 462,496). Mercury forms conjugates with thiol compounds such as glutathione and cysteine and causes depletion of glutathione, which is necessary to mitigate reactive damage. One study found that insertion of Amalgam fillings or nickel dental materials causes a supression of the number of T-lympocytes(270), and impairs the T-4/T-8 ratio. Low T4/T8 ratio has been found to be a factor in autoimmune conditions. 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). Metalloprotein(MT) are involved in metals transport and detoxification(114,442,464) What do you think would happen if the MT's were all knocked out? 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 (114,241,296,442,464,477,495). 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, but much higher percentages tested positive for autoimmune condition patients. In the MELISA laboratory, 12 out of 13 ALS patients tested showed positive immune reactivity lymphocyte responses to metals in vitro [87], indicating metals reactivity a likely major factor in their condition. A recent study assessed the possible causes of high ALS rates in Guam and similar areas and the recent decline in this conditions. One of the studies conclusions was that a likely major factor for the high ALS rates in Guam and similar areas in the past was chronic dietary deficiency since birth in Ca, Mg and Zn induced excessive absorption of divalent metal cations such as mercury which accelerates oxidant-mediated neuronal degenerations in a genetically susceptible population(466).

Mercury blocks the immune function of magnesium and zinc (198,427,43,38), (And what effect to you think that might produce?) whose deficiencies are known to cause significant neurological effects(461,463,430). The low Zn levels result in deficient CuZnSuperoxide dismustase (CuZnSOD), which in turn leads to increased levels of superoxide due to toxic metal exposure. This is in addition to mercury's effect on metallothionein and copper homeostasis as previously discussed(477). Copper is an essential trace metal which plays a fundamental role in the biochemistry of the nervous system(489,495463,,464). Several chronic neurological conditions involving copper metabolic disorders are well documented like Wilson's Disease and Menkes Disease. Mutations in the copper/zinc enzyme superoxide dismustase(SOD) have been shown to be a major factor in the motor neuron degeneration in conditions like familial ALS. Exposures to toxic metals such as mercury and cadmium have been found to cause such effects, and similar effects on Cu/Zn SOD have been found to be a factor in other conditions such as autism, Alzheimer's, Parkinson's, and non-familial ALS (489,495,464,469,111). This condition can result in zinc deficient SOD and oxidative damage involving nitric oxide, peroxynitrite, and lipid peroxidation(495,496,489), which have been found to affect glutamate mediated excitability and apoptosis of nerve cells and effects on mitochondria (495,496,119) These effects can be reduced by zinc supplementation(464,495,430), as well as supplementation with antioxidants and nitric oxide-suppressing agents and peroxynitrite scavengers such as Vit C, Vit E, lipoic acid, Coenzyme Q10, carnosine, gingko biloba, N-acetylcysteine, etc.(444,464,494,495,469,470). Ceruloplasmin in plasma can be similarly affected by copper metabolism disfunction, like SOD function, and is often a factor in neurodegeneration(489).

Calcium plays a major role in the extreme neurotoxicity of mercury and methyl mercury. Both inhibit cellular calcium ATPase and calcium uptake by brain microsomes at very low levels of exposure (270,288,329,333,432,56,). Protein Kinase C (PKC) regulates intracellular and extra cellular signals across neuronal membranes, and both forms of mercury inhibit PKC at micromolar levels, as well as inhibiting phorbal ester binding(43,432). They also block or inhibit calcium L-channel currents in the brain in an irreversable and concentration dependent manner. Mecury vapor or inorganic mercury exposure affects the posterior cingulate cortex and causes major neurological effects with sufficient exposure(428,453). Some of the resulting conditions include stomatitis, tremor, ADD, erythism, etc. Metallic mercury is much more potent than methyl mercury in such actions, with 50 % inhibitation in animal studies at 13 ppb(333,329).

Mercury exposure also degrades the immune system resulting in more susceptability to viral, bacterial, or parasitic effects along with candida albicans which are often present in those with chronic conditions and require treatment (404,468,470,485,500). Four such commonly found in ALS patients are mycoplasma AND echo-7 enterovirus(468,470), candida albicans(404), and parasites(485). Mercury from amalgam interferes with production of cytokines that activate macrophage and neutraphils, disabling early control of viruses or other pathogens and leading to enhanced infection(131,251).

Spatial and temporal changes in intracellular calcium concentrations are critical for controlling gene _expression and neurotransmitter release in neurons(432,438). Mercury alters calcium homeostasis and calcium levles in the brain and affects gene _expression and neurotransmitter release through its effects on calcium, etc. Mercury inhibits sodium and potassium (N,K)ATPase in dose dependent manner and inhibits dopamine and noreprenephrine uptake by synaptosomes and nerve implulse transfer(288,270,56,43,35). Mercury also interrupts the cytochrome oxidase system, blocking the ATP energy function (35,43,84), chronic flatigue syndrom, lowering immune growth factor IGF-I levels and impairing astrocyte function(119,131). Astrocytes are common cells in the CNS involved in the feeding and detox of nerve cells. Increases in inflamatory cytokines such as caused by toxic metals trigger increased free radical activity and damage to astrocyte and astrocyte function(152). IGF-I protects against brain and neuronal pathologies like ALS, MS, and Fibromyalgia by protecting the astrocytes from this destructive process.

Mercury lymphocyte reactivity and effects on glutamate in the CNS induce Chronic-Fatigue-Syndrome type symptoms including profound tiredness, musculoskeletal pain, sleep disturbances, gastrointestinal and neurological problems along with other Chronic-Fatigue-Syndrome symptoms and Fibromyalgia(342,346,369,375,496). Mercury has been found to be a common cause of Fibromyalgia(293,346,369) , which based on a Swedish survey occurs in about 12% of women over 35 and 5.5% of men(368). Glutamate is the most abundant amino acid in the body and in the CNS acts as excitory neurotransmitter (346,386,412,496,119), which also causes inflow of calcium. Astrocytes, a type of cell in the brain and CNS with the task of keeping clean the area around nerve cells, have a function of neutralizing excess glutamate by transforming it to glutamic acid. If astrocytes are not able to rapidly neutralize excess glutamate, most obviously because of the mercury's influence, then a buildup of glutamate and calcium occurs, causing swelling and neurotoxic effects(119,131,152,333,496). Mercury and other toxic metals inhibit astrocyte function in the brain and CNS(119,131), causing increased glutamate and calcium related neurotoxicity(119,152,333,226a,496) which are responsible for much of the Fibromyalgia symptoms and a factor in neural degeneration in MS and ALS. This is also a factor in conditions such as CFS, Parkinson's, and ALS(346,416,496). Animal studies have confirmed that increased levels of glutamate(or aspartate, another amino acid excitory neurotransmitter) cause increased sensitivity to pain , as well as higher body temperature- both found in CFS/Fibromyalgia. Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage(346,142,13). Medical studies and doctors treating Fibromyalgia have found that supplements which cause a decrease in glutamate or protect against its effects have a positive effect on Fibromyalgia and other chronic neurologic conditions. Some that have been found to be effective include CoQ10 (444), ginkgo biloba and pycnogenol(494a), NAC(54,494a), Vit B6, methyl cobalamine(B12), L-carnitine, choline, ginseng, vitamins C and E, nicotine, and omega 3 fatty acids(fish and flaxseed oil) (417,495e).

Another neurological effect of mercury that occurs at very low levels is inhibition of nerve growth factors, for which deficiencies result in nerve degeneration. 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 susceptability to toxic effects. Prenatal mercury vapor expsoure 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 neruons 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 pateients 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 supplenting both thyrotropin-releasing hormone and growth control hormone is more effective at increasing all of these hormone levels in the patient(499).

Tick-borne encephalitis, such as Lyme Diseaese, has been found to cause ALS in a significant portion of untreated acute cases(471). Lyme disease is widespread in the U.S.

Large numbers of patients diagnosed with ALS have been found to have treatable tick-borne encephaltis, and many have recovered after treatment.

Extremely toxic anerobic bacteria from root canals or cavitations formed at incompletely healed tooth extraction sites have also been found to be common factors in fibromyalgia and other chronic neurological conditions such as Parkinson's and ALS, with condensing osteitis which must be removed with a surgical burr along with 1 mm of bone around it(35,437,500). Have you had any teeth extracted in the last year or so? Cavitations have been found in 80% of sites from wisdom tooth extractions tested and 50% of molar extraction sites tested(35,437). The incidence is likely somewhat less in the general population. Medical studies and doctors treating fibromylagia have found that supplements which cause a decrease in glutamate or protect against its effects have a positive effect on fibromyalgia and other chronic neurologic conditions like ALS. Some that have been found to be effective include Vit B6, methyl cobalamine(B12), L-carnitine, choline, ginseng, Ginkgo biloba,vitamins C and E, CoQ10, nicotine, and omega 3 fatty acids(fish and flaxseed oil) (417,468).

Clinical tests of patients with ALS, MND, Parkinson's, Alzheimer's, Lupus(SLE), and Rheumatoid Arthritis have found that the patients generally have elevated plasma cysteine to sulphate ratios, with the average being 500% higher than controls(330,331,56,84), and in general being poor sulphur oxidizers. This means that these patients have blocked enzymatic processes for converting the basic cellular fuel cysteine to sulfates and glutathione, and thus insufficient sulfates available to carry out necessary bodily processes. Mercury has been shown to diminish and block sulphur oxidation and thus reducing glutathione levels which is the part of this process involved in detoxifying and excretion of toxics like mercury(33). Glutathione is produced through the sulphur oxidation side of this process. Low levels of available glutathione have been shown to increase mercury retention and increase toxic effects(111), while high levels of free cysteine have been demonstrated to make toxicity due to inorganic mercury more severe(333,194,56,33e). The deficiency in conjugation and detoxification of sulfur based toxins in the liver results in toxic metabolites and progressive nerve damage over time (331). Mercury has also been found to play a part in inducing intolerance and neuronal problems through blockage of the P-450 enzymatic process(84,33e). Patients with some of these conditions have found that bathing in Epsom Salts (magnesium sulfate) offers temporary relief for some of their symptoms by providing sulfates that avoid the blocked metabolic pathway. A test that some doctors treating conditions like ALS usually prescribe to measure the cysteine to sulfate ratio and other information useful in diagnosis and treatment is the Great Smokies Diagnostic Labs comprehensive liver detox test(386). The test results come with some recommendations for treatment. A hair test for toxic metals is also usually ordered to determine toxic exposures that might be involved(386). A more definitive test such as MELISA for immune reactivity to toxics is available by sending blood to a European lab(87). Other labs also have other useful tests such as Immune Reactivity Biocompatability Tests(445), ELISA or organic acid panels or amino acid panels(386). Treatment using IV glutathione, vitaminC, and minerals has been found to be very effective in the stabilizing and ammelioration of some of these chronic neurological conditions by neurologist such as Perlmutter in Florida(469).

In one subtype of ALS, damaged, blocked, or faulty enzymatic superoxide dimutase (SOD) processes appear to be a major factor in cell apoptosis involved in the codition(443). Mercury is known to damage or inhibit SOD actitivity(441,33,111).

Total dental revision(TDR) which includes replacing amalgam fillings, extracting root canaled teeth, and treating cavitations has been found to offer significant health improvements to many with ALS and other autoimmune conditions(35,293,437). root canals and cavitations have been found to harbor anerobic bacteria which give off toxins of extreme toxicity which block enzymatic processes at the cellular level causing degenerative processes according to the medical labs that do the tests(437,35), similar to mercury's effects but in some cases even more toxic . IGF-1 treatments have also been found to alleviate some of the symptoms of ALS(424). Medical studies and doctors treating fibromylagia have found that supplements which cause a decrease in glutamate or protect against its effects have a positive effect on fibromyalgia. Some that have been found to be effective in treating metals related autoimmune conditions include Vit B6, CoenzymeQ10, methyl cobalamine(B12), L-carnitine, choline, ginseng, Ginkgo biloba, vitamins C and E, nicotine, and omega 3 fatty acids(fish and flaxseed oil) (417,444,468).

One dentist with severe symptoms similar to ALS improved after treatment for mercury poisoning(246), and others treated for mercury poisoning or using TDR have also recovered or significantly improved (97,229,423,405,406,468-470,485,35).The Edelson Clinic in Atlanta which treats ALS patients reports similar experience(406), and the Perlmutter Clinic has also had success with treatment of ALS and other degenerative neurological coditions(469).

While there are many studies documenting effectiveness of chemical chelators like DMSA and DMPS at reducing metals levels and alleviating adverse effects for most conditions, and many thousands of clinical case results(500,501); there is also some evidence from animal studies that these chelators can result in higher levels of mercury in the motor neurons in the short term which might be a problem for ALS patients(). Thus other detox options might be preferable for ALS patients until enough clinical evidence is available treating ALS patients with them with mercury toxicity. Another chelator used for clogged arteries, EDTA, forms toxic compounds with mercury and can damage brain function(307). Use of EDTA may need to be restricted in those with high Hg levels. N-acetylcysteine(NAC) has been found to be effective at increasing cellular glutathione levels and chelating mercury(54). Experienced doctors have also found additional zinc to be useful when chelating mercury(222) as well as counteracting mercury's oxidative damage(43). Zinc induces metallothionein which protects against oxidative damage and increases protective enzyme activities and glutathione which tend to inhibit lipid peroxidation and suppress mercury toxicity(430,464). Also lipoic acid,LA, has been found to dramatically increase excretion of inorganic mercury(over 12 fold), but to cause decreased excretion of organic mercury(494d) and copper. Lipoic acid has a protective effect regarding lead or inorganic mercury toxicity through its antioxidant properties(494), but should not be used with high copper until copper levels are reduced. LA and NAC (N-acetylcysteine) also increase glutathione levels and protect against superoxide radical/ peroxynitrite damage, so thus have an additional neuroprotective effect(494ab,54). Zinc is a mercury and copper antagonist and can be used to lower copper levels and protect against mercury damage. Lipoic acid has been found to have protective effects against cerebral ischemic-reperfusion, excitotoxic amino acid(glutamate) brain injury, mitochondrial dysfunction, diabetic neuropathy(494). Other antioxidants such as carnosine(495a), Coenzyme Q10,Vitamins C & E, gingko biloba, and pycnogenol have also been found protective against degenerative neurological conditions(494,495e, 444).


(13) 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; & S.Tan et al, "Oxidative stress induces programmed cell death in nueronal cells", J Neurochem, 1998, 71(1):95-105. & J.S. Bains et al, "Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death", Brain Res Rev, 199, 25(3):335-58; & Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995; 18(2): 321-36.

(33) S.C. Langley-Evans et al, "SO2: a potent glutathion depleting agent", Comp Biochem Physiol Pharmocol Toxicol Endocrinol, 114(2):89-98; & (b)P.E. Emory et al, "Increased Prevalence of poor sulphuoxidation in patients with Rheumatoid Arthritis ", Ann Rheum Dis, 1992, 51(3): 318-20; & (c) 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; & (d)2S.A.McFadden, "Xenobiotic metabolism and adverse environmental response: sulfur- dependent detox pathways",Toxicology, 1996, 111(1-3):43-65;

(35) Huggins HA, Levy,TE, Uniformed Consent: the hidden dangers in dental care, 1999, Hampton Roads Publishing Company Inc; & Hal Huggins, Its All in Your Head, 1993; & Center for Progressive Medicine, 1999,

(43) Knapp LT; Klann E. Superoxide-induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem 2000 May 22; & B.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", & 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

(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.

(54) M.E. Lund et al, "Treatment of acute MeHg poisoning by NAC", J Toxicol Clin Toxicol, 1984, 22(1):31-49; & Livardjani F; Ledig M; Kopp P; Dahlet M; Leroy M; Jaeger A. Lung and blood superoxide dismustase activity in mercury vapor exposed rats: effect of N-acetylcysteine treatment. Toxicology 1991 Mar 11;66(3):289-95. & G.Ferrari et al, Dept. Of Pathology, Columbia Univ., J Neurosci,1995, 15(4):2857-66; & RR. Ratan et al, Dept. of Neurology, Johns Hopkins Univ., J Neurosci, 1994, 14(7): 4385-92;

(56) X.M.Shen et al, Neurolbehavioral 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; & A.Nicole et al, "Direct evidence for glutathione as mediator of apoptsosis in neuronal cells", Biomed Pharmacother, 1998; 52(9):349-55; & J.P.Spencer et al, "Cysteine & GSH in PD", mechinsms involving ROS", J Neurochem, 1998, 71(5):2112-22: & P.Jenner,"Oxidative mechanisms in PD", Mov Disord, 1998; 13(Supp1):24- 34; & D. Offen et al, "Use of thiols in treatment of PD", Exp Neurol, 1996,141(1):32-9; & A.D.Owen et al, Ann NY Acad Sci, 1996, 786:217-33; & JJ Heales et al, Neurochem Res, 1996, 21(1):35-39.

(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).

(87) 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.

(92) L. Tandon et al, "Elemental imbalance studies by INAA on ALS patients", J Radioanal Nuclear Chem 195(1):13-19,1995; & Y.Mano et al, "Mercury in the hair of ALS patients", Rinsho Shinkeigaku, 1989, 29(7): 844-848; & Mano et al, 1990, Rinsho Shinkeigaku 30: 1275-1277; & Khare et al, 1990, "Trace element imbalances in ALS", Neurotoxicology, 1990,11:521-532..

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

(97) Redhe O, Pleva J, "Recovery from ALS after removal of dental amalgam fillings", Int J Risk & Safety in Med 4:229-236, 1994; &Vanacore N, Corsi L, Fabrizio E, Bonifati V, Meco G, "Relationship between exposure to environmental toxins and motor neuron disease: a case report", Med Lav 1995 Nov-Dec; 86(6):522-33.

(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.

(111)T.W.Clarkson et al, "Billiary secretion of glutathione-metal complexes", Fundam Appl Toxicol, 1985, 5(5):816-31; & D.Quig, Doctors Data Lab,"Cysteine metabolism and metal toxicity", Altern Med Rev, 1998;3:4, p262-270, & Ceaurriz et al, Role of gamma- glutamyltraspeptidase(GGC) and extracellular glutathione in disopition 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; & R.K. Zulups et al, J Toxicol Environ Health, 1995, 44(4): 385-99; & Pocernich CB, Cardin AL, Racine CL, Lauderback CM, Allan Butterfield D. 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;

(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; & 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.

(119) L.Ronnback et al, "Chronic encephalopaties induced by low doses of mercury or lead", Br J Ind Med 49: 233-240, 1992; & H.Langauer-Lewowicka," Changes in the nervous system due to occupational metallic mercury poisoning" Neurol Neurochir Pol 1997 Sep-Oct;31(5):905-13; & 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.

(131) M.Kubicka-Muranyi et al, "Systemic autoimmune disease induced by mercuric chloride", Int Arch Allergy Immunol;1996, 109(1):11-20 & M.M.Christensen et al, Institute of Medical Microbiology, "Comparision of interaction of meHgCl2 and HgCl2 with murine macrophages", Arch Toxicol, 1993, 67(3):205-11; &

Christensen MM, Ellermann-Eriksen S, Mogensen SC. Influence of mercury chloride on resistance to generalized infection with herpes simplex virus type 2 in mice. Toxicology 1996, 114(1): 57-66; & S.Ellermann-Eriksen et al, "Effect of mercuric chloride on macrophage-mediated resistance mechinisms against infection", Toxicology, 93:269-297,1994;

(142) Ariza ME; Bijur GN; Williams MV. Lead and mercury mutagenesis: role of H2O2, superoxide dismutase, and xanthine oxidase. Environ Mol Mutagen 1998;31(4):352-61; & M.E. Ariza et al, "Mercury mutagenisis", Biochem Mol Toxicol, 1999, 13(2):107-12; & M.E.Ariza et al, "Mutagenic effect of mercury", InVivo 8(4):559-63,1994;

145) J.M.Gorell et al, "Occupational exposure to mercury, manganese, copper, lead, and therisk of Parkinson's disease", Neurotoxicology, 1999, 20(2-3):239-47

(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.

(149) 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

(152) 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; & Langworth et al, "Effects of low exposure to inorganic mercury on the human immune system", Scand J Work Environ Health, 19(6): 405-413.1993; J Biol Chem 2000 Dec 8;275(49):38620-5.

(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.

(175) 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.; & 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- .

(194) Lu SC, FASEB J, 1999, 13(10):1169-83, "Regulation of hepatic glutathione synthesis: current concepts and

controversies"; & R.B. Parsons, J Hepatol, 1998, 29(4):595-602; & R.K.Zalups et al,"Nephrotoxicity of inorganic mercury co-administered with L-cysteine", Toxicology, 1996, 109(1): 15-29. & T.L. Perry et al, "Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase defieciency", Ann Neural, 1985, 18(4):482-489.

(198) E.S. West et al, Textbook of Biochemistry, MacMillan Co, 1957,p853;& B.R.G.Danielsson et al,"Ferotoxicity of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus", Biol Res Preg Perinatal. 5(3):102-109,1984; & Danielsson et al, Neurotoxicol. Teratol., 18:129-134;

(207) Haley, B. Kasarskis, EJ; et al. GTP-binding proteins in amyotrophic lateral sclerosis cerebrospinal fluid. Ann Neurol, 1995; & "Mercury Vapor Inhaltion Inhibits Binding of GTP . Neurotoxicology 1997, 18(2)::315-24

(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 (amalgam replacement & DMPS, over 5,000 cases)

(226) 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;

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

March, 1994(case histories documented); & Kantarjian A, "A syndrome clininically resembling amyotrophic lateral sclerosis following chronic mercurialism", Neurology 11:639-644 (1961)

(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

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

(251) 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-Theraputics Research, 20(3):195-229, 1995; & "Mercury exposure from silver fillings", Acupunture & Electrotherapy Res, 1996, 133-

(254) al-Saleh I, Shinwari N. Urinary mercury levels in females: influence of dental amalgam fillings. Biometals 1997; 10(4): 315-23; & 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;

(270) D.W.Eggleston, "Effect of dental amalgam and nickel alloys on T-lympocytes",J Prosthet Dent. 51(5):617-623, 1984; & D.W.Eggleston et al, J Prosthet Dent, 1987,58(6),704-7; & J of the American Medical Assoc., Sept 96.

(288)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 Biochim 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 ; 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; & Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol 1992; 262(5 Pt2):F84308

(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.

(293) H.Huggins,Burton Goldberg, & Editors of Alternative Medicine Digest,Chronic Fatigue Fibromyalgia & Environmental Illness, Future Medicine Publishing, Inc, 1998, p197-;

(296) L.Bucio et al, Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line. Mutat Res 1999 Jan 25;423(1-2):65-72; & L.Verschaeve et al, "Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes", Muta Res, 1985, 157(2-3):221-6; & L.Verschaeve,"Genetic damage induced by low level mercury exposure", Envir Res,12:306-10,1976.

(305) S. Soederstroem et al, "The effect of mercury vapor on chloinergic neurons in the fetal brain" ,Developmental Brain Research,85(1):96-108.1995; & 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.

(307) Duhr EF, Pendergrass JC, Slevin JT, Haley BE: HgEDTA complex inhibits GTP interactions with the E-site of brain beta-tubulin. Toxicology & Applied Pharmacology 1993; 122 (2): 273-80.

(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.

(314) M.Goldman et al,1991,"Chemically induced autoimmunity ...",Immunology Today,12:223-; & K. Warfyinge et al, "Systemic autoimmunity due to mercury vapor exposure in genetically susceptible mice", Toxicol Appl Pharmacol, 1995, 132(2):299-309;& L.M. Bagentose et al, "Mercury induced autoimmunity in humans", Immunol Res, 1999,20(1): 67-78; &"Mercury-induced autoimmunity", Clin Exp Immunol, 1998, 114(1):9-12;

(325) B. Arvidson(Sweden), Inorganic mercury is transported from muscular nerve terminals to spinal and brainstem motorneurons. Muscle Nerve, 1992, 15(10);1089-94, & Mitchell JD. Heavy metals and trace elements in amyotrophic lateral sclerosis. Neurol Clin 1987 Feb;5(1):43-60; & M. Su et al, Selective involvement of large motor neurons in the spinal cord of rats treated with methylmercury. J Neurol Sci,1998, 156(1):12-7;

(327) G. Danscher et al, Environ Res, "Localization of mercury in the CNS", 1986, 41:29-43; & Exp Mol Pathol, 1990, 52: 291-299; & "Ultrastructural localization of mercury after expsoure to mercury vapor", Prog Histochem Cytochem, 1991, 23:249-255; & R.Pamphlett et al, "Entry of low doses of mercury vapor into the nervous system", Neurotoxicology, 1998, 19(1):39-47; & Pamphlett et al, "Oxidative damage to nucleic acids in motor neurons containing Hg", J Neurol Sci,1998,159(2):121-6. (rats & primates); & Pamphlett R, Waley P, "Motor Neuron Uptake of Low Dose Inorganic Mercury", J. Neurological Sciences 135: 63-67 (1996) ;

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) 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; & 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; & 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

(330) C.M. Tanner et al,"Abnormal Liver Enzyme Metablolism in Parkinson's",Neurology, 1991, 41(5): Suppl 2, 89-92; & M.Watanabe et al, Amino Acids, 1998, 15(2): 143-50 & M.T.Heafield et al, "Plasma cysteine and sulphate levels in patients with Motor neurone disease, Parkinson's Disease, and Alzheimer's Disease", Neurosci Lett, 1990, 110(1-2), 216,20; & A.Pean et al, "Pathways of cysteine metabolism in MND/ALS", J neurol Sci, 1994, 124, Suppl:59-61;

(331) C.Gordon et al, "Abnormal sulphur oxidation in systemic lupus erythrmatosus(SLE)", Lancet, 1992,339:8784,25-6; & P.Emory et al, "Poor sulphoxidation in patients with rheumatoid arthitis", Ann Rheum Dis, 1992, 51:3,318-20; & P.Emory et al, Br J Rheumotol, 1992, 31:7,449-51; & Steventon GB, et al; Xenobiotic metabolism in motor neuron disease, The Lancet, Sept 17 1988, p 644-47; & Neurology 1990,


(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, 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.

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

(342) V.Stejskal, "MELISA: A New Technology for Diagnosing and Monitoring of Metal Sensitivity", Proceedings: 33rd Annual Meeting of American Acadamy of Environmental Medicine, Nov. 1998, Baltimore, Maryland.

(346) Clauw DJ, "The pathogenesis of chronic pain and fatigue syndroms: fibromyalgia" Med Hypothesis, 1995, 44:369-78; & Hanson S, Fibromyalgia, glutamate, and mercury. Heavy Metal Bulletin, Issue 4, 1999, p5,6.

(368) Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al. Metal- specific memory lymphoctes: biomarkers of sensitivity in man. Neuroendocrinology Letters, 1999.

(369) Sterzl I, Prochazkova J, Stejskal VDM et al, Mercury and nickel allergy: risk facotrs in fatigue and autoimmunity. Neuroendocrinology Letters 1999; 20:221-228.

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

(386) Doctors Data Lab , , inquiries@doctors, &

Great Smokies Diagnostic Lab,; & MetaMatrix Lab, &

Biospectron/LMI, Lennart Månsson International .

(404) M. E. Godfrey, Candida, Dysbiosis and Amalgam. J. Adv. Med. vol 9 no 2 (1996); & Romani L, Immunity to Candida Albicans: Th1,Th2 cells and beyond. Curr Opin Microbiol 1999, 2(4):363-7

(405) Jenny Stejskal, Vera Stejskal. The role of metals in autoimmune diseases and the link to neuroendocrinology Neuroendocrinology Letters, 20:345-358, 1999.

(406) The Edelson Clinic, Atlanta, Ga. ( (see the testimonials)

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

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

(416) Rothstein JD, Martin LJ, Kuncl RW. Decreased glutamte transport by the brain and spinal cord in ALS. New Engl J Med 1992, 326: 1464-8.

(417) Folkers K et al, Biochemical evidence for a deficiency of vitamin B6 in subjects reacting to MSL-Glutamate. Biochem Biophys Res Comm 1981, 100: 972; & Felipo V et al, L-carnatine increases the affinity of glutamate for quisqualate receptors and prevents glutamate neurotoxicity. Neurochemical Research 1994, 19(3): 373-377; & Akaike A et al, Protective effects of a vitamin-B12 analog(methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons. European J of Pharmacology 1993, 241(1):1-6 .

(418) Srikantaiah MV; Radhakrishnan AN. Studies on the metabolism of vitamin B6 in the small intestine. Purification and properties of monkey intestinal pyridoxal kinase. Indian J Biochem 1970 Sep;7(3):151-6.

(423) C.R. Adams et al, "Mercury intoxication simulating ALS", JAMA, 1983, 250(5):642-5; & T.Barber, "Inorganic mercury intoxification similar to ALS", J of Occup Med, 1978, 20:667-9; &

Schwarz S, Husstedt I, Bertram HP, Kuchelmeister K. Amyotrophic lateral sclerosis after accidental injection of mercury. J Neurol Neurosurg Psychiatry. 1996 Jun;60(6):698; & Sienko DG, Brooks BR. Amyotrophic lateral sclerosis. A case-control study following detection of a cluster in a small Wisconsin communit Arch Neurol 1990 Jan;47(1):38-41; & 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.

(424) Cephalon, Inc. ,

(427) Chetty CS, McBride V, Sands S, Rajanna B. Effects in vitro on rat brain Mg(++)-ATPase. Arch Int Physiol Biochem 1990, 98(5):261-7; & M.Burk et al, Magnesium, 4(5-6): 325-332, 1985 ?

(428) O'Carroll RE, Masterton G, Goodwin GM. The neuropsychiatric sequelae of mercury poisoning. The Mad Hatter's disease revisited. Br J Psychiatry 1995, 167(1): 95-8; & PUBLIC HEALTH REPORTS, PUBLIC HEALTH BULLETIN #263. March 28, 1941. Mercurialism and its control in the felt hat industry.

(430) Fukino H, Hirai M, Hsueh YM, Yamane Y. Effect of zinc pretreatment on mercuric chloride-induced lipid peroxidation in the rat kidney. Toxicol Appl Pharmacol 1984, 73(3): 395-401.

(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;

(437) Affinity Labeling Technology, Inc.(Dental Lab), oral toxicity testing technology and tests,

see research web pages on amalgam toxicity, root canals, cavitaions. ; &

G. Mienig, root canal Coverup, 1997.

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

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

(441) P.Bulat, "Activity of Gpx and SOD in workers occupationally exposed to mercury", Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & D.Jay, "Glutathione inhibits SOD activity of Hg", Arch Inst cardiol Mex, 1998,68(6):457-61.

(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 dismutase causes apototic dealth 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 dismutase produces apoptotic death of spinal neurons. Proc Nat Acad Sci,USA, 1994, 91(10):4155-9.

(444) 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; & 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; & 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;

(445) Clifford Lab, Dental Materials Biocompatability Testing, Colorada Springs, Colo.; & Peak Energuy Performance, inc., Dental Materials Biocompatibility Testing,

(466) Chen KM, Department of Neurology, Guam Memorial Hospital; Disappearance of ALS from Guam: implications for exogenous causes, 2000.

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

(461) Rasmussen HH, Mortensen PB, Jensen IW. Depression and magnesium deficiency. Int J Psychiatry Med

1989;19(1):57-63: & Bekaroglu M, Aslan Y, Gedik Y, Karahan C. Relationships between serum free fatty

acids and zinc with ADHD. J Child Psychol Psychiatry 1996; 37(2):225-7; & Maes M, Vandoolaeghe E, Neels H, Demedts P, Wauters, A, Meltzer HY, Altamura C, Desnyder R. Lower serum zinc in major Depression is a sensitive marker of treatment resistance and of the immune/inflammatory response in that illness. Biol Psychiatry 1997;42(5):349-358.

(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.

(463) Johnson S. The possible role of gradual accumulation of copper, cadmium, lead and iron

depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty acids in multiple sclerosis. Med Hypotheses 2000 Sep;55(3):239-41.

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

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

(468) M.M. Van Benschoten and Associates, Reseda, Calif. Clinic;

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

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

(471) Umanekii KG, Dekonenko EP. Structure of progressive forms of tick-borne encephalitis. Zh Nevropatol Psikhiatr Im S S Korsakova 1983;83(8):1173-9. [article in Russian]; & B HEMMER, F X GLOCKER, R KAISER. Generalised motor neuron disease as an unusual manifestation of Borrelia burgdorferi infection. J Neurol Neurosurg Psychiatry 1997;63:257-258;& Fredrikson S, Link H. CNS-borreliosis selectively affecting central motor neurons. Acta Neurol Scand 1988;78:181-184[Medline]; & Halperin JJ, Kaplan GP, Brazinsky S, et al. Immunologic reactivity against Borrelia burgdorferi in patients with motor neuron disease. Arch Neurol 1990;47:586-594

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

(485) Hulda Clark , The Cure For All Diseases , 2000, (U.S. CDC confirms parasites common in those with chronic immune conditions)

(489) Waggoner DJ, Bartnikas TB, Gitlin JD. The role of copper in neurodegenerative disease. Neurobiol Dis 1999 Aug;6(4):221-30; & (b) Torsdottir G, Kristinsson J, Gudmundsson G, Snaedal J, Johannesson T. Copper, ceruloplasmin and superoxide dismustase (SOD) in amyotrophic lateral sclerosis. Pharmacol Toxicol 2000 Sep;87(3):126-30; & © Estevez AG,Beckman JS et al, Induction of nitric oxide-dependent apoptosis in motor neurons by zinc-deficient superoxide dismustase. Science 1999 Dec 24;286(5449):2498-500; & (d) Cookson MR, Shaw PJ. Oxidative stress and motor neurons disease. Brain Pathol 1999 Jan;9(1):165-86.

(494) (a)Kobayashi MS, Han D, Packer L. Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Free Radic Res 2000 Feb;32(2):115-24(PMID: 10653482); & Packer L, Tritschler HJ, Wessel K. Neuroprotection by the metabolic antioxidant alpha-lipoic acid. Free Radic Biol Med 1997;22(1-2):359-78(PMID: 8958163); & (b)Whiteman M, Tritschler H, Halliwell B. Protection against peroxynitrite-dependent tyrosine nitration and alpha 1-antiproteinase inactivation by oxidized and reduced lipoic acid. FEBS Lett 1996 Jan 22;379(1):74-6(PMID: 8566234); & © "Decreased phagocytosis of myelin by macrophages with ALA. Journal of Neuroimmunology 1998, 92:67- 75; & (d) & Z.Gregus et al, "Effect of lipoic acid on biliary excretion of glutathione and metals", Toxicol APPl Pharmacol, 1992, 114(1):88-96;

(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

(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.

(499) Van den Berghe G, Bowers C et al, Neuroendocrinology of prolonged critical illness: effects of

exogenous thyrotropin-releasing hormone and its combination with growth hormone secretagogues.

J Clin Endocrinol Metab 1998 Feb;83(2):309-19.

(500) B. Windham, Annotated bibliography: Exposure levels and health effects related to mercury/dental amalgam and results of amalgam replacement, 2001; (over 1000 medical study references documenting mechanism of causality of 40 chronic conditions and over 60,000 clinical cases of recovery or significant improvement of these conditions after amalgam replacement-documented by doctors)

(501) B. Windham, Cognitive and Behavioral Effects of Toxic Metal Exposures, 2001; (over 150 medical study references)


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