Mercury from Amalgam Fillings is a Common Cause of MS, ALS, PD, SLE, RA, MCS, AD, etc.

Bernard Windham (Ed.), Biostatistician/ Engineer 

                 Introduction- the Mercury/Toxic Metal/Dental Amalgam Connection (and other factors)             

Proper functioning of the human body and mind depends on interactions of the brain and CNS using neuronal signaling mechanisms with elaborate metabolic and enzymatic processes and respiration that occurs at the cellular level in the various organs and parts of the body, as controlled by low levels of hormones from the endocrine system. It will be shown that toxic substances, such as mercury that the body is chronically exposed to, accumulate in the brain, pituitary gland, CNS, liver, kidneys, etc. and can damage, inhibit, and cause imbalances at virtually any stage of these various processes at very low levels of exposure, which can have major neurological, immunological, and metabolic effects on an individual. Multiple Sclerosis (MS) is caused by the erosion of myelin, a substance which helps the brain send messages to the body. Metal particles entering the body can bind to this myelin. For those who are hypersensitive, this myelin-metal bond comes under attack from the immune system. This is called autoimmunity. In such cases, the progression of MS can be halted by removing the source of the metal or other toxic factor (369,303b,35).  MS prevalence has been increasing in recent years and is currently about 1 in 700, giving approx. 390,000 in the U.S. (1). 

According to the National Lupus Foundation, there are generally four recognized forms or types of lupus: Cutaneous (skin) Lupus Erythematosus, Systemic Lupus Erythematosus (SLE), Drug-induced Erythematosus and Neonatal Lupus. Both genetic susceptibility and environmental factors such as toxic metals and organic chemicals have been found to be factors in Lupus incidence. The prevalence of lupus is approx. 1 in every 194 or 1.4 million in the U.S. (1b).  A large occupational health study found that those exposed to mercury or pesticides occupationally had a significantly higher likelihood of having the autoimmune condition, lupus (SLE) (113c).


Mercury is known to be one of the most toxic substances commonly encountered and to be along with lead and arsenic the toxic substances 

adversely affecting the largest numbers of people(276). Dental amalgam is documented by medical studies and medical lab tests to be the 

largest source of both inorganic and methyl mercury in most people who have several mercury amalgam fillings (599). Bacteria, yeasts, and Vitamin B12 methylate inorganic mercury to methyl mercury in the mouth and intestines (599,510) and mercury inhibits functional methylation in the body, a necessary process (509). The main factors determining whether chronic conditions are induced by metals appear to be exposure and genetic susceptibility, which determines individuals immune sensitivity and ability to detoxify metals (405). Very low levels of exposure have been found to seriously affect relatively large groups of individuals who are immune sensitive to toxic metals, or have an inability to detoxify metals due to such as deficient sulfoxidation or metallothionein function or other inhibited enzymatic processes related to detoxification or excretion of metals. 

A large epidemiological study of 35,000 Americans by the National Institute of Health, the nation's principal health statistics agency, found that there was a significant correlation between having a greater than average number of dental amalgam surfaces and having the a chronic condition such as epilepsy, MS, or migraine headaches. Fewer of those with this condition have zero fillings than those of the general population while significantly more of those with the condition have 17 or more surfaces than in the general population(543). MS clusters in areas with high metals emissions from facilities such as metal smelters have been documented(184).

As far back as 1996 it was shown that the lesions produced in the myelin sheath of axons in cases of multiple sclerosis were related to excitatory receptors on the primary cells involved called oligodendroglia. The loss of myelin sheath on the nerve fibers characteristic of the disease are due to the death of these oligodendroglial cells at the site of the lesions (called plaques). Further, these studies have shown that the death of these important cells is as a result of excessive exposure to excitotoxins at the site of the lesions(576,598). Most of these excitotoxins are secreted from microglial immune cells in the central nervous system. This not only destroys these myelin-producing cells it also breaks down the blood-brain barrier (BBB), allowing excitotoxins in the blood stream to enter the site of damage. Some common exposures that cause such proliferation of such excitotoxins resulting in MS are mercury and aspartame, with additional effects from MSG and methanol. Mercury and other toxic metals inhibit astrocyte function in the brain and CNS(119), causing increased glutamate and calcium related neurotoxicity (119,333,416,496) which are factors in neural degeneration in MS and ALS. There is evidence that astrocyte damage/malfunction is a major factor in MS(544). Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage(142,13). Nitric oxide related toxicty caused by peroxynitrite formed by the reaction of NO with superoxide anions, which results in nitration of tyrosine residues in neurofilaments and manganese Superoxide Dimustase(SOD) has been found to cause inhibition of the mitochondrial respiratory chain, inhibition of the glutamate transporter, and glutamate-induced neurotoxicity involved in ALS(524,521). 

It is now known the cause for the destruction of the myelin in the lesions is overactivation of the microglia in the region of the myelin(598). An enzyme that converts glutamine to glutamate called glutaminase increases tremendously, thereby greatly increasing excitotoxicity. Any dietary excitotoxin can activate the microglia, thereby greatly aggravating the injury. This includes the aspartate in aspartame and MSG which is in many processed foods. The methanol in diet drinks adds to this toxicity as well. Now, the secret to treatment appears to be calming down inflammation of the microglia.

Mercury and cadmium inhibit magnesium and zinc levels as well as inhibiting glucose transfer are other mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance/diabetes (43,198,338,597). Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation and are protective against these conditions(595,43). 

According to neurologist Dr. RL Blaylock(598), the good news is that there are supplements and nutrients that calm the microglia-the most potent are: silymarin, curcumin and ibuprophen. Phosphatidylcholine helps re-myelinate the nerve sheaths that are damaged, as does B12, B6, B1, vitamin D, folate, vitamin C, natural vitamin E (mixed tocopherols) and L-carnitine (576). A study demonstrated protective effects of methylcobalamin, a vitamin B12 analog, against glutamate- induced neurotoxicity(508), and similarly for iron in those who are iron deficient DHA plays a major role in repairing the myelin sheath. Vitamin D may even prevent MS(463b,576), but it acts as an immune modulator, preventing further damage - the initial dose is 2000 IU a day. Magnesium, as magnesium malate, is needed in a dose of 500 mg 2X a day. They must avoid all excitotoxins, even natural ones in foods-such as soy, red meats, nuts, mushrooms and tomatoes. Avoid all fluoride and especially all vaccinations since these either inhibit antioxidant enzymes or triggers harmful immune reactions.  Intake of ≥400 IU/day of vitamin D from multivitamins was associated with a reduced risk whereas intake of whole milk, an important source of dietary vitamin D, was associated with an increased risk(463b).

It has also been found that the antibiotic minocycline powerfully shuts down the microglia. Dr. Blaylock tried this treatment on a patient who just came down with fulmanant MS. He was confined to a wheelchair. He was placed on minocycline and now, just a few weeks later, he is walking.

The various neurological, immune, and metabolic related diseases discussed together here are diagnosed and labeled clinically based primarily on symptoms, along with tests for some underlying conditions found common in each disease. But each individual will be seen to have their own unique combination of neurological, endocrine, and enzymatic imbalances along with autoimmunities that result in the functional problems that lead to symptoms that are diagnosed as multiple sclerosis(MS) or Amyotrophic Lateral Sclerosis(ALS) or Alzheimer’s Disease(AD), or Parkinson’s Disease(PD), or Systemic Lupus Erythematosus(SLE), rheumatoid arthritis(RA), chronic fatigue syndrome(CFS), or oral lichen planus(OLP), etc.(100) However, a lot of commonality among these factors has been documented, both within specific diseases and among the various diseases discussed here. In MS, an autoimmune T-cell attack on CNS myelin sheath results in demyelinated plaques (405,etc.). Activated T-cells, plasma cells, and macrophages have been found in the demyelinated areas. ALS is a systemic motor neuron disease that affects the corticospinal and corticobulbar tracts, ventral horn motor neurons, and motor cranial nerve nuclei(405,etc.). Approximately 10 percent of ALS cases are of the familial type that has been linked to a mutation of the copper/zinc super oxide dismustase gene(Cu/Zn SOD). The majority of ALS cases are of the sporadic type. There are many toxic substances as well as some common drugs(336) that have been found to be major factors in producing the functional conditions that result in these diseases. However mercury appears to be the most commonly implicated of these, and in particular mercury from amalgam fillings- as will be documented here. For the majority of cases there are now tests to identify the various factors involved in these types of diseases; and once an individual’s underlying causative factors have been identified, high success rates at cure or significant improvement are being achieved.

Toxic metals such as mercury, lead, cadmium, etc. have been documented to be neurotoxic, immunotoxic, reproductive/developmental toxins that 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(2,125,441,505,601,600,503). Exposure of humans and animals to toxic metals such as mercury, cadmium, lead, copper, aluminum, arsenic, chromium, manganese, etc. is widespread and in many areas increasing. The U.S. Center for Disease Control(276) ranks toxic metals as the number one environmental health threat to children. According to an EPA/ATSDR assessment, the toxic metals mercury, lead, and arsenic are the top 3 toxics having the most adverse health effects on the public based on toxicity and current exposure levels in the U.S., with cadmium, nickel and chromium also highly listed. 

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. The reason is that the public appears to be generally unaware that considerable scientific evidence supports that mercury is the metal causing the most widespread adverse health effects to the public, and amalgam fillings have been well documented to be the number one source of exposure of mercury to most people, with exposure levels often exceeding Government health guidelines and levels documented to cause adverse health effects. Much of the direct chronic exposure to toxic metals for persons with the autoimmune diseases discussed here appears to be from use of metals in dental work. The most common dental metals that have been documented to be causing widespread adverse health effects are mercury, nickel, palladium, gold, and copper. Although chronic exposure clearly is affecting a much larger population, nickel has been found to be a major factor in many cases of MS and lupus, with palladium having very similar effects to nickel. Likewise chronic exposures to manganese and copper have been implicated in some cases of Parkinson’s disease. Another group of toxic substance substances with widespread exposure that have been demonstrated to generate reactive oxygen species and have positive correlations to some of the diseases discussed here are the organochlorine pesticides. Toxic metals appear to be only one of the factors involved in chronic autoimmune conditions. Pathogens such as viruses, mycoplasma, bacteria and parasites have been found to usually be present and a factor to deal with in treating those with chronic degenerative conditions and weakened immune systems such as MS(448e,449,468,470,485,598, 303) and other autoimmune conditions. Studies have found high incidence of EBV and mycoplasma in MS patients, and treatment of such has been a factor in improvement of some according to Dr. Blaylock's and Dr. Nicholson's experience and papers. 


II. Documentation of High Common Exposures and Accumulation of Mercury in the Brain and Motor Neurons

Amalgam fillings are the largest source of mercury in most people with daily exposures documented to commonly be above government health guidelines (14,49,79,99,183,506,500,217). This is due to continuous vaporization of mercury from amalgam in the mouth, along with galvanic currents from mixed metals in the mouth that deposit the mercury in the gums and oral cavity (605). Mercury vapor is lipid soluble and volatile so crosses the blood brain barrier; as does methyl mercury, which results by the conversion from mercury vapor or inorganic mercury (589,32,606) by bacteria. Due to the high daily mercury exposure and excretion into home and business sewers of those with amalgam, dental amalgam is also the largest source of the high levels of mercury found in all sewers and sewer sludge, and thus according to government studies a significant source of mercury in rivers, lakes, bays, fish, and crops (603). People also get significant exposure from vaccinations, fish, and dental office vapor(600).

When amalgam was placed into teeth of monkeys and rats, within one year mercury was found to have accumulated in the brain, trigeminal ganglia, spinal ganglia, kidneys, liver, lungs, hormone glands, and lymph glands (22,303). People also commonly get exposures to mercury and other toxic metals such as lead, arsenic, nickel, and aluminum from food, water, and other sources (601). All of these are highly neurotoxic and are documented to cause neurological damage which can result in chronic neurological conditions over time, as well as ADHD, mood, and behavioral disorders (601,303).

Mercury is one of the most toxic substances in existence and is known to bioaccumulate in the body of people and animals that have chronic exposure (600). Mercury exposure is cumulative and comes primarily from 4 main sources: silver(mercury) dental fillings, food (mainly fish), vaccinations, and occupational exposure. Whereas mercury exposure from fish is primarily methyl mercury and mercury from vaccinations is thimerosal (ethyl mercury), mercury from occupational exposure and dental fillings is primarily from elemental mercury vapor. Developmental and neurological conditions occur at lower levels of exposure from mercury vapor than from inorganic mercury or methyl mercury(606). Mercury in amalgam fillings, because of its relatively high vapor pressure compared to its PEL safety limit and galvanic action with other metals in the mouth, has been found to be continuously vaporized and released into the body, and has been found to be the directly correlated to the number of amalgam surfaces and the largest source of mercury in the majority of people (14,49,183,199,209,79,99,500), typically between 60 and 90% of the total. The level of daily exposure of those with several amalgam fillings commonly exceeds the U.S. EPA health guideline for daily mercury exposure of 0.1 ug/kg body weight/day, and the oral mercury level commonly exceeds the mercury MRL of the U.S.ATSDR of 0.2 ug/ cubic meter of air(217,500). When amalgam fillings are replaced, levels of mercury in the blood, urine, and feces typically rise temporarily but decline between 60 to 85% within 6 to 9 months (79,600.).

Mercury has been found to accumulate preferentially in the brain, major organs, hormone glands, and 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(22,14,99,163,291,327,329,442,48,604). Mercury, with exposure either to vapor or organic mercury tends to accumulate in the glial cells in a similar pattern, and the pattern of deposition is the same as that seen from morphological changes(327g,287,305). Though mercury vapor and organic mercury readily cross the blood-brain barrier, mercury has been found to be taken up into neurons of the brain and CNS without having to cross the blood-brain barrier, since mercury has been found to be taken up and transported along nerve axons as well through calcium and sodium channels and along the olfactory path(329, 288,333,34). 


III. Mercury Toxicity: Summary of Neurological Effects

Mercury has been found to accumulate in the cerebellum and other brain areas, producing reactive oxygen species(ROS), including superoxide that cause damage to those parts of the brain(194,13). Mercury was also found to cause a reduction in antioxidant function such as superoxide dimustase(SOD) and glutathione peroxide(GPx) that tries to counter-balance the ROS(13,56a). Mercury, with exposure either to vapor or organic mercury tends to accumulate in the glial cells in a similar pattern, and the pattern of deposition is the same as that seen from morphological changes (327g,287a). Mercury(especially mercury vapor or organic mercury) penetrates and damages the blood brain barrier allowing penetration of the barrier by other substances that are neurotoxic (along with reduced amino acid uptake to brain) (22,38,85,604,162,301,311/262). Such damage to the blood brain barrier’s function has been found to be a major factor in chronic neurological diseases such as MS(286,289,291,302, 324,326,478). 

Programmed cell death(apoptosis) is documented to be a major factor in degenerative neurological conditions like MS, ALS, Alzheimer’s, 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(13,43a,56a,296b,495), reduced glutathione levels(56,126a,111a), liver enzyme effects and inhibition of protein kinase C and cytochrome P450(43,84,260), nitric oxide and peroxynitrite toxicity (43a,521,524), excitotoxicity and lipid peroxidation(490,496), excess free cysteine levels (56d,111a,33,330),excess glutamate toxicity(13b, 416), excess dopamine toxicity (56d,13a), beta-amyloid generation(462,56a), increased calcium influx toxicity (296b,333,416,432,462c,507) and DNA fragmentation(296,42,114,142) and mitochondrial membrane dysfunction (56de, 416).

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). Gluthathione 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 mechinsisms are disrupted by toxic exposures such as mercury, neuronal cell apoptosis results and neurological damage. Mercury has been shown to induce TNFa, deplete glutathione, and increase glutamate, dopamine, and calcium related toxicity, causing inflammatory effects and cellular apoptosis in neuronal and immune cells(126b,126c). Mercury’s biochemical damage at the cellular level include DNA damage, inhibition of DNA and RNA synthesis (42,114,142,197,296,392); alteration of protein structure (33,111,114,194,252,442); alteration of the transport and signaling functions of calcium(333,43b,254,416d,462,507); inhibition of glucose transport(338,254), and of enzyme function and other essential nutrients (96,198,254,263,264,33,330,331,338,339,347, 441,442); induction of free radical formation (13a,43b,54,405,424), depletion of cellular glutathione (necessary for detoxification processes) (56,111,126,424), inhibition of glutathione peroxidase enzyme(13a,442), inhibits glutamate uptake(119,416d), induces peroxynitrite and lipid peroxidation damage(521b), causes abnormal migration of neurons in the cerebral cortex(149), immune system damage (111,194, 226,252, 272,316,325,355); inducement of inflammatory cytokines(126,152,181) and autoimmunity (181,226,272,314,369,405,507,100,etc.)  A study of patients suffering from autoimmune conditions found that approx. 70% recovered or significantly improved after safe amalgam filling replacements(60c). Infectious agents such as Helicobacter pylori (Hp) may cause chronic inflammation and autoimmune reactivity in susceptible subjects. The results of in vitro experiments performed with lymphocytes from Hp infected patients indicate that Hp can cause immunosuppression which might be eliminated by successful eradication therapy(60c). Mercury, heavy metals and Hp infection may play an important role in AT and autoimmune conditions.

Patients with certain autoimmune and allergic diseases, such as systemic lupus, multiple sclerosis, autoimmune thyroiditis or atopic eczema, often show increased lymphocyte stimulation by low doses of inorganic mercury in vitro(65). Results of lymphocyte reactivity measured with MELISA indicate that in vitro reactivity after the replacement of dental amalgam decreased significantly to inorganic mercury, silver, organic mercury and lead. Out of 35 patients, 25 patients (71%) showed improvement of health. The highest rate of improvement was observed in patients with multiple sclerosis,

MS patients have been found to have much higher levels of mercury in cerebrospinal fluid compared to controls (163,291,35,139). German studies including studies at German universities have found that MS patients usually have high levels of mercury body burden, with one study finding 300% higher than controls (271,302). Most recovered after mercury detox, with some requiring additional treatment for viruses and intestinal dysbiosis.Very high levels of mercury are also found in brain memory areas such as the cerebral cortex and hippocampus of patients with diseases with memory related symptoms (158,34, 207,etc.). Studies have found mercury related neurological effects to be indistinguishable from those of MS (207,212,222,244,271,289, 291,302,183,184,303,324,326,406). 

Mercury has been shown to be a factor that can cause rheumatoid arthritis by activating localized CD4+ T-cells which trigger production of immune macrophages and immunoglobulin(Ig) producing cells in joints (405,513,514). 

IV. Mercury Related Neurological Damage: Mechanisms of Causality

Exposure to inorganic mercury has significant effects on blood parameters and liver function. Studies have found that in a dose dependent manner, mercury exposure causes reductions in oxygen consumption and availability, perfusion flow, biliary secretion, hepatic ATP concentration, and cytochrome P450 liver content(260), while increasing blood hemolysis products and tissue calcium content and inducing heme oxygenase, porphyria, platelet aggregation through interfering with the sodium pump.

Mercury vapor and methyl mercury penetrate and damage the blood brain barrier (311,22,85,105,162,600/262), also facilitating other toxic substances penetration of the BBB. Damage to the blood brain barrier's function has been found to be a major factor in chronic neurological diseases discussed here. Mercury also causes high levels of oxidative stress and reactive oxygen species(ROS)(13), which have been implicated as major factors in neurological disorders including stroke, ALS(501) PD(502), Alzheimer’s(503), CFS(504), Lupus(113,234,331,602). Studies have found mercury related neurological effects to be indistinguishable from those of MS (163,207,271,244,289,291,302,303,184,324,326). 

Metals like mercury bind to SH-groups(sulphydryl) in sulfur compounds like amino acids and proteins, changing the structure of the compound that it is attached to. This often results in the immune systems T-cells not recognizing them as appropriate nutrients and attacking them(181,226,314,507). Such binding and autoimmune damage has been documented in the fat-rich proteins of the myelin sheaths and collagen(405), which are affected in MS. Metals by binding to SH radicals in proteins and other such groups can cause autoimmunity by modifying proteins which via T-cells activate B-cells that target the altered proteins inducing autoimmunity as well as causing aberrant MHC II expression on altered target cells(425de,343). Studies have also found mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and myelin basic protein(MBP) (269ag,405,478,515,516). Mercury and cadmium also have been found to interfere with zinc binding to MBP(517b) which affects MS symptoms since zinc stabilizes the association of MBP with brain myelin(517a). MS has also been found to commonly be related to inflammatory activity in the CNS such as that caused by the reactive oxygen species and cytokine generation caused by mercury and other toxic metals (405,478,515,516). Antioxidants like lipoic acid which counteract such free radical activity have been found to alleviate symptoms and decrease demyalination(494,572). A group of metal exposed MS patients with amalgam fillings were found to have lower levels of red blood cells, hemoglobin, hemocrit, thyroxine, T-cells, and CD8+ suppressor immune cells than a group of MS patients with amalgam replaced, and more exacerbations of MS than those without(102a). Immune and autoimmune mechanisms are thus seen to be a major factor in neurotoxicity of metals. 

Na(+),K(+)-ATPase is a transmembrane protein that transports sodium and potassium ions across cell membranes during an activity cycle that uses the energy released by ATP hydrolysis. Mercury is documented to inhibit Na(+),K(+)-ATPase function at very low levels of exposure(288ab). Studies have found that in Ms cases there was an elevation in plasma serum digoxin and a reduction in serum magnesium and RBC membrane Na(+)-K+ ATPase activity (263). The activity of all serum free-radical scavenging enzymes, concentration of glutathione, alpha tocopherol, iron binding capacity, and ceruloplasmin decreased significantly in Ms, while the concentration of serum lipid peroxidation products and nitric oxide increased.  The inhibition of Na+-K+ ATPase can contribute to increase in intracellular calcium and decrease in magnesium, which can result in 1) defective neurotransmitter transport mechanism, 2) neuronal degeneration and apoptosis, 3) mitochondrial dysfunction, 4) defective golgi body function and protein processing dysfunction. It is documented in this paper that mercury is a cause of most of these conditions seen in MS (13a,111,288,442,521b,43,56,263etc.)

Autoimmunity has also been found to be a factor in chronic degenerative autoimmune conditions such as MS, ALS, Autoimmune Thyroiditis, etc., with genetic susceptibility a major factor in who is affected. One genetic factor in Hg induced autoimmunity is major histocompatibility complex(MHC) linked. Both immune cell type Th1 and Th2 cytokine responses are involved in autoimmunity(425c). One genetic difference found in animals and humans is cellular retention differences for metals related to the ability to excrete mercury (426). For example it has been found that individuals with genetic blood factor type APOE-4 do not excrete mercury readily and bioaccumulate mercury, resulting in susceptibility to chronic autoimmune conditions such as Alzheimer’s, Parkinson’s, etc. as early as age 40(437), whereas those with type APOE-2 readily excrete mercury and are less susceptible (437,35). Those with type APOE-3 are intermediate to the other 2 types. A study of 465 chronic mercury toxic patients with primarily fatigue, depression, or memory loss found a significant correlation between CMT and APOE-4 blood allele type, which appears to be less protective of metals toxicity(65). Removal of amalgam mercury fillings in these patients, combined with appropriate treatment, resulted in a significant symptom reduction (p<0.001) to levels reported by healthy subjects. The incidence of autoimmune conditions has increased to the extent this is now one of the leading causes of death among women(450). Also when a condition has been initiated and exposure levels decline, autoimmune antibodies also decline in animals or humans (233,234d,369,60,118,303,368,405). A retrospective cohort study in New Zealand found that MS had a 1.24 hazard risk relative to a measure of dental amalgam exposure(81).

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(333). 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). They also block or inhibit calcium L-channel currents in the brain in an irreversible and concentration dependent manner. Metallic mercury is much more potent than methyl mercury in these actions, with 50 % inhibition in animal studies at 13 ppb(333). 

A direct mechanism involving mercury’s inhibition of cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino acids appears to be a major part of the connection to allergic/immune reactive conditions. The binding of mercury from amalgam to the -SH groups often results in inactivation of sulfur and blocking of enzyme function, producing sulfur metabolites with extreme toxicity that the body is unable to properly detoxify(33,114). Sulfur is essential in enzymes, hormones, nerve tissue, and red blood cells. These exist in almost every enzymatic process in the body. Blocked or inhibited sulfur oxidation at the cellular level has been found in most with many of the chronic degenerative diseases, including Parkinson’s, Alzheimer’s, ALS, lupus, rheumatoid arthritis, CFS,FMS,MCS, autism, etc.(33,234,330,331,501-505,602)

Some studies of patients with major neurological or degenerative diseases have found evidence amalgam fillings may play a major role in development of conditions such as such as , 

MS(102,163,170,184,212,285,291,302,303,324,326), ALS(92,97,325,501), RA(600), AD(66,67,158,166,204,207,221,238,242,244,258,296,300,303,503), SLE (234,60,405), PD(56,84,98,169,218,248,250,258,303,502) , and many other conditions(600,303). 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). Only a few micrograms of mercury severely disturb cellular function (33,56,226). 

Mercury exposure causes high levels of oxidative stress/reactive oxygen species(ROS)(13), which has been found to be a major factor in neurological disease(56,501-505). Mercury and quinones form conjugates with thiol compounds such as glutathione and cysteine and cause depletion of glutathione, which is necessary to mitigate reactive damage. Such congugates are found to be highest in the brain substantia nigra with similar congugates formed with L-Dopa and dopamine in Parkinson’s disease(56,502). Mercury depletion of GSH and damage to cellular mitochrondria and the increased lipid perxodation in protein and DNA oxidation in the brain appear to be a major factor in Parkinson’s disease(33). A Canadian study found those with 15 or more amalgam fillings to have more than 250% greater risk of MS than controls, and likewise higher risk for those who have had amalgam fillings more than 15 years, and another study also found higher mrcury body burden in those with more fillings and increased risk of MS with more fillings(324). Another study(169) found blood and urine mercury levels to be very strongly related to Parkinson's with odds ratios of approx. 20. 

Exposure to mercury results in metalloprotein compounds that have genetic effects, having both structural and catalytic effects on gene 

expression(114). Some of the processes affected by such metalloprotein 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 metalloprotein formation also appears to cause a change in antigenicity and autoimmune reactions in a significant numbers of people(114,60,342,405). Much mercury in saliva and the brain is also organic, the most neurotoxic form (506,51,220,272), since mouth bacteria and other organisms in the body methylate inorganic mercury to organic mercury (506,51,254). Dental amalgam has been found to be the largest source of methyl mercury in most with mercury amalgam fillings (506,etc.).

Spatial and temporal changes in intracellular calcium concentrations are critical for controlling neurotransmitter release in neurons(432). Mercury alters calcium homeostasis and calcium levels in the brain and affects neurotransmitter release through its effects on calcium levels(270c,333,372,43). Low levels of toxic metals have been found to inhibit dihydroteridine reductase, which affects the neural system function by inhibiting neurotransmitters through its effect on phenylalanine, tyrosine and tryptophan transport into neurons(257,258). This was found to cause severe impaired amine synthesis and hypokinesis. Tetrahydro biopterin, which is essential in production of neurotransmitters, is significantly decreased in patients with Alzheimer's, Parkinson', and MS. Such patients have abnormal inhibition of neurotransmitter production.. 

Mercury at extremely low levels also interferes with formation of tubulin producing neurofibrillary tangles in the brain, similar to those observed in Alzheimer’s patients with high levels of mercury in the brain (207,303). Mercury and the induced neurofibrillary tangles also appear to produce a functional zinc deficiency in the of AD sufferers(242), as well as causing reduced

lithium levels which is another factor in such diseases. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide(463). Lithium protects brain cells against excess glutamate induced excitability and calcium influx(280). Also mercury binds with cell membranes interfering with sodium and potassium enzyme functions, causing excess membrane permeability, especially in terms of the blood brain barrier (159,207,311]. Less than 1ppm mercury in the blood stream can impair the blood  brain barrier. Mercury was also found to accumulate in the mitochondria and interfere with their vital functions, and to inhibit cytochrome C enzymes which affect energy supply to the brain. Persons with extra Apo E4 gene copies appear especially susceptible to this damage(207,221)

Mercury blocks the immune function of magnesium and zinc (198,427,43,38), 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 ALS (489,495,464,469,111,501-504). 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. (444,464,494,495,469,470,572). Some of the antioxidants such as ginkgo bilabo were also found to have protective effects through increasing catalase and SOD action, while reducing lipid peroxidations(494a) Ceruloplasmin in plasma can be similarly affected by copper metabolism dysfunction, like SOD function, and is often a factor in neurodegeneration (489). 

Excess zinc from products such as GSK Superpolygrip(before reformulated) can also cause demyelating conditions with effects similar to MS, Demyelinating Syndrome, and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)(530) 

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. There is some evidence that astrocyte damage/malfunction is the main factor in MS(544). 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 neurological 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). 


V. Endocrine System and Metabolic Enzymatic System Impairments

Mercury has been well documented to be an endocrine system-disrupting chemical(affecting hormonal processes(85,146,149,199,312,604) and enzyme production processes(33,111,194) at very low levels.  The pituitary gland, in which mercury has been documented to accumulate, controls many of the body’s endocrine system functions and secretes hormones involved in control of most bodily processes. The hypothalamus regulates body temperature and many metabolic processes. Such hormonal secretions are affected at levels of mercury exposure much lower than the acute toxicity effects normally tested for (146,199). Some of the common effects of mercury on the endocrine system include inhibiting human growth hormone, causing hormonal imbalances that affect the reproductive system and body temperature regulation, and causing hormonal imbalances resulting in imbalances in metabolism of important minerals such as calcium(333,21,25,35,280).

Calcium flux is inhibited in synoptic plasma membranes of the cerebellum and cerebrum cortex. A permanent increase in cytosolic calcium levels appears to be associated with various pathological conditions which result in cell death(333). All of the effects on hormonal regulation of the various bodily processes add to and reinforce the imbalances caused in the metabolic enzymatic processes.

All body functions depend on cellular enzymatic and respiratory processes that use Nutrients delivered by the blood, detoxify toxic substances, and eliminate waste products through the cellular respiratory process back through the lymph and blood to the lungs, kidneys, or liver for excretion. Proteins are converted by enzymatic processes to amino acids such as cysteine, cystine, glutamic acid, methionine, etc. for cellular metabolic processes and to organic compounds such as glutathione which is necessary to detoxify toxic substances such as mercury(13,111,194). Imbalances or blockages in any of several of these enzymatic processes have been documented to cause major neurological and immune damage that appears to be involved in most of the diseases being discussed here.

Mercury vapor of those with chronic exposure is continuously released into the blood stream through the lungs and distributed to cells throughout the body, where it creates metal-protein compounds and reactive oxidative species(ROS) such as superoxide, which must be detoxified. Cysteine and glutathione, which are produced and interchanged as required through enzymatic processes, are necessary for detoxification. Blockages or impairments caused by mercury or other toxic substances or processes can then result in cellular toxicity and damage to vital organs such as the brain, CNS, liver, or kidneys. 

Clinical tests of patients with motor neurone disease( MND),ALS, PD, AD, SLE, and RA have found that the patients generally have damaged enzymatic processes resulting in elevated plasma cysteine to sulphate ratios, with the average being 500% higher than controls (330,331), and in general are poor sulphur oxidizers (33,331). High levels of free cysteine have been found to result in major neurological damage to the brain, CNS, and cellular processes(194,330,331). The two main enzymatic processes that down regulate cysteine to taurine, sulfates, and glutathione are cysteine dioxygenese(CDO) and gamma-glutamylcysteine synthetase(GGCS). Impairment in CDO can result in high cysteine levels, high cysteine to sulfate ratio, low taurine levels, and neurological damage(194,330,331). GGCS converts cysteine to glutathione , which has been demonstrated to be necessary to detoxification of toxic substances like mercury(111). If this enzymatic process is blocked, inhibited, or overloaded by chronic high toxicity levels or autoimmune reactions, there is insufficient glutathione and toxic damage occurs due to immune inability to process the metal-organic compounds and the ROS created by exposure to mercury or other toxic substances(111,33,60,56). Another enzymatic process necessary for proper cellular metabolism is sulfite oxidase(SO) which is involved in conversion of toxic sulfur forms such as sulfites, sulfur dioxide(SO2), hydrogen sulfide(H2S), etc. to nontoxic sulfates(33). SO can be blocked or inhibited by mercury or other toxic exposures, resulting in more of these very toxic sulfur compounds. SO is commonly found to be totally blocked or inhibited in patients with MND,PD,AD,SLE,RA, etc.(330,331). Glutathione peroxidase(GPx) is another enzymatic process in this loop that is often affected, as well as the process involved in converting Vitamin B6 through the essential coenzyme pyrodoxal 5-phosphate(P5P) in the synthesis of neurotransmitters. Impairment in this process results in brain neurotransmitter imbalances. Individual patients with any of these diseases who commonly have been shown to have high ratio of cysteine to sulfate can thus have several different individual enzymatic blockages or imbalances that result in such high ratios, and different levels of neurological, immune, and cellular damage due to high cysteine levels or low glutathione levels. Autoimmune reactions have also been found to be commonly involved in such blockages or imbalances, particularly for those with the major diseases being considered here. This aspect will thus be further discussed.

V. Autoimmunity, Neurological and Immune Diseases, and Mercury

Mercury has been documented to cause autoimmune disease (45,91,234,269,270,291, 328,405) and many researchers have concluded that autoimmunity is a factor in the major chronic neurological diseases such as MS, ALS, PD, SLE,RA,etc..  Mercury and other toxic metals also form inorganic compounds with OH, NH2, CL, in addition to the SH radical and thus inhibits many cellular enzyme processes, coenzymes, hormones, and blood cells(405,600). Mercury has been found to impair conversion of thyroid T4 hormone to the active T3 form as well as causing autoimmune thyroiditis common to such patients(369,382). In general, immune activation from toxic metals such as mercury resulting in cytokine release and abnormalities of the hypothalamus pituitary adrenal(HPA) axis can cause changes in the brain, fatigue, and severe psychological symptoms (342,369,379 382,385,405,118) such as profound fatigue, muscosketal pain, sleep disturbances, gastrointestinal and neurological problems as are seen in CFS, fibromyalgia, and autoimmune thyroidititis. Such hypersensitivity has been found most common in those with genetic predisposition to heavy metal sensitivity(60,342,369,382,405), such as found more frequently in patients with human lymphocyte antigens (HLA DRA) (381-383). A significant portions of the population appear to fall in this category.

The enzymatic processes blocked by such toxic substances as mercury also result in chronic formation of metal protein compounds (HLA antigens 

or antigen-presenting macrophages) that the body’s immune system(T-lymphocytes) does not recognize, resulting in autoimmune reactions 

(114,342,405). The metals bind to SH-groups on proteins which can then be recognized as “foreign” and attacked by immune lymphocytes. Such has 

been extensively documented by studies such as the documentation of the autoimmune function test MELISA, a sophisticated immune/autoimmune test which was developed to test for such reactions(60,405). 

Very low doses and short term exposures of inorganic Hg (20-200 mug/kg) exacerbates lupus and accelerates mortality in mice. low dose Hg exposure increases the severity and prevalence of experimental autoimmune myocarditis induced by other factors. A strong significant correlation was found between occupational exposure to mercury or pesticides to lupus (SLE), with dental personal having a very high risk factor(113c). In a study of small-scale gold mining using mercury, there was a positive interaction between Hg autoimmunity and malaria. These results suggest a new model for Hg immunotoxicity, as a co-factor in autoimmune disease, increasing the risks and severity of clinical disease in the presence of other triggering events, either genetic or acquired(234f). 


Autoimmune reactions to inorganic and methyl mercury have been found to be relatively independent, occurring in over 10% of controls. In the population of over 3,000 patients tested by MELISA, the following percentages tested positive for lymphocyte reactivity:

nickel-34%, inorganic mercury-22%, phenyl mercury-15%, methyl mercury-8%, gold-10%, palladium-10%, cadmium-11%, silver-1%. Groups with autoimmune symptoms such as oral lichen planus, CFS, MS, autoimmune thyroiditis, etc. generally have high percentages with lymphocyte reactivity to metals(60,342,369,405). Among a population of patients being tested for autoimmune problems, 94% of such patients had significant immune reactions to inorganic mercury(MELISA test,60,342,369,405) and 72% had immune reactions to low concentrations of HgCl2(<0.5 ug/ml). Of a population of 86 patients with CFS symptoms who had amalgam fillings replaced, 78% reported significant health improvement in a relatively short time period after replacent, and MELISA test scores had a significant reduction in lymphocyte reactivity compared to pre- replacement(369). Similar results were experienced for those with MS, lupus, and autoimmune thyroiditis(369). The MELISA test has proved successful in diagnosing and treating environmentally caused autoimmune diseases such as MS, SLE, oral lichen planus, CFS,etc. (60,313,342,369,405). A high percentage of patients subjectively diagnosed with CNS and systemic symptoms suggestive of mercury intoxication have been found to have immune reactivity to inorganic mercury(MELISA test,118), and likewise for MRI positive patients for brain damage. Controls without CNS problems did not have such positive correlations. Nickel, palladium, and gold have also been found to induce autoimmunity in genetically predisposed or highly exposed individuals (60,118,313,314,234,369,130). Tests have found a significant portion of people(over 10%) to be in this category and thus more affected by exposure to amalgam than others. Once compromised by a toxic substance that depletes the immune protectors and causes autoimmunity, the immune system is more susceptible to being sensitized to other toxic chemicals, a factor in multiple chemical sensitivity(MCS). Mercury also causes a reduction in thyroid production(50) and an accumulation in the thyroid of radiation. Among those with chronic immune system problems with related immune antibodies, the types showing the highest level of antibody reductions after amalgam removal include glomerular basal membrane, thyroglobulin, and microsomal thyroid antigens(91). 

Mercury and toxic metals block enzymes required to digest milk casein and wheat gluten, resulting in increased IgA and IgG to gluten and IgA to casein ,as well as dumping morphine like substances in the blood that are neurotoxic and psychotic, as a major factor in schizophrenia, autism, ADHD, and MS (24-26). A higher level of milk consumption has been found to be correlated with higher MS incidence(463b). Likewise for wheat gluten, and a casein/gluten free diet has been found to result in improvements in conditions like MS and autism. 

A mechanism in MS occurs due to a reduction in immune system activity. Specifically, it is the reduction in the number of the suppressor T-cells within the immune system that allows CD4 helper T-cells to do damage (102a,181,226, 314,405,507,513,514,20). Thus, during an acute relapse the overall number of T-cells is reduced, the normal balance of helper and suppressor T-cells is disrupted, and helper T-cells tend to predominate.  This is most pronounced during an acute relapse, but a similar situation occurs although perhaps to a lesser extent, in chronic progressive MS. A double blind study using a potent opiate antagonist, naltrexone (NAL), produced significant reduction in neurological symptomology among the 56% most responsive to opioid effects in a population of autism patients(18,19). The behavioral improvements was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase in the T-helper-inducers and a significant reduction of the T-cytotoxic-suppressors and a normalization of the CD4/CD8 ratio.  Low dose naltrexone (LDN) has been found to commonly be effective in reducing MS symptoms and exerbations, apparently due its opioid suppressive effects(20).


VI. Recovery from Chronic Neurological and Immune Related Diseases After Amalgam Removal and Mercury Detoxification

There are extensive documented cases (many thousands) where removal of amalgam fillings led to cure of serious health problems such as MS(369,35,94,95,102,163,170,212,222,271,291,302,468,470,34,229, 406,485,523), SLE(369,12,35,113,222,229,233,323,60), Chronic Fatigue Syndrome (8,35,60,212,293,229,222,232, 233,271,317,323,342,369, 376,382,440,470,523), muscular/joint pain/Fibromyalgia (35,222,293,317,322,369,440,468,470,523,94), depression (94,107,222,271,294,212,229,233,285e,317,322,376,453,465,468,485, 523,35,40), Rheumatoid Arthritis(35,95,103,212, 222,271, 322,358,470, 523), autoimmune thyroiditis (369,382,91), OralLichenPlanus(60,75,78,82,86, 87,90,94,101,133, 168,313), ALS(97,229,405,406,468-470,485,35), Parkinson’s/ muscle tremor (222,248,229,271,470,212,94,98,35), Alzheimer’s’s(204,35), and many other chronic conditions(600). In several of the studies, over 75% of those with MS and having amalgams replaced recovered or had significant improvement( 369,212(a),(b),(e),302,222,35). Some of the studies reported similar success rates for SLE and autoimmune thyroiditis, but with lower number of cases treated. There is consensus that dental amalgam is the main cause of oral lichen planus and most recover after amalgam replacement.

In one study all 6 of those tested for autoimmunity by the MELISA blood lymphocyte immune reactivity test were found to be immune reactive to mercury, and all had significant improvement in their condition after amalgam replacement, as well as reduction in immune reactivity(369). Out of 15 patients with lupus (SLE), 73% had significant improvement in health, and out of 8 with autoimmune thyroiditis 75% had significant improvement after amalgam replacement. The patients who did not have significant improvement were found to have immune reactivity to nickel which did not improve after amalgam replacement as the amalgam was not the source of the nickel exposure (369). 

Clinical studies have found that patch testing is not a good predictor of success of amalgam removal, as a high percentage of those testing negative also recovered from chronic conditions after replacement of fillings (86,87,90). Follow up tests for autoimmune reaction to inorganic mercury after amalgam replacement have found that in most patients tested, the immune reaction as well as most symptoms disappear over time (60,313,405, etc.).

The level of mercury in the gums is often 1200 ppm near a gold cap on an amalgam filling (30,35,48,194). These levels are among the highest levels ever measured in tissues of living organisms, exceeding the highest levels found in chronically exposed chloralkali workers, those who died from mercury in Minamata, or animals that died from mercury poisoning. The FDA/EPA action level for warnings of dangerous levels in fish or food is 1 ppm.

Tests and Treatment

In a large German study of MS patients after amalgam revision, extraction resulted in 85% recovery rate versus only 16% for filling replacement alone (302,222). Other clinics have found that recovery from serious autoimmune diseases, dementia, or cancer may require more aggressive mercury removal techniques than simple filling replacement due to body burden. This appears to be due to migration of mercury into roots & gums that is not eliminated by simple filling replacement. Also, toxic metals, formaldehyde, and other toxic substances have been documented to accumulate in the jaw bone and tissue near teeth with multiple metals, as well as in pockets from extracted teeth and form cavitations (areas of toxic materials and diseased bone). Such cavitations and toxic bacteria accumulating from root-canaled teeth sometimes must be cleaned out before significant recovery can occur (573,200,302,222,207,etc.). There is a direct connection between the teeth and gums with the brain and CNS by both travel along nerve fibers and through the cranio-vertebral venous system for either toxic substances such as mercury or for bacteria (34,325,207,etc.), The following protocol is perhaps the most used protocol for treating these conditions and has had considerable success:

Huggins Total Dental Revision Protoco/IAOMT Safe Replacement Protocol(35)

(a) history questionnaire and panel of tests.

(b) replace amalgam fillings starting with filling with highest negative current or highest negative quadrant, with supportive vitamin/mineral supplements.

© extract all root canaled teeth using proper finish protocol (573). [root canaled teeth can harbor extremely toxic bacterial toxins and are

                      a major factor or cause of chronic neurological or immune conditions (573)]

(d) test and treat jawbone cavitations and amalgam tattoos where relevant (573)

(e) supportive supplementation, periodic monitoring tests, evaluate need for further treatment (not usually needed).

note: after treatment of many cases of chronic autoimmune conditions such as MS, ALS, Parkinson’s, Alzheimer’s, CFS, Lupus, Rheumatoid Arthritis, etc., it has been observed that often mercury along with root canal toxicity or cavitation toxicity are major factors in these conditions, and most with these conditions improve after TDR if protocol is followed carefully (35,200,600). Other measures in addition to TDR that have been found to help in treatment of MS in clinical experience are avoidance of milk products (463b, etc.), get lots of sunlight, supplementation of calcium AEP(448) and alpha lipoic acid(448b). Progesterone creme has been found to promote regrowth of myelin sheaths in animals(448c).

Tests suggested by Huggins/Levy (35) for evaluation and treatment of mercury toxicity:

(a) hair element test (386) (low hair mercury level does not indicate low body level)(more than 3 essential minerals out of normal range indicates likely metals toxicity)

(b) CBC blood test with differential and platelet count

© blood serum profile

(d) urinary mercury (for person with average exposure with amalgam fillings, average mercury level is 3 to 4 ppm;

lower test level than this likely means person is poor excretor and accumulating mercury, often mercury toxic(35) 

(e) fractionated porphyrin (note test results sensitive to light, temperature, shaking)

(f) individual tooth electric currents (replace high negative current teeth first)

(g) patient questionnaire on exposure and symptom history

Based on the known mechanisms of damage found in these conditions, the authors of the study(463) suggest that supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100 & mgr;g Se, 180 mg EPA nd 120 mg DHA per day between 14 and 16 years of age may prevent MS, and reduce futher damage for those with the condition. 

An Oregon researcher, Dr. R. Swank, found a significant correlation between MS and dietary fat (274) . He developed a low fat diet, with animal meat mostly replaced by fish or fish oil (with EPA/DHA) and olive oil.  Studies found the Swank diet effective at reducing the effects of MS.   European studies have confirmed his findings regarding connection of MS to high fat animal diets, and effectiveness of the Swank diet. Studies have also found deficiency in essential fatty acids to be associated with demyelination, again consistent with the Swank findings. Studies have also found protective effects of diets high in vegetable protein, dietary fiber, cereal fiber, vit C, vit D, thiamin, riboflavin, calcium, potassium, and magnesium. A study found increased vit D helpful in reducing MS effects. Additionaly curcumin and Acetyl-L-Carnitine were found by studies to be neuroprotective.   Both reduce inflammation/ oxidative stress.   Extracts of green tea (EGCG) and black tea(theaflavins) also have been found to be highly effective at reducing inflammatory effects(274). A study comparing alternative treatment of MS to conventional treatment found the majority using alterntive treatments were satisfied with their treatment, and much lower adverse health effects from alternative treatments compared to convention treatments (273). Amalgam replacement was one of the alternatives used by some. 

More information on causes, prevention, and treatment of autoimmune conditions can be found at the following review (100). Information on test and treatment options and doctors and dentists with experience at dealing with toxic metal related conditions can be obtained from DAMS (800-311-6265) or the dental and medical association IAOMT (

Causes and Treatments of MS other than Mercury or Toxic Metals:

See Conditions:    [webpage search for Multiple Sclerosis or (MS)   ]



(1)Understanding Autoimmune Disease: NIAID, 2010; & (b) NWHIC,


(2)U.S. Environmental Protection Agency(EPA), 1999, "Integrated Risk Information System, National Center for Environmental Assessment, Cincinnati, Ohio,; & United States Environmental Protection Agency, Office of Water, November 2000, The National Listing of Fish and Wildlife Advisories: Summary of 1999 Data, EPA 823 F 00 20,

(12) Dimaval Scientific monograph, sixth Ed., Jan 1997, Dr Johann Ruprecht, Heyl Corporation

(13)(a) S.Hussain et al, “Mercuric chloride induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain”,J Environ Sci Health B 1997 May;32(3):395 409; & P.Bulat, “Activity of Gpx and SOD in workers occupationally exposed to mercury”, Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med 1995; 18(2): 321-36 ; & D.Jay, “Glutathione inhibits SOD activity of Hg”, Arch Inst cardiol Mex, 1998,68(6):457-61 & El-Demerdash FM. Effects of selenium and mercury on the enzymatic activities and lipid peroxidation in brain, liver, and blood of rats. J Environ Sci Health B. 2001 Jul;36(4):489-99. &(b) S.Tan et al, “Oxidative stress induces programmed cell death in neuronal cells”, J Neurochem, 1998, 71(1):95-105; & Matsuda T, Takuma K, Lee E, et al. Apoptosis of astroglial cells [Article in Japanese] Nippon Yakurigaku Zasshi. 1998 Oct;112 Suppl 1:24P-; & & Lee YW, Ha MS, Kim YK.. Role of reactive oxygen species and glutathione in inorganic mercury-induced injury in human glioma cells. Neurochem Res. 2001 Nov;26(11):1187-93; & (c)Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002 Dec 1;70(5):694-702. 

(14) (a) M.Nylander et al, "Mercury concentrations in the human brain and kidneys and exposure from amalgam fillings", Swed Dent J 1987; 11:179-187, & (b) D.W.Eggleston et al, Correlation of dental amalgam with mercury in brain tissue. J Prosthet Dent, 1987,58(6),704-7; & J.A.Weiner et al,“The relationship between mercury concentration in human organs and predictor variables", Sci Tot Environ, 138(1-3):101-115,1993

(18) Scifo R, Marchetti B, et al. Opioid-immune interactions in autism: behavioral and immunological assessment during a double-blind treatment with naltexone. Ann Ist Super Sanita 1996; 32(3): 351-9.

(19) Eedy DJ, Burrows D, Dlifford T, Fay A. Elevated T cell subpopulations in dental students. J prosthet Dent 1990; 63(5):593-6; &  & Yonk LJ et al, CD+4 helper T-cell depression in autism. Immunol Lett, 1990, 25(4):341-5. 

(20) LDN for MS Trials/Experience

(21) Goyer RA Toxic effects of metals. Cassarett and Doull's toxicology  The basic science of poisons , ed3, New York , MacMillan Publ.Co 1986, pp582 609

(22) (a) Galic N, Ferencic Z et al, Dental amalgam mercury exposure in rats. Biometals. 1999 Sep;12(3):227-31; & Arvidson B, Arvidsson J, Johansson K,. Mercury deposits in neurons of the trigeminal ganglia after insertion of dental amalgam in rats. Biometals. 1994 Jul;7(3):261-3; & (b)Danscher G, Horsted-Bindslev P, Rungby J. Traces of mercury in organs from primates with amalgam fillings. Exp Mol Pathol. 1990 Jun;52(3):291-9; & L.Hahn et al, Distribution of mercury released from amalgam fillings into monkey tissues”, FASEB J.,1990, 4:5536

(24) J.R. Cade et al, Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999. ;& Autism and Schizophrenia: Intestinal Disorders, Cade R et al. Nutritional Neuroscience, March 2000. & ; & "Beta-casomorphin induces Fos-like immunoreactivity in discrete brain regions relevant to schizophrenia and autism" Autism March 1999 vol 3(1) 67-83; Sun, ZJ, Cade JR, et al & A Peptide Found in Schizophrenia and Autism Causes Behavioral Changes in Rats, J.R. Cade, Z. Sun , Univ of Florida, USA , Autism, Vol. 3, No. 1, 85-95 (1999) DOI: 10.1177/1362361399003001007 © 1999 The National Autistic Society, SAGE Publications ; & Opiate hypothesis in infantile autism? Therapeutic trials with naltrexone, Leboyer M, et al., Encephale 1993 Mar-Apr;19(2):95-102; & Food allergy and infantile autism. Lucarelli S, et al., Panminerva Med 1995 Sep;37(3):137-41;  & Application of the Exorphin Hypothesis to Attention Deficit Hyperactivity Disorder: A Theoretical Framework by Ronald Hoggan A Thesis Submitted To The Faculty Of Graduate Studies In Partial Fulfilment Of The Requirements For The Degree Of Master Of Arts, Graduate Division Of Educational Research,Calgary, April, 1998 University of Calgary 

(25) Reichelt KL. Biochemistry and psycholphisiology of autistic syndromes. Tidsskr Nor Laegeforen 1994, 114(12):1432-4; & Reichelt KL et al, Biologically active peptide-containing fractions in schizophrenia and childhood autism. Adv Biochem Psychopharmocol 1981; 28: 627-43; Lucarelli S, Cardi E, et al, Food allergy and infantile autism. Panminerva Med 1995; 37(3):137-41; & Shel L, Autistic disorder and the endogenous opioid system. Med Hypotheses 1997, 48(5): 413-4.

(26)The mercury/casein/gluten factor effect on opioid peptides as a mechanism in causing autism, schizophrenia, ADHD, MS, and other neurological conditions, B Windham (Ed),; & (b) IgA antibodies against gliadin and gluten in multiple sclerosis, Reichelt KLJensen D.Acta Neurol Scand. 2004 Oct;110(4):239-41; & (c) Gluten sensitivity in Japanese patients with adult-onset cerebellar ataxia, Ihara M, Makino F, et al; Intern Med. 2006;45(3):135-40; & (d) Multiple sclerosis and occult gluten sensitivity , Pengiran Tengah CD, Lock RJ, Unsworth DJ, Wills AJ. Neurology. 2004 Jun 22;62(12):2326-7.



(28) F.Schmidt et al, “Mercury in urine of employees exposed to magnetic fields”, Tidsskr Nor Laegeforen, 1997, 117(2): 199-202; & Sheppard AR and EisenbudM., Biological Effects of electric and magnetic fields of extremely low frequency. New York university press. 1977; & Ortendahl T W, Hogstedt P, Holland RP, "Mercury vapor release from dental amalgam in vitro caused by magnetic fields generated by CRT's", Swed Dent J 1991 p 31 Abstract 22.

(30) Till et al.,Zahnarztl. Welt/reform, 1978:87;1130 1134; & S.Olssonl, "Release of elements due to electrochemical corrosion of dental amalgam" J of Dental Research, 1994, 73:33 43

(32)   B. Windham, DAMS,  Mercury or metals exposure and health effects, & Dental Amalgam Mercury Page, (over 5000 peer-reviewed studies cited)

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

(34) PatrickStörtebecker,Associate Professor of Neurology, Karolinska Institute, Stockholm. Mercury Poisoning from Dental amalgam-A Hazard to the Human Brains, ISBN: 0-941011001-1  & J Canadian Dental Assoc, 33(6): 300-; & Henriksson J, Tjalve H. Uptake of inorganic mercury in the olfactory bulbs via olfactory pathways in rats. Environ Res. 1998 May;77(2):130-40.

(35) (a) Huggins HA, Levy,TE,  Solving the MS Mystery: Help, hope and recovery, 2002; & (b) Huggins HA, Levy,TE, Uniformed Consent: the hidden dangers in dental care, 1999, Hampton Roads Publishing Company Inc; & (c)Hal Huggins, Its All in Your Head, 1993; & (d) Center for Progressive Medicine,

& Dr. T Levy, Curing the Incurable: Vitamin C, Infectious Diseases, and Toxins PaperbackSeptember, 2002

(38)S.Ziff and M.Ziff, Infertility and Birth Defects: Is Mercury from Dental Fillings a Hidden Cause? , Bio Probe, Inc. ISBN: 0 941011 03 8.1987,

(42) Rodgers JS, Hocker JR, et al, Mercuric ion inhibition of eukaryotic transcription factor 

binding to DNA. Biochem Pharmacol. 2001 Jun 15;61(12):1543-50; & K.Hansen et al A survey of metal induced mutagenicity in vitro and in vivo, J Amer Coll Toxicol , 1984:3;381 430; 

(43) (a)Knapp LT; Klann E. Superoxide induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem 2000 May 22; & P.Jenner,“Oxidative mechanisms in PD”, Mov Disord, 1998; 13(Supp1):24-34;&(b) Rajanna B et al, “Modulation of protein kinase C by heavy metals”, Toxicol Lett, 1995, 81(2-3):197-203: & Badou A et al, “HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels”J Biol Chem. 1997 Dec 19;272(51):32411-8., & D.B.Veprintsev, 1996, Institute for Biological Instrumentation, Russian Academy of Sciences, Pb2+ and Hg2+ binding to alpha lactalbumin”.Biochem Mol Biol Int 1996 ;39(6): 1255 65; & M. J. McCabe, University of Rochester School of Medicine & Dentistry, 2002, Mechanisms of Immunomodulation by Metals,; & Buzard GS, Kasprzak KS. Possible roles of nitric oxide and redox cell signaling in metal-induced toxicity and carcinogenesis: a review. Environ Pathol Toxicol Oncol. 2000;19(3):179-99

(45) Pelletier,L et al., In  vivo self reactivity of mononuclear cells to T cells and macrophages exposed to Hg Cl2 Eur. J Immun.,1985: 460 465; & Pelletier et al, "Autoreactive T cells in mercury induced autoimmune disease",J Immunol, 1986, 137(8): 2548 54 & Scand J of Immunology, 1990, 31:65 74 & M. Kubicka et al, "Autoimmune disease induced by mercuric choride", Int Arch Allergy Immunol, Jan 1996, 109(1):11 20. 

(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. 

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

(50) J.Kawada et al, “Effects of inorganic and methyl mercury on thyroidal function”, J Pharmacobiodyn, 1980, 3(3):149-59.

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

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

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

(60) V.D.M. Stejskal,Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden "MEMORY LYMPHOCYTE IMMUNO STIMULATION ASSAY  MELISA

( & VDM Stejskal et al, "MELISA: tool for the study of metal allergy", Toxicology in Vitro, 8(5):991 1000, 1994: & (b) Metal-specific lymphocytes: biomarkers of sensitivity in man. Stejskal VD, Danersund A, Lindvall A, Lindh U.Neuroendocrinology Letters 1998; & ©The role of environmental factors in autoimmune thyroiditis. Hybenova M et al: Neuro Endocrinol Lett. 2010;31(3):283-9;

(65) Mercury toxicity presenting as chronic fatigue, memory impairment and depression: diagnosis, treatment, susceptibility, and outcomes in a New Zealand general practice setting (1994-2006). Wojcik DP, Godfrey ME, et al; Neuro Endocrinol Lett. 2006 Aug;27(4):415-23; &(b) Increased frequency of delayed type hypersensitivity to metals in patients with connective tissue disease(SLE,RA,SS). Stejskal V, Bjorklund G et al; J Trace Elem Med Biol. 2015;31:230-6; & (c ) The beneficial effect of amalgam replacement on health in patients with autoimmunity. Prochazkova J, Stejskal VD, et al;Neuro Endocrinol Lett. 2004 Jun;25(3):211-8.

(66)"Regional brain trace element studies in Alzheimer's disease",Thompson, CM Markesbery, et al, Univ. Of Kentucky Dept. Of Chemistry, Neurotoxicology (1988 Spring) 9(1):1 7 & Hock et al, "Increased blood mercury levels in Alzheimer's patients",Neural. Transm. 1998, 105:59 68 & Cornett et al, "Imbalances of trace elements related to oxidative damage in Alzheimer's diseased brain", Neurotoxicolgy, 19:39.

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

(79)L.Bjorkman et al, “Mercury in Saliva and Feces after Removal of Amalgam Fillings", J Dent Res 75: 38- IADR Abstract 165, 1996; & Toxicology and Applied Pharmacology, May 1997, 144(1), p156-62; & & G. Sandborgh-Englund et al,  Mercury in biological fluids after amalgam removal. J Dental Res, 1998, 77(4): 615-24 & Berglund A, Molin M, "Mercury levels in plasma and urine after removal of all amalgam restorations: the effect of using rubber dams", Dent Mater 1997 Sep;13(5):297-304; & J.Begerow et al,"Long-term mercury excretion in urine after removal of amalgam fillings", Int Arch Occup Health 66:209-212, 1994.

(81) Health effects of dental amalgam exposure: a retrospective cohort study. Bates MN et al; Int J Epidemiol. 2004 Aug;33(4):894-902.

(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).

& Itoh ; K ; “Defects of cytochrome c oxidase in the substantia nigra of Parkinson's disease: and immunohistochemical and morphometric study” ; Mov Disord ; 1997 ; 12(1) ; 9 16

(85) J.A.Weiner et al,"The relationship between mercury concentration in human organs and predictor variables",138(1 3):101 115,1993; & "An estimation of the uptake of mercury from amalgam fillings", Sciemce of the Total Environment, v168,n3, p255 265, 1995.

(86) E.R.Smart et al, "Resolution of lichen planus following removal of amalgam restorations", Br Dent J 178(3):108-112,1995(12 cases); & H.Markow,” Regression from orticaria following dental filling removal:,New York State J Med, 1943: 1648-1652; & G. Sasaki et al, “Three cases of oral lichenosis caused by metallic fillings”, J. Dermatol, 23 Dec, 1996; 12:890-892; & J.Bratel et al, “Effect of Replacement of Dental Amalgam on OLR”, Journal of Dentistry, 1996, 24(1-2):41-45(161 cases). 

(87) A. Skoglund, Scand J Dent Res 102(4): 216 222, 1994; and 99(4):320 9,1991; & 

P.O.Ostman et al,"Clinical & histologic changes after removal of amalgma",Oral Surgery, Oral Medicine, and Endodontics, 1996, 81(4):459 465.

(90) P.Koch et al, “Oral lesions and symptoms related to metals”, Dermatol, 1999,41(3):422-430; & "Oral lichenoid lesions,mercury hypersensitity, ...", Contact Dermatitis, 1995, 33(5): 323-328; & S.Freeman et al, “Oral lichenoid lesions caused by allergy to mercury in amalgam”, Contact Dermatitis, 33(6):423-7, Dec 1995 

(Denmark) & H.Mobacken et al, Contact Dermatitis, 10:11-15,1984; & M.Jolly et al, “Amalgam related chronic ulceration of oral mucosa”, Br Dent J, 1986,160: 434-437; & C.Camisa et al, “Contact hypersensitivity to mercury”, Cutis, 1999, 63(3):189-

(91) B. Lindqvist et al, "Effects of removing amalgam fillings from patients with diseases affecting the immune system", Med Sci Res 24(5): 355 356, 1996.

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; & Carpenter DO. Effects of metals on the nervous system of humans and animals. Int J Occup Med Environ Health 2001;14(3):209-18.

(94) F.BerglundCase reports spanning 150 years on the adverse effects of dental amalgam, Bio-Probe, Inc.,Orlando,Fl,1995;ISBN 0-9410011-14-3(245 cured)

(95) Lichtenberg, HJ "Elimination of symptoms by removal of dental amalgam from mercury poisoned patients", J Orthomol Med 8:145-148, 1993; & Lichtenberg H, "Symptoms before and after proper amalgam removal in relation to serum-globulin reaction to metals", Journal of Orthomolecular Medicine,1996,11(4):195-203.(119 cases)

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

(97) O. Redhe et al, "Recovery from ALS after removal of dental amalgam fillings", Int J Risk & Safety in Med 4:229 236, 1994; & N.Vanacore et al, Dirparimento di Scienze Neurologiche, Univer. La Sapienza, Roma, Med Lav (Italy), 1995, Nov, 86(6): 522 533.

(98) A. Seidler et al, "Possible environmental factors for Parkinson's disease",Neurology, 46(5):1275 1284, 1996; & F.O.Vroom et al, "Mercury vapor intoxication", 95: 305 318, 1972 ;& Ohlson et al, "Parkinsons Disease and Occupational Exposure to Mercury", Scand J. Of Work Environment Health, Vol7, No.4: 252 256, 1981.

(99) M. Nylander et al,Mercury and selenium concentrations and their interrelations in organs from dental staff and the general population. Br J Ind Med 1991, 48(11):729-34; 

(100) Review: Autoimmune Diseases: Causes and Treatment, B Windham (Ed) & 

Life Enhancement Foundation, Disease Prevention and Treatment, Expanded 4th Edition, 2003.

(102) R.L. Siblerud et al,"Evidence that mercury from silver fillings may be an etiological factor in multiple sclerosis", Sci Total Environ, 1994, 142(3):191-205 , & “Mental health, amalgam fillings, and MS”, Psychol Rep,1992, 70(3 Pt2), 1139-51;& Siblerud R.L. and Kienholz E., Evidence that mercury from dental amalgam may cause hearing loss in MS patients, J. Orthomol. Med, v12#4 pp 240-4 (1997); & (b) Amalgam dental fillings and hearing loss, International Journal of Audiology 2008; 47:770_776, Janet A. Rothwell, Paul J. Boyd

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

(111) (a) Quig D, Doctors Data Lab,"Cysteine metabolism and metal toxicity", Altern Med Rev, 1998;3:4, p262 270, & (b) Ceaurriz et al, Role of gamma  glutamyltraspeptidase(GGC) and extracellular glutathione in dissipation of inorganic mercury",J Appl Toxicol,1994, 14(3): 201 ; & W.O. Berndt et al, "Renal glutathione and mercury uptake", Fundam Appl Toxicol, 1985, 5(5):832 9; & Zalups RK, Barfuss DW.  Accumulation and handling of inorganic mercury in the kidney after coadministration with glutathione, J Toxicol Environ Health, 1995, 44(4): 385-99; & T.W.Clarkson et al, "Billiary secretion of glutathione metal complexes", Fundam Appl Toxicol, 1985, 5(5):816 31; 

(113)T.A.Glavinskiaia et al, “Complexons in the treatment of lupus erghematousus”, Dermatol Venerol, 1980, 12: 24-28; & A.F.Hall, Arch Dermatol 47, 1943, 610-611; & 

(c ) Cooper GS, Parks CG, et al, Occupational risk factors for the development of systemic lupus erythematosus. J Rheumatol. 2004 Oct;31(10):1928-33


(114) M.Aschner et al, “Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury vapor”, Brain Research, 1997, dec 5, 778(1):222-32; &  Aschner M, Rising L, Mullaney KJ.  Differential sensitivity of neonatal rat astrocyte cultures to mercuric chloride (MC) and methylmercury (MeHg): studies on K+ and amino acid transport and metallothionein (MT) induction. Neurotoxicology. 1996 Spring;17(1):107-16. & (b)T.V. O’Halloran, “Transition metals in control of gene expression”, Science, 1993, 261(5122):715-25; & (c) Matts RL, Schatz JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction of disulfide bonds. J Biol Chem 1991; 266(19): 12695-702; Boot JH. Effects of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes. Cell Struct Funct 1995; 20(3): 233-8; & Baauweegers HG, Troost D. Localization of metallothionein in the mammilian central nervous system.. Biol Signals 1994, 3:181-7. 

(118) L.Tibbling et al, Immunolocial and brain MRI changes in patients with suspected metal intoxication", Int J Occup Med Toxicol 4(2):285 294,1995.

(119)(a) 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; &(b) Kim P, Choi BH. “Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes”, Yonsei Med J 1995; 36(3): 299-305; & Brookes N. In vitro evidence for the role of glutatmate in the CNS toxicity of mercury. Toxicology 1992, 76(3):245-56; & Albrecht J, Matyja E. Glutamate: a potential mediator of inorganic mercury toxicity. Metab Brain Dis 1996; 11:175-84.

(125) U.S. CDC, National Center for Environmental Health , National Report on Human Exposure to Environmental Chemicals, 2001, ;& U.S. CDC, 

Second National Report on Human Exposure to Environmental Chemicals,

(126)(a) Singh I, Pahan K, Khan M, Singh AK. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatory cytokine-mediated apoptosis in demyelinating diseases. J Biol Chem. 1998 Aug 7;273(32):20354-62; & Pahan K, Raymond JR, Singh I. Inhibition of phosphatidylinositol 3-kinase induces nitric-oxide synthase in lipopolysaccharide- or cytokine-stimulated C6 glial cells. J. Biol. Chem. 274: 7528-7536, 1999; & Xu J, Yeh CH, et al, Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death. J Biol Chem. 1998 Jun 26;273(26):16521-6; & Dbaibo GS, El-Assaad W, et al, Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death. FEBS Lett. 2001 Aug 10;503(1):7-12; & Liu B, Hannun al, Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell death.J Biol Chem. 1998 May 1;273(18):11313-20; & (b)Noda M, Wataha JC, et al, Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes. Dent Mater. 2003 Mar;19(2):101-5; & Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production but activates proinflammatory cytokine expression in murine macrophage: differential modulation of NF-kappaB and p38 MAPK signaling pathways. Nitric Oxide. 2002 Aug;7(1):67-74; & Dastych J, Metcalfe DD et al, Murine mast cells exposed to mercuric chloride release granule-associated N-acetyl-beta-D-hexosaminidase and secrete IL-4 and TNF-alpha. J Allergy Clin Immunol. 1999 Jun;103(6):1108-14; & (c) Tortarolo M, Veglianese P, et al, Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression.. Mol Cell Neurosci. 2003 Jun;23(2):180-92.

(130) S. Enestrom et al, "Does amalgam affect the Immune System?" Int Arch Allergy Immunol 106:180 203,1995.

(139 )G.Sallsten et al, “Mercury in cerebrospinal fluid in subjects exposed to mercury vapor”, Environmental Research, 1994; 65:195-206.

(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; 

(146) T.Colborn(Ed.),Chemically Induced Atlerations in Functional Development, Princeton Scientific Press,1992 & Developmental Effects of Endocrine  Disrupting Chemicals", Environ Health Perspectives, V 101, No.5, Oct 1993; 

& E.Roller et al, J Fert Reprod, 1995, 3: 31&33.

(152) 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; & Walum E et al, Use of primary cultures to sutdy astrocytic regulatory functions. Clin Exp Pharmoacol Physiol 1995, 22:284-7; &  J Biol Chem 2000 Dec 8;275(49):38620-5; & (b)Kerkhoff H, Troost D, Louwerse ES. Inflammatory cells in the peripheral nervous system in motor neuron disease. Acta Neuropathol 1993; 85:560-5; & (c)Appel Sh, Smith RG. Autoimmunity as an etiological factor in amyotrophic lateral sclerosis. Adv Neurol 1995; 68:47-57.

& 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; ?

(158) Wenstrup et al, "Trace element imbalances in the brains of Alzheimers patients", 

Research, Vol 533,p125 131,1990; & F.L.Lorscheider, B.Haley et al, "Mercury vapor inhibits tubulin binding...", FASEB J, 9(4):A 3485.,1995; 

& Vance et al, 1988, Neurotoxicology, 9:197 208;

(159) L.D. Koller, Immunotoxicity of heavy metals”, Int J of Immunopharmacology, 2,p269,1980; & Amer j Vet Res, Vol 34,1457,1973.

(160) B.Windham(Ed), "Health Effects of Toxic Metals: An Anotated Bibliography",1998,

(162) N.K.Mottet et al, "Health Risks from Increases in Methylmercury Exposure",vol63:133 140,1985.

(163) Ahlrot-Westerlund B. Multiple Sclerosis and mercury in cerebrospinal fluid. Second Nordic Symposium on Trace Elements and Human Health, Odense, Denmark, Aug 1987; & Monica Kauppi and Dr Britt Ahlrot-Westerlund, Heavy Metal Bulletin 2(3):11-12 December 1995. (Vit B12)

(166) H.Basun et al, J Neural Transm Park Dis Dement Sect, "Metals in plasma and 

cerebrospinal fluid in normal aging and Alzheimer's disease", 1991,3(4):231 58

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

(170)R.L.Siblerud,"A commparison of mental health of multiple schlerosis patients with silver dental fillings and those with fillings removed", Psychol Rep, 1992, 70(3),Pt2, 1139 51; & (b)Birgitta Brunes, Adima Bergli,  From MS diagnosis to better health ,1996.

(181) Mathieson PW, “Mercury: god of TH2 cells”,1995, Clinical Exp Immunol.,102(2):229-30; & (b) Heo Y, Parsons PJ, Lawrence DA, Lead differentially modifies cytokine production in vitro and in vivo. Toxicol Appl Pharmacol, 1996; 138:149-57; & (c) Murdoch RD, Pepys J; Enhancement of antibody and IgE production by mercury and platinum salts. Int Arch Allergy Appl Immunol 1986 80: 405-11;

(183) World Health Organization(WHO),1991, Environmental Health criteria 118, Inorganic Mercury, WHO, Geneva; & Envir. H. Crit. 101, Methyl Mercury; & Halbach, 1995, "estimation of mercury dose ...", Int. Archives of Ocuupational & Environmental Health, 67: 295 300; 

(184)(a) T.H.Ingalls, Clustering of multiple sclerosis in Galion, Ohio, 1982-1985. Amer J Forensic Med Pathol 1989; 10: 213-5; & “Endemic clustering of multiple sclerosis in time and place”, Am J.Fors Med Path, 1986,7:3-8; & J Forsenic Medicine and Pathology, Vol 4, No 1, 1953; & Epidemiology, etiology and prevention of MS”,Am J Fors Med & Pathology, 1983, 4:55-61;& (b) EL PASO MULTIPLE SCLEROSIS CLUSTER INVESTIGATION- EL PASO, TEXAS,Environmental Epidemiology and Toxicology, Texas Department of Health  August 2001,

&(c) Craelius W, Comparative epidemiology of multiple sclerosis and dental caries”, J of Epidemiological and Community Health 32:155-65; 

(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.Zulups 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) Cd2+ and Hg2+ affect glucose release and cAMP-dependent transduction pathway in isolated eel hepatocytes. Aquat Toxicol. 2003 Jan 10;62(1):55-65, Fabbri E, Caselli F, Piano A, Sartor G, Capuzzo A. & Fluctuation of trace elements during methylmercury toxication and chelation therapy. Hum Exp Toxicol. 1994 Dec;13(12):815-23, Bapu C, Purohit RC, Sood PP; & 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;

(199) Dr. P.Kraub & M.Deyhle, Universitat Tubingen  Institut fur Organische Chemie, "Field Study on the Mercury Content of Saliva", 1997 (20,000 patients tested) www.uni; 

(200) Kulacz & Levy , The Roots of Disease. Xlibris Corporation at 1-888-795-4274; & B.E. haley, ; & G Mienig, Root Canal Coverup, 1997.

(204) Tom Warren, Beating Alzheimer's, Avery Publishing Group, 1991.

(207) Boyd Haley, Univ. Of Kentucky, "The Toxic Effects of Mercury on CNS Proteins: 

Similarity to Observations in Alzheimer's Disease", IAOMT Symposium paper, March 1997 & (b)"Mercury Vapor Inhaltion Inhibits Binding of GTP ... Similarity to Lesions in Alzheimers Diseased Brains", Neurotoxicology, 18:315  June 1997; & (c) Met Ions Biol Syst,1997,34:461 78 (* web page & dental lab:cavitations,root &(d) Palkiewicz P, Zwiers H, Lorscheider FL; ADP Ribosylation of Brain Neuronal Proteins Is Altered by In Vitro and In Vivo Exposure to Inorganic Mercury, Journal of Neurochemistry. 62(5):2049 2052, 1994 May

(209) Mark Richardson, Environmental Health Directorate,Health Canada, Assessment of 

Mercury Exposure and Risks from Dental Amalgam, 1995, Final Report, & 

G.M. Richardson et al,"A Monte Carlo Assessment of Mercury Exposure and Risks from Dental Amalgam", Human and Ecological Risk Assessment, 2(4): 709 761. 

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

Inc., ISBN 0-941011-04-6; & Dental Mercury Detox, Bio-Probe, Inc. 

[ (a)FDA Patient Adverse Reaction Reports-762 cases reported, 1992 (b)Dr.M.Hanson-Swedish patients-519 cases, (c) Dr. H.Lichtenberg- 100 Danish patients, (d) Dr. P.Larose- 80 Canadian patients, (e) Dr. R.Siblerud, 86 Colorado patients, 

(f) Dr. A.V.Zamm, 22 patients]

(217)Agency for Toxic Substances and Disease Registry, U.S. Public Health Service, 

Toxicological Profile for Mercury , 1999; & Jan 2003 Media Advisory, New MRLs for toxic substances, MRL:elemental mercury vapor/inhalation/chronic & MRL: methyl mercury/ oral/acute; &

(218) A. Seidler et al, "Possible environmental or occupational factors for Parkinson's Disease", Neurology, 1996; 46(5): 1275 84.

(220) Sellars WA, Sellars R. Univ. Of Texas Southwestern Medical School “Methyl mercury in dental amalgams in the human mouth”, Journal of Nutritional & Environmental Medicine 1996; 6(1): 33-37; & C Arch Environmental Health, 19,891-905, Dec 1969.

(221) R. Golden et al, Duke Univ., "Dementia and Alzheimer's" Disease", Minnesota 

Medicine, 78:p25 29, 1995; & Schofield P, Dementia associated with toxic causes and autoimmune disease. Int Psychogeriatr. 2005;17 Suppl 1:S129-47.

(222) M. Daunderer, “Improvement of Nerve and Immunological Damages after Amalgam 

Removal”, Amer. J. Of Probiotic Dentistry and Medicine, Jan 1991; & Handbuch der Amalgamvergiftung, Ecomed Verlag, Landsberg 1998, ISBN 3 609 71750 5 (in German); & Toxicologische erfahrungen am menchen; Quecksilber in der umwelf-hearing zum amalgamproblem”,Niedersachsiscles Umweltministerium, 1991; 

(amalgam removal & DMPS,over 3,000 cases)

(223) J.K.Nicholson et al, Cadmium and mercury exposure and nephrotoxicity”,. Nature 

1983 Aug 18 24;304(5927):633 5 

(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; &(b) 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; 

( 1999 , 20(1): 67-78; &“Mercury-induced autoimmunity”, Clin Exp Immunol, 1998, 114(1):9-12.?

(229) M.Davis,editor, Defense Against Mystery Syndromes", Chek Printing Co., March, 1994(case histories documented) & lDAMS & Kantarjian A, "A syndrome clininically resembling amyotrophic lateral sclerosis following chronic mercurialism", Neurology 11:639 644 (1961) 

(233) Sven Langworth et al,”Amalgamnews and Amalgamkadefonden”, 1997.

& F.Berglund,Bjerner/Helm,Klock,Ripa,Lindforss,Mornstad,Ostlin), “Improved Health after Removal of dental amalgam fillings”, Swedish Assoc. Of Dental Mercury Patients, 1998. ( (over 1000 cases) (Sweden Gov’t has voted to phase out use of amalgam)

(234) (a) Cooper GS, Dooley MA., et al, NIEHS, Occupational risk factors for the development of systemic lupus erythematosus, J Rheumatol. 2004 Oct;31(10):1928-33; & (b) P.E. Bigazzi, “Autoimmunity and Heavy Metals”, Lupus, 1994; 3: 449-453; & (c)Pollard KM, Pearson Dl, Hultman P. Lupus-prone mice as model to study xenobiotic-induced autoimmunity. Environ Health Perspect 1999; 107(Suppl 5): 729-735; & Nielsen JB; Hultman P. Experimental studies on genetically determined susceptibility to mercury induced autoimmune response. Ren Fail 1999 May Jul;21(3 4):343 8; & Hultman P, Enestrom S, Mercury induced antinuclear antibodies in mice, Clinical and Exper Immunology, 1988, 71(2): 269-274; & (d)Robbins SM, Quintrell NA, Bishop JM. Mercuric chloride activates the Src-family protein tyrosine kinase, Hck in myelomonocytic cells. Eur J Biochem. 2000 Dec;267(24):7201-8; & (e) Via CS, Nguyen P, Silbergeld EK, et al, Low-dose exposure to inorganic mercury accelerates disease and mortality in acquired murine lupus, Environ Health Perspect. 2003, 111(10):1273-7; & (f) Silbergeld EK, Silva IA, Nyland JF. Mercury and autoimmunity: implications for occupational and environmental health. Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):282-92. 

(242) J.Constantinidis et al, Univ. Of Geneva Medical School, "Hypothesis regarding amyloid and zinc in the pathogenisis of Alzheiemer Disease", Alzheimer Dis Assoc Disord , 1991, 5(1):31 35; & G. Bjorklund,"Can mercury cause Alzheimer's",Tidsskr Nor Laegeforen,1991 

(244) H.Basun et al, Dept. Of Geriatric Medicine, Huddinge Hospital, Sweeden, "Trace metals in plasma and cerebrospinal fluid in Alzheimer's disease", J Neural Transm Park Dis Dement Sect 1991; 3(4):231 

(248) Y.Finkelstein et al, "The enigma of parkinsonism in chronic borderline mercury intoxication, resolved by challenge with penicillamine", Neurotoxicology, 1996, Spring, 17(1): 291 5.

(250) J.M. Gorell et al,"Occupational exposures to metals as risk factors for Parkinson's disease", Neurology, 1997 Mar, 48:3, 650 8; & B.A.Rybicki et al,"Parkinson's disease mortality and the industrial use of heavy metals in Michigan",Mov Disord, 1993, 8:1,87 92. & Yamanaga H, "Quantitative analysis of tremor in Minamata disease", Tokhoku J Exp Med, 1983 Sep, 141:1, 13 22

(252) B.J.Shenker et al, Dept. of Pathology, Univ. of Pennsylvania, “Immunotoxic effects of mercuric compounds on human lymphoctes and monocytes: Alterations in cellular glutathione content”, Immunopharmacol Immunotoxicol 1993, 15(2-3):273-90.

(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.

(257) C.Eggar et al, "Effect of Lead on Tetrahydrobiopterin metabolism: A mechinism for neurotoxicity", Clin Chim Acta 161(1); 103 109, 1986. & I. Smith et al, "Pteridines and mono amines: relevance to neurological damage", Postgrad Med J, 62(724): 113 123,1986.

(258) Clinical Management of Poisoning, 3rd Ed.,(p753) Haddad, Shannon, and Winchester, W.B. Saunders and Company, Philadelphia, 1998; & A.D.Kay et al, "Cerebrospinal fluid biopterin is decreased in Alzheimer's disease", Arch Neurol, 43(10): 996 9, Oct 1986; & T.Yamiguchi et al, 

"Effects of tyrosine administreation on serum bipterin In patients with Parkinson's Disease and normal controls", Scinece, 219(4580):75 77, Jan 1983.

(260) Woods JS et al, Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity”, Physiol Pharmocol, 1996,74(2):210-15, & Strubelt O, Kremer J, et al, Comparative studies on the toxicity of mercury, cadmium, and copper toward the isolated perfused rat liver. J Toxicol Environ Health. 1996 Feb 23;47(3):267- 83; & Kaliman PA, Nikitchenko IV, Sokol OA, Strel'chenko EV. Regulation of heme oxygenase activity in rat liver during oxidative stress induced by cobalt chloride and mercury chloride. Biochemistry (Mosc). 2001 Jan;66(1):77-82.; & Kumar SV, Maitra S, Bhattacharya S. In vitro binding of inorganic mercury to the plasma membrane of rat platelet affects Na+-K+-Atpase activity and platelet aggregation. Biometals. 2002 Mar;15(1):51-7

(262) L.W.Chang, "Neurotoxic effects of mercury", Environ. Res.,1977, 14:329 

(263) Kumar AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase activity: a common pathway in central nervous system disorders.  J Assoc Physicians India. 2002 Mar;50:400-6; & Kumar AR, Kurup PA. Membrane Na+ K+ ATPase inhibition related dyslipidemia and insulin resistance in neuropsychiatric disorders. Indian J Physiol Pharmacol. 2001 Jul;45(3):296-304. 

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

(269) (a)C.J.G.Robinson et al, “Mercuric chloride induced anitnuclear antibodies In mice”, Toxic Appl Pharmacology, 1986, 86:159-169. &(b) P.Andres, IgA-IgG disease in the intestines of rats ingesting HgCl”, Clin Immun Immunopath, 30:488-494, 1984; &(c) F.Hirsch et al, J Immun.,136(9), 3272-3276, 1986 & (d)J.Immun.,136(9):3277-3281; & (e)J Immun., 137(8),1986,2548- & (f)Cossi et al, “Beneficial effect of human therapeutic IV-Ig in mercury induced autoimmune disease” Clin Exp Immunol, Apr, 1991; & (g) El-Fawai HA, Waterman SJ, De Feo A, Shamy MY. Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune Mechanisms. Contact Dermatitis 1999; 41(1): 60-1. .

(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; &  Tan XX, Tang C, Castoldi AF, Costa Lg. Effects of inorganic and organic mercury on intracellular calcium levels in rat T lymphocytes. J Toxicol Environ Health 1993, 38(2):159-70. 

(271) B.A.Weber, “The Marburg Amalgam Study”, Arzt und Umwelt, Apr, 1995; (266 cases)

& B.A.Weber, “Alternative treatment of Multiple Schlerosis, Tumor, or Cancer”, Institute for Naturopathic Medicine 1997 (40 MS cases), http://home,t"

(272) BJ Shenker,“Low-level MeHg exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial disfunction”, Environ Res, 1998, 77(2):149-159; & O.Insug et al, “Mercuric compounds inhibit human monocyte function by inducing apoptosis: evidence for formation of reactive oxygen species(ROS), development of mitochondrial membrane permeability, and loss of reductive reserve”, Toxicology, 1997, 124(3):211-24; 

(273) Complementary and alternative medicine for multiple sclerosis

Schwarz S, Knorr C, Geiger H, Flachenecker P. Mult Scler. 2008 Sep;14(8):1113-9. Epub 2008 Jul 16.

(274) Life Extension Foundation, Disease Prevention and Treatment, Expanded 4th Edition. 2003,

(276)ATSDR/EPA Priority List for 2003: Top 20 Hazardous Substances, Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services,; & (b) U.S. Environmental Protection Agency, Hazardous Air Pollutant Hazard Summary, Fact Sheets, EPA: In Risk Information System, 1998, & &(c) U.S. EPA, Region I, 2001,

(280) S.Nonaka et al, Nat. Inst. of Mental Health, Bethesda Md., “Lithium treatment protects neurons in CNS from glutamate induced excitibility and calcium influx”, Neurobiology, Vol 95(5):2642-2647, Mar 3, 1998.

(285) R.C.Perlingeiro et al, "polymorphonuclear phagentosis in workers exposed 

to mercury vapor", Int J Immounopharmacology, 16(12):1011 7,1994. 

(286) M. Lai et al, "Sensiitivity of MS detections by MRI", Journal of 

Neurology, Neruosurgury, and Psychiatry, 1996, 60(3):339 341.

(287)M.C. Newland et al,”Behavioral consequences of in utero exposure to mercury vapor in squirrel monkeys”, Toxicology & Applied Pharmacology, 1996, 139: 374-386; & “Prolonged behavioral effects of in utero exposure to methyl mercury or lead”, Toxicol Appl Pharmacol, 1994, 126(1):6-15;

& K.Warfvinge et al, “Mercury distribution in neonatal cortical areas ...after exposure to mercury vapor”, Environmental Research, 1994, 67:196-208.

(288) (a)Hisatome I, Kurata Y, et al; Block of sodium channels by divalent mercury: role of specific cysteinyl residues in the P-loop region. Biophys J. 2000 Sep;79(3):1336-45; & Bhattacharya S, Sen S et al, Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction. Biometals. 1997 Jul;10(3):157-62; & Anner BM, Moosmayer M, Imesch E. Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism. Am J Physiol. 1992 May;262(5 Pt 2):F830-6. & Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol 1992; 262(5 Pt2):F84308; & Wagner CA, Waldegger S,et al; Heavy metals inhibit Pi-induced currents through human brush-border NaPi-3 cotransporter in Xenopus oocytes.. Am J Physiol. 1996 Oct;271(4 Pt 2):F926-30;  & Lewis RN; Bowler K. Rat brain (Na+ K+)ATPase: modulation of its ouabain sensitive K+ PNPPase activity by thimerosal. Int J Biochem 1983;15(1):5 7 

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

(289) Mai J, Sorensen PS, Hansen JC.  High dose antioxidant supplementation to MS patients. Effects on glutathione peroxidase, clinical safety, and absorption of selenium. Biol Trace Elem Res. 1990 Feb;24(2):109-17. 

(291) H.A. Huggins,  Solving the MS Mystery, 2002, & ; &

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

(294) “Do amalgam fillings influence manic depression?”,Journal of Orthomol. Medicine, 1998,

(296) L.Bucio et al, Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line. Mutat Res 1999 Jan 25;423(1 2):65 72; & (b) Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA 

damage. J Neurosci Res. 2002 Dec 1;70(5):694-702; &(c) & Snyder RD; Lachmann PJ; Thiol involvement in the inhibition of DNA repair by metals in mammalian cells. Source Mol Toxicol, 1989 Apr Jun, 2:2, 117 28 L.Verschaeve et al, “Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes”, Muta Res, 1985, 157(2-3):221-6; & L.Verschaeve,“Genetic damage induced by low level mercury exposure”, Envir Res,12:306-10,1976.; &  Harrison's Principles Of Internal Medicine, 14th Ed., McGraw Hill, N.y., 1998.

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

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

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

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

(305) Soderstrom S, Fredriksson A, Dencker L, Ebendal T, “The effect of mercury vapor on cholinergic neurons in the fetal brain, Brain Research & Developmental Brain Res, 1995, 85:96-108; & Toxicol Lett 1995; 75(1-3): 133-44.; &  (b)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: &(c) Leong CC, Syed NI, Lorscheider FL.  Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury. Neuroreport 2001 Mar 26;12(4):733-7

(311) L.W. Chang et al, Acta Neurolpathol(Berlin), 30(3): 211 214; & Exp Neurol 35(1): 122 37 & Blood brain barrier dysfunction in mercury Intoxication" Acta Neuropathol (Berlin), 1972,21(3):179 84; & Adv Pharmacol Chemother., 1980, 17:195 231.

(312) Richard Hanson, The Key to Ultimate Health, 1999; & J.Lee(mD), What Your Doctor May Not Tell You About Hormones, DAMS, (800-311-6265).

(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.Kubicka-Muranyi et al, “Systemic autoimmune disease induced by mercuric chloride”, Int Arch Allergy Immunol;1996, 109(1):11-20 & 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;& (b)L.M. Bagenstose 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;

(316)B.J.Shenker et al, Dept. Of Pathology, Univ. Of Pennsylvania School of Dental Medicine, “Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in B-cell function and viability” Immunopharmacol Immunotoxicol, 1993, 15(1):87-112; & J.R.Daum,”Immunotoxicology of mercury and cadmium on B-lymphocytes”, Int J Immunopharmacol, 1993, 15(3):383-94; & Johansson U, et al, "The genotype determines the B cell response in mercury-treated mice", Int Arch Allergy Immunol, 116(4):295-305, (Aug 1998) 

(317) S.Zinecker, “Amalgam: Quecksilberdamfe ...”, der Kassenarzt, 1992, 4:23;

Praxiproblem Amalgam”, Der Allgermeinarzt, 1995,17(11):1215-1221. (1800 patients)

(320) U.F.Malt et al, “Physical and mental problems attributed to dental amalgam fillings”, Psychosomatic medicine, 1997, 59:32-41. (99 cured)

(322) P.Engel, “Beobachtungen uber die gesundheit vor und nach amalgamentfernug”, Schweiz 

Monatschr Zuhbmed, 1998, vol 108(8).(75 cases) 

(324) Dental amalgam and multiple sclerosis: a systematic review and meta-analysis.  J Public Health Dent. 2007 Winter;67(1):64-6; Aminzadeh KK, Etminan M;& (b)

Bangsi D, Krewski D. Dental amalgam and multiple sclerosis: a case-control study in Montreal, Canada. Int J Epidemiol 1998 Aug;27(4):667-71; & (c) McGrother CW, Baird WO. Multiple sclerosis, dental caries and fillings: a case control study. Br Dent J 1999 Sep 11;187(5):261 264 &(d) E. Mauch et al, "umweltgifte und multiple sklerose", Der Allgremeinarzt, 1996, 20:2226 2220.

(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; 

(326) E.Baasch, "Is multiple sclerosis a mercury allergy?", Schweiz arch Neurol Neurochir Psichiatr, 1966, 98:1 19; & J. Clausen, "Mercury and MS", Acta Neurol Scand, 1993; 87:461 464; & P. Le Quesne, ", "Metal induced diseases of the nervous system", 1982, Br J Hosp Med, 28:534 38.

(327) G. Danscher et al, Environ Res, “Localization of mercury in the CNS”, 1986, 41:29-43; & Danscher G; Horsted Bindslev P; Rungby J. Traces of mercury in organs from primates with amalgam fillings. Exp Mol Pathol 1990;52(3):291 9; & ”Ultrastructural localization of mercury after exposure 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); &(g) Schionning JD, Danscher G, "Autometallographic inorganic mercury correlates with degenerative changes in dorsal root ganglia of rats intoxicated with organic mercury", APMIS 1999 Mar;107(3):303 10

(328) P.McKeever et al, "Patterns of antigenic expression in human glioma cells", Crit Rev Neurobiology, 1991, 6:119 147.

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

(330) Wilkinson LJ, Waring RH. Cysteine dioxygenase: modulation of expression in human cell lines by cytokines and control of sulphate production. Toxicol In Vitro. 2002 Aug;16(4):481-3; & (b) 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; & Steventon GB, et al; Xenobiotic metabolism in motor neuron disease, The Lancet, Sept 17 1988, p 644-47; & Neurology 1990, 40:1095-98. 

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

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

(334) T.Nguyen et al, Mol Immunol,1996,3(4):379-86; & P.Eggleton et al, “Pathophysicological roles of calreticulin in autoimmune disease”, Scand J Immunol, 1999, 49(5): 466-73.

(336) G.S. Hill, “Drug Associated glomerulopathies” Toxicol Pathol, 1986, 14(1):37-44; & M.Monestier et al, European J Immunology, 1994, 29(3): 723-30.

(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; &(e) H.Iioka et al, “The effect of inorganic mercury on placental amino acid transport”, Nippon sanka Fujinka Gakkai Zasshi, 1987, 39(2): 202-6.

(342) Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al. Metal- specific memory lymphocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters, 1999; 20: 289-98; & Metal-specific lymphocyte reactivity is downregulated after dental metal replacement. Yaqob A, Danersund A, Stejskal VD, Lindvall A, Hudecek R, Lindh U., Neuro Endocrinol Lett. 2006 Feb-Apr;27(1-2):189-97. (patients with fatigue)

(343) P.L.Bigazzi, “Autoimmunity induced by metals”, in Chang, L., Toxicology of Metals, Lewis Publishers, CRC Press Inc. 1996., p835-52.

(344) G.A.Caron et al, “Lymphocytes transformation induced by inorganic and organic mercury”, Int Arch Allergy, 1970, 37:76-87.

(345) N.H.Nielsen et al,“The relationship between IgE-mediated and cell-mediated hypersensities”, The Glostrup Allergy Study, Denmark, British J of Dermatol, 1996,

(346) D.J.Clauw, “The pathogenesis of chronic pain and fatigue syndroms: fibromyalgia”

Med Hypothesis, 1995, 44:369-78.

(368) Olin R, Paulander J, Axelsson P; FMS,CFS, and TMS- Prevalences in a Swedish County, An oral examination based study, Preventive Dental Health Care Center, Karlstad, Sweden, 1998.

(369) Sterzl I, Prochazkova J, Stejskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Neuroendocrinology Letters 1999; 20:221-228; & (b)Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; The beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuro Endocrinol Lett. 2004 Jun;25(3):211-8:; & Šterzl I, Procházková J, Hrdá P, Matucha P, Bártová J, Stejskal VDM: Removal of dental amalgam decreases anti-TPO and anti-Tg autoantibodies in patients with autoimmune thyroiditis. Neuro Endocrinol Lett, 2006, 27(Suppl.1): 25-30; & (c) Dagmar Magnusson, Dentist, Samos, Greece, 1000 patients with amalgam replacement with over 80% significantly improved, ; & (d) Dr. E. Valentine-Thon, Head-Immunology Department, Laboratory Center, Bremen, Friedrich-Karl-Str.22 28205 Germany; & Valentine-Thon et al, Neuroendocrinol Lett 27:17-24,2006.


(372) Atchison WD. Effects of neurotoxicants on synaptic transmission. Neuroltoxicol Teratol 1998; 10(5):393-416.

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

(380) Komaroff AL, Buchwald DS. Chronic fatigue syndrom: an update. Ann Rev Med 1998; 49: 1-13; & Buchwald DS, Wener MH, Kith P. Markers of inflamation and immune activation in CFS. J Rheumatol 1997; 24:372-76.

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

(382) Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi 1998; 44: 456-60; &(b) Sterzl I, Hrda P, Prochazkova J, Bartova J, Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitr Lek 1999 Sep;45(9):527 31; & (c)Kolenic J, Palcakova D, Benicky L, Kolenicova M - "The frequency of auto-antibody occurrence in occupational risk (mercury)" Prac Lek 45(2):75-77 (1993) 

(383) Saito K. Analysis of a genetic factor of metal allergy-polymorphism of HLA-DR-DO gene. Kokubyo Gakkai Zasschi 1996; 63: 53-69; & Prochazkova J, Ivaskova E, Bartova J, Stejskal VDM. Immunogentic findings in patients with altered tolerance to heavy metals. Eur J Human Genet 1998; 6: 175; & Prochazkova J, Bartova J, Ivaskova E, Kupkova L, Sterzl I, Stejskal VD. HLA-association in patients with intolerance to mercury and other metals in dental materials.  Dis Markers. 2000;16(3-4):135-8.

& Prochazkova J, Bartova J, et al, HLA-association in patients with intolerance to mercury and other metals in dental materials. Dis Markers, 2000, 16(3-4):135-8. 

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

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

(386) Great Smokies Diagnostic Lab, research web pages (by condition); & Doctors Data Lab , , inquiries @doctors, & MetaMetrix Lab,; & Biospectron Lab, LMI, Lennart Månsson International AB,

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

(406) The Edelson Clinic, Atlanta, Ga. 

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

(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 .

(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; 

(425) (a) Hu H; Abedi Valugerdi M; Moller G. Pretreatment of lymphocytes with mercury in vitro induces a response in T cells from genetically determined low responders and a shift of the interleukin profile. Immunology 1997 Feb;90(2):198 204; & (b) Hu H;Moller G; Abedi Valugerdi M. Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro. J Autoimmun 1997 Oct;10(5):441 6; & (c) Hu H; Moller G; Abedi Valugerdi M. Mechanism of mercury induced autoimmunity: both T helper 1  and T helper 2 type responses are involved. Immunology 1999 Mar;96(3):348 57; & (d) HultmanP, Johansson U, Turley SJ; Adverse immunological effects and autoimmunit induced by dental amalgam in mice. FASEB J 1994; 8: 1183-90; &(e) Pollard KM, Lee DK, Casiano CA; The autoimmunity-inducing xenobiotic mercury interacts with the autoantigen fibrillarin and modifies its molecular structure ad antigenic properties. J Immunol 1997; 158: 3421-8.

(426) Hultman P, Nielsen JB. The effect of toxicokinetics on murine mercury-induced autoimmunity. Environ Res 1998, 77(2): 141-8. 

(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 ?

(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, cavitations.;

&(b) Thomas E. Levy , MD, FACC, and Hal A. Huggins, DDS, MS; Routine Dental Extractions Routinely Produce Cavitations, Journal of Advancement in Medicine Volume 9, Number 4, Winter 1996 &

&(c) American College of Medical Genetics Working Group findings on ApoE4 strong connection to Alzheimer’s, JAMA, 1995,274:1627-29. ; & Duke Univ. Medical Center,

&(d) Godfrey ME, Wojcik DP, Krone CA. Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity. J Alzheimers Dis. 2003 Jun;5(3):189-95. 

&(e) Joachim Mutter et alAlzheimer Disease: Mercury as pathogenetic factor and apolipoprotein E as a moderator,  Neuroendocrinol Lett 2004; 25(5):331–339;

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

(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.

(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; &  C. Gooch et al, Eleanor & Lou Gehrig MDA/ALS Center at Columbia-Presbyterian Medical Center in New York; ALS Newsletter Vol. 6, No. 3 June 2001

(445) Clifford Consulting & Research, Inc, Dental Materials Reactivity Testing, Colorada Springs, Colo.; &

Peak Energy Performance, inc., Dental Materials Biocompatibility Testing, 

(446) P.W.PhillipsSkinner’s Science of Dental Materials, 1980; & ImmunoSciences Lab; www.immuno sci

(448) Dr. J. Mercola, Optimal Center Newsletter, Aug 2000, &(b) “Decreased phagocytosis of myelin by macrophages with ALA. Journal of Neuroimmunology 1998, 92:67-75; & (c)(Human Reproduction Jun 2000, Supp1:1-13, & J Steroid Biochem Mol Biol 1999, 69:97-107; & Mult Scler 1997, 3:105-12); & (e) Neurology July 25, 2000; 55:178-84;

(449) Primary infection with the Epstein-Barr virus and risk of multiple sclerosis; 

Levin LI, Munger KL, O'Reilly EJ, Falk KI, Ascherio A. Ann Neurol. 2010 Jun;67(6):824-30; &(b) Epstein-Barr virus and multiple sclerosis: epidemiological evidence.99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: Ascherio A, Munger KL. Clin Exp Immunol. 2010 Apr;160(1):120-4; & (c ) Human endogenous retrovirus-K18 Env as a risk factor in multiple sclerosis; Tai AK, O'Reilly EJ, Alroy KA, Simon KC, Munger KL, Huber BT, Ascherio A.Mult Scler. 2008 Nov;14(9):1175-80; & (d) Infectious mononucleosis and risk for multiple sclerosis: a meta-analysis. Thacker EL, Mirzaei F, Ascherio A. Ann Neurol. 2006 Mar;59(3):499-503; & (e) Epidemiology of multiple sclerosis: from risk factors to prevention. Ascherio A, Munger K. Semin Neurol. 2008 Feb;28(1):17-28.

(450) Dr. S J Walsh and L M Rau, University of Connecticut Health Center, “Autoimmune Disease Overlooked as a Leading Cause of Death in Women. Am J Public Health 2000;90:1463 1466.

(456) Panasiuk J , Peripheral blood lymphocyte transformation test in various skin diseases of allergic origin. (nickel & lupus) Przegl Dermatol 1980;67(6):823 9 [Article in Polish] ; & Barnett JH, Discoid lupus erythematosus exacerbated by contact dermatitis. Cutis 1990 Nov;46(5):430 2 (nickel & lupus) & Nickel Allergy Is Found in a Majority of Women with Chronic Fatigue Syndrome and Muscle Pain– And May Be Triggered by Cigarette Smoke and Dietary Nickel Intake; Journal of Chronic Fatigue Syndrome, Vol. 8(1) 2001

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

(463) Johnson S. The possible role of gradual accumulation of copper, cadmium, lead and iron and 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; & (b) Dietary intake of vitamin D during adolescence and risk of multiple sclerosis; Munger KL, Ascherio A. et al, J Neurol. 2011 Mar;258(3):479-85; & Diet, Vitamin D and multiple sclerosis; Ascherio A, Munger KL, Simon KC. Lancet Neurol. 2010 Jun;9(6):599-612.

(464) Metal Metabolism and Human Functioning, 2000, Nutrient Power, Dr. W Walsh, 2018,

(468) M.M. van Benschoten, ““Acupoint Energetics of Mercury Toxicity and Amalgam Removal with Case Studies,”” American Journal of Acupuncture, Vol. 22, No. 3, 1994, pp. 251-262; & M.M. Van Benschoten and Associates, Reseda, Calif. Clinic;

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

& Michael Guthrie, R.Ph. 07 18 2001 Mycoplasmas – The Missing Link in Fatiguing Illnesses,; & D.Cooper,, Professor Garth Nicolson’s Studies and Treatments Explained,

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

(478) Ganser, AL; Kirschner, DA. The interaction of mercurials with myelin: Comparison of

in vitro and in vivo effects. Neurotoxicol, 6(1):63 77, 1985; & Windebank, AJ. Specific Inhibition of Myelination by Lead in vitro; Comparison with Arsenic, Thallium, and Mercury. Exp Neurol, 94(1):203 12, 1986; & International Labor Organization (ILO). Encyclopaedia of Occupational Health and Safety, 3rd Ed., Vol. 2. ED: Parmeggiani, L., pp. 1332 59 1983.

(485) Hulda Clark, The Cure for all Diseases, 2000,; (amalgam replacement, dental cleanup, detoxification, and treatment for brain fluke parasite and shigella bacteria- commonly from milk products)  & 

 (U.S. CDC confirms parasites and pathogenic infections common in those with chronic immune conditions) High-consequence pathogens include viruses, bacteria, and prions. They cause many chronic 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.

(490) Shibata N, Nagai R, Kobayashi M. Morphological evidence for lipid peroxidation and protein glycoxidation in spinal cords from sporadic amyotrophic lateral sclerosis patients. Brain Res 2001 Oct 26;917(1):97-104 & 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; & Bridi R, Crossetti FP, Steffen VM, Henriques AT. The antioxidant activity of standardized extract of Ginkgo biloba (EGb 761) in rats. Phytother Res 2001 Aug;15(5):449-51; 

(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.

(500) Amalgam Dental Fillings- the Largest Source of Inorganic Mercury in Most People and of Methyl Mercury in Many, B.Windham(Ed),

(501) Mercury- A Common Significant Factor in Amyotropic Lateral Sclerosis(ALS), 2001, B.Windham(Ed.), over 100 medical study references,

(502) Mercury- A Common Significant Factor in Parkinson’s Disease(PD), 2001, B.Windham(Ed.),

(503) Alzheimer’s Disease(AD): the Mercury Connection, 2001, B.Windham(Ed.),

(504) Chronic Fatigue Syndrome(CFS) and Fibromyalgia(FMS): the Mercury Connections to CFS,FMS,RA, and Lupus, B.Windham(Ed),

(505) Autism: the Mercury Connection, 2001, B.Windham(Ed.),

(506) Leistevuo J, Pyy L, Osterblad M, Dental amalgam fillings and the amount of organic mercury in human saliva. Caries Res 2001 May Jun;35(3):163 6; Leistevuo J et al., Dental amalgam fillings and the amount of organic mercury in human saliva, Corks Res, 35(3):163-6 (2001 May-Jun)

(507) Niebroj-Dobosz I, Jamrozik Z, Janik P, Hausmanowa-Petrusewicz I, Kwiecinski H. Anti-neural antibodies in serum and cerebrospinal fluid of amyotrophic lateral sclerosis (ALS) patients. Acta Neurol Scand 1999 Oct;100(4):238-43; & Appel SH, Stockton-Appel V, Stewart SS, Kerman RH. Amyotrophic lateral sclerosis. Associated clinical disorders and immunological evaluations. Arch Neurol 1986 Mar;43(3):234-8: Pestronk A, Choksi R. Multifocal motor neuropathy. Serum IgM anti-GM1 ganglioside antibodies in most patients detected using covalent linkage of GM1 to ELISA plates. Neurology 1997 Nov;49(5):1289-92; & Pestronk A, Adams RN, Cornblath D, Kuncl RW, Drachman DB, Clawson L. Patterns of serum IgM antibodies to GM1 and GD1a gangliosides in amyotrophic lateral sclerosis. Ann Neurol 1989 Jan;25(1):98-102

(508) Protective effects of methylcobalamin, a vitamin B12 analog, against glutamate- induced neurotoxicity in retinal cell culture.  Kikuchi M,Kashii S, Honda Y, Tamura Y, Kaneda K, Akaike A. Invest Ophthalmol Vis Sci. 1997 Apr;38(5):848-54; &  van Rensburg SJ, Kotze MJ, Hon D, Haug P,Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha T, Erasmus RT. Metab Brain Dis. 2006 Sep;21(2-3):121-37; & van Rensburg SJ, Kotze MJ, Hon D,Haug P, Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha T, Erasmus RT. Metab Brain Dis. 2006 Sep;21(2-3):121-37.

(509) Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal,  Waly M,Olteanu H, Deth RC et al, Mol Psychiatry. 2004 Apr;9(4):358-70; & Mercury and multiple sclerosis, Clausen J. Acta Neurol Scand. 1993 Jun;87(6):461-4

(510) Chemical methylation of inorganic mercury with methylcobalamin, a vitamin B12 analogImura N,  Pan SK,  Ukita T et alScience. 1971 Jun 18; 172(989): 1248-9; & Cobalamin-mediated mercury methylation by Desulfovibrio desulfuricans LS, Choi SC, Bartha R. Appl Environ Microbiol. 1993 Jan;59(1):290-5, & Isolation of the provisionally named Desulfovibrio fairfieldensis from human periodontal pockets, Loubinoux J.; Bisson-Boutelliez C.; Miller N.; Le Faou A.E. Oral Microbiology and Immunology, Volume 17, Number 5, October 2002 , pp. 321-323(3)

(513) Chen M, von Mikecz A. Specific inhibition of rRNA transcription and dynamic relocation of fibrillarin induced by mercury. Exp Cell Res 2000 Aug 25;259(1):225 238; & © Dieter MP, Luster MI, Boorman GA, Jameson CW, Dean JH, Cox JW. Immunological and biochemical responses in mice treated with mercuric chloride.. Toxicol Appl Pharmacol 1983 Apr;68(2):218 228; & (d) Hansson M, Djerbi M, et al; Exposure to mercuric chloride during the induction phase and after the onset of collagen-induced arthritis enhances immune/autoimmune responses and exacerbates the disease in DBA/1 mice.
Immunology. 2005 Mar;114(3):428-37; & (e)Arnett FC, Fritzler MJ, Ahn C, Holian A. Urinary mercury levels in patients with autoantibodies to U3-RNP (fibrillarin). J Rheumatol. 2000 Feb;27(2):405-10

(514) Kusaka Y. Occupational diseases caused by exposure to sensitizing metals. Sangyo Igaku 1993, 35:75-87; &

(b) Firestein GS. Rheumatoid arthitis, in:Kelley G, HarrisL, Sledge J, (Eds( Textbook of Rheumatology, USA:

WB Saunders Company 1997; p851-88; & (c) Parnham M, Blake D. Antioxidants as antirheumatics. Agents Actions Suppl 1993, 44:189-95; & (d Karatas GK, Tosun AK, Karacehennem E, Sepici V. Mercury poisoning: an unusual cause of polyarthritis. Clin Rheumatol. 2002 Feb;21(1):73-5.

(515) Casspary EA. Lymphocyte sensitization to basic protein of brain in multiple scherosis and other neurological diseases. J Neurol Neurosurg Psychiatry 1974; 37:701-3; & (b) el-Fawal HA, Gong Z, Little AR. Exposure to methyl mercury results in serum autoantibodies to neuro typic and gliotypic proteins. Neurotoxicology 1996, 17:267-76; & (c) Schwyzer RU, Henzi H. Multiple sclerosis: plaques caused by 2-step demyelization? Med Hypothesis, 1983, 12:129-42. 

(516) Fassbender K, Schmidt R, Mossner R. Mood disorders and dysfunction of the hypothalamic-pituitary-adrenal axis in conditions such as MS: association with cerebral inflammation. Arch Neurol 1998, 55: 66-72; & (b) Wilder RL. Neuroendocrine-immune system interactions and autoimmunity. Annu Rev Immunol 1995; 13:307-38. 

(517) Earl C, Chantry A, Mohammad N. Zinc ions stabilize the association of basic protein with brain myelin membranes. J Neurochem 1988; 51:718-24; & Riccio P, Giovanneli S, Bobba A. Specificity of zinc binding to myelin basic protein. Neurochem Res 1995; 20: 1107-13; & Sanders B. The role of general and metal-specific cellular responses in protection and repair of metal-induced damage: stress proteins and metallothioneins. In: Chang L(Ed.), Toxicology of Metals. Lewis Publishers, CRC Press Inc, 1996, p835-52; & Mendez-Alvarez E, Soto-Otero R, et al, Effects of aluminum and zinc on the oxidative stress caused by 6-hydroxydopamine autoxidation: relevance for the pathogenesis of Parkinson's disease. Biochim Biophys Acta. 2002 Mar 16;1586(2):155-68. 

(519) Kong J, Xu Z. Mitochondrial degeneration in motor neurons triggers the onset of ALS in mice expressing a mutant SOD1 gene. J Neurosci 1998; 18:3241-50; & (b)Cassarino DS, Bennett JPJ,Mitochrondrial mutations and oxidative pathology, protective nuclear responses, and cell death in neurodegeneration. Brain Res Brain Res Rev 1999; 29:1-25. 

(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; & & (b)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. & Miyamoto K, Nakanishi H, et al, Involvement of enhanced sensitivity of N-methyl-D-aspartate receptors in vulnerability of developing cortical neurons to methylmercury neurotoxicity. Brain Res. 2001 May 18;901(1-2):252-8; & (c) Anuradha B, Varalakshmi P. Protective role of DL-alpha-lipoic acid against mercury-induced neural lipid peroxidation. Pharmacol Res. 1999 Jan;39(1):67-80. 

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

(524) 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; & 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; & 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; & 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

(526) Ahlbom II, Cardis E, Green A, Linet M, Savitz D, Swerdlow A. Review of the Epidemiologic Literature on EMF and Health. Environ Health Perspect 2001 Dec;109 Suppl 6:911-933. 

(530) American Academy of Neurology: An unusual source of excess zinc, leading to hypocupremia and neurologic disease, 2010; & Press Release - 2/18/2010 - Parker Waichman Alonso LLP Commends GlaxoSmithKline for its Decision to Voluntarily Stop the Manufacture, Distribution and Advertising of all

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

(544) Behan P and Chaudhuri A, Astrocyte malfunction as cause of MS, Journal of the Royal College of Physicians of Edinburgh; Nov 2002,

(572) (b) “Decreased phagocytosis of myelin by macrophages with ALA. Journal of Neuroimmunology 1998, 92:67-75; & (c) 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); & McCarty MF. Versatile cytoprotective activity of lipoic acid may reflect its ability to activate signaling intermediates that trigger the heat-shock and phase II responses. Med Hypotheses 2001 Sep;57(3):313-7 & 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); & (d) Z.Gregus et al, “Effect of lipoic acid on biliary excretion of glutathione and metals”, Toxicol APPl Pharmacol, 1992, 114(1):88-96;


(573) Toxic Root Canals, Dr. T. Levy, The Toxic Tooth;& Dr. J. Mercola, Root Canals Linked to Heart Disease and Inflammatory Conditions,; & TOXIC BACTERIA IN TEETH CONTRIBUTES TO ILLNESS THROUGHOUT THE BODY, & Root Canal Coverup, Dr. G.Meinig DDS; & & Weston Price findings, & The Roots of Disease, Dr. T Levy, & Hidden Epidemic, Silent Oral Infections cause most heart attacks and Breast Cancer, Dr. T Levy,2017

(576) Sannchez-Gomez MV, Malute C. AMPA and kainate receptors each mediate excitotoxicity in oligodendroglial cultures. Neurobiology of Disease 6:475-485, 1999; & (b)Yoshika A, et al. Pathophysiology of oligodendroglial excitotoxicity, J Neuroscience Research 46: 427-437, 1996.; &(c) Singh P, et al. Prolonged glutamate excitotoxicity: effects on mitochondrial antioxidants and antioxidant enzymes. Molecular Cell Biochemistry 243: 139-145, 2003; & (d)Leuchtmann EA, et al. AMPA receptors are the major mediators of excitotoxin death in mature oligodendrocytes. Neurobiology of Disease 14:336-348, 2003; & Takahashi JL, et al. Interleukin1 beta promotes oligodendrocyte death through glutamate excitotoxicity. Annal Neurology 53: 588-595, 2003; & (e)Pitt D, et al Glutamate uptake by oligodendrocytes: implications for excitotoxicity in multiple sclerosis. neurology 61: 1113-1120, 2003; &(f) Soto A, et al. Excitotoxic insults to the optic nerve alter visual evoked potentials. Neuroscience 123: 441-449, 2004; & (g)Blaylock RL. Interactions of cytokines, excitotoxins and reactive nitrogen and oxygen species in autism spectrum disorders. Journal of American Nutraceutical Association 6: 21-35, 2003; & Blaylock RL. Chronic microglial activation and excitotoxicity secondary to excessive immune stimulation: possible factors in Gulf War Syndrome and autism. Journal American Physicians and Surgeons, Summer, 2004; & (h) Sodium-mediated axonal degeneration in inflammatory demyelinating disease.
Bechtold DA, Smith KJ., J Neurol Sci. 2005 Jun 15;233(1-2):27-35

(577) Joachim Mutter et alAlzheimer 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. 

(589) Mercury Involvement in Neuronal Damage and in Neurodegenerative Diseases. Cariccio VL et al; Biol Trace Elem Res. 2019 Feb;187(2):341-356. & (b) Associations of blood mercury, inorganic mercury, methyl mercury and bisphenol A with dental surface restorations in the U.S. population, NHANES 2003–2004 and 2010–2012. Lei Yin et al; Ecotoxicology and Environmental Safety, 2016; 134: 213 

(595) High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. Magnes Res. 2006 Dec;19(4):237-43. Rayssiguier Y, Gueux E, et al; & (b) Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am J Clin Nutr. 2006 Nov;84(5):1062-9 Bo S, Durazzo M, Pagano G. et al; & (c) Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome.  Diabetes Metab Res Rev. 2006 Nov-Dec;22(6):471-6. Guerrero-Romero F, Rodríguez-Morán 

(596) Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein. Mayo Clin Proc. 2008 Mar;83(3):333-42, Dandona P; & Role of advanced glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell Biochem Biophys. 2007;49(1):48-63, Vasdev S,Gill V, Singal P.

(597) Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes. Toxicol In Vitro. 2005 Mar;19(2):207-14.  Barnes DM, Kircher EA; & Effects of inorganic HgCl2 on adipogenesis. Toxicol Sci. 2003 Oct;75(2):368-77. Epub 2003 Jul 25, Barnes DM, Hanlon PR, Kircher EA; & (b) Heavy metal-induced inhibition of active transport in the rat small intestine in vitro. Interaction with other ions. Comp Biochem Physiol C. 1986;84(2):363-8, Iturri SJ, Peña A; & Interaction of the sugar carrier of intestinal brush-border membranes with HgCl2. Biochim Biophys Acta. 1980 May 8;598(1):100-14, Klip A, Grinstein S, Biber J, Semenza G.

(598) Overcoming Depression, Dr. Russell Blaylock, The Blaylock Wellness Report, Vol 5, No. 3, March 2008, & Food Additives, What you eat can kill you, Vol 4, No. 10,

(599) Documentation that dental amalgam is the largest source of both organic and inorganic mercury in most people who have several amalgam fillings, DAMS FS,

(600) Annotated bibliography: Exposure levels and health effects related to mercury/dental amalgam and results of amalgam replacement, 2004;B Windham(Ed.), (over 4000 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)

(601) Cognitive and Behavioral Effects of Toxic Metal Exposures, 2002;B. Windham(Ed), (over 150 medical study references)

(602) The mechanisms by which mercury causes chronic immune and inflamatory 

condtions, B.Windham(Ed.), 2002,

(603) The environmental effects of mercury from amalgam affect everyone. B. 

Windham(Ed.) (Gov’t studies)

(604) "Health, Hormonal, and Reproductive Effects of Endocrine Disrupting Chemicals" (including mercury), Annotated Bibliography ,2002, B.Windham,

(605) Mechanisms of mercury release from amalgam dental fillings: vaporization, oral galvanism, and effects of Electromagnetic fields,

(606) Developmental and neurological effects of mercury vapor, B.Windham(Ed)


Note: etc. when it is used in a list of references means that Author knows of several more references supporting the statement, in #600 for example, but doesn’t think them necessary here.