Immune Reactive Conditions: The mercury connection to eczema, psoriasis, lupus, asthma, scleroderma, rheumatoid arthritis, and allergies 

                             Bernard Windham (Ed.)

 I.  Introduction.

     This paper documents that a significant percentage of people are allergic or immune reactive to mercury to varying degrees, and that millions are adversely affected by such conditions, including many disabled by related autoimmune conditions.   The incidence of allergic and immune reactive conditions such as allergies, asthma, eczema, lupus, psoriasis, MS, etc. have been increasing rapidly in recent years (1-3,21,23).  

Toxic metals such as mercury, lead, cadmium, etc. have been documented to be highly toxic and endocrine disrupting  and damage the immune system.  The health effects of toxic metals are  synergistic  with other toxic exposures such as  pesticides , herbicides , & other  endocrine disrupting substances like organochlorine compounds , POP s, PAHs , PCBs, etc. There are also synergistic effects with the various types of parasites, bacteria, viruses to which people have common exposures and commonly become infected when the immune system is weakened by toxic exposures (485,469b,470,581). Studies have found considerable genetic variability in  susceptibility  to toxic metals as well.   While there is considerable commonality to the health effects commonly caused by these toxic metals, and effects are cumulative and  synergistic  in many cases, this paper will concentrate primarily on the health effects of elemental mercury from amalgam fillings. 

 Autism incidence rate had a 10- fold increase in the last decade and ADHD had major increases likewise (16,115b). At least 50 million have allergies (19%) (1d) and according to the U.S. CDC(1c) approximately 20 million have asthma (7.7%). The largest increase has been in infants (1,2,6,7,21,23,16), and approximately 10 % of infants- approximately 15 million in the U.S. with systemic eczema(1ab,9,16).  Studies researching the reason for these rapid increases in infant reactive conditions seem to implicate earlier and higher usage of vaccines containing mercury (thimerasol) as a likely connection (2,6,21,23,16), plus fetal and neonatal exposure from mother�s blood and milk (115).  It has been estimated that by age 3 the typical child has received over 235 micrograms of mercury thimerasol from vaccinations which is considerably more than Federal mercury safety guidelines, in addition to significant levels of mercury exposure from other sources for many (2,21,23,16). Infants during this period have undeveloped immune systems and blood brain barriers, and much of the mercury goes to the brain, resulting in significant adverse neurological effects in those that are most susceptible.  Many thousands of parents have reported that their child got such conditions after vaccination, and tests have confirmed high levels of mercury in many of those tested, along with other toxic exposures. Many of those diagnosed with high mercury levels have also been found to have significant improvement after mercury detoxification (16,23,11,12,116, etc.). Thimerasol had been previously removed from similar preservative uses in eye drops and eye medications after evidence of a connection to chronic degenerative eye conditions.  After over 15,000 law suits were filed in France over adverse effects of the Hepatitis B vaccine, the French Minister of Health ended the mandatory hepatitis B vaccination program for all school children. Adverse effects included neurological disorders and autoimmune disorders such as multiple sclerosis and lupus.

 People with chronic and immune reactive problems are increasingly finding dental materials are a factor in their problems (159, etc.) and getting biocompatibility tests run to test their immune reactivity to the various dental materials used.  Of all patients tested in a German medical lab (12e), approximately 11% were found to have significant mercury allergy, and most of these had significant health improvement after amalgam replacement.   A high percentage of such patients test immune reactive to mercury and some of the other toxic metals.  Of the many thousands who have had the Clifford immune reactivity test and the similar Peak Lab test, over 90% tested immune reactive to mercury and often to other metals as well(46).  The extreme immunotoxicity of mercury and resulting damage to immune system cells and the immune system by mercury exposure is likely a factor in this. MELISA is an immune reactivity test developed to measure �significant� immune reactivity to substances to the degree that often results in autoimmune reactions and autoimmune conditions like CFS, Fibromyalgia, oral lichen planus, MS, rheumatoid arthritis, lupus, etc.  Of  a population of over 3000 with chronic health problems tested by the immune lymphocyte reactivity test(MELISA,12a), 20% tested positive for inorganic mercury, 13% for phenyl mercury, 8% for methyl mercury, and 7% for mercury thimerasol.  For people with autoimmune conditions such as CFS, Fibromyalgia, or Multiple Chemical Sensitivity, the percentage testing immune reactive to mercury was much higher-  28% percent were immune reactive to palladium, 26% to gold, 23% to inorganic mercury, 23% to phenyl mercury, and 12% to methyl mercury, as compared to less than 5% for controls.  Of 98 patients who had amalgam fillings replaced, 76% had long term health improvement and significant improvement in MELISA scores.  Other clinics have reported similar results (39-43,159, etc.).

 II.  Allergic health effects related to mercury exposure .

        Many studies including hundreds of thousands of clinical cases as well as Scientific Panels have found that the number one source of mercury in adults is  mercury amalgam fillings  and exposures to those with amalgam commonly exceed government health guidelines for mercury (199,134). Amalgam has also been found to be the largest source of methyl mercury in most who have amalgam fillings (134,199). Amalgam fillings of mothers is also a significant source of exposure to infants as mercury in the mother crosses the placenta in levels higher than in the mother and significant exposure also occurs through breast milk(115).   EMF and Wi-fi  have been found to increase mercury vapor exposure from amalgams and to increase chronic damage.  Susceptability  factors have also been found to exert a major effect on who is affected and to what extent. 

Studies have found mercury to be a major factor in allergic/immune reactive conditions including lupus(27-32,46d,47,88,159), contact dermatitis (3-10,91,159),eczema (3-9,18-20, 34,31), psoriasis(33-38,54,31, 11) , oral lichen planus (11,39-42,159), systemic eczematous contact-type dermatitis (baboon syndrome)(7), stomatitis(10b,54,159), scleroderma(47,87), allergies(11-15,31,43-49), asthma (47-51,65,16), autoimmune renal effects(26b), and rheumatoid arthritis(47,49,88).  Mercury has been found to accumulate in connective tissue, resulting in lupus or scleroderma (157,159).  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( 12,513,514).  

 Allergic contact eczema is the most frequent occupational disease (1,91), occurring in over 10% of children in some areas; and the most common cause of contact eczema is exposure to toxic metals(1, 5-9).  The metals most commonly causing allergic immune reactivity are nickel, mercury, chromium, cobalt, and palladium(5-15,60,91,159,200).   Nickel in stainless steel braces and crowns is a source of reactivity and autoimmunity along with gold and palladium in crowns(32bc,11,12)    The highest level of sensitization is to Infants, who are most reactive to thimerosal, a form of mercury that has been used as a preservative in vaccines and eye drops(6,5b,16).    There is strong suggestive and clinical evidence for a connection between toxic metals and autism (16,21,2,23-25,81,86).     Although nickel has historically been the number one source of metal allergy and contact allergy, with many dozens of medical studies documenting the connection to conditions such as contact eczema, in recent years the largest increase in infant reactivity appears to be related to mercury exposure(6,7, 32,86,16). Also mercury has been found to be the most significant factor in large numbers of reactive autoimmune allergic and neurological conditions(11-15,201)  Thus in assessing mechanisms by which these conditions are related to metals, this paper will focus more on mercury.  Some of this would be similar for other metals however. 

Mercury causes release of inflammatory cytokines such as Tumor Necrosis Factor-alpha(TNFa) and Interleukin-4 which are documented to be factors in the chronic inflammatory conditions discussed here, including asthma, lupus, rheumatoid arthritis, scleroderma, celiac and chron�s disease, etc. (47,49,65,87-92) and also is involved in chronic heart problems.  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(101a).  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 mechanisms 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(101b,101c)

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(94). Studies have found that in asthma, lupus, rheumatoid arthritis, scleroderma, celiac/chron�s/IBS, and eczema cases there was a reduction in serum magnesium and RBC membrane Na(+)-K+ ATPase activity and an elevation in plasma serum digoxin  (87-90,65).   The activity of some free-radical scavenging enzymes, concentration of glutathione decreased significantly, 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 that mercury is a cause of most of these conditions (30,29,65,87-90,95,96,etc.)

Dental staff have been found to have significantly higher prevalence of eye problems, conjunctivitis, atopic dermatitis, and contact urticaria(91c). Finnish dental staff have the highest occupational risk of contact dermatitis with 71% affected over time(91b) with plastics, rubber, and mercury the most common causes of sensitization.  Korean dental technicians have a high incidence of contact dermatitis, with dental metals the most common sensitizers. Over 25% had contact dermatitis with over 10% sensitive to 5 metals, chromium, mercury, nickel, cobalt, and palladium(91a).  16.3% were immune reactive to mercury. 

One mechanism of mercury�s affect on contact sensitivities is the inhibition of glutathione S- transferase(92), which is a modulator of inflammation. Mercury also causes intestinal damage and leaky gut, causing metabolic damage and increasing food sensitivities(93,157,84).  

   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 these allergic/immune reactive conditions(13,15,16,23-31,56-58).  For example mercury has been found to strongly inhibit the activity of dipeptyl peptidase (DPP IV) which is required in the digestion of the milk protein casein(25,26a,16). Studies involving a large sample of autistic and schizophrenic patients found that over 90 % of those tested had high levels of the milk protein beta-casamorphin-7 in their blood and urine and defective enzymatic processes for digesting milk protein(24). Casamorphin is a morphine like compound that results in neural disfunction.   Elimination of milk products from the diet has been found to improve the condition.  As noted previously, such populations have also been found to have high levels of mercury and to recover after mercury detox (23,11,12,16,116).  As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs (16,200). Additional cellular level enzymatic effects of mercury�s binding with proteins include blockage of sulfur oxidation processes, enzymatic processes involving vitamins B6 and B12, effects on the cytochrome-C energy processes, along with mercury�s adverse effects on cellular mineral levels of calcium, magnesium, zinc, and lithium(16,200).  And along with these blockages of cellular enzymatic processes, mercury has been found to cause additional neurological and immune system effects in many through immune/autoimmune reactions(11-15,201).   But the effect on the immune system of exposure to various toxic substances such as toxic metals and environmental pollutants has also been found to have additive or  synergistic effects  and to be a factor in increasing eczema,  allergies, asthma, and sensitivity to other lesser allergens.   Many of the immune reactive children tested for toxic exposures have found high or reactive levels of other toxic metals, and organochlorine compounds(11,12,4).  Other than the organochlorines or toxic metals which are discussed later, four common pollutants that have been documented to have effects on such conditions are traffic and industrial pollutants nitrogen oxide, sulfur dioxide, power plant residual oil fly ash, and organochlorine pollutants(4).

        Mercury vapor exposure at very low levels adversely affects the 

immune system (11-15,44-46,56-62,157,159).  From animal studies it has 

been determined that mercury damages T-cells by generating reactive 

oxygen species(ROS), depleting the thiol reserves of cells, damaging and 

decreasing the dimension of mitochondria, causing destruction of 

cytoplasmic organelles with loss of cell membrane integrity, inhibiting 

ability to secrete interleukin IL-1 and IL-2R, causing activation of glial cells 

to produce superoxide and nitric oxide, and inactivating or inhibiting 

enzyme systems involving the sulphydryl protein groups(13-6,45,57,200). 

Mercury caused adverse effects on both neutrophil and macrophage 

function and after depletion of thiol reserves, T-cells were susceptible to 

Hg induced cellular death (apoptosis)(15,63,64).   Interferon syntheses 

was reduced in a concentration dependent manner with either mercury or 

methyl mercury as well as other immune functions(13-15,200), and low 

doses also induce aggregation of cell surface proteins and dramatic 

tyrosine phosporlation of cellular proteins related to asthma(49-51) and 

allergic diseases such as eczema and lupus(27-38,201), and

autoimmunity (11-15,56-58).  One study found that insertion of amalgam 

fillings or nickel dental materials causes a suppression of the number of T-

lymphocytes(60), and impairs the T-4/T-8 ratio.  Low T4/T8 ratio has been 

found to be a factor in lupus, anemia, MS, eczema, inflammatory bowel 

disease, and glomerulonephritis.  Mercury induced autoimmunity in 

animals and humans has been found to be associated with mercury�s 

expression of major histocompatibility complex(MHC) class II genes 

(56,14,15,57c). Both mercuric and methyl mercury chlorides caused dose 

dependent reduction in immune B-cell production (59).  B-cell expression 

of IgE receptors were significantly reduced(59), with a rapid and sustained 

elevation in intracellular levels of calcium induced(59,65).  Antigen specific 

LST-test was performed on a large number of patients with atopic 

eczema (33), using T-cells of peripheral blood. 87% showed LST positive 

reactions to Hg, 87% to Ni, 38% to Au and 40% to Pd   They removed LST 

positive dental metals from the oral cavities of patients. Improvement of 

symptoms was obtained in 82% (160/196) of the patients within 1-10 

months.  Similar results have been obtained at other clinics(11,34-38).

Mercury and toxic substances effects on suppressing the immune system also are documented to cause increased susceptibility to other pathogens such as viruses, mycoplasma, bacterial infections, and parasites(157,98-100). The majority of those with autoimmune conditions like ALS, CFS, FMS, MS have been found to also be infected with mycoplasma and other pathogens. Clinical experience by physicians treating people with chronic conditions has found that the pathogens generally cannot be eliminated without detoxification of mercury and toxic metals (157, 116,etc.)

Many studies have found that the body�s basic building blocks, amino acids with SH hydroxyl radicals form strong bonds with the toxic metals such as mercury, resulting in compounds which the immune system recognizes as foreign or non-functional in the basic digestive enzymatic processes that use them as fuel and building blocks in cell structure.  This results in activation of the immune system, and when there is a chronic exposure can lead to an autoimmune process that results in significant symptoms and various autoimmune diseases and conditions such as these systemic allergic conditions as well as others such as chronic fatigue (CFS), multiple chemical sensitivities (MCS), and fibromyalgia (11-15,84,157,201).

As previously noted, many occupational and children�s studies have found mercury and other toxic metals to be a common cause of immune reactivity and contact and systemic skin conditions including eczema (4-12,31-38).  One of the confusions about mercury is that there are several forms of mercury, with different mechanisms of exposure for the different forms, as well as different mechanisms in which the forms of mercury affect the body and immune system.  However all have been documented to be extremely neurotoxic and immunotoxic, and to cause autoimmunity in susceptible individuals.   Many studies including patch tests and immune reactivity tests have been carried out to assess the level of mercury sensitivity in different populations. They have found that there is a significant portion of the population that are reactive and sensitive to mercury and such have significant effects.   In a group of medical students tested by patch test, 12.8 % were sensitive to mercury(17).  The mercury sensitized students were found to have more than average number of amalgam fillings, higher urine mercury than non-sensitized students, and more allergic reactions to other things such as cosmetics, soaps, shampoos, etc.   Many other studies have found similar levels of sensitization in recent years, with those populations with higher exposures such as those with many fillings or dental staff tending to have higher levels of sensitization(11,12,200) and more adverse health effects.   In a group of 8 with contact eczema patch tested for mercury in Spain, all were positive for mercurochrome, six to inorganic mercury, and some to thimerosal(18).  This study like several others noted the danger in patch tests for mercury as 2 of the patients suffered anaphylactic shock after the patch test due to the extreme immune reactivity of some to mercury. Patch tests have also been found to not be a reliable test of mercury or toxic metal sensitivity, since most studies find many with negative patch tests recover from chronic conditions such as OLP(303,etc.)  Inorganic mercury was found to be a cause of systemic eczema and digestive problems by a  Japanese study(19).  There is consensus among researchers and dental authorities that amalgam fillings is the main cause of oral lichen planus(OLP) and the condition is usually cured by amalgam removal(39-42,54). 

        Mercury  blocks the immune function of  magnesium and zinc (125-128), whose deficiencies are known to cause significant neurological effects(129-131). The low Zn levels result in deficient  CuZnSuperoxide  dismustase (CuZnSOD), which in turn leads to increased levels of superoxide due to toxic metal exposure.  

III.  Autoimmunity caused by Mercury: Connection to Immune and Neurological Conditions

       Mercury has been documented to cause autoimmune disease (139,140,159,118,60,82,141,11,12)  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(12b,200).   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(140,142,156,157,12).  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 (12,140,143,144-147,156,157,12b,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 (11,12,142,157), such as found more frequently in patients with human lymphocyte antigens (HLA‑DRA) (142,146,147,12).  A significant portions of the population appear to fall in this category.  Mercury accumulation in areas of sensory ganglia and the Autonomic Nervous System has been found to commonly be a cause of such pain and fatigue(157). 

         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 (103,12a,12b).  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(11,12b).   

        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.  In a study of small-scale gold mining using mercury, there was a  positiveinteraction 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(28e). 

      Autoimmune reactions to inorganic and methyl mercury have been found to be relatively independent, occurring in over 10% of controls.  Among a population of patients being tested for autoimmune problems, 94% of such patients had significant immune reactions to inorganic mercury(MELISA test,11,12a,12b) 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 replacement, and MELISA test scores had a significant reduction in lymphocyte reactivity compared to pre- replacement(12).   The MELISA test  has proved successful in diagnosing and treating environmentally caused autoimmune diseases such as MS, SLE, oral lichen planus, CFS,etc. (11,12,148).     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,148), 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 (11,12,13,149).  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(150) 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(140,142,12).

        Toxic metals appear to be only one of the factors involved in chronic autoimmune conditions and appear to often be cofactors with other triggering effects(28e). 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.  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(28e).   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(97e,98 ,99,100) and other autoimmune conditions. 

        Mercury�s biochemical damage at the cellular level include DNA damage, inhibition of DNA and RNA synthesis (102-105);  induction of free radical formation (12,95), depletion of cellular glutathione (necessary for detoxification processes) (30de,106,101,116), inhibition of glutathione peroxidase enzyme(95), inhibition of glutamate uptake(108), induces peroxynitrite and lipid peroxidation damage(109),  inducement of inflammatory cytokines(101,111,14), causes abnormal immune system damage (15,63,69,107,110); and autoimmunity (12-15,63,112,etc.) Some of these effects can also result in  cancer . 

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 (13-15,112).  Such binding and autoimmune damage has been documented in the fat-rich proteins of the myelin sheaths and of collagen(12b), 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(115de,117).     Studies have also found mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and myelin basic protein(MBP) (118ag,12,119,120,121).  Mercury and cadmium also have been found to interfere with zinc binding to MBP(122b) which affects MS symptoms since zinc stabilizes the association of MBP with brain myelin(122a).  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 (12,119,120,121). Antioxidants like lipoic acid which counteract such free radical activity have been found to alleviate symptoms and decrease demyelization(123,124).   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(80).  Immune and autoimmune mechanisms are thus seen to be a  major factor in neurotoxicity of metals.    

Autoimmunity has also been found to be a factor in chronic degenerative autoimmune conditions such as MS,ALS, 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(57c).  One genetic difference found in animals and humans is cellular retention differences for metals related to the ability to excrete mercury(58).  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(132), whereas those with type APOE-2 readily excrete mercury and are less susceptible  (132).  Those with type APOE-3 are intermediate to the other 2 types.   The incidence of autoimmune conditions has increased to the extent this is now one of the leading causes of death among women(135).   Also when a condition has been initiated and exposure levels decline, autoimmune antibodies also decline in animals or humans (136,28c,11,118,137,12)

        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 

significant numbers of people(103,11,12a,12b).  Much mercury in saliva 

and the brain is also organic, the most neurotoxic form(138,63), since 

mouth bacteria and other organisms in the body methylate inorganic 

mercury to organic mercury(134,133). Dental amalgam has been found to 

be the largest source of methyl mercury in most with mercury amalgam 

fillings(134,199,etc.).

Mucocutaneous lymph node syndrome(Kawasaki syndrome) is an autoimmune disease that manifests as a multisystemic necrotizing medium vessel vasculitis that is largely seen in children under 5 years of age, which affects many organs, including the skin, mucous membranes,  lymph nodes , and  blood vessel  walls, but the most serious effect is on the heart where it can cause severe aneurysmal dilations in untreated children.   Medical literature, epidemiological findings, and some case reports have suggested that mercury may play a pathogenic role(158). Several patients with Kawasaki's Disease have presented with elevated urine mercury levels compared to matched controls. Most symptoms and diagnostic criteria which are seen in children with acrodynia, known to be caused by mercury, are similar to those seen in Kawasaki's Disease. Genetic depletion of glutathione S-transferase , a susceptibility marker for Kawasaki's Disease, is known to be also a risk factor for acrodynia and may also increase susceptibility to mercury . Coinciding with the largest increase (1985-1990) of thimerosal (49.6% ethyl mercury) in vaccines, routinely given to infants in the U.S. by 6 months of age (from 75microg to 187.5microg), the rates of Kawasaki's Disease increased ten times, and, later (1985-1997), by 20 times. Since 1990 88 cases of patients developing Kawasaki's Disease some days after vaccination have been reported to the Centers of Disease Control (CDC) including 19% manifesting symptoms the same day.

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

        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.  

        Many clinics and studies involving thousands of patients have found that patients with allergic reactive conditions such as oral lichen planus, eczema, chronic allergies etc. usually recover or have significant improvements after amalgam replacement.  Of a group of 86 patients with CFS symptoms, 78% reported significant health improvements after replacement of amalgam fillings within a relatively short period, and MELISA test found significant reduction in lymphocyte reactivity compared to pre removal tests (11,12,116cd). The improvement in symptoms and lymphocyte reactivity imply that most of the Hg-induced lymphocyte reactivity is allergenic in nature.     Patients with other systemic neurological or immune symptoms such as arthritis, myalgia, CFS, MCS, MS, etc. also often recover after amalgam replacement(11,12,200).

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 (155)

    There are extensive documented cases (many thousands) where removal of amalgam fillings led to cure of serious health problems such as 

eczema (22,33,34,38,52-54,67-69,11,12,156,159),  psoriasis(33-38,12), asthma(49-52,68,72,98),  lupus(12,27,32,33,68,70,71,31,156,157,159), allergies(31,32,43,48,51,49,52,53,66-74,84,157), oral lichen planus(39-42), chronic multiple chemical sensitivities (32,68,70,71,73,75-77,84,154,157, 11,12,31), ALS(51,99,154,31), arthritis(31,52,67,68,72,73,78,79,98,157,11), MS(52,67-70,73,80-83,31c,99,100,151-154,156,157),  CFS (11,12,31,33,52-54,66-68,70,71,75,84,85,98,99,153,154,157), autoimmune thyroiditis (140,156,157,12c), muscular/joint pain/fibromyalgia (11,12,31,53,68,69,72,84,85,98,99,151) and over 20 other chronic health conditions(200).  Any references not found in this paper can be found in the bigger paper (200), from which much of this paper is excerpted and which contains clinical documentation of over 60,000 cases of recoveries after amalgam replacement. In several of the studies, over 75% of those with MS and having amalgams replaced recovered or had significant improvement (212abe,302,222,*31).   Some of the studies reported similar success rates for SLE but with lower number of cases treated.

       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 (11,313,12b, etc.)

V. Arthritis   

        Osteoarthritis is characterized by degeneration of the articular cartilage or synovial membrane and bone next to the cartilage of knees, hips, and spine, or hand).  Cracking or thinning of cartilage leads to loss of shock absorption ability and resulting thickening of bone and development of bone spurs, and inflammatory reactions.  The result in stiffness and pain.

        Rheumatoid arthritis is an autoimmune condition, characterized by chronic inflammation and thickening of the synovial lining and cartilage destruction. The majority with RA have positive rheumatoid factor in serum. (186) Copper deficiency can be a factor in RA and supplementation can be helpful in such circumstances. 

        Arthritis is chronic inflammation of joints, characterized by high levels in the joints of archidonic acid products, which are metabolized along 2 enzymatic pathways- PGE-2 & LTB4. The destruction of bone and cartilage in both osteoarthritis (OA) and rheumatoid arthritis (RA) is related to pro-inflammatory cytokines such as TNFa, Interleukin-1 and IL6.  It has been found that there is an excess of TNFa in both OA and RA, and some treatments attempt to inhibit TNFa.  While NSAIDs relieve symptoms, they do not alleviate the underlying problems and usually result in more damage to joints in the long run (186).  Celebrex and Vioux are COX-2 inhibitors but do not block inflammation and damage through the LTB4 pathway, plus have significant adverse health effects.  Embrel is an expensive TNFa blocker, but can also block useful purposes of TNFa such as for fighting infections and does not suppress other inflammatory cytokines. Other natural options are more effective and safer.  DHA from fish oil is an effective anti-inflammatory with no adverse effects.  For those for whom this is not sufficient, the drug pentoxifylline (PTX) (Trental) is often helpful (186).  

             As has been seen, toxic metals like mercury cause pro-inflammatory cytokines and inflammation, so reductions in exposure and body burden such as amalgam replacement, avoidance, and detoxification have been found to be effective at reducing such inflammation(116). 

Several natural supplements have been found to be beneficial in reducing arthritis pain and damage by reducing inflammatory cytokines and. Inflammation.  These include nettle leaf, SAMe, ginger, glucosamine and chondroitin sulfate, willow bark (pain relief), EFAs, antioxidants, Gamma-Linolenic Acid (GLA), MSM, chlorella, and curcumin (186). Inflacin is a topically applied compound that has been found to relieve arthritic pains. Nexrutine is a natural anti-inflammatory that inhibits COX-2 and has been found to be helpful, while 5-Loxin (Boswellic Acid) inhibits the 5-LOX pathway.  Both can be beneficial in extreme cases. 

        Food allergens that can increase inflammation include grain gluten, nightshades, corn, dairy products (casein), and red meats. Fish is a preferred protein. Generally vegetarian diets with probiotics are often helpful for arthritis relief (186). Uncooked vegen diets rich in berries, fruits, vegetable, nuts, and seeds often benefit arthritis sufferers. 

VI. Asthma

Asthma is a chronic inflammatory disorder of the airways, characterized by wheezing, shortness of breath, chest tightness, mucus production, etc. At least 7.2% of the adult population has asthma and asthma in children has become much more prevalent. (186)  Asthma is closely tied to immune system reactions of the humoral system, as controlled by cell signaling cytokines. Allergic antigens bind to immune mast cells and basophils, and when these come into contact with IgE antibody, a hypersensitivity response of the immune system occurs leading to inflammation and bronchoconstriction.  

        Current pharmaceutical treatments are bronchodilators or anti-inflammatory compounds. As previously seen, toxic metal exposures increase inflammatory cytokines and inflammation, so reductions in toxic exposures can significantly improve such conditions.   Natural supplements that have been found effective in reducing asthma effects include essential fatty acids (DHA,EPA, GLA), curcumin, flavinoids such as silybin, lycopene, pycogenol, quercetin, Ginkgo extracts, licorice(coughs & congestion), Yerba mate, bee pollen (186). 

        Breastfeeding for at least 6 months and low levels of cereals has been found to be protective against asthma and allergies,  Probiotics for the breastfeeding mother has also been found to be a preventive factor. (186)  Food allergies often related to asthma include cereal grains.  Other foods that produce common allergies are milk, nuts, chocolate, eggs, MSG, aspirin.  High intake of red meat and fats also are related to asthma. Anti-inflammatories like vit C, E, and NAC are usually beneficial in asthma prevention. The minerals selenium and magnesium are protective against asthma. (186)

                        References

(1) American Academy of Dermatology, Press Release, February, 2000;  &(b) National Institute of Arthritis and Musculoskeletal and Skin Diseases, (U.S.) National Institute of Health, 2003; &(c) CDC. Behavioral Risk Factor Surveillance System Survey. Atlanta, Georgia: U.S. Department of Health and Human Services, CDC, 2001; &(d) American Academy of Allergy, Asthma and Immunology (AAAAI).  The Allergy Report: Science Based Findings on the Diagnosis & Treatment of Allergic Disorders , 1996-2001; & (e) S. Redd, U.S. Centers for Disease Control, National Center for Environmental Health, 1998.

(2) Gary Null,  Second Opinion: Vaccinations , Gary Null and Associates,Inc., 2000.  www.garynull.com.

(3) Silhan P, Arenberger P.  Standard epicutaneous tests in ambulatory care of patients. Cas Lek Cesk 1999, 138(15):469-73; & Lindemayr H, Drobil M.  Eczema of the lower leg and contact allergy. [German] Hautarzt, 1985, 36(4): 227-3.  

(4) Reichrtova E et al, Cord Serum Immunoglobulin E Related to Environmental Contamination of Human Placentas with Oganochlorine Compounds, Envir Health Perspec, 1999, 107(11):895-99; & Gavett SH et al.  Residual Oil Fly Ash Amplifies Allergic Cytokines, Airway Responsiveness, and Inflamtion in Mice.  Am J Respir Crit Care Med, 1999, 160(6):1897-1904; & Kramer U et al, Traffic-related air pollution is associated with atopy in children living in urban areas.  Epidemiology 2000, 11(1): 64-70; & S.C. Langley-Evans et al,  � SO2: a potent glutathione depleting agent, Comp Biochem Physiol Pharmocol Toxicol Endocrinol, 114(2):89-98

(5) Romaguera C, Vilaplana J.  Contact dermatitis in children: 6 years experience. Contact Dermatitis 1998; 39(6): 277-8aZ0; & Manzini BM, Ferdani G, Simonetti V, Donini M, Sedernari S.  Contact sensitization in children.  Pediatr Dermatol 1998; 15(1): 12-17.    

(6)  Brasch J, Geier J, Schnuch A.   Differentiated contact allergy lists serve in quality improvement.  Hautarzt 1998; 49(3): 184-91; & Audicana MT, Munoz D, del Pozo MD, Fernandez E, Gastaminza G, Fernandez de Corres L. Allergic contact dermatitis from mercury antiseptics and derivatives: study protocol of tolerance to intramuscular injections of thimerosal. Am J Contact Dermat. 2002 Mar;13(1):3-9.; &  Patrizi A, Rizzoli L, Vincenzi C, Trevisi P, Tosti A.   Sensitization to thimerosal in atopic children.  Contact Dermatitis, 1999, 40(2): 94-7.

(7)  Nakada T, Higo N, Iijima M, Nakayama H, Maibach HI. Contact Dermatitis. 1997 May;36(5):237-9.;

(8) Sun CC.  Allergic contact dermatitis of the face from contact with nickel and ammoniated mercury.  Contact Dermatitis 1987, 17(5):306-9;. &  Schafer T, Bohler E, et al, Epidemiology of contact allergy in adults.   Allergy. 2001 Dec;56(12):1192-6.

(9) Xue C, He Z, Zhang H, Li S.   Study on the contact allergen in patients with dermatitis and eczema.   Wei Sheng Yen Chiu 1997, 26(5): 296-8;  & Meding B, Jarvholm B. Hand eczema in Swedish adults and children -  J Invest Dermatol 2002 Apr;118(4):719-23; &  Lindemayr H, Drobil M, .[Eczema of the lower leg and contact allergy]  [German]  Hautarzt. 1985 36(4): 227-31.

(10) Aberer W, Holub H, Strohal R, Slavicek R.  Palladium in dental alloys- the dermatologists responsibility to warn?   Contact Dermatitis 1993.  28(3): 163-5; & Veien NK.  Stomatitis and systemic dermatitis from mercury in amalgam dental restorations.Dermatol Clin. 1990 Jan;8(1):157-60.

(11) V.D.M. Stejskal, Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden, LYMPHOCYTE IMMUNO‑STIMULATION ASSAY ‑MELISA, & VDM Stejskal et al, "MELISA: tool for the study of metal allergy", Toxicology in Vitro, 8(5):991-1000, 1994; & 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. www.melisa.org ; & (b) Alanko K, Estlander T.  Oral mucosal diseases investigated by patch testing with a dental screening series. Contact Dermatitis.1996 Apr;34(4):263-7. 

(12)  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; & (b) Jenny Stejskal, Vera Stejskal. The role of metals in autoimmune diseases and the link to neuroendocrinology, Neuroendocrinology Letters, 20:345‑358, 1999. &(c) Sterzl I, Prochazkova J, Stejaskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity. Neuroendocrinology Letters 1999; 20:221-228; &(d) 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;  www.melisa.org ;  & (e)Valentine-Thon E, Schiwara HW, Validity of MELISA for metal sensitivity testing; Neuroendocrinol Lett, 2003, Feb-Apr, 24(1-2): 57-64. 

(13) S.Ellermann-Eriksen et al, "Effect of mercuric chloride on macrophage-mediated resistance mechinisms against infection", Toxicology, 93:269-297,1994; & M.Kubicka-Muranyi et al, Systemic autoimmune disease induced by mercuric chloride�, Int Arch Allergy Immunol;1996, 109(1):11-20  & M.M.Christensen et al, Institute o Medical Microbiology, Comparision of interaction of meHgCl2 and HgCl2 with murine macrophages, Arch Toxicol, 1993, 67(3):205-11; & 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;

(14) P.W. Mathieson, Mercury: god of TH2 cells,1995, Cliical Exp Immunol.,102(2):229-30; & Parronchi P, Maggi E. Genetic and Environmental Factors Contributing to the Onset of Allergic Disorders. Int Arch Allergy Immunol 2000 Jan; 121(1):2-9.

(15) L.M. Bagentose et al, Mercury induced autoimmunity in humans, Immunol Res, 1999,20(1): 67-78; & Mercury-induced autoimmunity, Clin Exp Immunol, 1998, 114(1):9-12; B.J. Shenker et al, Dept. Of Pathology, Of Pathology,Univ. Of Penn. School of Dental Med., Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes:Alterations in cell viability and Immune suppression of human T-cell activation, Immunopharmacologicol Immunotoxical, 1992, 14(3):555-77;  & Mercury-induced autoimmunity, Clin Exp Immunol, 1998, 114(1):9-12.

(16) Windham, B. Annotated Bibliography: The mercury connection to childhood neurological and developmental conditions .  

 (17) Sato K, Kusaka Y, Miyakoshi S. An epideomological study of factors relating to mercury sensitization. Arerugi 1995; 44(2):86-92; & Chen L, Nordlind K, Liden S, Sticherling M., Increased expression of keratinocyte interleukin-8 in human contact eczematous reactions to heavy metals.  APMIS. 1996 Jul-Aug;104(7-8):509-14. 

(18) Galindo PA, Feo F, Fernadez F.  Mercurochrome allergy: immediate and delayed hypersensity. Allergy 1997; 52(11): 1138-41;

(19) Koizumi A et al, Mercury poisoning as cause of smelter disease. Lancet 1994; 343(8910): 1411-2. 

(20) Ulukapi I. Mercury hypersensitivity from amalgam: report of case. ASDC J Dent Child 1995;62(5):363-4.

(21) Halsey, NA.  Limiting Infant Exposure to Thimerosal in vaccines.   J. of the Amer. Medical Assoc., 282: 1763-66.

(22) Recovery from asthma and allergies after removal of dental amalgam fillings.  Int J of Risk & Safety in Medicine 1994; 4:229-236, Redhe O, Pleva J.

(23) Autism: a unique form of mercury poisoning . & (b) Thimerosal: a versatile sulfhydryl reagent, calcium mobilizer, and cell function‑modulating agent.  Gen Pharmacol 1999 Jul;33(1):1‑6, Elferink JG.; & Merthiolate hypersensitivity and vaccination. Contact Dermatitis. 1980 Jun;6(4):241-5, Forstrom L, Lehmuskallio E.; & Epidemiology of contact allergy in adults.  Allergy.2001 Dec;56(12):1192-6. Schafer T, Bohler E, et al,

(24) Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999, J.R. Cade et al, . http://www.hsc.ufl.edu/post/post0399/post03_19/1.html

(25) 'Isolation and characterization of dipeptidyl peptidase IV from human   placenta',  Eur J Biochem  1982 Aug;126(2):359-65, Puschel G, Mentlein R, Heymann E; & Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties.  J Clin Lab Anal. 1996;10(6):435-40, Shibuya-Saruta H, Hashimoto Y; &  Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993 Jul;44(1):13-8, Blais A, Le Grimellec C.

(26) Stefanovic V. et al, Kidney ectopeptidases in mercuric chloride-induced renal failure.  Cell Physiol Biochem 1998; 8(5): 278-84; & (b) Guzzi, G., et al. (2008). Mercury dental amalgam and renal autoimmunity. J. Environ. Pathol. Toxicol. Oncol. 27, 147�155.

(27) 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.

(28) P.E. Bigazzi, Autoimmunity and Heavy Metals, Lupus, 1994; 3: 449-453; & (b)Pollard KM, Pearson Dl, 

          Hultman P.  Lupus-prone mice as model to study xenobiotic-induced autoimmunity.  Envriron 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) 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; &(e) 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.

(29)   C.Gordon et al, �Abnormal sulphur oxidation in systemic lupus erythrmatosus(SLE)�, Lancet, 1992,339:8784,25-6; & P.Emory et al, �Poor sulphoxidation in patients with rheumatoid arthitis�, Ann Rheum Dis, 1992,  51:3,318-20; & P.Emory et al, Br J Rheumotol, 1992, 31:7,449-51; &    C.M. Tanner et al,�Abnormal Liver Enzyme Metablolism in Parkinson�s�,Neurology,  1991, 41(5): Suppl 2, 89-92;   &  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; & Hisatome I, 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.

(30) Xenobiotic metabolism and adverse environmental response: sulfur-dependent detox pathways,Toxicology, 1996, 111(1-3):43-65, S.A. McFadden, ;& (b) “Heavy metals (Hg, Cd) inhibit the activity of the liver and kidney sulfate transporter Sat‑1", Toxicol  Appl Pharmacol, 1999,154(2):181‑7, Markovich et al,";&(c) Sulphation deficit in low-functioning autistic children. Biol Psychiatry 1999, 46(3):420-4, Alberti A, Romano C; &(d)  Quig D, Doctors Data Lab, "Cysteine metabolism and metal  toxicity", Altern Med Rev, 1998;3:4, p262‑270, & (e)   Role of gamma‑glutamyltraspeptidase (GGC) and extracellular glutathione in dissipation of inorganic mercury", J Appl Toxicol,1994, 14(3): 201‑ J.de  Ceaurriz et al;  

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

(32) 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)

& (b)  Schultz JC, Connelly E, Glesne L, Warshaw EM. Cutaneous and oral eruption from oral exposure to nickel in dental braces.   Dermatitis. 2004 Sep;15(3):154-7; &  Genelhu MC, Marigo M et al; Characterization of nickel-induced allergic contact stomatitis associated with fixed orthodontic appliances, Am J Orthod Dentofacial Orthop. 2005 Sep;128(3):378-81; & (c) &(c) Marcusson JA,  Contact allergies to nickel sulfate, gold sodium thiosulfate and palladium chloride in patients claiming side-effects from dental alloy components,  Contact Dermatitis, 1996 May, 34:5, 320-3

(33) Dr. Kohdera, Faculty of Dentistry, Osaka Univ, International Congress of Allergology and Clinical Immunology, EAACI, Stockholm, June 1994;  & Heavy  Metal Bulletin, Vol 1, Issue 2, Oct 1994.   (160 cases cured-eczema); Tsunetoshi Kohdera, MD, dermatology, allergology,  31 Higashitakada‑cho Mibu Nakagyo‑ku Schimazu Clinics Kyoto 604 Japan  e‑mail:smc‑inet@mbox.kyoto‑inet.or.jp & P.Dallmann, kon nen durch Quecksilber entstehen? PeDa_Eigenverisg, 1995;& SS Tsyganok, Unithiol in treatment of dermatoses, Vestn.Dermatol.Venerol., 1978, (9): 67-69. Neukirchen (clinic) (Germany, near Czech border). Director; Gruia Ionescu, owns 2 Clinics, cases paid by insurance companies in Germany.  Email: Spezialklinik‑Neukirchen@toolpool.de   fax: 0049 9947 10 51 11

       (these clinics use MELISA test for diagnosis of immune reactivity)

(34) Kohdera T, Koh N, Koh R.  Antigen-specific lympocyte stimulation test on patients with psoriasis vulgaris. XVI International Congress of Allergology and Clinical Immunology, Oct 1997, Cancoon, Mexico; & Ionescu G. Schwermetallbelastung bei atopischer Dermatitis und Psoriasis.  Biol Med 1996; 2:65-68

(35) Wehner‑Caroli J; Scherwitz C; Schweinsberg F;   Fierlbeck G. Exacerbation of pustular psoriasis in mercury poisoning. Hautarzt 1994 Oct;45(10):708‑10; & Britschgi M, Pichler WJ.  Acute generalized exanthematous pustulosis, a clue to neutrophil-mediated inflammatory processes orchestrated by T cells.   Curr Opin Allergy Clin Immunol. 2002 Aug;2(4):325-31.

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

(37) Metal Profiles in 25 Patients with Long-Term Illness. Presented at Eurotox 93 Congress, Lindvall A, Lindh U, Danersund A, & Lindh, U. Nucl Instr and Meth B30:404. 1988 & Hallgren, R; Feltelius, N; Lindh, U.J. Rheumatol. 15:308. 1988

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

(39) (a) Guzzi, G., C., Pigatto, P. et al, (2003). Toxicol. Lett. 144(Suppl. 1), 35-36; &A Dunsche et al, "Oral lichenoid reactions associated with amalgam: improvement after amalgam removal." British Journal of Dermatology  2003 Jan;148:1:70-6; & (b) 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); & Mutter, J. et al (2007).  Nummular dermatitis,  Crit. Rev. Toxicol. 37, 537-549;

(40)A. Skoglund, Scand J Dent Res 102(4): 216-222, 1994; and 99(4):320-9,1991(40 cases); & P.O.Ostman et al, Clinical & histologic changes after removal of amalga m ,  Oral Surgery, Oral Medicine,  and Endodontics, 1996, 81(4):459-465;  &  S.H. Ibbotson et al, The relevance of amalgam replacement on oral lichenoid reaction, British Journal of Dermatology, 134(3):420-3, 1996; (270 cases)    

(41)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-

(42) J.Laine et al, Immunocompetent cells in amalgam-associated oral licheinoid contact lesions, Oral Pathol Med 1999; 28(3): 117-21; &  Contact allergy to dental restorative materials in patients with oral lichenoid lesions, Contact Dermatitis, 1997,36:3,141-6; & Resolution of OLL after replacement of amalgam restorations, Br J Dermatol, 1992,126(1):10-15(20 cases); &  A. Adachi et al, Efficacy of dental metal elimination  in the management of atopic dermatitis � , J Dermatology, 1997, 24:1,141-6;

(43)Veron et al, Amalgam Dentaires et Allergies, J Biol Buccale., 1986 : 14; 83‑100 (41 cases); & D.E. Swartzendruber, Med Hyptheses, 1993, v41,n1, p31-34.

(44) K.Sato et al, "An epidemiological study of factors relating to mercury sensitization",  Arerugi 44(2): 86-92, 1995; &         T.Mori et al,  � Mercury sensitization caused by environmental factors � , Nippon Eiseigaku Zasshi, 1998, 52(4):661-6.

(45) E.G.Miller et al, Prevelence of Mercury Hypersensitivity among Dental Students � , J Dent   Res. 64:Abstract 1472, p338,1985; & D.Kawahara et al, Epidemiologic Study of occupational Contact Dermatitis in the Dental Clinic, Contact Dermatitis, Vol 28, No.2, pp114-5,1993; & Lewezuk E et al, Occupational health problems in dental practice, [Polish] Med Pr 2002, 53(2): 161-5.

(46) Clifford Consulting & Research, Inc, Dental Materials Reactivity Testing, Colorado Springs, www.ccrlab.com; & Immunosciences Lab; & Peak Energy Performance, inc., Dental Materials Biocompatibility Testing, www.peakenergy.com

 & (d) Great Smokies Diagnostic Lab, research web pages (by condition) www.gsdl.com; & Doctors Data Lab,  www.doctorsdata.com , inquiries @doctors data.com,

(47)  (a)Noda M, Wataha JC, Lockwood PE, Volkmann KR, Kaga M, Sano H.  Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes Dent Mater. 2003;19(2):101-5; &(b) 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; &  (c) 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, 103(6):1108-14; & Hide I.
[Mechanism of production and release of tumor necrosis factor implicated in inflammatory diseases] Nippon Yakurigaku Zasshi. 2003 Mar;121(3):163-73; & (e) Increased expression of keratinocyte interleukin-8 in human contact eczematous reactions to heavy metals.  APMIS. 1996 Jul-Aug;104(7-8):509-14. Chen L, Sticherling M.,

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

(49) (a) Hunter I, Cobban HJ, et al; Tumor necrosis factor-alpha-induced activation of RhoA in airway smooth muscle cells: role in the Ca2+ sezation of myosin light chain20 phosphorylation. Mol Pharmacol. 2003 Mar; 63(3): 714-21;  & Walczak-Drzewiecka A, Wyczolkowska J, Dastych J. Environmentally Relevant Metal and Transition Metal Ions Enhance Fc Epsilon RI-Mediated Mast Cell Activation. Environ Health Perspect. 2003 May;111(5):708-13; & Halasz A, Cserhati E, Kosa L, Cseh K. Relationship between the tumor necrosis factor system and the serum interleukin-4, interleukin-5, interleukin-8, eosinophil cationic protein, and immunoglobulin E levels in the bronchial hyperreactivity of adults and their children, Allergy Asthma Proc. 2003 Mar-Apr;24(2):111-8; & Kurup RK, Kurup PA. Hypothalamic digoxin, cerebral chemical dominance, and pathogenesis of pulmonary diseases Int J Neurosci. 2003 Feb;113(2):235-58; &(b)Wu Z, Turner DR, Oliveira DB. IL-4 gene expression up-regulated by mercury in rat mast cells: a role of oxidant stress in IL-4 transcription. Int Immunol. 2001 Mar;13(3):297-304; & Strenzke N, Gibbs BF, et al,  Mercuric chloride enhances immunoglobulin E-dependent mediator release from human basophils.Toxicol Appl Pharmacol. 2001 Aug 1;174(3):257-63; & Gillespie KM, Mathieson PW, et al, Interleukin-4 gene      expression in mercury-induced autoimmunity. Scand J Immunol. 1995 Mar;41(3):268-72; & Beghe B, Holloway J, et al.  Polymorphisms in the interleukin-4 and interleukin-4 receptor alpha chain genes confer susceptibility to asthma and atopy in a Caucasian population. Clin Exp Allergy. 2003 Aug;33(8):1111-1117; & (c) Wu Z, Turner DR, Oliveira DB.  IL-4 gene expression up-regulated by mercury in rat mast cells: a role of oxidant stress in IL-4 transcription. Int Immunol. 2001 Mar;13(3):297-304; & Strenzke N, Gibbs BF, et al, Mercuric chloride enhances immunoglobulin E-dependent mediator release from human basophils. Toxicol Appl Pharmacol. 2001 Aug 1;174(3):257-63; & Gillespie KM, Mathieson PW, et al, Interleukin-4 gene expression in mercury-induced autoimmunity. Scand J Immunol. 1995 Mar;41(3):268-72; & Beghe B, Holloway J, et al. Polymorphisms in the interleukin-4 and interleukin- 4 receptor alpha chain genes confer susceptibility to asthma and atopy in a Caucasian population. Clin Exp Allergy. 2003 Aug;33(8):1111-1117; & Fireman P.  Understanding asthma pathophysiology. Allergy Asthma Proc. 2003 Mar- Apr;24(2):79-83. 

(50) Anaphylaxis improvement after removal of amalgam fillings, Annals of Allergy, 1990, 64(5):472-75, Katsunuma et al; & Amalgam allergy associatiated with exacerbation of aspirin-intolerant asthma. Clin Exp Allergy 1999; 29(10): 1412-4, Yoshida S, Amayasu H; Is mercury a respiratory tract allergen?, Allerg Immunol(Paris),1990; 22(3):81, Yoshida S,

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

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

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

(54) A.Tosti et al, Contact stomatitis, Semin Cutan Med Surg, 1997, 16(4):314-9; & T.Nakada et al, Patch test  materials for mercury allergic contact dematitis, Dermatitis, 1997, 36(5):237-9.

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

(57)  Hu H; Abedi‑Valugerdi M; Moller G.  retreatment 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 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 Autoimmune 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.

(58) Hultman P, Nielsen JB.  The effect of toxicokinetics on murine mercury-induced autoimmunity. Environ Res 1998, 77(2): 141-8; & P.Hultman et al,Dept. Of Pathology, Linkoping Univ., Sweden, Adverse immunological effects and immunity induced by  dental amalgam" FASEB J 8:1183-1190, 1994; & Toxicol Appl Pharmacol, 1992, 113(2):199-208; & 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. 

(59) 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; & .R.Daum, Immunotoxicology of mercury and cadmium on B-lymphocites, Int J Immunopharmacol, 1993, 15(3):383-94; & Johansson U, Hansson-Georgiadis H, Hultman P. The genotype determines the B cell response in mercury-treated mice. Int Arch Allergy Immunol. 1998 Aug;116(4):295-305.

(60) 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.

(61) R.C.Perlingeiro et al, Polymorphonuclear phagentosis in workers exposed  to mercuryvapor, Int J Immounopharmacology � , 16(12):1011-7,1994; & Hum Exp Toxicol 1995, 14(3):281-6;   & M.L. Queiroz et al, Pharmacol Toxicol, 1994, 74(2):72-5      on B-lumphocutes � , Int J Immunopharmacol,  1993, 15(3):383-94..

(62) L.Pelletier 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 .

(63)  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 hunan moncyte 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; 

  (64) W.Kostler, Beeinflubung der zellularen Immunabwehr drch Quecksilberfreisetzung, Forum Prakt. Allgem. Arzt,          1991, 30(2):62-3; & P.Schleicher,  � Schwermetalle schadigen das Immunsystem, Mineraloscope, 1996, (1):    37; & Immunschaden durch Toxine �  Argumente+Fakten der Medizin, 1992, 05; & W. Scheicher, Dissertation, Universitat Karlsruhe, 1977.

(65)  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;&  A. Szucs et al, Cell Mol Neurobiol, 1997,17(3): 273-8; & D.Busselberg, 1995,  � Calcium channels as target sites of heavy metals � ,Toxicol Lett, Dec;82‑83:255‑61; Rajanna B et al, Modulation of protein kinase C by heavy metals � , Toxicol Lett, 1995, 81(2-3):197-203.

(66) A multicenter survey of amalgam fillings and subjective   complaints in non-selected patients in the dental practice. Eur J Oral Sci 1998 Melchart D, Wuhr E, Kremers L.; 106:770-77 (6,744 patients in 34 clinics)

(67) Ziff, M.F., Documented Clinical Side Effects to Dental Amalgams, ADV. Dent. Res.,1992; 1(6):131-134; & S.Ziff, Dentistry without Mercury , 8th Edition, 1996, Bio-Probe, Inc., ISBN 0-941011-04-6; &  Dental Mercury  Detox , Bio-Probe, Inc.  http://www.bioprobe.com. (cases:FDA Patient Adverse Reaction Reports-762, Dr.M.Hanson-Swedish patients-519,  Dr. H. Lichtenberg-100 Danish patients,Dr. P.Larose- 80 Canadian patients,  Dr. R.Siblerud, 86 Colorado patients,Dr. A.V.Zamm, 22 patients)

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

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

(70) M.Davis,editor,  Defense Against Mystery Syndromes � , Chek Printing Co., March, 1994 (case histories)

(71)  Sven Langworth et al, Amalgamnews and Amalgamkadefonden, 1997 and Svenska Dogbladet,1997 (286 cases) & Improved Health after Removal of dental amalgam fillings, Swedish Assoc. Of Dental Mercury Patients, 1998. (www.tf.nu) (over 1000 cases) (Sweden Gov � t maintains health records on all citizens); & Heavy Metal Bulletin, No.3,1996 and No.1, 1999, p7,8; &  Klock B, Blomgren J, Ripa U, Andrup B, "Effekt av amalgamavl gsnande p patienter som misst nker att de lider eller har lidit av amalgamf � rgiftning", Tandl � kartidn 81(23):1297-1302 (1989)       .

(72)  P.Engel, Beobachtungen uber die gesundheit vor und nach  amalgamentfernug,Separatdruck aus Schweiz. Monatsschr Zahnm. 1998, vol 108(8). (75 cases amalgam removal) http://soho.globalpoint.ch/paul‑engel (89% sigificant improvement)

(73)   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)

(74)  F.Perger, Amalgamtherape, in  Kompendiu der Regulationspathologie und Therapie , Sonntag-Verlag, 1990; &  � Belastungen durch toxische Schwermetalle, 1993, 87(2): 157-63; & K.H.Friese, Homoopathische Behandlung der Amalgamvergiftung, Allg. Homoopathische Z, 241(5); 184-187, & Erfahrungsheikunde, 1996, (4): 251-253; & Amalgamvergiftung_moglicher Der Naturazt,1995,135(8):13-15; & M. Strassburg et al, Generalized allergic reaction from silver amalgam filling, Dtsche Zahnarztliche Zeit, 22:3-9, 1967(total: over 1200 cases)

(75) Adolph Coors Foundation, Coors Amalgam Study: Effects of placement and removal of amalgam fillings, 1995. (www) & Internations DAMS Newsletter, p17, Vol VII, Issue 2, Spring 1997. (31 cases)

(76) G.Hall, V-TOX, Mercury levels excreted after Vit C IV as chelator‑ by number of fillings  Int Symposium "Status Quo and Perspectives of Amalgam and Other Dental Materials" European  Academy, Ostzenhausen/Germany. April 29 ‑ May 1, 1994; & Heavy Metal Bulletin, Apr 1996, Vol.3,Issue 1, p6-8 (200 cured or significantly improved)

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

(78)A.P.Tanchyk, "Amalgam Removal for Treatment of Arthritis", Gen Dent,v42,n4, July 1994, p354-

(79) N.I. Shtelmakh et al, Comparative treatments of rheumatoid arthities � , Vrasch. Delo.,1982, (1):49-52. 

(80)  R.L. Siblerud et al,"Evidence that mercury from silver fillings may be an etiological factor in multiple sclerosis", Sci Total Environ, 1994, v142,n3, p191-, & A commparison of mental health of multiple sclerosis patients with silver   dental fillings and those with fillings  removed, 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 Multiple Schlerosis Patients. J. Orthomol. Med, v12#4 pp 240-4 (1997).

(81)  T. Engalls, Am J Forensic Med Pathol, 4(1):1983, Mar, 55-61

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

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

(84)  Kidd RF.  Results of dental amalgam removal and mercury detoxification.  Altern Ther Health Med 2000 Jul;6(4):49‑55.

(85) H.Huggins, Burton Goldberg, & Editors of Alternative Medicine Digest, Chronic Fatigue  Fibromyalgia & Environmental Illness , Future Medicine Publishing, Inc,   1998, p197-;      &     U.Dorffer,  � Anorexia Hydragyra: ..., Monatsschr. Kinderheilkd., 1989, 137(8): 472.  

(86) Geier M.R., Geier DA; Timerosal in Childhood Vaccines, Neurodevelopmental Disorders, and Heart Disease in the U.S. ; J of Amer Physicians and Surgeons, Vol 8(1), Spring 2003

(87)  Overzet K, Gensler TJ, et al;  Small nucleolar RNP Scleroderma      autoantigens associate with  phosphorylated serine/arginine splicing factors during apoptosis.  Arthritis Rheum 2000 Jun;43(6):1327‑36 ;

   & Mayes MD. Epidemiologic studies of environmental agents and systemic autoimmune diseases. Environ Health Perspect. 1999 Oct;107 Suppl 5:743-8; &. Bigazzi PE.   Metals and kidney autoimmunity.  Environ Health Perspect. 1999 Oct;107 Suppl 5:753-65

(88) Feighery L, Collins C, Feighery C, Mahmud N, Coughlan G, Willoughby R, Jackson J. Anti-transglutaminase antibodies and the serological diagnosis of coeliac disease.  Br J Biomed Sci. 2003;60(1):14-8; & Kurup RK, Kurup PA. Hypothalamic digoxin, cerebral chemical dominance, and regulation of gastrointestinal/hepatic function.     Int J Neurosci. 2003 Jan;113(1):75-105; & Kumar AR, Kurup PA. Hypothalamic digoxin and irritable bowel syndrome.   Indian J Gastroenterol. 2001 Sep-Oct;20(5):173-6.

(89)  Kurup RK, Kurup PA.   Hypothalamic digoxin, hemispheric dominance, and neuroimmune integration.    Int J Neurosci. 2002 Apr;112(4):441-62; & 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; 

(90) Hide I. [Mechanism of production and release of tumor necrosis factor implicated in inflammatory diseases] Nippon Yakurigaku Zasshi. 2003 Mar;121(3):163-73; & Straub RH, Pongratz G,et al; Long-term anti-tumor necrosis factor antibody therapy in rheumatoid arthritis patients sensitizes the pituitary gland and favors adrenal androgen secretion.. Arthritis Rheum. 2003 Jun;48(6):1504-12; &  Kurup RK, Kurup PA, Hypothalamic digoxin and hemispheric chemical dominance--relation to the pathogenesis of senile osteoporosis, degenerative osteoarthritis, and spondylosis.   Int J Neurosci. 2003 Mar;113(3):341-59;   

(91) Lee JY, Yoo JM, Cho BK, Kim HO. Contact dermatitis in Korean dental technicians.  Contact Dermatitis. 2001 Jul;45(1):13-6; & (b) Increase in occupational skin diseases of dental personnel.  Contact Dermatitis. 1999 Feb;40(2):104-8) Kanerva L, Jolanki R; &(c) "Adverse health reactions in skin, eyes, and respiratory tract among dental personnel in Sweden", Swed Dent J, 1998, 22(1-2): 33-45, E.C. Lonnroth et al,

(92) Inhibition of the human erythrocytic glutathione-S-transferase T1 (GST T1) by thimerosal., Int J Hyg Environ Health. 2001 Jul;203(5-6):479-81, Muller M, Hallier E; & [Genetic polymorphism of glutathione s-transferase as a factor predisposing to allergic dermatitis]   [ Polish], Med Pr. 2001;52(1):45-51 Lutz W, Nowakowska E.. 

(93) Watzl B, Abrahamse SL, Treptow-van Lishaut S, Neudecker C, Hansch GM, Rechkemmer G, Pool-Zobel BL., Enhancement of ovalbumin-induced antibody production and mucosal mast cell response by mercury.  Food Chem Toxicol. 1999 Jun;37(6):627-37.

(94) 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;79(3):1336-45; & BhattacharyaS, Sen S et al,  Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction.   Biometals. 1997;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;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  

(95)  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

(96) 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.  &  (c) Anuradha B, Varalakshmi P.  Protective role of DL-alpha-lipoic acid against mercury-induced  lipid peroxidation.    Pharmacol Res. 1999 Jan;39(1):67-80.

(97)   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 (MS) July 25, 2000; 55:178-84;

(98)  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;  http://www.mmvbs.com/

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

  &  Michael Guthrie, R.Ph. ImmuneSupport.com     07‑18‑2001  Mycoplasmas  The Missing Link in Fatiguing Illnesses

(100)  Hulda Clark ,  The Cure for all Diseases , 2000,

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

(102)   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; 

(103)   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

(104)  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;

(105)   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;

(106)   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.

(107)  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..

(108)  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;

(109) 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

(110)  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;

(111)  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.

(112)  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

(113)       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; & (b)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; &(c) 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;

(114)  ) 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.

(115)  B. Windham (Ed), Annotated bibliography, Effects of fetal/neonatal mercury exposures,  & B. Windham (Ed);  Neurological and Developmental Effects of Toxic Metal Exposures

 (116) (a) The Long-Term Algae Extract ( Chlorella and Fucus sp ) and Aminosulphurate Supplementation Modulate SOD-1 Activity and Decrease Heavy Metals (Hg ⁺⁺ , Sn) Levels in Patients with Long-Term Dental Titanium Implants and Amalgam- Fillings Restorations. Antioxidants (Basel). 2019 Apr 16;8(4). Merino JJ ; & (b) N -acetyl-cysteine affords protection against lead-induced cytotoxicity and oxidative stress in human liver carcinoma (HepG ₂ ) cells. Int J Environ Res Public Health 4:132_137, Yedjou GC, TchounwouPB (2008)

&( c ) Detoxification: Heavy Metals Testing and Chelation Therapy-Lyn Patrick, ND (DMSA for challenge test & chelation or MCP)- https://cdn.simplecast.com/audio/4ed1adc9-1b56-4d5d-a2fb-9106997393d4/episodes/6c148e92-bf66-424f-9431-e1a01dbf870d/audio/8773d9e9-9e26-4b2f-aec6-a2004e921e66/default_tc.mp3?aid=rss_feed&feed=1NYUFSRI & (d) Take Charge of Your Health (Testing & Chelation of Heavy Metals) - Dr. Chris Shade - CEO of Quicksilver Scientific https://s115.podbean.com/pb/1860a0ddeed2ad45db31477355f265e8/60103875/data1/fs48/6936790/uploads/Take_Charge_1218208ati1.mp3?pbss=f02615a5-91d0-5c11-8e0e-81cca9f7c721

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

(118)  (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. .

(119)  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.

(120) 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.  

(121) 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.  

(122) 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.

(123)   (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;

(124)  (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 signalling intermediates that  triggerthe 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;

(125)   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;

(126)  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

(127) (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

(128)  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,   www.bioprobe.com

(129)   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, et al,  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.

 (130)  Johnson S.     The possible role of gradual accumulation of copper, cadmium, lead and     iron depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and essential fatty    acids in multiple        sclerosis.     Med Hypotheses 2000 Sep;55(3):239‑41.

(131)   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.

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

see research web pages on amalgam toxicity, root canals, cavitations.  http://www.altcorp.com; 

&(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

&     www.flcv.com/damspr11.html

&(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, www.genomics.duke.edu/pdf/Alzheimer.pdf

&(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 al ,  Alzheimer Disease: Mercury as pathogenetic factor and apolipoprotein E as a moderator,  Neuroendocrinol Lett 2004;  25 (5):331�339;

(133) H eintze 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. 

(134)  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)

(135)  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.

(136)   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. (www.tf.nu) (over 1000      cases) (Sweden Gov�t has voted to phase out  use of amalgam)

(137)   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.

(138)  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.

(139)   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. 

(140)   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.

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

(142)   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) 

(143)  Stejskal V, Hudecek R, Mayer W, "Metal-specific lymphocytes: risk factors in CFS and other related diseases", Neuroendocrinology Letters, 20: 289-298, 1999

(144)   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.

(145) 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.

(146) 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; & (d) Guzzi G, Mazzi B, Tomasi S, Fleischhauer K, Pigatto PD.  Association between HLA- class II and mercury  sensitization. RMZ & Materials and Geoenvironment   2004;51:136-140.

(147)  .(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. 

(148)  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.

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

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

(151)   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)

(152)  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;   & Birgitta Brunes, Adima Bergli,   From MS diagnosis to better health  ,1996. www.melisa.org

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

(154)  The Edelson Clinic, Atlanta, Ga.  

(155)   U.S. Centers for Disease Control, National Center for Health Statistics,  NHANES III study(thousands of people�s health monitored), http://www.myflcv.com/NHANES3.html

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

(156)  The beneficial effect of amalgam replacement on health in patients with autoimmunity. Prochazkova J, Sterzl I, Kucerova H, Bartova J,StejskalVD; Neuro Endocrinol Lett. 2004 Jun;25(3):211-8; &  terzl  I, Prochzkov J, Hrd P, Matucha P, Bartov 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; 

http://www.melisa.org/pdf/Mercury-and-autoimmunity.pdf

& (b)  Dagmar Magnusson, Dentist, Samos, Greece, 1000 patients with amalgam replacement with over 80% significantly improved, http://md24.embarq.synacor.com/service/home/~/Dagmars%20contribution.doc?auth=co&id=47020&part=2

(157) Heavy Metal and Chemical Toxicity,  Dietrich Klinghardt, MD, Ph.D.   www.klinghardtacadamy.com :  �& 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

(158)  Kawasaki's disease, acrodynia, and mercury. Mutter J , Yeter D . Curr Med Chem. 2008;15(28):3000-10.

(159) Pigatto PD, Guzzi G, Persichini P. Nummular lichenoid dermatitis from mercury dental amalgam. Contact Dermatitis. 2002;46: 355-6; &

Guzzi G, Minoia C, Pigatto P, et al. Safe dental amalgam removal in patients with immuno-toxic reactions to mercury. Toxicol Letters 2003;

& Guzzi G, Minoia C, Pigatto PD, Lucchiari S, Severi G. Mercury and dental patients: toxicology, immunology and genetic connection. Toxicol

Letters; 2005; 158S: S239;&  Guzzi G, Pigatto PD, Brambilla L. Fever of unknown cause and dental amalgams. EAACI 2006 XXV Congress of the European Academy of Allergology and Clinical Immunology, Vienna, Austria, 10 � 14 June 2006; 389.

(186) Life Extension Foundation,  Disease Prevention and Treatment , Expanded 5 ^th  Edition, 2013 & Life Extension Foundation,  Life Extension, Jan 2009 (citing many studies). &  www.lifeextension.com 

(199) Documentation that mercury amalgam dental fillings are the largest source of both methyl and toal mercury in most who have amalgam fillings,   http://www.myflcv.com/damspr1.html

     & & World Health Organization(WHO),1991, Environmental Health criteria 118,  Inorgtanic  Mercury,

(200) Annotated bibliography: Exposure levels and health effects related to mercury/dental          amalgam and results of amalgam replacement, 2002;B Windham(Ed.), (over 2000 medical      study references documenting mechanism of causality of 30 chronic conditions and over          60,000 clinical cases of recovery or significant improvement of these conditions after               amalgam replacement-documented by doctors)  ;                                                                  www.myflcv.com/amalg6.html

(201)  Documentation of the mechanisms by which mercury causes over 30 chronic health conditions, (over 4000 medical study references documenting mechanism of causality of 30 chronic conditions and over 60,000 clinical cases of recovery or significant improvement of these conditions after  amalgam replacement-documented by doctors)  www.myflcv.com/indexa.html

**********