Immune Reactive Conditions: The Mercury Connection to Eczema, Psoriasis, Lupus, Asthma, Scleroderma, Rheumatoid Arthritis, and Allergies

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A significant percentage of people are allergic or immune reactive to mercury to varying degrees, and 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, and MS, has been increasing rapidly in recent years.

The autism incidence rate had a tenfold increase in the last decade, and ADHD had major increases likewise. At least 50 million have allergies (19%), and according to the U.S. CDC, approximately 20 million have asthma (7.7%). The largest increase has been in infants, and approximately 10% of infants—approximately 15 million in the U.S.—have systemic eczema. Studies implicate earlier and higher usage of vaccines containing mercury (thimerasol) as a likely connection, plus fetal and neonatal exposure from mother’s blood and milk. It has been estimated that by age three the typical child has received over 235 micrograms of mercury thimerasol from vaccinations, which is considerably more than the federal mercury safety guidelines states is safe, in addition to significant levels of mercury exposure from other sources for many. 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 developed such conditions after being vaccinated, 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. 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.

Dental materials are a factor in many people’s development of chronic immune problems. Of all patients tested in a German medical lab, approximately 11% were found to have significant mercury allergy, and most of these had significant health improvements after amalgam replacement. A high percentage of patients tested immune reactive to mercury and 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. The extreme immunotoxicity of mercury and resulting damage to the immune system exposure is likely a factor. 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, and lupus. Within a population of over 3000 with chronic health problems tested by the immune lymphocyte reactivity test, 20% tested positive for inorganic mercury; 13% for phenyl mercury; 8% for methyl mercury; and 7% for mercury thimerasol. For people with autoimmune conditions, 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 methylmercury, 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.

Allergic Health Effects Related to Mercury Exposure

Many studies, clinical cases, and 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. Amalgam fillings expose those with fillings to methylmercury. Amalgam fillings of mothers is also a significant source of exposure to infants as mercury in the mother crosses the placenta in high levels, and significant exposure occurs through breast milk.

Studies have found mercury to be a major factor in allergic/immune reactive conditions, including lupus, contact dermatitis, eczema, psoriasis, oral lichen planus, systemic eczematous contact-type dermatitis (baboon syndrome), stomatitis, scleroderma, allergies, asthma, autoimmune, renal effects, and rheumatoid arthritis. Mercury has been found to accumulate in connective tissue, resulting in lupus or scleroderma. 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.

Allergic contact eczema is the most frequent occupational disease, occurring in over 10% of children in some areas; the most common cause of contact eczema is exposure to toxic metals. The metals most commonly causing allergic immune reactivity are nickel, mercury, chromium, cobalt, and palladium. Nickel, typically found in stainless steel braces and crowns, is a source of reactivity and autoimmunity, along with gold and palladium in crowns. The highest level of sensitization is to infants, who are most reactive to thimerosal, a form of mercury used as a preservative in vaccines and eye drops. There is strong suggestive and clinical evidence for a connection between toxic metals and autism. 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. Also, mercury has been found to be the most significant factor in large numbers of reactive autoimmune allergic and neurological conditions.

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 Crohn’s disease, etc. 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. Glutathione is an amino acid that helps control apoptosis. When glutathione is depleted in the brain, reactive oxidative species increases, and CNS and cell signaling mechanisms are disrupted by toxic exposures such as mercury, resulting in neuronal cell apoptosis 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.

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. Studies have found that in asthma, lupus, rheumatoid arthritis, scleroderma, celiac/Crohn’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. 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, and 4) defective golgi body function and protein processing dysfunction. It is documented that mercury is a cause of most of these conditions.

Dental staff members have been found to have significantly higher prevalence of eye problems, conjunctivitis, atopic dermatitis, and contact urticaria. Finnish dental staff members have the highest occupational risk of contact dermatitis with 71% affected over time by plastics, rubber, and mercury. 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. 16.3% were immune reactive to mercury. One mechanism of mercury’s effect on contact sensitivities is the inhibition of glutathione S-transferase, which is a modulator of inflammation. Mercury also causes intestinal damage and leaky gut, causing metabolic damage and increasing food sensitivities.

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. 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. 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. Casamorphin is a morphine-like compound that results in neural dysfunction. Elimination of milk products from the diet has been found to improve the condition. Such populations have also been found to have high levels of mercury and to recover after mercury detox. As mercury levels are reduced the protein binding is reduced and improvement in the enzymatic process occurs. 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. 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. The effect on the immune system of exposure to various toxic substances 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. Other than the organochlorines or toxic metals four common pollutants that have been documented to have effects on such conditions are: traffic and industrial pollutants, sulfur dioxide, power plant residual oil fly ash, and organochlorine pollutants.

Mercury vapor exposure at very low levels adversely affects the immune system. 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 systems involving the sulphydryl protein groups. Mercury causes adverse effects on both neutrophil and macrophage, and after depletion of thiol reserves, T-cells are susceptible to Hg-induced cellular death. Interferon syntheses was reduced in a concentration dependent manner with either mercury or methylmercury as well as other immune functions, and low doses induce aggregation of cell surface proteins and dramatic tyrosine phosporlation of cellular proteins related to asthma, allergic diseases, such as eczema and lupus, and autoimmunity. One study found that insertion of amalgam fillings or nickel dental materials causes a suppression of the number of T-lymphocytes, 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. Both mercuric and methylmercury chlorides caused dose dependent reduction in immune B-cell production. B-cell expression of IgE receptors were significantly reduced, with a rapid and sustained elevation in intracellular levels of calcium induced. Antigen specific LST-test was performed on a large number of patients with atopic eczema, 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% of the patients within one to ten months. Similar results have been obtained at other clinics.

Mercury and toxic substances’ effects on suppressing the immune system are documented to cause increased susceptibility to other pathogens, such as viruses, mycoplasma, bacterial infections, and parasites. The majority of those with autoimmune conditions, like ALS, CFS, FMS, and 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.

Many studies have found that the body’s basic building blocks—amino acids with SH hydroxyl radicals—form strong bonds with the toxic metals, 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.

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. 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 forms 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 is reactive and sensitive to mercury.

In a group of medical students tested by patch test, 12.8 % were sensitive to mercury. 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 tending to have higher levels of sensitization and more adverse health effects. In a group of eight with contact eczema patch tested for mercury in Spain, all were positive for mercurochrome, six to inorganic mercury, and some to thimerosal. This study like several others noted the danger in patch tests for mercury as two 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 be an unreliable test of mercury or toxic metal sensitivity. Inorganic mercury was found to be a cause of systemic eczema and digestive problems. 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. Mercury blocks the immune function of magnesium and zinc, whose deficiencies are known to cause significant neurological effects. The low Zn levels result in deficient CuZnSuperoxide dismutase (CuZnSOD), which in turn leads to increased levels of superoxide due to toxic metal exposure.

Autoimmunity Caused by Mercury: Connection to Immune and Neurological Conditions

Mercury has been documented to cause autoimmune disease, 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 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. Mercury has been found to impair conversion of thyroid T4 hormone to the active T3 form as well as to cause autoimmune thyroiditis common to such patients. 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 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, such as found more frequently in patients with human lymphocyte antigens (HLA-DRA). A significant portion of the population appears 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.

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. 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.

Very low doses and short-term exposures of inorganic Hg (20-200 mug/kg) exacerbate lupus and accelerate 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.

Autoimmune reactions to inorganic and methylmercury 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 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. MELISA test scores saw a significant reduction in lymphocyte reactivity compared to pre-replacement. The MELISA test has proven successful in diagnosing and treating environmentally caused autoimmune diseases such as MS, SLE, oral lichen planus, CFS, etc. A high percentage of patients subjectively diagnosed with CNS and systemic symptoms suggestive of mercury intoxication has been found to have immune reactivity to inorganic mercury and for MRI positive patients for brain damage as well. 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. 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 MCS. Mercury also causes a reduction in thyroid production 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.

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. Such binding and autoimmune damage has been documented in the fat-rich proteins of the myelin heaths and of collagen, 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. Studies have also found mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and myelin basic protein (MBP). Mercury and cadmium also have been found to interfere with zinc binding to MBP which affects MS symptoms since zinc stabilizes the association of MBP with brain myelin. 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. Antioxidants like lipoic acid which counteract such free radical activity have been found to alleviate symptoms and decrease demyelization. A group of metal-exposed MS patients with amalgam fillings was 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. 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 with genetic susceptibility being a major factor in who is affected. One genetic factor in Hg-induced autoimmunity is major histocompatibility complex (MHC). Both immune cell types Th1 and Th2 cytokine responses are involved in autoimmunity. One genetic difference found in animals and humans is cellular retention differences for metals related to the ability to excrete mercury. For example it has been found that individuals with genetic blood factor type APOE-4 do not excrete mercury readily and bio-accumulate mercury, resulting in susceptibility to chronic autoimmune conditions such as Alzheimer’s, Parkinson’s, etc. as early as age 40, whereas those with type APOE-2 readily excrete mercury and are less susceptible. 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. Also when a condition has been initiated and exposure levels decline, autoimmune antibodies also decline in animals or humans.

Exposure to mercury results in metalloprotein compounds that have genetic effects, having both structural and catalytic effects on gene expression. Some of the processes affected by such metalloprotein control of genes include cellular respiration, metabolism, enzymatic processes, metal-specific homeostasis, and adrenal stress response. 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. Dental amalgam has been found to be the largest source of methylmercury in most with mercury amalgam fillings.

Mucocutaneous lymph node syndrome (Kawasaki syndrome) is an autoimmune disease that manifests as a multi-systemic necrotizing medium vessel vasculitis that is largely seen in children under five. The disorder 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. Several patients with Kawasaki’s disease have presented 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 six months of age (from 75microg to 187.5microg), the rates of Kawasaki’s Disease increased ten times, and, later (1985-1997) by twenty 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.

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 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, and chronic allergies, 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. 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, and MS, also often recover after amalgam replacement. 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 seventeen or more surfaces than in the general population.

There are extensive documented cases (many thousands) where removal of amalgam fillings led to cure of serious health problems such as eczema, psoriasis, asthma, lupus, allergies, oral lichen planus, chronic multiple chemical sensitivities, ALS, arthritis, MS, CFS, autoimmune thyroiditis, muscular/joint pain/fibromyalgia, and over twenty other chronic health conditions. In several of the studies, over 75% of those with MS who had their amalgams replaced recovered or had significant improvement. Some of the studies reported similar success rates for SLE, but a lower number of cases were 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. 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 disappeared over time.


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 results in thickening of bone, development of bone spurs, and inflammatory reactions. The result is 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. 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 and 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. 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. 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.

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, and curcumin. 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. Uncooked vegen diets, rich in berries, fruits, vegetable, nuts, and seeds, often benefit arthritis sufferers.


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. 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 and congestion), Yerba mate, and bee pollen.

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


1. Silhan P, Arenberger P. Standard epicutaneous tests in ambulatory care of patients. Cas Lek Cesk. 1999; 138(15): 469-73.

2. Lindemayr H, Drobil M. Eczema of the lower leg and contact allergy. Hautarzt. 1985; 36(4): 227-3.

3. Reichrtova E, et al. Cord serum immunoglobulin E related to environmental contamination of human placentas with oganochlorine compounds. Environ Health Perspect. 1999; 107(11): 895-99.

4. Gavett SH, et al. Residual oil fly ash amplifies allergic cytokines, airway Responsiveness, and inflammation in mice. Am J Respir Crit Care Med. 1999; 160(6): 1897-1904.

5. Kramer U, et al. Traffic-related air pollution is associated with atopy in children living in urban areas. Epidemiology. 2000; 11(1): 64-70.

6. Romaguera C, Vilaplana J. Contact dermatitis in children: 6 years’ experience. Contact Dermatitis. 1998; 39(6): 277-80.

7. Manzini BM, Ferdani G, Simonetti V, Donini M, Sedernari S. Contact sensitization in children. Pediatr Dermatol. 1998; 15(1): 12-17.

8. Brasch J, Geier J, Schnuch A. Differentiated contact allergy lists serve in quality improvement. Hautarzt. 1998; 49(3): 184-91.

9. Audicana MT, Munoz D, del Pozo MD, et al. Allergic contact dermatitis from mercury antiseptics and derivatives: study protocol of tolerance to intramuscular injections of thimerosal. Am J Contact Dermat. 2002; 13(1): 3-9.

10. Patrizi A, Rizzoli L, Vincenzi C, Trevisi P, Tosti A. Sensitization to thimerosal in atopic children. Contact Dermatitis. 1999; 40(2): 94-7.

11. Sun CC. Allergic contact dermatitis of the face from contact with nickel and ammoniated mercury. Contact Dermatitis. 1987; 17(5): 306-9.

12. 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.

13. Meding B, Jarvholm B. Hand eczema in Swedish adults and children. J Invest Dermatol. 2002; 118(4): 719-23.

14. Lindemayr H, Drobil M. Eczema of the lower leg and contact allergy. Hautarzt. 1985 36(4): 227-31.

15. Aberer W, Holub H, Strohal R, Slavicek R. Palladium in dental alloys: The dermatologists responsibility to warn? Contact Dermatitis. 1993; 28(3): 163-5.

16. Veien NK. Stomatitis and systemic dermatitis from mercury in amalgam dental restorations. Dermatol Clin. 1990; 8(1): 157-60.

17. Stejskal VDM, et al. MELISA: Tool for the study of metal allergy. Toxicology in Vitro. 1994; 8(5): 991-1000.

18. Stejskal VDM, et al. Mercury-specific lymphocytes: An indication of mercury allergy in man. J. of Clinical Immunology. 1996; 16(1): 31-40.

19. Alanko K, Kanerva L, Jolanki R, Kannas L, Estlander T. Oral mucosal diseases investigated by patch testing with a dental screening series. Contact Dermatitis. 1996; 34(4): 263-7.

20. Stejskal VDM, Danersund A, Lindvall A, et al. Metal-specific memory lymphocytes: Biomarkers of sensitivity in man. Neuroendocrinology Letters. 1999.

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

22. Sterzl I, Prochazkova J, Stejaskal VDM, et al. Mercury and nickel allergy: Risk factors in fatigue and autoimmunity. Neuroendocrinology Letters. 1999; 20: 221-228.

23. Valentine-Thon E, Schiwara HW. Validity of MELISA for metal sensitivity testing; Neuroendocrinology Letters. 2003; 24(1-2): 57-64.

24. Ellermann-Eriksen S, et al. Effect of mercuric chloride on macrophage-mediated resistance mechanisms against infection. Toxicology. 1994; 93: 269-297.

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

26. Christensen MM, et al. Comparison of interaction of meHgCl2 and HgCl2 with murine macrophages. Arch Toxicol. 1993; 67(3): 205-11.

27. Goldman M, et al. Chemically induced autoimmunity. Immunology Today. 1991; 12: 223.

28. Warfyinge K, et al. Systemic autoimmunity due to mercury vapor exposure in genetically susceptible mice. Toxicol Appl Pharmacol. 1995; 132(2): 299-309.

29. Mathieson PW. Mercury: God of TH2 cells. Clinical Exp Immunol. 1995; 102(2): 229-30.

30. Parronchi P, Brugnolo F, Sampognaro S, Maggi E. Genetic and Environmental Factors Contributing to the Onset of Allergic Disorders. Int Arch Allergy Immunol. 2000; 121(1): 2-9.

31. Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cell viability immune suppression of human T-cell activation. Immunopharmacologicol Immunotoxical. 1992; 14(3): 555-77.

32. Sato K, Kusaka Y, Miyakoshi S. An epideomological study of factors relating to mercury sensitization. Arerugi. 1995; 44(2): 86-92.

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

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

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

36. Halsey NA. Limiting Infant Exposure to Thimerosal in vaccines. JAMA. 1999; 282: 1763-66.

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

38. Elferink JG. Thimerosal: A versatile sulfhydryl reagent, calcium mobilizer, and cell function-modulating agent. Gen Pharmacol. 1999; 33(1): 1-6.

39. Forstrom L, Hannuksela M, Kousa M, Lehmuskallio E. Merthiolate hypersensitivity and vaccination. Contact Dermatitis. 1980; 6(4): 241-5.

40. Schafer T, Bohler E, et al. Epidemiology of contact allergy in adults. Allergy. 2001; 56(12): 1192-6.

41. Cade JR, et al. Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism. 1999.

42. Puschel G, Mentlein R, Heymann E. Isolation and characterization of dipeptidyl peptidase IV from human placenta. Eur J Biochem. 1982; 126(2): 359-65.

43. Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV (DPPIV) and its unique properties. J Clin Lab Anal. 1996; 10(6): 435-40.

44. Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary culture of rabbit proximal tubules as a cellular model to study nephrotoxicity of xenobiotics. Kidney Int. 1993; 44(1): 13-8.

45. Stefanovic V, et al. Kidney ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem. 1998; 8(5): 278-84.

46. Guzzi G, et al. Mercury dental amalgam and renal autoimmunity. J. Environ. Pathol. Toxicol. Oncol. 2008; 27: 147–155.

47. Glavinskiaia TA, et al. Complexons in the treatment of lupus erghematousus. Dermatol Venerol. 1980; 12: 24-28.

48. Pollard KM, Pearson Dl, Hultman P. Lupus-prone mice as model to study xenobiotic-induced autoimmunity. Environ Health Perspect. 1999; 107(5): 729-735.

49. Nielsen JB, Hultman P. Experimental studies on susceptibility to mercury-induced autoimmune response. Ren Fail. 1999; 21(3-4): 343-8.

50. Hultman P, Enestrom S. Mercury induced antinuclear antibodies in mice. Clinical and Exper Immunology. 1988; 71(2): 269-274.

51. 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.

52. Silbergeld EK, Silva IA, Nyland JF. Mercury and autoimmunity: Implications for occupational and environmental health. Toxicol App Pharmacol. 2005; 207(2): 282-92.

53. Gordon C, et al. Abnormal sulphur oxidation in systemic lupus erythrmatosus (SLE). Lancet. 1992; 339: 8784-6.

54. Emory P, et al. Poor sulphoxidation in patients with rheumatoid arthritis. Ann Rheum Dis. 1992; 51(3): 318-20.

55. Tanner CM, et al. Abnormal liver enzyme metabolism in Parkinson’s. Neurology. 1991; 41(5.2): 89-92.

56. Wilkinson LJ, Waring RH. Cysteine dioxygenase: modulation of expression in human cell lines by cytokines and control of sulphate production. Toxicol In Vitro. 2002; 16(4): 481-3.

57. Hisatome I, 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.

58. McFadden SA. Xenobiotic metabolism and adverse environmental response: Sulfur-dependent detox pathways. Toxicology. 1996; 111(1-3): 43-65.

59. Markovich, et al. Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat-1. Toxicol App Pharmacol. 1999; 154(2): 181-7.

60. Alberti A, Pirrone P, Elia M, Waring RH, Romano C. Sulphation deficit in “low-functioning” autistic children. Biol Psychiatry. 1999; 46(3): 420-4.

61. Quig D. Cysteine metabolism and metal toxicity. Altern Med Rev. 1998; 3(4): 262-270.

62. de Ceaurriz J, et al. Role of gamma-glutamyltraspeptidase (GGC) and extracellular glutathione in dissipation of inorganic mercury. J Appl Toxicol. 1994; 14(3): 201.

63. Huggins HA, Levy TE. Uniformed Consent: The Hidden Dangers in Dental Care. Hampton Roads Publishing Company Inc; 1999.

64. Panasiuk J. Peripheral blood lymphocyte transformation test in various skin diseases of allergic origin. Przegl Dermatol. 1980; 67(6): 823-9.

65. Barnett JH, Discoid lupus erythematosus exacerbated by contact dermatitis. Cutis. 1990; 46(5): 430-2.

66. Schultz JC, Connelly E, Glesne L, Warshaw EM. Cutaneous and oral eruption from oral exposure to nickel in dental braces. Dermatitis. 2004; 15(3): 154-7.

67. Genelhu MC, Marigo M, et al. Characterization of nickel-induced allergic contact stomatitis associated with fixed orthodontic appliances. Am J Orthod Dentofacial Orthop. 2005; 128(3): 378-81.

68. 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; 34(5): 320-3.

69. Tsyganok SS. Unithiol in treatment of dermatoses. Vestn. Dermatol. Venerol. 1978; 9: 67-69.

70. Ionescu G. Schwermetallbelastung bei atopischer dermatitis und Psoriasis. Biol Med. 1996; 2: 65-68.

71. Wehner-Caroli J, Scherwitz C, Schweinsberg F, Fierlbeck G. Exacerbation of pustular psoriasis in mercury poisoning. Hautarzt. 1994; 45(10): 708-10.

72. 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; 2(4): 325-31.

73. Lipozencic J, Milavec-Puretic V, Pasic A. Contact allergy and psoriasis. Arh Hig Rada Toksikol. 1992; 43(3): 249-54.

74. Roujeau JC, et al. Acute generalized exanthematous pustulosis: Analysis of 63 cases. Arch Dermatol. 1991; 127(9): 1333-8.

75. Yiannias JA, Winkelmann RK, Connolly SM. Contact sensitivities in palmar plantar pustulosis (acropustulosis). Contact Dermatitis. 1998; 39(3): 108-11.

76. Dunsche A, et al. Oral lichenoid reactions associated with amalgam: improvement after amalgam removal. British Journal of Dermatology. 2003; 148(1): 70-6.

77. Smart ER, et al. Resolution of lichen planus following removal of amalgam restorations. Br Dent J. 1995; 178(3): 108-112.

78. Markow H. Regression from orticaria following dental filling removal. New York State J Med. 1943: 1648-1652.

79. Sasaki G, et al. Three cases of oral lichenosis caused by metallic fillings. J. Dermatol. 1996; 12: 890-892.

80. Bratel J, et al. Effect of replacement of dental amalgam on OLR. Journal of Dentistry. 1996; 24(1-2): 41-45.

81. Mutter J, et al. Nummular dermatitis. Crit. Rev. Toxicol. 2007; 37: 537-549.

82. Ostman PO, et al. Clinical & histologic changes after removal of amalgam. Oral Surgery, Oral Medicine, and Endodontics. 1996; 81(4): 459-465.

83. Ibbotson SH, et al. The relevance of amalgam replacement on oral lichenoid reactions. British Journal of Dermatology. 1996; 134(3): 420-3.

84. Koch P, et al. Oral lesions and symptoms related to metals. Dermatol. 1999; 41(3): 422-430.

85. Freeman S, et al. Oral lichenoid lesions caused by allergy to mercury in amalgam. Contact Dermatitis. 1995; 33(6): 423-7.

86. Jolly M, et al. Amalgam related chronic ulceration of oral mucosa. Br Dent J. 1986; 160: 434-437.

87. Camisa C, et al. Contact hypersensitivity to mercury. Cutis. 1999; 63(3): 189.

88. Laine J, et al. Immunocompetent cells in amalgam-associated oral licheinoid contact lesions. Oral Pathol Med. 1999; 28(3): 117-21.

89. Laine J. Contact allergy to dental restorative materials in patients with oral lichenoid lesions. Contact Dermatitis. 1997; 36(3): 141-6.

90. Adachi A, et al. Efficacy of dental metal elimination in the management of atopic dermatitis. Dermatol. 1997; 24(1): 141-6.

91. Sato K, et al. An epidemiological study of factors relating to mercury sensitization. Arerugi. 1995; 44(2): 86-92.

92. Mori T, et al. Mercury sensitization caused by environmental factors. Nippon Eiseigaku Zasshi. 1998; 52(4): 661-6.

93. Miller EG, et al. Prevelence of mercury hypersensitivity among dental students. J Dent Res. 1985: 338.

94. Kawahara D, et al. Epidemiologic study of occupational contact dermatitis in the dental clinic. Contact Dermatitis. 1993; 28(2): 114-5.

95. Lewezuk E, et al. Occupational health problems in dental practice. Med Pr. 2002; 53(2): 161-5.

96. Noda M, Wataha JC, Lockwood PE, Volkmann KR, Kaga M, Sano H. Dental material components alter TNF-alpha secretion of THP-1 monocytes. Dent Mater. 2003; 19(2): 101-5.

97. 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; 7(1): 67-74.

98. Chen L, Nordlind K, Liden S, Sticherling M. Increased expression of keratinocyte interleukin-8 in human contact eczematous reactions to heavy metals. APMIS. 1996; 104(7-8): 509-14.

99. Zamm AF. Removal of dental mercury: often an effective treatment for very sensitive patients. J Orthomolecular Med. 1990; 5(53): 138-142.

100. Cutler E. Winning the War Against Asthma & Allergies. 1st ed. Delmar Learning; 1997.

101. Hunter I, Cobban HJ, et al. Tumor necrosis factor-alpha-induced activation of RhoA in airway smooth cells: role in the Ca2+ sensitization of myosin light chain20 phosphorylation. Mol Pharmacol. 2003; 63(3): 714-21.

102. 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; 111(5): 708-13.

103. 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 hyper-reactivity of adults and their children. Allergy Asthma Proc. 2003; 24(2): 111-8.

104. 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; 13(3): 297-304.

105. Gillespie KM, Mathieson PW, et al. Interleukin-4 gene expression in mercury-induced autoimmunity. Scand J Immunol. 1995; 41(3): 268-72.

106. Strenzke N, Gibbs BF, et al. Mercuric chloride enhances immunoglobulin E-dependent mediator release from human basophils. Roxicol Appl Pharmacol. 2001; 174(3): 257-63.

107. Gillespie KM, Mathieson PW, et al. Interleukin-4 gene expression in mercury-induced autoimmunity. Scand J Immunol. 1995; 41(3): 268-72.

108. 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; 33(8): 1111-1117.

109. Fireman P. Understanding asthma pathophysiology. Allergy Asthma Proc. 2003; 24(2): 79-83.

110. Katsunuma, et al. Anaphylaxis improvement after removal of amalgam fillings. Annals of Allergy. 1990; 64(5): 472-75.

111. Yoshida S, Mikami H, Nakagawa H, Amayasu H. Amalagam allergy associatiated with exacerbation of aspirin-intolerant asthma. Clin Exp Allergy. 1999; 29(10): 1412-4.

112. Drouet M, et al. Is mercury a respiratory tract allergen? Allerg Immunol (Paris). 1990; 22(3): 81.

113. Redhe O, Pleva J. Recovery from ALS and from asthma after removal of dental amalgam fillings. Int J Risk & Safety in Med. 1994; 4: 229-236.

114. 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; 86(6): 522-33.

115. Weber BA. The Marburg amalgam study. Arzt und Umwelt. 1995.

116. Zinecker S. Amalgam: Quecksilberdamfe bis ins Gehirn. Der Kassenarzt. 1992; 32(4): 23.

117. Tosti A, et al. Contact stomatitis. Semin Cutan Med Surg. 1997; 16(4): 314-9.

118. Nakada T, et al. Patch test materials for mercury allergic contact dermatitis. Dermatitis. 1997; 36(5): 237-9.

119. Goldman M, et al. Chemically induced autoimmunity. Immunology Today. 1991; 12: 223.

120. Warfyinge K, et al. Systemic autoimmunity due to mercury vapor exposure in genetically susceptible mice. Toxicol App Pharmacol. 1995; 132(2): 299-309.

121. Bagentose LM, et al. Mercury induced autoimmunity in humans. Immunol Res. 1999; 20(1): 67-78.

122. 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.

123. Hu H, Moller G, Abedi-Valugerdi M. Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in vitro. J Autoimmun. 1997; 10(5): 441-6.

124. 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. 96(3): 348-57.

125. HultmanP, Johansson U, Turley SJ. Adverse immunological effects and autoimmunit induced by dental amalgam in mice. FASEB J. 1994; 8: 1183-90.

126. 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.

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

128. Hultman P, et al. Adverse immunological effects and immunity induced by dental amalgam. FASEB J. 1994; 8: 1183-1190.

129. Robbins SM, Quintrell NA, Bishop JM. Mercuric chloride activates the Src-family protein tyrosine kinase, Hck in myelomonocytic cells. Eur J Biochem. 2000; 267(24): 7201-8.

130. Daum R. Immunotoxicology of mercury and cadmium on B-lymphocutes. Int J Immunopharmacol. 1993; 15(3): 383-94.

131. Johansson U, Hansson-Georgiadis H, Hultman P. The genotype determines the B cell response in mercury-treated mice. Int Arch Allergy Immunol. 1998; 116(4): 295-305.

132. Eggleston DW. Effect of dental amalgam and nickel alloys on T-lympocytes. J Prosthet Dent. 1984; 51(5): 617-623.

133. Perlingeiro RC, et al. Polymorphonuclear phagentosis in workers exposed to mercury vapor. Int J Immounopharmacology. 1994; 16(12): 1011-7.

134. Pelletier, et al. Autoreactive T cells in mercury induced autoimmune disease. J Immunol. 1986; 137(8): 2548-54.

135. Kubicka M, et al. Autoimmune disease induced by mercuric chloride. Int Arch Allergy Immunol. 1996; 109(1): 11-20.

136. Shenker BJ. Low-level MeHg exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial dysfunction. Environ Res. 1998; 77(2): 149-159.

137. Insug O, 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.

138. Kostler W. Beeinflubung der zellularen immunabwehr drch quecksilberfreisetzung. Forum Prakt. Allgem. Arzt. 1991; 30(2): 62-3.

139. Veprintsev DB. Pb2+ and Hg2+ binding to alpha-lactalbumin. Biochem Mol Biol Int. 1996; 39(6): 1255-65.

140. Busselberg D. Calcium channels as target sites of heavy metals. Toxicol Lett. 1995; 82-83: 255-61.

141. Rajanna B, et al. Modulation of protein kinase C by heavy metals. Toxicol Lett. 1995; 81(2-3): 197-203.

142. Melchart D, Wuhr E, Weidenhammer W, Kremers L. A multicenter survey of amalgam fillings and subjective complaints in non-selected patients in the dental practice. Eur J Oral Sci. 1998; 106: 770-77.

143. Ziff MF. Documented clinical side effects to dental amalgams. Adv. Dent. Res. 1992; 1(6): 131-134.

144. Ziff S. Dentistry without Mercury. 8th ed. Bio-Probe, Inc; 1996.

145. Berglund F. Case Reports Spanning 150 years on the Adverse Effects of Dental Amalgam. Orlando, FL: Bio-Probe; 1995.

146. Davis M, ed. Defense Against Mystery Syndromes. Chek Printing Co; 1994.

147. Berglund F, et al. Improved health after removal of dental amalgam fillings. Heavy Metal Bulletin. 1996; 3.

148. Klock B, Blomgren J, Ripa U, Andrup B. Effekt av amalgamavl ägsnande på patienter som misst änker att de lider eller har lidit av amalgamf örgiftning. Tandl ä kartidn. 1989; 81(23): 1297-1302.

149. Engel P. Beobachtungen uber die gesundheit vor und nach amalgamentfernug, separatdruck aus schweiz. Monatsschr Zahnm. 1998; 108(8).

150. Lichtenberg HJ. Elimination of symptoms by removal of dental amalgam from mercury poisoned patients. J Orthomol Med. 1993; 8: 145-148.

151. Lichtenberg H. Symptoms before and after proper amalgam removal in relation to serum-globulin reaction to metals. J Orthomol Med. 1996; 11(4): 195-203.

152. Strassburg M, et al. Generalized allergic reaction from silver amalgam fillings. Dtsche Zahnarztliche Zeit. 1967; 22: 3-9.

153. Hall G. V-TOX, mercury levels excreted after vit C IV as chelator by number of fillings. Heavy Metal Bulletin. 1993; 3(1): 6-8.

154. Malt UF, et al. Physical and mental problems attributed to dental amalgam fillings. Psychosomatic Medicine. 1997; 59: 32-41.

155. Tanchyk AP. Amalgam removal for treatment of arthritis. Gen Dent. 1994; 42(4): 354.

156. Shtelmakh NI, et al. Comparative treatments of rheumatoid arthritis. Vrasch. Delo. 1982; (1): 49-52.

157. Siblerud RL, et al. Evidence that mercury from silver fillings may be an etiological factor in multiple sclerosis. Sci Total Environ. 1994; 142(3): 191.

158. Siblerud RL, Kienholz E. Evidence that mercury from dental amalgam may cause hearing loss in multiple sclerosis patients. J. Orthomol. Med. 1997; 12(4): 240-4.

159. Huggins HA, TE Levy. Cerebrospinal fluid protein changes in MS after Dental amalgam removal. Alternative Med Rev. 1998; 3(4): 295-300.

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

161. Dorffer U. Anorexia hydragyra. Monatsschr. Kinderheilkd. 1989; 137(8): 472.

162. Geier MR, Geier DA. Timerosal in childhood vaccines, neurodevelopmental disorders, and heart disease in the U.S. J of Amer Physicians and Surgeons. 2003; 8(1).

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

164. Mayes MD. Epidemiologic studies of environmental agents and systemic autoimmune diseases. Environ Health Perspect. 1999; 107(5): 743-8.

165. Bigazzi PE. Metals and kidney autoimmunity. Environ Health Perspect. 1999; 107(5): 753-65.

166. 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.

167. Kurup RK, Kurup PA. Hypothalamic digoxin, cerebral chemical dominance, and regulation of gastrointestinal/hepatic function. Int J Neurosci. 2003; 113(1): 75-105.

168. Kumar AR, Kurup PA. Hypothalamic digoxin and irritable bowel syndrome. Indian J Gastroenterol. 2001; 20(5): 173-6.

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

170. Kumar AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase activity: a common pathway in central nervous system disorders. J Assoc Physicians India. 200; 50: 400-6.

171. Hide I. Mechanism of production and release of tumor necrosis factor implicated in inflammatory diseases. Nippon Yakurigaku Zasshi. 2003; 121(3): 163-73.

172. 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; 48(6): 1504-12.

173. Lee JY, Yoo JM, Cho BK, Kim HO. Contact dermatitis in Korean dental technicians. Contact Dermatitis. 2001; 45(1): 13-6.

174. Kanerva L, Lahtinen A, Toikkanen J, et al. Increase in occupational skin diseases of dental personnel. Contact Dermatitis. 1999; 40(2): 104-8.

175. Lonnroth EC, et al. Adverse health reactions in skin, eyes, and respiratory tract among dental personnel in Sweden. Swed Dent J. 1998; 22(1-2): 33-45.

176. Muller M, Westphal G, Vesper A, Bunger J, Hallier E. Inhibition of the human erythrocytic glutathione-S-transferase T1 (GST T1) by thimerosal. Int J Hyg Environ Health. 2001; 203(5-6): 479-81.

177. Lutz W, Tarkowski M, Nowakowska E. Genetic polymorphism of glutathione s-transferase as a factor predisposing to allergic dermatitis. Med Pr. 2001; 52(1): 45-51.

178. Watzl B, Abrahamse SL, Treptow-van Lishaut S, et al. Enhancement of ovalbumin-induced antibody production and mucosal mast cell response by mercury. Food Chem Toxicol. 1999; 37(6): 627-37.

179. 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.

180. Bhattacharya S, Sen S, et al. Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction. Biometals. 1997; 10(3): 157-62.

181. Anner BM, Moosmayer M, Imesch E. Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism. Am J Physiol. 1992; 262(5.2): F830-6.

182. Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol. 1992; 262(5.2): F84308.

183. 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; 271(4.2): F926-30.

184. 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.

185. Hussain S, 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; 32(3): 395-409.

186. Bulat P. Activity of Gpx and SOD in workers occupationally exposed to mercury. Arch Occup Environ Health. 1998; 71: S37-9.

187. Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of metal ions. Free Radic Biol Med. 1995; 18(2): 321-36.

188. Jay D. Glutathione inhibits SOD activity of Hg. Arch Inst Cardiol Mex. 1998; 68(6): 457-61.

189. 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; 36(4): 489-99.

190. 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; 60(4): 838-46.

191. 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; 36(5): 687-97.

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

193. van Benschoten MM. Acupoint energetics of mercury toxicity and amalgam removal with case studies. American Journal of Acupuncture. 1994; 22(3): 251-262.

194. 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; 273(32): 20354-62.

195. 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. 1999; 274: 7528-7536.

196. 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; 273(26): 16521-6.

197. Dbaibo GS, El-Assaad W, et al. Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death. FEBS Lett. 2001; 503(1): 7-12.

198. Liu B, Hannun YA, et al. Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell death. J Biol Chem. 1998; 273(18): 11313-20.

199. 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; 19(2): 101-5.

200. Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production but activates pro-inflammatory cytokine expression in murine macrophage: differential modulation of NF-kappaB and p38 MAPK signaling pathways. Nitric Oxide. 2002; 7(1): 67-74.

201. 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.

202. 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; 23(2): 180-92.

203. Rodgers JS, Hocker JR, et al. Mercuric ion inhibition of eukaryotic transcription factor binding to DNA. Biochem Pharmacol. 2001; 61(12): 1543-50.

204. Hansen K, et al. A survey of metal induced mutagenicity in vitro and in vivo. J Amer Coll Toxicol. 1984; 3: 381-430.

205. Aschner M, et al. Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury vapor. Brain Research. 1997; 778(1): 222-32.

206. 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.

207. Bucio L, et al. Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line. Mutat Res. 1999; 423(1-2): 65-72.

208. Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002; 70(5): 694-702.

209. Nicole A, et al. Direct evidence for glutathione as mediator of apoptosis in neuronal cells. Biomed Pharmacother. 1998; 52(9): 349-55.

210. Spencer JP, et al. Cysteine and GSH in PD, mechanisms involving ROS. J Neurochem. 1998; 71(5): 2112-22.

211. Bains JS, et al. Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death. Brain Res Rev. 1997; 25(3): 335-58.

212. 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; 36(11): 1179-84.

213. Lu SC, Regulation of hepatic glutathione synthesis: Current concepts and controversies. FASEB J. 1999; 13(10): 1169-83.

214. Zulups RK, et al. Nephrotoxicity of inorganic mercury co-administered with L-cysteine. Toxicology. 1996; 109(1): 15-29.

215. Perry TL, et al. Hallevorden-Spatz disease: Cysteine accumulation and cysteine dioxygenase deficiency. Ann Neural. 1985, 18(4): 482-489.

216. 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.

217. 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.

218. Leigh PN. Pathologic mechanisms in ALS and other motor neuron diseases. In: Calne DB, ed. Neurodegenerative Diseases. WB Saunder Co; 1997: 473-88.

219. 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; 60(4): 838-46.

220. 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; 36(5): 687-97.

221. Langworth, et al. Effects of low exposure to inorganic mercury on the human immune system. J Work Environ Health. 1993; 19(6): 405-413.

222. Kerkhoff H, Troost D, Louwerse ES. Inflammatory cells in the peripheral nervous system in motor neuron disease. Acta Neuropathol. 1993; 85: 560-5.

223. Appel Sh, Smith RG. Autoimmunity as an etiological factor in amyotrophic lateral sclerosis. Adv Neurol. 1995; 68: 47-57.

224. 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; 100(4): 238-43.

225. Appel SH, Stockton-Appel V, Stewart SS, Kerman RH. Amyotrophic lateral sclerosis: Associated clinical disorders and immunological evaluations. Arch Neurol. 1986; 43(3): 234-8.

226. 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; 49(5): 1289-92.

227. 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; 25(1): 98-102.

228. 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; 114(3): 428-37.

229. Arnett FC, Fritzler MJ, Ahn C, Holian A. Urinary mercury levels in patients with autoantibodies to U3-RNP (fibrillarin). J Rheumatol. 2000; 27(2): 405-10.

230. Luster MI, Boorman GA, Jameson CW, Dean JH, Cox JW. Immunological and biochemical responses in mice treated with mercuric chloride. Toxicol App Pharmacol. 1983; 68(2): 218-228.

231. Kusaka Y. Occupational diseases caused by exposure to sensitizing metals. Sangyo Igaku. 1993; 35: 75-87.

232. Parnham M, Blake D. Antioxidants as antirheumatics. Agents Actions. 1993; 44: 189-95.

233. Karatas GK, Tosun AK, Karacehennem E, Sepici V. Mercury poisoning: An unusual cause of polyarthritis. Clin Rheumatol. 2002; 21(1): 73-5.

234. Bigazzi PL. Autoimmunity induced by metals. In: Chang L, ed. Toxicology of Metals. Lewis Publishers, CRC Press Inc; 1996: 835-52.

235. Robinson CJG, et al. Mercuric chloride induced antinuclear antibodies in mice. Toxic App Pharmacology. 1986; 86: 159-169.

236. Andres P. IgA-IgG disease in the intestines of rats ingesting HgCl. Clin Immun Immunopath. 1984; 30: 488-494.

237. Cossi, et al. Beneficial effect of human therapeutic IV-Ig in mercury induced autoimmune disease. Clin Exp Immunol. 1991.

238. 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.

239. Ganser, AL; Kirschner, DA. The interaction of mercurials with myelin: Comparison of in vitro and in vivo effects. Neurotoxicol. 1985; 6(1): 63-77.

240. Windebank AJ. Specific inhibition of myelination by Lead in vitro: Comparison with arsenic, thallium, and mercury. Exp Neurol. 1986; 94(1): 203-12.

241. Casspary EA. Lymphocyte sensitization to basic protein of brain in multiple sclerosis and other neurological diseases. J Neurol Neurosurg Psychiatry. 1974; 37: 701-3.

242. el-Fawal HA, Gong Z, Little AR. Exposure to methylmercury results in serum autoantibodies to neuro typic and gliotypic proteins. Neurotoxicol. 1996; 17: 267-76.

243. Schwyzer RU, Henzi H. Multiple sclerosis: Plaques caused by 2-step demyelization? Med Hypothesis. 1983; 12: 129-42.

244. 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.

245. Wilder RL. Neuroendocrine-immune system interactions and autoimmunity. Annu Rev Immunol. 1995; 13: 307-38.

246. Earl C, Chantry A, Mohammad N. Zinc ions stabilize the association of basic protein with brain myelin membranes. J Neurochem. 1988; 51: 718-24.

247. Riccio P, Giovanneli S, Bobba A. Specificity of zinc binding to myelin basic protein. Neurochem Res. 1995; 20: 1107-13.

248. 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: 835-52.

249. 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; 1586(2): 155-68.

250. Kobayashi MS, Han D, Packer L. Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Free Radic Res. 2000; 32(2): 115-24.

251. Bridi R, Crossetti FP, Steffen VM, Henriques AT. The antioxidant activity of standardized extract of Ginkgo biloba (EGb 761) in rats. Phytother Res. 2001; 15(5): 449-51.

252. Packer L, Tritschler HJ, Wessel K. Neuroprotection by the metabolic antioxidant alpha-lipoic acid. Free Radic Biol Med. 1997; 22(1-2): 359-78.

253. McCarty MF. Versatile cytoprotective activity of lipoic acid may reflect its ability to activate signaling intermediates that trigger the heat-shock and phase II responses. Med Hypotheses 2001 Sep; 57(3):313-7

254. 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; 379(1): 74-6.

255. Gregus Z, et al. Effect of lipoic acid on biliary excretion of glutathione and metals. Toxicol APPl Pharmacol. 1992; 114(1): 88-96.

256. Danielsson BRG, et al. Ferotoxicity of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus. Biol Res Preg Perinatal. 1984; 5(3): 102-109.

257. 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.

258. Knapp LT, Klann E. Superoxide-induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem. 2000.

259. Jenner P. Oxidative mechanisms in PD. Mov Disord. 1998; 13: 24-34.

260. Rajanna B, et al. Modulation of protein kinase C by heavy metals. Toxicol Lett. 1995; 81(2-3): 197-203.

261. 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; 272(51): 32411-8.

262. Rasmussen HH, Mortensen PB, Jensen IW. Depression and magnesium deficiency. Int J Psychiatry Med. 1989; 19(1): 57-63.

263. 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.

264. 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.

265. 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; 55 (3): 239-41.

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

267. Levy TE, Huggins HA. Routine dental extractions routinely produce cavitations. J Adv Med. 1996; 9(4).

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

269. Mutter J, et al. Alzheimer’s disease: Mercury as pathogenetic factor and apolipoprotein E as a moderator. Neuroendocrinology Letters. 2004; 5: 331–339.

270. Heintze, et al. Methylation of mercury from dental amalgam and mercuric chloride by oral Streptococci. Scan. J. Dent. Res. 1983, 91: 150-152.

271. Rowland, Grasso, Davies. The methylation of mercuric chloride by human intestinal bacteria. Experientia. Basel. 1975; 31: 1064-1065.

272. Hamdy MK, et al. Formation of methyl mercury by bacteria. App Microbiol. 1975.

273. 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; 47(1): 23-9.

274. Ludwicki JK. Studies on the role of gastrointestinal tract contents in the methylation of inorganic mercury compounds. Bull Env Contam Toxicol. 1989; 42: 283-288.

275. Choi SC, Bartha R. Cobalamin-mediated mercury methylation by desulfovibrio desulfuricans LS. Appl Environ Microbiol. 1993; 59(1): 290-5.

276. Wang J, Liu Z. In vitro study of strepcoccus mutans in the plaque on the surface of amalgam fillings on the conversion of inorganic mercury to organic mercury. Shanghai Kou Qiang Yi Xue. 2000; 9(2): 70-2.

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

278. Leistevuo J, et al. Dental amalgam fillings and the amount of organic mercury in human saliva. Corks Res. 2001; 35(3): 163-6.

279. Walsh SJ, Rau LM. Autoimmune disease overlooked as a leading cause of death in women. Am J Public Health. 2000; 90: 1463-1466.

280. Sellars WA, Sellars R. Methyl mercury in dental amalgams in the human mouth. Journal of Nutritional & Environmental Medicine. 1996; 6(1): 33-37.

281. 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.

282. Pelletier et al, Autoreactive T cells in mercury induced autoimmune disease. J Immunol. 1986; 137(8): 2548-54.

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

284. McKeever P, et al. Patterns of antigenic expression in human glioma cells. Crit Rev Neurobiology. 1991; 6: 119-147.

285. Sterzl I, Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with polyglandular activation of autoimmunity. Vnitrni Lekarstvi. 1998; 44: 456-60.

286. Sterzl I, Hrda P, Prochazkova J, Bartova J. Reactions to metals in patients with chronic fatigue and autoimmune endocrinopathy. Vnitrni Lekarstvi. 1999; 45(9): 527-31.

287. Kolenic J, Palcakova D, Benicky L, Kolenicova M. The frequency of auto-antibody occurrence in occupational risk (mercury). Prac Lek. 1993; 45(2): 75-77.

288. Stejskal V, Hudecek R, Mayer W. Metal-specific lymphocytes: risk factors in CFS and other related diseases. Neuroendocrinology Letters. 1999; 20: 289-298.

289. MacDonald EM, Mann AH, Thomas HC. Interferons as mediators of psychiatric morbidity. Lancet. 1978: 1175-78.

290. Hickie I, Lloyd A. Are cytokines associated with neuropsychiatric syndrome in humans? Int J Immunopharm. 1995; 4: 285-294.

291. Komaroff AL, Buchwald DS. Chronic fatigue syndrome: An update. Ann Rev Med. 1998; 49: 1-13.

292. Buchwald DS, Wener MH, Kith P. Markers of inflammation and immune activation in CFS. J Rheumatol. 1997; 24: 372-76.

293. 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.

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

295. Ng TB, Liu WK. Toxic effect of heavy metals on cells isolated from the rat adrenal and testis. In Vitro Cell Dev Biol. 1990; 26(1): 24-8.

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

297. Ionescu G. Heavy metal load with atopic dermatitis and psoriasis. Biol Med. 1996; 2: 65-68.

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

299. Enestrom S, et al. Does amalgam affect the immune system? Int Arch Allergy Immunol. 1995; 106: 180-203.

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

301. Siblerud RL. A comparison of mental health of multiple schlerosis patients with silver dental fillings and those with fillings removed. Psychol Rep. 1992; 70(3.2): 1139-51.

302. Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD. Beneficial effect of amalgam replacement on health in patients with autoimmunity. Neuroendocrinology Letters. 2004; 25(3): 211-8.

303. Šterzl I, Procházková J, Hrdá P, Matucha P, Bártová J, Stejskal VDM. Removal of dental amalgam decreases anti-TPO and anti-Tg autoantibodies in patients with autoimmune thyroiditis. Neuroendocrinology Letters. 2006, 27(1): 25-30.

304. Pigatto PD, Guzzi G, Persichini P. Nummular lichenoid dermatitis from dental amalgam. Contact Dermatitis. 2002; 46: 355-6.

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

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