Immune Reactive Conditions: The Mercury Connection to Inflammatory & Immune Reactive Conditions

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Increasing Incidence of Inflammatory, Immune Reactive Conditions

The incidence of allergic and immune reactive conditions, such as allergies, asthma, lupus, and allergic contact disease has been increasing rapidly in the United States over the last decade.
The prevalence of asthma doubled over the last decade to approximately 31 million (11.5% of the total population). At least 50 million have allergies (19%), and the largest increase has been in infants, with approximately 10% of infants—approximately 15 million in the U.S. with systemic eczema. Approximately 12% have had chronic sinusitis.

Inflammation has been found to be a major factor in many chronic health conditions, including cardiovascular problems, diabetes, arthritis, depression, osteoporosis, periodontal disease, joint stiffness, chronic fatigue, fibromyalgia, age-related immune dysfunction, etc. Many studies have found exposure to mercury and other heavy metals to be common causes of such conditions.

Oral Metal Exposures from Dental Materials and Oral Effects

Exposure to metals has been found to be one of the most common causes of allergic contact diseases (ACD) and other allergic and immune reactive conditions. One of the largest sources of exposure to the metals that commonly causes inflammatory, immune reactive conditions is from dental metals. Having dissimilar metals in the teeth, e.g. amalgam (mercury, copper, tin, silver), gold alloys (gold, palladium), nickel or stainless steel crowns(nickel, cobalt), causes galvanic electrical currents and much higher mercury vapor levels in oral air and metal levels in oral tissues.

Government agencies and medical studies have found that the largest source of mercury exposure in most people is from dental amalgam fillings. For those with amalgam dental fillings, exposure from fillings amounts to 50 to 90 % of exposure, with the average being about 75 % of total exposure. Mercury is an unusual metal because it is commonly a liquid at room temperature and vaporizes to a gas from its liquid or solid states. Studies found that mercury amalgams are unstable due to mercury’s vaporization and galvanic action, leaking mercury vapor continuously into the lungs and saliva at levels exceeding government health standards. Dental amalgam is also a major source of methylmercury exposure for many since oral and intestinal mercury is methylized by oral bacteria and other methyl donors. The other most common sources of mercury exposure are methylmercury from fish or mercury thimerosal from vaccines, which is a major source of exposure mostly for infants or those frequently receiving flu shots.

The amount of mercury released into saliva has been found by large studies to be about 1.5 to 1.9 micrograms per liter for each additional amalgam filling, resulting in an increase of about 1 microgram per liter in urine and even higher levels excreted in feces. Average mercury levels in gum tissue near amalgam fillings are over 100 ppm and are the result of mercury flow into the mucous membrane because galvanic currents with the mucous membrane serve as cathodes and amalgam metals serve as anodes. Concentrations of mercury in oral mucosa for a population of patients with 6 or more amalgam fillings taken during oral surgery were 20 times the level of controls. Amalgam also releases significant amounts of silver, tin, and copper, which also have toxic effects, with organic tin compounds formed in the body being even more neurotoxic than organic mercury.

Mercury and other metals accumulate in the oral cavity in fibroblasts, macrophages, and multinuclear giant cells of connective tissue, in blood vessel walls, along nerve sheath fibers, in basement membranes of mucosal epithelium, striated muscle fibers, along collagen bundles and elastic tissue, in acini of salivary glands, and in tooth roots and jaw bones. Such mercury including that in the commonly formed amalgam tattoos moves to other parts of the body over time in significant amounts and more rapidly than the other metals. Macrophages remove mercury by phagocytosis and the mercury moves to other parts of the body through the blood and along nerves. Oral galvanism—where electric currents caused by mixed metals in the mouth take the metals into the gums and oral mucosa—results in accumulating mercury and other dental metals at the base of teeth with large amalgam fillings or metal crowns over amalgam base. Such metals are documented to cause local and systemic lesions and health effects such as inflamed tissues, metal mouth, burning mouth, discomfort, tooth pain, gingivitis, oral lichen planus, and orofacial granulomatosis. Most usually improve from these conditions after removal of amalgam fillings and/or the amalgam tattoos by surgery. The high levels of accumulated mercury also are dispersed to other parts of the body. Some studies have also found persons with chronic exposure to electromagnetic fields (EMF) to have higher levels of mercury exposure and excretion. Such fields are known to induce current in metals and would increase the effects of galvanism.

Mechanisms by Which Mercury & Heavy Metals Cause Chronic Inflammatory Conditions

Metals like mercury bind to SH-groups (sulfhydryl) in sulfur compounds like amino acids and proteins, changing the structure of the compound that it is attached to. This often results in suppression of the immune system and in the immune systems T-cells not recognizing them as appropriate nutrients and attacking them with chronic exposure resulting in autoimmunity. Such binding and autoimmune damage has also been documented in collagen. 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 cause aberrant MHC II expression on altered target cells.

Mercury and other toxic metals cause release of inflammatory cytokines such as Tumor Necrosis Factor-alpha (TNFa), Interleukin-8, Interleukin-4, which are factors in the chronic inflammatory conditions, including asthma, lupus, rheumatoid arthritis, Scleroderma, celiac and Crohn’s disease, etc. Studies have demonstrated that low concentrations of mercury (HgCl2, i.e. 10(-9)-10(-15) M) significantly enhanced chemiluminescence, as well as stimulated H2O2 production by polymorphonuclear leukocytes. These studies clearly demonstrate the ability of extremely low levels of HgCl2 not only to suppress various PMN leukocyte functions involved in host defense but also to stimulate reactive oxygen metabolism. In vivo, these HgCl2 effects would not only compromise host defense but also promote tissue injury via the local production of reactive oxygen metabolites. This has been demonstrated to increase effects of factors in cardiovascular disease and neurological disease. Melatonin, vitamin E, and vitamin C have been found to counter these adverse effects. Theaflavins from black tea, EGCG from green tea, and curcumin have also been found effective at inhibiting inflammatory effects.

HgCl2 induces a protein kinase C-dependent Ca2+ influx through L-type calcium channels. The calcium/calcineurin-dependent pathway and protein kinase C activation are both implicated in HgCl2-induced IL-4 gene expression, and HgCl2 can activate directly the protein kinase C, which is one of the main intracellular targets for HgCl2. Inorganic mercury exposure results in T cell polyclonal activation and the expansion of pathogenic autoreactive anti-class II Th2 cells. These cells produce interleukin (IL)-4 and induce a B cell polyclonal activation that is responsible for autoimmune disease. These effects of HgCl2 appear to be independent of antigen-specific recognition. Mercury from amalgam fillings has also been documented to cause proliferation of the inflammatory cytokine IL-8. IL-8 is responsible for much of the acute inflammation in inflammatory conditions such as asthma, gum disease, inflammatory bowel disease (IBS), etc. Theaflavins from black tea have been found to block such effects of IL-8 and C-reactive protein (CFP) and to have beneficial effects for many inflammatory conditions, including asthma, gum disease, IBS, strokes, pancreatitis, colitis, cancer, cardiovascular disease, etc.

Supplemented patients also show significantly reduced levels of the inflammation-generating transcription factor NFkB, the cytokine-generating enzyme COX-2, and the adhesion molecule ICAM-1. Digestive problems are common and increase with aging, as generation of enzymes necessary for proper digestion decline and proliferation of pathogenic biological agents in the intestines increases. Such problems often decrease absorption of minerals and nutrients and cause increases in inflammatory processes. Supplementing with digestive enzymes and enteric coated probiotics such as bacillus coagulans have been found to offer significant improvement in inflammatory conditions such as rheumatoid arthritis, IBS, Crohn’s disease, influenza, etc.

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, nickel, aluminum, and other toxic metals are 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 red blood cell (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 and toxic metals are common causes of these conditions. Also, they have synergistic effects.

A study found that 39% of a group of Crohn’s disease patients tested were immune reactive to nickel. Nickel is the most common cause of ACD, approximately 20% of total. Nickel (Ni), chromium (Cr), and cobalt (Co), as ions and compounds, are well recognized skin sensitizers. Cobalt positive reactions are associated with nickel sulfate and/or potassium dichromate sensitivity. In 2594 subjects, Co sensitivity was seen in association with positive reactions to Ni and Cr in 95.2% of cases. Patients tested to Co, Cr, and Ni, sensitized to any one of the metals, had significantly higher odds of sensitization to an additional metal.

Gold was found to be the sixth most frequent cause of positive patch test reactions in the U.S. Similar prevalence was observed in Europe and Japan. In a large Swedish study, 8.6% of 832 patients with suspected contact allergy on routine patch testing gave a positive response with gold sodium thiosulfate (GST). Other patients with contact allergy to GST also gave positive reactions to potassium dicyanoaurate, but were negative to gold sodium thiomalate (GSTM) and metallic gold. These findings were confirmed by another group of investigators, who found that 4.6% of 278 patients in United Kingdom had positive reactions to GST on routine testing. All of these patients were females, with a mean age of 37 years and most frequent site of eczema was the head and neck. In Japan, 8.4% of 653 patients tested from 1990 to 2001 showed a positive reaction to gold chloride, and significantly more women (10.2%) than men (0.8%) reacted. A study by Bruze, et al. reported that a large percentage was long-lasting, and 35% developed late reactions. In a number of cases, positive test sites were seen to remain negative after 3 days, but to turn positive by day 7. These findings emphasize the necessity of a second patch test reading at a distance of 1 week, at least.

Gold salt therapy, restorative materials in dentistry, orthopedic appliances, and jewelry are the most accepted causes for Au ACD. Medical practitioners have long recognized the adverse effects, including ACD, in the risk-benefit of the usage of Au in anti-inflammatory therapy. In particular, an increasing incidence of delayed skin reactions has been noted since the introduction of GST and GSTM in the treatment of rheumatoid arthritis. Allergy to Au was seen in more than 50% of patients so treated, as indicated by patch testing with GSTM. Patients developed dermatitis, stomatitis, and eosinophilia, and less commonly immune complex glomerulonephritis, lymphadenopathy, antinuclear antibody, increased serum IgE, and other blood disorders.

Gold-based dental restoration appeared to be an important risk factor for Au ACD. Several authors have found that a positive patch test to Au is significantly correlated with Au dental restorations. The saliva may slowly dissolve Au and transport it through the mucous membranes into the bloodstream, and the amount of dental Au has been found to be correlated qualitatively and quantitatively to the blood level of Au. Oral lichenoid mucositis, clinically and histologically similar to oral lichen planus, was observed at sites directly adjacent to Au dental restorations.

A study of Yiannias, et al. retrospectively reviewed 46 patients with oral lichenoid lesions who had also been patch tested; 2 patients who were sensitized only to Au showed marked clinical improvement with removal of their dental Au restorations. Hypersensitivity to Au has been reported in students involved in the manufacture of prosthetic materials in a dental clinic in Japan, and 3 of 12 individuals tested had positive reactions to sodium thiosulfatoaurate. Moreover, implanting an Au-plated stent seemed to represent a risk of sensitizing the patients to Au. In the stent, 45.5% of patients had a contact dermatitis to Au; while in the control group, 20.0% of subjects reacted, and this difference was significant.

Lymphocyte proliferation in vitro shows good correlation to allergic epicutaneous test reactions to Au. There are several reports on palladium (Pd) sensitivity associated with exposure to Pd containing dental restorations. Symptoms observed included signs of contact dermatitis, stomatitis, mucositis, and oral lichen planus. General symptoms like swelling of the lips and cheeks, dizziness, asthma, chronic urticaria, and other symptoms have also been reported. In some case reports, patients’ complaints disappeared after replacement with Pd-free or metal-free constructions. Another aspect of Pd2+ sensitization is its frequent specific cross-sensitization with nickel. During a 10-year period, the trend of sensitization to Pd in a clinic population increased to a maximum of 9.7% in the year 2000, with a higher percentage in females than in males. Of Pd-sensitized patients, 40.5% complained of hand dermatitis, 47.4% complained of body dermatitis, and 1.7% complained of burning mouth syndrome. The similarities in chemistry of Ni2+ and Pd2+ support the idea of a similar mechanism involving common protein binding sites and conformational alterations. A study with 10,000 participants tested with about 25 allergens confirmed that of all patients 5.4% reacted to palladium dichloride alone, whereas all other patients also had a positive reaction to nickel sulphate. There are also reports of allergic reactions from non-dermatological causes such as glasses frames.

Titanium has also been found to be a common immune sensitizer. It has been proposed that the optimized version of LLT, i.e., MELISA, had a greater potentiality in diagnosing hypersensitivity to Ti. In a recent study, 56 patients chronically exposed to Ti via dental or endoprosthetic implants presented clinical symptoms and were subjected to the MELISA test against 10 metals, including Ti. Of the 56 patients tested, 21 (37.5%) were positive to Ti. On the contrary, when patients were patch-tested, all resulted to be negative to Ti. Following removal of the implants, patients showed remarkable clinical improvement.

Studies have also found mercury and lead cause autoantibodies to neuronal proteins and neurofilaments. The thymus gland plays a significant part in the establishment of the immune system and lymphatic system from the 12th week of gestation until puberty. Inhibition of thymus function can thus affect proper development of the immune and lymphatic systems. Lymphocyte differentiation, maturation, and peripheral functions are affected by the hormone thymulin. Mercury at very low concentrations has been seen to impair some lymphocytic functions, causing subclinical manifestations in exposed workers. Animal studies have shown mercury significantly inhibits thymulin production at very low micromolar levels of exposure. The metal allergens mercuric chloride and nickel sulfate were found to stimulate DNA synthesis of both immature and mature thymocytes at low levels of exposure, so chronic exposure can have long-term effects. Nickel in stainless steel braces and crowns is a source of reactivity and autoimmunity along with gold and palladium in crowns. Also, micromolar levels of mercuric ions specifically blocked synthesis of ribosomal RNA, causing fibrillarin relocation from the nucleolus to the nucleoplasm in epithelial cells as a consequence of the blockade of ribosomal RNA synthesis. This appears to be a factor in deregulation of basic cellular events and in autoimmunity caused by mercury.

There were specific immunotoxic and biochemical alterations in lymphoid organs of mice treated at the lower doses of mercury. The immunological defects were consistent with altered T-cell function as evidenced by decreases in both T-cell mitogen and mixed leukocyte responses. Mercury caused increased immune-reactivity for glial fibrillary protein at 1 nanamole (0.2 ppb) concentration and microglial response at even lower levels. There was a particular association between the T-cell defects and inhibition of thymic pyruvate kinase, the rate-limiting enzyme for glycolysis. Pyruvate and glycolysis problems are often seen in mercury toxic children being treated for autism. 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, leading to metabolic damage and increased food sensitivity. Inorganic mercury was found to be a cause of systemic eczema and digestive problems by Japanese study

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, 13 % were sensitive to mercury. The mercury sensitized students were found to have more than average number of amalgam fillings, higher hair 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 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. 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.

The 1998–2000 North American Contact Dermatitis Group (NACDG) data base reported thiomersal to have a definite or probable relevance in 2.9% of the patients with a positive patch test. Thiomersal may be found in topical medications, especially ophthalmic and nasal preparations, cosmetics, and as a preservative in vaccines and contains organic Hg and thiosalicylate. Positive patch test reactions to one or both the constituents of thiomersal have been frequently encountered. Thiomersal resulted to be the fifth most common allergen in patients. The main target of autoantibodies is the ribonucleoprotein fibrillarin, which may also be a target in scleroderma patients. Mercuric chloride causes antifibrillarin antibodies and immune complex glomerulonephritis in susceptible mouse strains. Antifibrillarin antibodies occur in a subset of scleroderma patients and preliminary evidence suggests that mercury levels may be higher in this group of individuals.

Positive responses to phenylmercury, a bactericidal agent in root fillings and in pharmaceutical preparations, were also noted in the oral lichen group but not in the control groups. Thus, low-grade chronic exposure to Hg may induce a state of systemic sensitization as verified by Hg-specific lymphocyte reactivity.

Wöhrl, et al. suggested that a high percentage (15.2%) of children sensitized to copper (Cu) was due to the increased use of this metal in dental amalgam. In the same way, a woman developed Cu ACD of the oral mucosa caused by the long-term exposure to Cu enriched dental amalgam fillings. Houger, et al. observed a relationship between intraoral metal ACD (i.e., mucositis) and pathogenesis of squamous cell carcinoma. Because of this high prevalence, Cu was considered an additional risk factor in the evolution of cancer. Additionally, a case of a woman with lesions of oral lichen planus due to the Cu contained in her prosthesis has been reported. The change of the prosthesis made the lesions improved. In light of the possible Cu-Ni cross-sensitization, it is unsafe to suggest covering nickel goods with a layer of Cu to protect individuals allergic to Ni. In 30 patients known to be contact sensitive to Ni but patch-test negative to Cu, the severity of patch test reaction to a Cu/Ni mixture was greater (p 0.001) than to Ni alone, suggesting that ions enhanced the sensitivity reaction to Ni.

Allergic contact eczema is the most frequent occupational disease, and the most common cause of contact eczema is exposure to metals. The metals most commonly causing allergic immune reactivity are nickel, mercury, copper, chromium, cobalt, and palladium. 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.

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 1-10 months. Similar results have been obtained at other clinics.

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 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. 16.3% were immune reactive to mercury.

In asthma allergen related T-lymphocytes cause release of inflammatory mediators from mast cells, esinophils, and lymphocytes, along with inflammatory cytokins such as Interleulin-4(Il-4), TNF-alpha, histamine, and increased IgE. It has also been documented that the majority of cases have decreased serum magnesium levels, decreased NA+K+ATPase levels, and increased digoxin levels (an inhibitor of NA+K+ATPase). Mercury exposure has been documented to cause an increase in inflammatory cytokines such as TNF-alpha and IL-4. TNFA-alpha has been found to increase the Ca(2+) sensitivity of agonist-stimulated phosphorylation and contractility in airway smooth muscle (ASM) and increase airway hyper-responsiveness. TNFa levels have also been found to be significantly correlated to levels of the inflammatory cytokines Il-4, Il-8, and Il-13 released from histamine-containing basophils, which results in histamine releases and increased IgE levels, as well as airway reactivity and asthmatic attacks. The release of these inflammatory cytokines has also been shown to be a factor in mercury’s inducement of autoimmunity that is involved in the development of airway inflammation.

Asthmatic patients are especially susceptible to air pollution. Upon contact with an allergen, sensitized mast cells release highly active pro-inflammatory mediators. Allergen-mediated mast cell activation is an important mechanism in the pathogenesis of atopic asthma. Epidemiologic studies found a positive correlation between severity of symptoms among asthmatic patients and the level of particulate matter (PM) in the air. Among the constituents of PM are metals and transition metals. A Polish study observed that several metal and transition metal ions activated mast cells and enhanced allergen-mediated mast cell activation.

Metal and transition metal ions also induced significant secretion of interleukin (IL)-4 and increased antigen-mediated IL-4 secretion in mast cells. These effects of metal and transition metal ions on mast cells were observed at concentrations that do not result in direct cytotoxicity. 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. 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, OLP, MCS, MS, etc. also often recover after amalgam replacement. Cases of documented clinical cases with recovery after amalgam replacement include:

  • eczema and contact dermatitis,
  • psoriasis,
  • asthma,
  • lupus,
  • allergies,
  • chronic multiple chemical sensitivities,
  • oral lichen planus,
  • CFS,
  • muscular/joint pain/fibromyalgia, and
  • MS.

Mercury has been found to accumulate in connective tissue, resulting in lupus or scleroderma.

As an example of experience of those with allergic conditions after amalgam replacement, a German study followed a large group of patients. Over 50% followed indicated they experienced significant improvement after amalgam replacement for 5 chronic conditions: asthma, chronic bronchitis, polymyosis, eczema, contact allergy, and food allergy. The study showed that skin allergy (patch) test apparently is not a reliable indicator of those with mercury related health problems. Patch test was positive in only 13.1 % of patients, whereas more than 50% of patients had significant health improvement for most conditions.

Arthritis-Toxic Metal & Pathogen Factors in 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, 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. Pathogens, such as Lyme disease, parvovirus, and chlamydia, have also been found to be factors in rheumatoid arthritis, especially in patients with immune systems weakened by toxic exposures such as mercury.

Treatment of Arthritis

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 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. Rifampin is known to attenuate chlamydial gene transcription, including the heat shock proteins that prepare infected cells for apoptosis. Combining this effect with antibiotics that block chlamydial protein synthesis (e.g., doxycycline or azithromycin) may allow for successful eradication of the cell harboring persistently infecting intracellular organisms, such as chlamydia.

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. 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.

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 vegan 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, silybin, lycopene, pycogenol, quercetin, Ginkgo extracts, licorice (coughs and congestion), Yerba mate, and bee pollen.

Breastfeeding for at least 6 months and low levels of cereals have been found to be protective against asthma and allergies; probiotics for the breastfeeding mother have also been found to be a preventive factor. 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.

Chronic Digestive Problems (Crohn’s Disease, Colitis, IBS, Leaky gut, etc.)

Crohn’s Disease occurs when the gastrointestinal tract becomes inflamed and weak. Toxic exposures such as mercury or other substances cause activation of inflammatory cytokines and/or autoimmune condition where immune system attacks intestine areas. Treatment includes:

  • Reduce toxic exposures and treat inflammation.
  • Eliminate diet and avoid food allergens (dairy, gluten, eggs, nuts, fruit, nightshades, corn, red meat, refined carbohydrates).
  • Treat candida as necessary.
  • Take good multivitamin and lots of probiotics/ FOS
  • Consider colonics probiotics.
  • Repair intestinal damage by taking glutamine, B5, zinc, tructose oligosaccharides, vit C, and fish oil.

DHEA lowers inflammation. Butyrate enemas are beneficial usually.

Ulcerative colitis is where the large intestine becomes inflamed and ulcerated, and it is caused by inflammation, inflammatory cytokines. Treat inflammation by using fish oil, butyrate enemas, glutamine, yeast RNA, DHEA, vit K, curcumin, etc.

Irritable Bowel Syndrome (IBS) occurs with chronic or reoccurring bowel disease (abdominal fullness, bloating, flatulence, diarrhea alternating with constipation, cramps, etc.) Often patients also have depression or anxiety.


1. National Institute of Arthritis and Musculoskeletal and Skin Diseases.

2. Rudikoff D, Lebwohl M. Atopic dermatitis. Lancet. 1998; 351(9117): 1715-21.

3. The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee. Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema: ISAAC. Lancet. 1998; 351: 1225-32.

4. Center for Disease Control. Vital health and statistics: Current estimates from the National Interview Survey, 1996. 1999; PHS 99-1528.

5. Redd S. Asthma in the United States: Burden and current theories. Environmental Health Perspectives. 2002; 110(4).

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

7. 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.

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

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

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

11. Guo YL, Wang BJ, Lee JY, Chou SY. Occupational hand dermatoses of hairdressers in Tainan City. Occup Environ Med. 1994; 51(10): 689-92.

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

13. Gliski W. Allergic contact dermatitis. Pol Merkur Lekarski. 2003; 14(84): 605-8.

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

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

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

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

18. 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.

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

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

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

22. Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al. Metal- specific memory lymphocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters. 1999; 20: 289-98.

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

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

25. Mori T, Hirai T, Tomiyama T, et al. Mercury sensitization induced by environmental exposure. Nippon Eiseigaku Zasshi. 1998; 52(4): 661-6.

26. Galindo PA, Feo F, Fernadez F. Mercurochrome allergy: Immediate and delayed hypersensitivity. Allergy. 1997; 52(11): 1138-41.

27. 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.

28. Bigazzi PE. Autoimmunity and heavy metals. Lupus. 1994; 3: 449-453.

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

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

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

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

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

34. 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.

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

36. 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.

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

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

39. 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.

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

41. Huggins HA. Solving the MS Mystery: Help, Hope and Recovery. Matrix; 2002.

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

43. 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.

44. 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.

45. 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.

46. Dallmann P. Kon nen durch quecksilber entstehen? PeDa_Eigenverisg. 1995.

47. Guarneri F, Marini H. Perioral dermatitis after dental filling in a 12-year-old girl: involvement of cholinergic system in skin neuroinflammation? Scientific World Journal. 2008; 6(8): 157-63.

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

49. 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.

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

51. Kal BI, Evcin O, Dundar N, Tezel H, Unal I. A case of immediate hypersensitivity reaction associated with an amalgam restoration. Br Dent J. 2008; 205(10): 547-50.

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

53. Roujeau JC, Bioulac-Sage P, Bourseau C, et al. Acute generalized exanthematous pustulosis: Analysis of 63 cases. Arch Dermatol. 1991; 127(9): 1333-8.

54. 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.

55. Wong L, Freeman S. Oral lichenoid lesions (OLL) and mercury in amalgam fillings. Contact Dermatitis. 2003; 48(2): 74-9.

56. Ostman PO, Anneroth G, Skoglund A. Amalgam-associated oral lichenoid reactions. Clinical and histologic changes after removal of amalgam fillings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996; 81(4): 459-65.

57. Pezelj-Ribari S, Prpi J, Mileti I, Brumini G, Soski MS, Ani I. Association between oral lichenoid reactions and amalgam restorations. J Eur Acad Dermatol Venereol. 2008; 22(10): 1163-7.

58. Skoglund A. Value of epicutaneous patch testing in patients with oral, mucosal lesions of lichenoid character. Scand J Dent Res. 1994; 102(4): 216-22.

59. Koch P, Bahmer FA. Oral lesions and symptoms related to metals used in dental restorations: a clinical, allergological, and histologic study. J Am Acad Dermatol. 1999; 41(3.1): 422-30.

60. Ibbotson SH, Speight EL, Macleod RI, Smart ER, Lawrence CM. The relevance of amalgam replacement on oral lichenoid reactions. British Journal of Dermatology. 1996; 134(3): 420-3.

61. 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.

62. 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.

63. 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.

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

65. 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.

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

67. Cutler E. Winning the War Against Asthma & Allergies. Delmar Learning; 1997.

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

69. Walczak-Drzewiecka A, Wyczolkowska J, Dastych J. Environmentally relevant metal and transition metal ions enhance Fc epsilon RI-mediated mast cell activation. Environmental Health Perspectives. 2003; 111(5): 708-13

70. 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.

71. Kurup RK, Kurup PA. Hypothalamic digoxin, cerebral chemical dominance, and pathogenesis of pulmonary diseases. Int J Neurosci. 2003; 113(2): 235-58.

72. 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.

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

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

75. 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.

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

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

78. Halasz A, Cserhati E, Cseh K. Role of the TNF system in the pathomechanism of bronchial asthma. Orv Hetil. 2002; 143(11): 553-7.

79. Gorrie MJ, Qasim FJ, Whittle CJ, Gillespie KM, Szeto CC, Nicoletti F, Bolton EM, Bradley JA, Mathieson PW. Exogenous type-1 cytokines modulate mercury-induced hyper-IgE in the rat. Clin Exp Immunol. 2000; 121(1): 17-22.

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

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

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

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

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

85. 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.

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

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

88. Szucs, et al. Effects of inorganic mercury and methylmercury on the ionic currents of cultured rat hippocampal neurons. Cell Mol Neurobiol. 1997; 17(3): 273-8.

89. 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.

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

91. Ziff S. Dentistry Without Mercury. 8th ed. Orlando, FL: Bio-Probe; 1996.

92. von Nerven B. und Immunschaden nach Amalgamsanierung. Dtsch.Aschr. F. Biologische Zahnmedzin. 1990; 6(4): 152-7.

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

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

95. Klock B, Blomgren J, Ripa U, Andrup B, Effekt av amalgamavlägsnande på patienter som misstänker att de lider eller har lidit av amalgamförgiftning. Tandläkartidn. 1989; 81(23): 1297-1302.

96. Engel P. Beobachtungen uber die gesundheit vor und nach amalgamentfernug. Separatdruck aus Schweiz. Monatsschr Zahnm. 1998; 108(8).

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

98. 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.

99. Friese KH. Homoopathische behandlung der amalgamvergiftung. Allg. Homoopathische Z. 1993; 241(5): 184-187.

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

101. G.Hall. V-TOX: Mercury levels excreted after Vit C IV as chelator by number of fillings. Heavy Metal Bulletin. 1996; 3(1): 6-8.

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

103. Shenker BJ, Berthold P, Decker S, Mayro J, Rooney C, Vitale L, Shapiro IM. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes. II. Alterations in cell viability. Immunopharmacol Immunotoxicol. 1992; 14(3): 555-77.

104. Robinson CJG, et al. Mercuric chloride induced antinuclear antibodies in mice. Toxicol App Pharmacol. 1986; 86: 159-169.

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

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

107. 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.

108. Annau Z, et al. Mechanisms of neurotoxicity and their relationships to behavioral changes. Toxicology. 1988; 49(2): 219-25.

109. Hu H, Abedi-Valugerdi M, Moller G. Pretreatment of lymphocytes with mercury in vitro induces a response in T cells from genetically determined low-responders and a shift of the interleukin profile. Immunology. 1997; 90(2): 198-204.

110. 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.

111. 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.

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

113. Pollard KM, Lee DK, Casiano CA. The autoimmunity-inducing xenobiotic mercury interacts with the autoantigen fibrillarin and modifies its molecular structure and antigenic properties. J Immunol. 1997; 158: 3421-8.

114. Abedi-Valugerdi M, Hansson M, Moller G. Genetic control of resistance to mercury-induced immune/autoimmune activation. Scand J Immunol. 2001; 54(1-2): 190-7.

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

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

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

118. 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.

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

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

121. Feighery L, Collins C, Feighery C, et al. Anti-transglutaminase antibodies and the serological diagnosis of coeliac disease. Br J Biomed Sci. 2003; 60(1):14-8.

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

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

124. Kumar AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase activity: A common pathway in central nervous system disorders. J Assoc Physicians India. 2002; 50: 400-6.

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

126. 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.

127. 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; 113(3): 341-59.

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

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

130. 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.

131. 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.

132. 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.

133. 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.

134. 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.

135. 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.

136. 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.

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

138. 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.

139. 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.

140. Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem. 2005; 12(10): 1161-208.

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

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

143. 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.

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

145. 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.

146. 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.

147. 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.

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

149. Silva VS, Duarte AI, Rego AC, et al. Effect of chronic exposure to aluminum on isoform expression and activity of rat (Na+/K+)ATPase. Gonçalves Toxicological Sciences. 2005; 88(2): 485-494.

150. Yokel RA. Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration. J Alzheimer’s Dis. 2006; 10(2-3): 223-53.

151. Charney et al. An in vitro inhibitor of Na-K-ATPase present in an adenosinetriphosphate preparation. J Appl Physiol. 1975; 39: 156-158.

152. Schofer H, Rosenberger G, Hottenrott C, et al. Sensitization to nickel sulfate in patients with ileitis terminalis (Crohn’s disease). Zentren der Dermatologie und Venerologie. 1988; 36(5): 157-62.

153. Nogi N. Electric current around dental metals as a factor producing allergic metal ions in the oral cavity. Nippon Hifuka Gakkai Zasshi. 1989; 99(12): 1243-54.

154. Certosimo AJ, O’Connor RP. Oral electricity. Gen Dent. 1996; 44(4): 324-6.

155. Pleva J. Mercury-A public health hazard. Reviews on Environmental Health. 1994; 10: 1-27.

156. Buchner A, Hansen LS. Amalgam tattoo of the oral mucosa: a clinicopatholigic study of 268 cases. Surg Oral Med Oral Pathol. 1980; 49(2): 139-47.

157. Forsell M, Larsson B, Ljungqvist A, Carlmark B, Johansson O. Mercury content in amalgam tattoos of human oral mucosa and its relation to local tissue reactions. Euro J Oral Sci. 1998; 106(1): 582-7.

158. Weaver T, Auclair PL, Taybos GM. Amalgam tattoo as a cause of local and systemic disease? Oral Surg. Oral Med. Oral Pathol. 1987; 63: 137-40.

159. Rose MD, Costello JP. The tarnished history of a posteria restoration. Br Dent J. 1998; 185(9): 436.

160. Arvidson K, Johansson EG. Corrosion studies of dental gold alloy in contact with amalgam. Swed. Dent. J. 1984; 68: 135-139.

161. Raue H. Resistance to therapy: Think of tooth fillings. Medical Practice. 1980; 32(72): 2303-2309.

162. Pizzichini M, Fonzi M, Sugherini L, et al. Release of mercury from dental amalgam and its influence on salivary antioxidant activity. Sci. Total Environ. 2002; 284(1-3): 19-25.

163. Nadarajah V, Neiders ME, Aguirre A, Cohen RE. Localized cellular inflammatory responses to subcutaneously implanted dental mercury. J Toxicol Environ Health. 1996; 49(2): 113-25.

164. Willershausen B, et al. Mercury in the mouth mucosa of patients with amalgam fillings. Dtsch Med Wochenschr. 1992; 117(46): 1743-7.

165. Monaci F, Bargagli E, Bravi F, Rottoli P. Concentrations of major elements and mercury in unstimulated human saliva. Biol Trace Elem Res. 2002; 89(3): 193-203.

166. Omura Y. Abnormal deposits of Al, Pb, and Hg in the brain, particularly in the hippocampus, as one of the main causes of decreased cerebral acetylcholine, electromagnetic field hypersensitivity, pre-Alzheimer’s disease, and autism in children. Acupuncture & Electro-Therapeutics Research. 2000; 25(3/4): 230.

167. Schmidt F, et al. Mercury in urine of employees exposed to magnetic fields. Tidsskr Nor Laegeforen. 1997; 117(2): 199-202.

168. Sheppard AR, Eisenbud M. Biological Effects of Electric and Magnetic Fields of Extremely Low Frequency. New York University Press; 1977.

169. Ortendahl TW, Hogstedt P, Holland RP. Mercury vapor release from dental amalgam in vitro caused by magnetic fields generated by CRT’s. Swed Dent J. 1991: 31.

170. Bergdahl J, Anneroth G, Stenman E. Description of persons with symptoms presumed to be caused by electricity or visual display units—oral aspects. Scand J Dent Res. 1994; 102(1): 41-5.

171. Heintze U, Edwardsson S, Derand T, Birkhed D. Methylation of mercury from dental amalgam and mercuric chloride by oral streptococci in vitro. Scand J Dent Res. 1983; 91(2): 150-2.

172. Kingman A, Albertini T, Brown LJ. Mercury concentrations in urine and blood associated with amalgam exposure in the U.S. military population. J Dent Res. 1998; 77(3): 461-71.

173. Lichtenberg H. Mercury vapor in the oral cavity in relation to the number of amalgam surfaces/gold/ porcelain and the classic symptoms of chronic mercury poisoning. Journal of Orthomolecular Medicine. 1996; 11(2): 87-94.

174. Barregard L, Sallsten G, Jarvholm B. People with high mercury uptake from their own dental amalgam fillings. Occup Envir Med. 1995; 52: 124-128.

175. Langworth S, Stromberg R. A case of high mercury exposure from dental amalgam. Eur J Oral Sci. 1996; 104(3): 320-1.

176. Bjorkman L, Sandborgh-Englund G, Ekstrand J. Mercury in saliva and feces after removal of amalgam fillings. Toxicol App Pharmacol. 1997; 144(1): 156-162.

177. Sandborgh-Englund G, Elinder CG, Langworth S, Schutz A, Ekstrand J. Mercury in biological fluids after amalgam removal. J Dent Res. 1998; 77(4): 615-24.

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

179. Valentino M, Santarelli L, Pieragostini E, Soleo L, Mocchegiani E. In vitro inhibition of thymulin production in mercury-exposed thymus of young mice. Sci Total Environ. 2001; 270(1-3): 109-112.

180. Nordlind K. Stimulating effect of mercuric chloride and nickel sulfate on DNA synthesis of thymocytes and peripheral lymphoid cells. Int Arch Allergy Appl Immunol. 1983; 72(2): 177-179.

181. Chen M, von Mikecz A. Specific inhibition of rRNA transcription and dynamic relocation of fibrillarin induced by mercury. Exp Cell Res. 2000; 259(1): 225-238.

182. Monnet-Tschudi F, Zurich MG, Honegger P. Comparison of the developmental effects of two mercury compounds on glial cells and neurons in aggregate cultures of rat telencephalon. Brain Res. 1996; 741(1-2): 52-9.

183. Dieter MP, 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.

184. Bernard S, Enayati A, Redwood L, Roger H, Binstock T. Autism: A novel form of mercury poisoning. Med Hypotheses. 2001; 56(4): 462-71.

185. Contrino J, Marucha P, Bigazzi PE, et al. Effects of mercury on human polymorphonuclear leukocyte function in vitro. Am J Pathol. 1988; 132(1): 110-8.

186. Schofer H, Rosenberger G, Hottenrott C, et al. Sensitization to nickel sulfate in patients with ileitis terminalis (Crohn disease). Zentren der Dermatologie und Venerologie. 1988; 36(5): 157-62.

187. Metal allergens of growing significance: Epidemiology, immunotoxicology, strategies testing and prevention antiseptics and disinfectants. In Rietschel RL, Fowler JR, Jr. eds. Fisher’s Contact Dermatitis. Philadelphia: Lippincott Williams & Wilkins; 2001: 149-155.

188. Life Enhancement.
189. Klinghard D, Mercola J. Mercury toxicity and systemic elimination agents. J of Nutritional and Environmental Medicine. 2001; 11: 53-62.

190. Buckland J. Lyme arthritis: Direct and indirect actions of borrelia burgdorferi. Nat Rev Rheumatol. 2010; 6(11): 615.

191. Pancewicz S, Zwierz K, et al. Activity of lysosomal exoglycosidases in serum and synovial fluid in patients with chronic Lyme and rheumatoid arthritis. Scand J Infect Dis. 2009; 41(8): 584-9.

192. Tuuminen T, Hedman K, Seppälä I. Acute parvovirus B19 infection frequently causes non-specificity in Borrelia, and less often in Salmonella and Campylobacter serology: A problem of diagnosis of infectious arthropathy. Clin Vaccine Immunol. 2010.

193. Rihl M, et al. A cure for Chlamydia-induced reactive arthritis? Arthritis and Rheumatism. 2010.

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