Mercury is a common cause of chronic conditions related to intestinal dysfunction, such as ulcerative colitis, IBS, Chohn’s, and psoriasis. Mercury and food intolerances are linked as a common causes of chronic conditions related to leaky gut and intestinal dysfunction, such as ulcerative colitis, IBS, Crohn’s, eczema, psoriasis, food allergies, arthritis, ADHD, and autoimmune disease; treatments that improve these conditions.
When intestinal permeability is increased, food and nutrient absorption is impaired. Dysfunction in intestinal permeability can result in leaky gut syndrome, where larger molecules and toxins in the intestines can pass through the membranes and into the blood, triggering immune response. Progressive damage can occur to the intestinal lining, eventually allowing disease-causing bacteria, undigested food particles, and toxins to pass directly into the blood stream. Dysfunctions in intestinal permeability have been found to be associated with diseases, such as leaky gut syndrome (LGS), ulcerative colitis, irritable bowel syndrome (IBS), Crohn’s disease, CFS, eczema, psoriasis, food allergies, autoimmune disease, and arthritis.
Symptoms commonly associated with LGS include: abdominal pain, indigestion, diarrhea, anxiousness, chronic joint pain, chronic muscle pain, mental confusion, mood swings, poor memory, poor immunity and recurrent infections, bloating, fatigue.
Although there are also other causes of LGS, mercury and toxic metals have been found to be common toxic exposures that can cause increased intestinal permeability and intestinal dysfunction, as well as of the kidney epithelial and brush border cells. Mercury exposure also reduced the mucosal entry of sugars and amino acids to 80-90% of control levels in the small intestine cells within several minutes. Mercury exposure blocks intestinal nutrient transport by interacting directly with brush border membrane transport proteins. Mercury also causes increase of inflammatory cytokines such as TNFa, IL-6, and IL-1b.
Mercury causes significant destruction of stomach and intestine epithelial cells, resulting in damage to stomach lining which along with mercury’s ability to bind to SH hydroxyl radical in cell membranes alters permeability and adversely alters bacterial populations in the intestines causing leaky gut syndrome with toxic, incompletely digested complexes in the blood and accumulation of heliobacter pylori, a suspected major factor in ulcers and stomach cancer and Candida albicans, as well as poor nutrient absorption.
Dental amalgam has been found by thousands of medical lab tests and by medical studies to be the largest source of mercury exposure in most people who have several amalgam fillings. Replacement of amalgam fillings and metal detoxification have been found to significantly improve the health of most with conditions related to bowel dysfunction and leaky gut syndrome.
Other common causes or factors in leaky gut and the related conditions include food allergies and intolerances; drugs(NSAIDs, aspirin, stomach h2 blockers, steroids, etc.); Dysbiosis (overgrowth of organisms due to antibiotic use and/or low probiotic levels); alcohol consumption; synergistic toxic exposures and chemical sensitivity; chronic infections; and inadequate digestive enzymes. While food allergies mediated by IgE can cause significant health effects, including leaky gut syndrome, these are usually easily identified by the immediateness of reactions or skin tests. Food intolerances mediated by IgG also commonly cause effects, including leaky gut syndrome, but the reactions are delayed and can be systemic and harder to identify. Tests based on IgE, such as skin test or RAST, do not reliably identify such problems that are common factors in chronic health conditions and tests, such as ELISA, that measure both IgE and IgG are more reliable. Common causes of food intolerances include failure to breast feed babies for at least the first year of life, feeding table food in first year of life, use of antibiotics without adequate addition of probiotics, and eating the same foods every day. Food intolerances and food additives or processed foods that contain glutamate, aspartame, high-fructose corn syrup, dyes, etc. are common causes of leaky gut syndrome and neurological conditions such as ADHD.
Food intolerances and IgG reactions lead to long lasting “immune complexes” that are factors in leaky gut related conditions as well as other conditions, such as Lupus, rheumatoid arthritis, CFS, fibromyalgia, ADHD, etc. Inflammatory reactions to toxic metals, vaccines, food additives, food intolerances not only cause immune reactions but also reactions in the neurological microglial system. This can cause brain fog, memory problems, and degenerative neurological conditions if prolonged chronic exposures. For example, virtually 100% of those with schizophrenic symptoms are found, when tested, to have food intolerance to wheat gluten or milk casein. Enzymatic blockages by chronic toxic metal exposures, such as vaccines or mercury, have been found to be a factor in food intolerances. Similarly this is the most common cause or factor in celiac disease and common cause of ataxia and diabetes.
Similarly food allergies or additives, food intolerances, high sugar consumption, and antibiotic use with adequate probiotics have been found to be the most common causes of children’s ear infections. Clinical studies have found that diets high in flavonoids and cartenoids, including nutritional supplements such as buffered Vit C and natural E, selenium, omega-3 oils, probiotics are effective in preventing ear infections and other chronic conditions. These in addition to multiple B vitamins, the flavanoids curcumin, hesperidin, and quercetin are effective in preventing and treating leaky gut related conditions.
Crohn’s disease usually occurs at a relatively young age and results when an immune or autoimmune response cause increased inflammatory cytokines like TNFa, IL-6, and IL-1b, resulting in inflammation of the ileum or colon. This usually results in thinning of the bowel wall and often formation of ulcers on the intestinal lining. Functional neutrophil deficiencies are often a factor in Crohn’s disease. In addition to improvements in many patients after amalgam replacement and detoxification, diet and nutritional measures are usually effective at improving Crohn’s Disease. The 4-R program has seen good success in many patients. The program removes all foods where there is suspicion of allergy that might produce inflammation. Common allergens include wheat/gluten, dairy, eggs, peanuts, tomatoes, corn, and red meat.
Additionally, elimination of gastrointestinal parasites, undesirable bacteria, fungus, and yeasts are carried out. Sometimes a treatment such as nystantin is used to eliminate yeast. Then vital nutrients are replaced by dietary measures and supplementation of a good multivitamin and mineral, minerals found deficient such as iron, magnesium, calcium, selenium, zinc, iodine and vitamins, such as B-complex, B6, B12, and folic acid. Next the intestines are re-inoculated with friendly bacteria (Lactobacillus acidophilus and Lactobacilus bulgaricus.) Finally, measures are taken to repair the intestine to correct for the increased permeability. This is done by adding nutrients such as glutamine, pathothenic acid (B5), zinc, FOS, and vitamin C. DHEA and Butyrate have also been found effective in many patients at reducing inflammation.
Supplements and other treatments that reduce intestinal permeability have also been found to be protective against and improve these conditions. Glutamine, berberine, probiotics, and vitamin D have been found to decrease intestinal permeability and protect against effects caused by leaky gut syndrome. Butyrate has been found to inhibit inflammation and carcinogenesis in the intestines and low butyrate levels are found in colon cancer, ulcerative colitis, and Crohn’s disease. Butyrate and phosphatidylcholine have been found to be protective against these conditions, and increased fiber content in diet promotes increased butyrate levels, through the effect on fermentation pattern.
Supplementation with chlorella has been found to result in beneficial effects when used in patients’ chronic conditions such as ulcerative colitis, hypertension, or Fibromyalgia. Doctors have suggested that the mechanism by which chlorella improves treatment of such conditions is metal detoxification, which is the main mechanism of action of chlorella and has been found to greatly improve intestinal function.
Brain inflammation or hypoglycemia related to toxic metal exposures, food intolerances, etc. have been found to be common causes of ADHD, impulsivity, juvenile delinquency, criminality, and violence. Detoxification, diet measures, and supplementation for deficient vitamins and minerals have been found to usually improve such conditions.
1. Mankertz J, Schulzke JC. Altered permeability in inflammatory bowel disease: pathophysiology and clinical implications. Curr Opin Gastroenterol. 2007 Jul; 23(4): 379-83.
2. Welcker K, Martin A, Kölle P, Siebeck M, Gross M. Increased intestinal permeability in patients with inflammatory bowel disease. Eur J Med Res. 2004 Oct; 9(10): 456-60.
3. Soeters PB, Luyer MD, Greve JW, Buurman WA. The significance of bowel permeability. Curr Opin Clin Nutr Metab Care. 2007 Sep; 10(5): 632-8.
4. Cereijido M, Contreras RG, Flores-Benítez D, Flores-Maldonado C, Larre I, Ruiz A, Shoshani L. New diseases derived or associated with the tight junction. Arch Med Res. 2007 Jul; 38(5): 465-78.
5. Weber P, Brune T, Ganser G, Zimmer KP. Gastrointestinal symptoms and permeability in patients with juvenile idiopathic arthritis. Clin Exp Rheumatol. 2003 Sep-Oct; 21(5): 657-62.
6. Ventura MT. Intestinal permeability in patients with adverse reactions to food. Dig. Liver Dis. 2006 Oct; 38(10):732-6.
7. Sandek A. Altered intestinal function in patients with chronic heart failure. J Am Coll Cardiol. 2007 Oct; 50(16):1561-9.
8. Fasano A, Shea-Donohue T. Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Nat Clin Pract Gastroenterol Hepatol. 2005 Sep; 2 (9):416-22.
9. Böhme M, Diener M, Mestres P, Rummel W. Direct and indirect actions of HgCl2 and methyl mercury chloride on permeability and chloride secretion across the rat colonic mucosa. Toxicol Appl Pharmacol. 1992 Jun;114(2): 285-94.
10. Watzl B, Abrahamse SL, Treptow-van Lishaut S, Neudecker C, Pool-Zobel BL. Enhancement of ovalbumin-induced antibody production and mucosal mast cell response by mercury. Food Chem Toxicol. 1999 Jun; 37(6): 627-37.
11. Aduayom I, Denizeau F, Jumarie C. Multiple effects of mercury on cell volume regulation, plasma membrane permeability, and thiol content in the human intestinal cell line Caco-2. Cell Biol Toxicol. 2005 May-Jul; 21(3-4):163-79.
12. van Hoek AN, de Jong MD, van Os CH. Effects of dimethylsulfoxide and mercurial sulfhydryl reagents on water and solute permeability of rat kidney brush border membranes. Biochim Biophys Acta. 1990 Dec;1030(2): 203-10.
13. Stirling CE. Mercurial perturbation of brush border membrane permeability in rabbit ileum. J Membr Biol. 1975 Aug 11; 23(1):33-56.
14. Miller DS. HgCl2 inhibition of nutrient transport in teleost fish small intestine. J Pharmacol Exp Ther. 1981 Jan; 216(1): 70-6.
15. De-Souza DA. Intestinal permeability and systemic infections in critically ill patients, effect of glutamine. Crit Care Med. 2005 May; 33(5):1175-8.
16. Jiang HP. Protective effect of glutamine on intestinal barrier function in patients receiving chemotherapy. Zhonghua Wei Chang Wai Ke Za Zhi. 2006, Jan; 9(1):59-61.
17. Alzamora R. Berberine inhibits ion transport in human colonic epithelia. Eur J Pharmocol. 1999 Feb; 368(1):111-8.
18. Zareie M, Jury J, Yang PC, Sherman PM. Probiotics prevent bacterial translocation and improve intestinal barrier function in rats following chronic stress. Gut. 2006 Nov; 55(11):1553-60.
19. Bai AP, Ouyang Q. Probiotics and inflammatory bowel diseases. Postgrad Med J. 2006 Jun; 82(968): 376-82.
20. Kong J, Zhang Z, Musch MW, et al. Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. Am J Physiol Gastrointest Liver Physiol. 2008 Jan; 294(1): G208-16.
21. Melietis CD. Hidden Causes of GI Dysfunction. Vitamin Research News. 2008; 22(4).
22. Blaylock, RL. Are you the victim of hidden allergies?. The Blaylock Wellness Report. 2007; 4(11): 1. w3.newsmax.com/newsletters/blaylock/issues/nov07/blaylock_nov07_41.pdf
23. Blaylock, RL. Food additives: What you eat can kill you. The Blaylock Wellness Report. 2007; 4(10).
24. Hamer HM, Jonkers D, et al. The role of butyrate on colonic function. Aliment Pharmocol Ther. 2008 Jan; 27(2):104-119.
25. Kim YS, Milner JA. Dietary modulation of colon cancer risk. J Nutr. 2007; 137( Suppl 11): 2576S-2579S.
26. Duffy MM. Mucosal metabolism in ulcerative colitis and Crohn’s Disease. Dis Colon Rectum. 1998 Nov; 41(11):1399-1405.
27. Thibault R. Down-regulation of the onocarboxylate transporter 1 is involved in butyrate deficiency during intestinal inflammation. Gastroenterology. 2007; 133(6): 1916-27.
28. Rose DJ. Influence of dietary fiber on inflammatory bowel disease and colon cancer: importance of fermentation pattern. Nutr Rv. 2007 Feb; 65(2):51-62.
29. Hossain Z. Effect of polyunsaturated fatty acid-enriched phosphatidylcholine and phosphatidylserine on butyrate-induced growth inhibition, differentiation, and apoptosis in Caco-2 cells. Cell Bichem Funct. 2006 Mar-Apr; 24(2):159-65.
30. Di Sabatino A, Morera R, Corazza GR, et al. Oral butyrate for mildly to moderately active Crohn’s disease. Aliment Pharmacol Ther. 2005 Nov 1; 22(9): 789-94.
31. R.A.Goyer, Toxic effects of metals. In: Caserett, Doull, ed. Toxicology: The Basic Science of Poisons. New York: McGraw-Hill Inc., 1993.
32. Goodman, Gillman. The Pharmacological Basis of Therapeutics. New York, Mac Millan Publishing Company, 1985.
33. International Labour Organization. Encyclopedia of occupational health and safety. www.ilo.org/safework/WCMS_113329/lang–en/index.htm
34. Markovich, et al. Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat-1. Toxicol Appl Pharmacol. 1999; 154(2):181-7.
35. McFadden A. Xenobiotic metabolism and adverse environmental response: Sulfur-dependent detox pathways. Toxicology. 1996; 111(1-3):43-65.
36. Alberti A, Pirrone P, Elia M, Waring RH, Romano C. Sulphation deficit in “low-functioning” autistic children. Biol Psychiatry. 1999; 46(3): 420-4.
37. Levy TE, Huggins HA. Uniformed Consent: The Hidden Dangers in Dental Care. Hampton Roads Publishing Company Inc., 1999.
38. Knapp LT, Klann E. Superoxide-induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem. 2000 May; 39: 22.
39. Rajanna B, et al. Modulation of protein kinase C by heavy metals. Toxicol Lett. 1995; 81(2-3):197-203.
40. Badou A, et al. HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels. J Biol Chem. 1997 Dec 19; 272(51): 32411-8.
41. Veprintsev DB. Pb2+ and Hg2+ binding to alpha-lactalbumin. Biochem Mol Biol Int. 1996 Aug; 39(6):1255-65.
42. Heintze et al. Methylation of Mercury from dental amalgam and mercuric chloride by oral Streptococci. Scan. J. Dent. Res. 1983; 91:150-152.
43. 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 [Article in Chinese]. Shanghai Kou Qiang Yi Xue. 2000 Jun; 9(2): 70-2.
44. Liang L, et al. Mercury reactions in the human mouth with dental amalgams. Water, Air, and Soil Pollution. 1995; 80:103-107.
45. Rowland, Grasso, Davies. The methylation of mercuric chloride by human intestinal bacteria. Experientia. Basel. 1975; 31:1064-1065.
46. Hamdy MK, et al. Formation of methyl mercury by bacteria. App Microbiol. 1975.
47. 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.
48. Choi SC, Bartha R. Cobalamin-mediated mercury methylation by desulfovibrio desulfuricans LS. Appl Environ Microbiol. 1993 Jan; 59(1): 290-5.
49. Lund M, et al. Treatment of acute MeHg poisoning by NAC. J Toxicol Clin Toxicol. 1984; 22(1): 31-49.
50. Livardjani F, Ledig M, Kopp P, Dahlet M, Leroy M, Jaeger A. Lung and blood superoxide dismustase activity in mercury vapor exposed rats: Effect of N-acetylcysteine treatment. Toxicology. 1991 Mar 11; 66(3): 289-95.
51. Goyer RA, National Institute of Environmental Health Sciences. Toxic and essential metal interactions. Annu Rev Nutr. 1997; 17: 37-50.
52. Goyer RA, et al. Environmental Risk Factors for Osteoporosis. Environmental Health Perspectives. 1994; 102(4): 390-394.
53. Lindh U, Carlmark B, Gronquist SO, Lindvall A. Metal exposure from amalgam alters the distribution of trace elements in blood cells and plasma. Clin Chem Lab Med. 2001 Feb; 39(2):134-142.
54. Goldberg AF, et al. Effect of Amalgam restorations on whole body potassium and bone mineral content in older men. Gen Dent; 1996, 44(3): 246-8.
55. Schirrmacher K, Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+]I in bone cells. Calcif Tissue Int. 1998 Aug; 63(2): 134-9.
56. Quig D, Doctors Data Lab. Cysteine metabolism and metal toxicity. Altern Med Rev. 1998; 3(4): 262-270.
57. 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.
58. Berndt WO, et al. Renal glutathione and mercury uptake. Fundam Appl Toxicol. 1985, 5(5): 832-9.
59. Zalups RK, Barfuss DW. Accumulation and handling of inorganic mercury in the kidney after co-administration with glutathione. J Toxicol Environ Health. 1995; 44(4): 385-99.
60. Clarkson TW, et al. Billiary secretion of glutathione-metal complexes. Fundam Appl Toxicol. 1985; 5(5): 816-31.
61. Walsh WJ, Isaacson Hr, Hall A. Elevated blood copper to zinc ratios in assaultive young males. Physiol Behav. 1997 Aug; 62(2): 327-9.
62. Liebert CA, Wireman J, Smith T, Summers AO. The impact of mercury released from dental silver fillings on antibiotic resistance in the primate oral and intestinal bacterial flora. Met Ions Biol Syst. 1997; 34: 441-60.
63. Summers AO, et al. Mercury released from dental “silver” fillings provokes an increase in mercury- and antibiotic-resistant bacteria in oral and intestinal floras of primates. Antimicrobial Agents and Chemotherapy. 1993; 37(4):825-834.
64. Poiata A, Badicut I, Indres M, Biro M, Buiuc D. Mercury resistance among clinical isolates of Escherichia coli. Roum Arch Microbiol Immunol. 2000 Jan-Jun; 59(1-2): 71-9.
65. Edlund C, Bjorkman L, Ekstrand J, Sandborgh-Englund G, Nord CE. Resistance of the normal human microflora to mercury and antimicrobials after exposure to mercury from dental amalgam fillings. Clin Infect Dis. 1996 Jun; 22(6): 944-50.
66. Vimy M, et al. Silver dental fillings provoke an increase in mercury and antibiotic resistant bacteria in the mouth and intestines of primates. APUA Newsletter. 1991.
67. Milatovic D, Aschner JL, Syversen T, et al. Methylmercury induces oxidative injury, alterations in permeability and glutamine transport in cultured astrocytes. Brain Res. 2007 Feb 2; 1131(1): 1-10.
68. Singh I, Pahan K, Khan M, Singh AK. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatory cytokine-mediated apoptosis in demyelinating diseases. J Biol Chem. 1998 Aug 7; 273(32): 20354-62.
69. 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.
70. Xu J, Yeh CH, et al. Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death. J Biol Chem. 1998 Jun 26; 273(26):16521-6.
71. Dbaibo GS, El-Assaad W, et al. Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death. FEBS Lett. 2001 Aug 10; 503(1): 7-12.
72. Liu B, Hannun YA, et al. Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell death. J Biol Chem. 1998 May 1; 273(18):11313-20.
73. Noda M, Wataha JC, et al, Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes. Dent Mater. 2003 Mar;19(2):101-5
74. Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production but activates proinflammatory cytokine expression in murine macrophage: Differential modulation of NF-kappaB and p38 MAPK signaling pathways. Nitric Oxide. 2002 Aug; 7(1): 67-74.
75. Dastych J, Metcalfe DD, et al. Murine mast cells exposed to mercuric chloride release granule-associated N-acetyl-beta-D-hexosaminidase and secrete IL-4 and TNF-alpha. J Allergy Clin Immunol. 1999 Jun; 103(6):1108-14.
76. Tortarolo M, Veglianese P, et al. Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression. Mol Cell Neurosci. 2003 Jun; 23(2):180-92.
77. Mathieson PW. Mercury: God of TH2 cells. Clinical Exp Immunol. 1995; 102(2): 229-30.
78. Murdoch RD, Pepys J. Enhancement of antibody and IgE production by mercury and platinum salts. Int Arch Allergy Appl Immunol. 1986; 80: 405-11.
79. Parronchi P, Brugnolo F, Sampognaro S, Maggi E. Genetic and environmental factors contributing to the onset of allergic disorders. Int Arch Allergy Appl Immunol. 2000 Jan; 121(1): 2-9.
80. Lu SC, Regulation of hepatic glutathione synthesis: current concepts and controversies. FASEB J. 1999; 13(10): 1169-83.
81. Zalups RK, et al. Nephrotoxicity of inorganic mercury co-administered with L-cysteine, Toxicology. 1996; 109(1): 15-29.
82. Yannai S, et al. Transformations of inorganic mercury by candida albicans and Saccharomyces cerevisiae. Applied Envir Microbiology. 1991; 7: 245-247.
83. Zorn NE, et al. A relationship between Vit B-12, mercury uptake, and methylation. Life Sci. 1990; 47(2):167-73.
84. Ridley WP, Dizikes L, Cheh A, Wood JM. Recent studies on biomethylation and demethylation of toxic elements. Environmental Health Perspectives. 1977 Aug;19: 43-6.
85. Yamada, Tonomura. Formation of methyl Mercury Compounds from inorganic Mercury by Clostridium cochlearium. J Ferment Techno. 1972; 50:159-1660.
86. Zamm AF. Removal of dental mercury: often an effective treatment for very sensitive patients. J Orthomolecular Med. 1990, 5(53):138-142.
87. Shenker BJ, et al. Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes: Alterations in cellular glutathione content. Immunopharmacol Immunotoxicol. 1993; 15(2-3): 273-90.
88. Perlingeiro RC, et al. Polymorphonuclear phagentosis in workers exposed to mercury vapor. Int J Immounopharmacology. 1994; 16(12):1011-7.
89. Albers JW, et al. Neurological abnormalities associated with remote occupational elemental mercury exposure. Ann Neurol. 1988; 24(5): 651-9.
90. Kidd RF. Results of dental amalgam removal and mercury detoxification. Alternative Therapies. 2000; 6(4):49-55.
91. Klinghard D, Mercola J. Mercury toxicity and systemic elimination agents. J of Nutritional and Environmental Medicine. 2001; 11: 53-62.
92. Merchant RE, Andre, CA. Dietary supplementation with chlorella pyrenoidosa produces positive results in patients with cancer or suffering from certain common chronic illnesses. Townsend Letter for Doctors & Patients.
93. Kubicka-Muranyi M, et al. Systemic autoimmune disease induced by mercuric chloride. Int Arch Allergy Immunol. 1996; 109(1):11-20.
94. Goldman M, et al.1Chemically induced autoimmunity. Immunology Today. 1991; 12: 223.
95. Warfyinge K, et al. Systemic autoimmunity due to mercury vapor exposure in genetically susceptible mice. Toxicol Appl Pharmacol. 1995; 132(2):299-309.
96. Bagenstose LM, et al. Mercury induced autoimmunity in humans. Immunol Res. 1999; 20(1): 67-78.
97. Boadi WY, et al. In vitro effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta. Environ Res. 1992; 57(1): 96-10.
98. Boadi WY. In vitro exposure to mercury and cadmium alters term human placental membrane fluidity. Pharmacol. 1992; 116(1): 17-23.
99. Urbach J, et al. Effect of inorganic mercury on in vitro placental nutrient transfer and oxygen consumption. Reprod Toxicol. 1992; 6(1): 69-75.
100. Karp W, Gale TF, et al. Effect of mercuric acetate on selected enzymes of maternal and fetal hamsters. Environ Res. 1985; 36: 351-358.
101. Karp W, et al. Correlation of human placental enzymatic activity with trace metal concentration in placenta. Environ Res. 1977; 13: 470- 477.
102. Boot JH. Effects of SH-blocking compounds on the energy metabolism and glucose uptake in isolated rat hepatocytes. Cell Struct Funct. 1995 Jun; 20(3): 233-8.
103. Semczuk M, Semczuk-Sikora A. New data on toxic metal intoxication (Cd, Pb, and Hg in particular) and Mg status during pregnancy. Med Sci Monit. 2001Mar; 7(2): 332-340.
104. Iioka H, et al. The effect of inorganic mercury on placental amino acid transport. Nippon sanka Fujinka Gakkai Zasshi. 1987; 39(2): 202-6.
105. Sterzl I, Prochazkova J, Stejskal VDM, et al. Mercury and nickel allergy: Risk factors in fatigue and autoimmunity. Neuroendocrinology Letters. 1999; 20: 221-228.
106. 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 Jun; 25(3): 211-8.
107. Godfrey ME. Candida, dysbiosis and amalgam. J. Adv. Med. 1996; 9(2).
108. Romani L, Immunity to Candida albicans: Th1,Th2 cells and beyond. Curr Opin Microbiol. 1999; 2(4): 363-7.
109. Zamm AV. Candida albicans theraphy: Dental mercury removal, an effective adjunct. J. Orthmol. Med. 1986; 1(4): 261-5.
110. Stejskal V. The role of metals in autoimmune diseases and the link to neuroendocrinology. Neuroendocrinology Letters. 1999; 20: 345-358.
111. Heise LA, Wagener BM, Vigil JR, Othman M, Shaninpoor P. Hemorrhagic colitis secondary to acute elemental mercury vapor poisoning. Am J Gastroenterol. 2009 Feb; 104(2): 530-1.
112. Cade JR, et al. Autism and schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism. 1999.
113. Puschel G, Mentlein R, Heymann E. Isolation and characterization of dipeptyl peptidase IV from human placenta. Eur J Biochem. 1982 Aug; 126(2): 359-65.
114. Kar NC, Pearson CM. Dipeptyl peptidases in human muscle disease. Clin Chim Acta. 1978; 82(1-2): 185-92.
115. 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.
116. 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 Jul; 44(1):13-8.
117. Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V. Plasma excitatory amino acids in autism. Invest Clin. 1996; 37(2):113-28.
118. Carlsson ML. Is infantile autism a hypoglutamatergic disorder? J Neural Transm. 1998; 105(4-5): 525-35.
119. Rolf LH, Haarman FY, Grotemeyer KH, Kehrer H. Serotonin and amino acid content in platelets of autistic children. Acta Psychiatr Scand. 1993; 87(5): 312-6.
120. Naruse H, Hayashi T, Takesada M, Yamazaki K. Metabolic changes in aromatic amino acids and monoamines in infantile autism and a new related treatment. No To Hattatsu. 1989, 21(2):181-9.
121. van Benschoten MM. Acupoint energetics of mercury toxicity and amalgam removal with case studies. American Journal of Acupuncture. 1994; 22(3): 251-262.
122. M. M. Van Benschoten, O. M. D. A., C.A., and Associates Website. http://www.mmvbs.com/
123. Guthrie M. Mycoplasmas—The missing link in fatiguing illness, Alternative Medicine. 2001; 43. www.immunesupport.com/library/showarticle.cfm?ID=3066
124. Zweers MM, Douma CE, van der Wardt AB, Krediet RT, Struijk DG. Amphotericin B, HgCl2 and peritoneal transport in rabbits. 7 April 1998.
125. Savage DF, Stroud RM. Structural basis of aquaporin inhibition by mercury. J Mol Biol. 2007 May 4; 368(3):607-17.
126. Yukutake Y, Tsuji S, Hirano Y, Adachi T, Takahashi T, et al. Mercury chloride decreases the water permeability of aquaporin-4-reconstituted proteoliposomes. Biol Cell. 2008.
127. Leistevuo J, Pyy L, Osterblad M. Dental amalgam fillings and the amount of organic mercury in human saliva. Caries Res. 2001 May-Jun; 35(3):163-6.
128. Leistevuo J, et al. Dental amalgam fillings and the amount of organic mercury in human saliva. Corks Res. 2001; 35(3):163-6.