The President’s Cancer Panel Report for 2008-2009 found that the true burden of environmentally-induced cancers has been grossly underestimated. Other studies and documentation have similar findings. As seen here, in addition to cancers caused by radiation, pesticides, and other organic chemicals, toxic metals such as mercury have major effects on weakening the immune system and facilitating cancer.
Medical labs, medical studies, and government agencies have documented that dental amalgam is the largest source of mercury in most people who have several amalgam fillings. Fish, vaccinations, and occupational exposure, such as dental offices, are other sources of significant mercury exposures. A nationwide survey found that over 22 percent of those tested for mercury levels in the hair had dangerous levels higher than the U.S. EPA mercury health reference level. Toxic metal levels were measured in 6-24 hours urinary samples of 100 randomly chosen patients with chronic conditions at the Institute of Integrative Medicine, following a combined EDTA/DMSA provocation challenge. Over 70% had levels of lead, arsenic, mercury, or cadmium outside the Laboratory Reference Level.
A large U.S. Centers for Disease Control epidemiological study, NHANES found that those with more amalgam fillings (more mercury exposure) have significantly higher levels of chronic health conditions. The conditions in which the number of dental amalgam surfaces were most highly correlated with disease incidence were MS, epilepsy, migraines, mental disorders, diseases of the nervous system, disorders of the thyroid gland, cancer, and infectious diseases.
Mercury and other toxic metals such as copper and lead cause breaks in and also have synergistic effects with x-rays. Several toxic metals, including arsenic, cadmium, chromium, and nickel, have been documented to be carcinogenic. Some of the mechanisms by which toxic metals such as mercury cause cancer have been documented by many medical studies. Low non-cytotoxic levels of mercury induce dose dependent binding of mercury to and significantly increased cell mutations and birth defects. In addition, mercury also promotes cancer by weakening the immune system, which contributes to increased chronic diseases like cancer.
Nobel Prize winner Dr. Otto Warburg determined that cancer has only one prime cause. It is the replacement of normal oxygen respiration of the body’s cells by an anaerobic (i.e., oxygen-deficient) cell respiration. Porphyrins are precursors to heme, the oxygen carrying component of blood. Mercury inhibits the conversion of specific porphyrins to heme. Mercury has been documented to bind to oxygen carrying sites in the blood, reducing a person’s available oxygen supply. Mercury binds with hemoglobin, which is located inside the red blood cell and carries oxygen for transport to tissues. Mercury binding to hemoglobin results in red blood cells carrying less oxygen and therefore less oxygen reaches tissues. The body senses the need for more oxygen and may attempt to compensate for this by increasing the production of hemoglobin. A normal or increased hemoglobin level combined with symptoms of lack of oxygen (fatigue, weakness, appearing pale, rapid heart rate, shortness of breath, etc) could indicate mercury toxicity. This can confuse some doctors since the patient seems like they are anemic but have seemingly fine blood counts. A new, well-documented book has more information on causes of cancer and effective natural treatments for cancer, including the toxic teeth connection.
At the energetic-molecular level, the boundary between health and the state of absence of health is marked by oxidosis, acidosis, and dysoxygenosis (dysox). There is but one fundamental difference between a healthy cell and an unhealthy cell: a healthy cell has a well preserved oxygen homeostasis. A healthy cell utilizes oxygen well, without incremental oxidative stress and without accumulating organic acids (acidosis). In contrast, an unhealthy cell cannot utilize oxygen well and gets clogged up with Krebs cycle metabolites and other organic acids. At the bioenergetic cellular level, all inflammatory, autoimmune, and neurodegenerative disorders are caused by the oxygen disorder (dysfunctional oxygen utilization) caused by cellular toxicity in the cells.
Mercury from dental amalgams appears to be one of the most, if not the most, potent disrupters of oxygen metabolism in the oral cavity. Other such disrupters are thioethers related to root canal teeth or cavitations and other microbial toxins. Those factors also alter the local conditions that either inhibit or foster microbial growth, thus facilitating biofilm formation. Such dynamics seem to play crucial roles in the pathogenesis of systemic disorders rooted in the oral cavity. The crucial importance of oral toxicity in triggering, amplifying, and perpetuating systemic inflammatory and infectious disorders has largely been ignored by most doctors and dentists.
The presence of the cellular dysox state can be readily documented by the measurement of 24-hour urinary excretion of organic acids.
Mercury has been found to bind oxygen binding sites in hemoglobin, thus reducing access to oxygen carried by the blood. Oxyhemoglobin saturation levels in venous blood should be at least 60% for normal levels. The majority of a group of 27 patients with amalgam dental fillings suffering from chronic fatigue whose oxyhemoglobin was tested had lower than normal oxyhemoglobin saturation levels. After amalgam replacement the majority of those with oxyhemoglobin levels equal to or less than 45% had significant increases in oxyhemoglobin saturation levels, on average about 15%. Heme is used for 2 main functions, in red blood cells and in production of energy by enzymatic processes in the ATP cytochrome oxidaze system. Mercury and other toxics have been documented to block these enzymatic processes, resulting in dumping porphyrin wastes into the urine rather than completing the proper heme functions. The level of these porphyrins in the urine can be measured by a standard urine test and the fractionated porphrin test. Levels indicate the level of toxic disruption of the basic enzymatic ATP production process. The majority of the patients in the study had high levels of porphyrins in the urine, which decreased significantly after amalgam replacement. This has also been confirmed by other studies.
Mercury from amalgam binds to the -SH (sulfhydryl) groups, resulting in inactivation of sulfur and blocking of enzyme functions such as cysteine dioxygenase, gamma-glutamyltraspeptidase and sulfite oxidase, producing sulfur metabolites with extreme toxicity that the body is unable to properly detoxify, along with a deficiency in sulfates required for many body functions. Sulfur is essential in enzymes, hormones, nerve tissue, and red blood cells. These exist in almost every enzymatic process in the body. Mercury also blocks the metabolic action of manganese and the entry of calcium ions into cytoplasm. Mercury from amalgam thus has the potential to disturb all metabolic processes. Mercury is transported throughout the body in blood and can affect cells in the body and organs in different ways causing numerous types of chronic health conditions, including blood conditions and cancer.
Mercury has a high affinity for and readily binds to selenium and to the thiol or sulfhydryl (sulfur/hydrogen combination) sites in living tissues. The higher the attraction between chemicals or elements, the stronger they bond to each other, and the harder it is to separate them. The thiol combination is extremely common in the human body. It occurs as part of certain amino acids, which are building blocks of proteins. Since these amino acids are used to build cells, hormones, and enzymes, the occurrence of the combination in the body is not only common but extremely important, as normal function is altered. There are several sites in the hemoglobin molecule in the red blood cells used to transport oxygen throughout the body. Mercury accumulates in red blood cells in humans and other animals. When mercury attaches to the thiol sites, the hemoglobin can’t carry as much oxygen as it could. This results in decreased availability of oxygen (hypoxia) that is needed by all body cells and explains one way that mercury toxicity can cause chronic fatigue symptoms and other effects of low oxygen levels in the cells.
Toxic metal exposure’s adverse influence on thyrocytes can play a major role in thyroid cancer etiology. Among those with chronic immune system problems with related immune antibodies, the types showing the highest level of antibody reductions after amalgam removal include thyroglobulin and microsomal thyroid antigens. Similar results regarding mercury have been found for treatment of other types of cancer. Studies have found conventional chemotherapy (alone) to be only a little more effective than no treatment, and clinical cases have demonstrated that detoxification and nutritional support can be effective in treating multiple myeloma and other cancers.
Exposure to mercury vapor causes decreased zinc and methionine availability, depresses rates of methylation, and increased free radicals—all factors in increased susceptibility to cancer and other chronic conditions. Amalgam fillings have also been found to be positively associated with oral cancer. Mercury from amalgam fillings has also been found to cause increase in white blood cells and in some cases to result in leukemia. There is evidence that some forms of leukemia are abnormal response to antigenic stimulation by mercury or other such toxics, and total dental revision including removal of amalgam has led to remission very rapidly in some cases. Among a group of patients testing positive as allergic to mercury, low level mercury exposure was found to cause adverse immune system response, including effects on vitro production of tumor necrosis factor TNF alfa and reductions in interleukin-1.
Mercury has been found to cause decreased sperm volume and motility, increased sperm abnormalities and spontaneous abortions, increased uterine fibroids/endometritis, and decreased fertility in animals and in humans. In studies of women having miscarriages or birth defects, husbands were found to typically have low sperm counts and significantly more visually abnormal sperm. It’s now estimated that up to 85% of the sperm produced by a healthy male is DNA-damaged. Abnormal sperm is also being blamed for a global increase in testicular cancer, birth defects, and other reproductive conditions.
There are extensive documented cases where removal of amalgam fillings led to cure or significant improvement of serious health problems such as oral keratosis (pre-cancer) and cancer (breast, leukemia, etc.). Some studies have found increased risk of lung, kidney, brain, and system cancers among dental workers. Other studies reviewed found increased rates of brain cancer related to mercury exposure. Dr. Max Daunderer’s serial biopsies on malignant tumors in-patients that had amalgam fillings found toxic metals contained in amalgam in the tumor. The concentration is highest in the center of the tumor (malignant melanoma, brain cancer, bladder, stomach, colon, and tongue cancer). An occupational study found that occupations with likely exposure to mercury or arsenic, such as dental nurses, displayed increased risk of melanoma.
Some studies have also found persons with chronic exposure to electromagnetic fields(EMF) to have higher release of mercury from dental amalgam, higher levels of mercury exposure and excretion, and higher likelihood of getting chronic conditions, like ALS, Alzheimer’s, and cancer.
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 intestine. This may cause leaky gut syndrome with toxic, incompletely digested complexes in the blood and accumulation of heliobacter pylori, a suspected major factor in stomach ulcers and stomach cancer and candida albicans, as well as poor nutrient absorption.
From extensive clinical experience, the spread of cancer has been commonly found to be related to fungal/Candida incidence, and treating Candida through blood alkalinity balance and reduction of toxic metals has been found to reduce the spread of cancer. Such treatments also increase oxygen supply to the cells. An anaerobic environment favors the development of yeast infections and cancer, since yeast is a fermenting spore and cancer is a fermenting cell rather than a normal respiratory (oxygen-using) cell.
Mercury has a symbiotic relation to Candida in the body and promotes the proliferation of Candida. Mercury impairs the body’s ability to kill Candida by impairment of the lytic activity of neutrophils and myeloperoxidase in workers whose mercury excretion levels are within current safety limits. Immune Th1 cells inhibit Candida by cytokine related activation of macrophages and neutrophils. Development of Th2 type immune responses deactivates such defenses. Mercury inhibits macrophage and neutrophil defense against Candida by its effects on Th1 and Th2 cytokine effects. Candida also methylates inorganic mercury to the highly toxic methyl-mercury form, which like mercury vapor readily crosses the blood-brain barrier, causes neurological damage, and weakens the immune system. Candidiasis is often observed in immunocompromised individuals such as those with toxic metal exposures, especially those who are found by test to be immune reactive to mercury or other toxic metals. Amalgam replacement cures or significantly improves Candida.
Nickel and beryllium are two other metals commonly used in dentistry that are very carcinogenic and toxic and cause malformations. Nickel ceramic crowns, root canals, and cavitations have also been found to be factors in some breast and other cancers. Some have recovered after dental treatments, which includes amalgam replacement, replacement of metal crowns over amalgam, nickel crowns, extraction of root canaled teeth, and treatment of cavitations where necessary. Nickel depletes intracellular ascorbate, which leads to the inhibition of cellular hydroxylases, manifested by the loss of hypoxia-inducible factor (HIF)-1alpha and -2alpha hydroxylation and hypoxia-like stress. Proline hydroxylation is crucial for collagen and extracellular matrix assembly as well as for assembly of other protein molecules that have collagen-like domains, including surfactants and complement. Thus, the depletion of ascorbate by chronic exposure to nickel could be deleterious for lung cells and may lead to lung cancer.
Root canals and cavitations also facilitate cancer by affecting the immune system. As more information is accumulated, it is apparent that these areas (bone cavitations) of chronic infection in the craniofacial area are very real and the probable cause of multiple painful conditions in the head, neck, and tooth area. This is due in part to the progressive loss of vascularity in the jaw bones and associated structures. This allows the pathogenic anaerobic microbial population to exist and create a chronic infected, inflamed area. This area is effectively isolated from the circulatory system which is responsible for delivering any anti-microbial medications to the infected area. These types of bone cavities have also been shown to have accumulations of toxic heavy metals, as well as the pathogenic microbes. There have been considerable numbers of cases documented of recovery from cancer after dealing with oral infections, such as root canals and cavitations.
Prostate cancer is the most commonly diagnosed cancer in men in the U.S. Over 300,000 new prostate cancer cases are diagnosed annually, constituting about 30% of all new male cancer cases, and more than 40,000 men die from the disease each year. Both breast cancer and prostate cancer are hormonally responsive, containing estrogen, androgen, and progesterone receptors. Genetic susceptibility and environmental factors that promote the sequence that results in clinical prostate cancer have been found to be factors in prostate cancer, with environmental factors being the larger with exposures in early life facilitating later effects. Low-level developmental exposures to substances that modulate endocrine activity can have life-long impacts if the exposure occurs during window(s) of unique vulnerability.
Cadmium and arsenic are known human carcinogens and are linked to prostate and breast cancer in epidemiologic and laboratory animal studies. Cadmium and arsenic have also been found to be associated with lung cancer. Food, cigarette smoke, and well water are 3 sources of cadmium exposure. Selenium (Se) in a large-scale human supplementation trial has been shown to significantly reduce the incidence of prostate cancer in elderly men. Because Se is known to interact with cadmium, it has been suggested that its cancer protective action could be attributable in part to its interaction with cadmium. The excessive accumulation of Cd in the prostates of smokers, along with sub-optimal Se intakes, could explain why smokers develop more aggressive and lethal forms of prostate cancer than nonsmokers. Toxic metals, such as mercury, lead, cadmium, and nickel, have been found to promote prostate cancer, and reducing toxic metal exposures and detoxification with nutritional support have been found to cure or result in significant improvement in the condition.
Dietary factors, such as consumption level of red meat smf refined carbohydrates, and environmental exposures to estrogenic chemicals have been found to increase the incidence of both prostate and breast cancer. Many occupational studies show an increased incidence of prostate cancer incidence and/or mortality among farmers and pesticide applicators. One in vitro study of human prostate cancer cells showed that several organochlorine pesticides, a pyrethroid, and a fungicide each caused proliferation of androgen-dependent cancer cells. Another “environmental estrogen,” bisphenol A (BPA, a component of epoxy resins, polycarbonate plastic, and dental sealants to which the general population is exposed at low levels) has been found to affect the prostate and be related to development of prostate cancer.
The toxic metals mercury, lead, cadmium, copper, cobalt, nickel, lead, aluminum, and tin have been found to have reproductive and endocrine system disrupting effects, as well as synergistic effects. The ability of metals to activate estrogen receptor-alpha (ERalpha) was measured in the human breast cancer cell line, MCF-7. Similar to estradiol, treatment of cells with the divalent metals copper, cobalt, nickel, lead, mercury, tin, and chromium or with the metal anion vanadate stimulated cell proliferation; by day six, there was a 2- to 5-fold increase in cell number. The metals also decreased the concentration of ERalpha protein and mRNA by 40-60% and induced expression of the estrogen-regulated genes progesterone receptor and pS2 by1.6- to 4-fold. Furthermore, there was a 2- to 4-fold increase in chloramphenicol acetyltransferase activity after treatment with the metals in COS-1 cells transiently cotransfected with the wild-type receptor and an estrogen-responsive chloramphenicol acetyltransferase reporter gene. The ability of the metals to alter gene expression was blocked by an antiestrogen, suggesting that the activity of these compounds is mediated by ERalpha. Aluminum in the form of aluminum chloride or aluminum chlorhydrate, which are used in antiperspirants, can interfere with the function of oestrogen receptors of MCF7 human breast cancer cells, both in terms of ligand binding and in terms of oestrogen-regulated reporter gene expression.
As previously seen, there are several estrogenic or carcinogenic metals, and clinical experience has found metals detoxification to be beneficial in cancer case treatment. There are also diet measures and supplements that have been found to be beneficial in preventing or treating cancer. A comprehensive and well-documented summary of natural cancer treatments clinically documented to be effective in treating cancer is Outsmarting Your Cancer. Many effective options are covered, with considerable detail and documentation.
Vit K2, Vit D, zinc, and green tea have all been found to be effective in preventing or treatment of prostate cancer and other types of cancer. Black tea theaflavins have been found to be effective at prevention of cigarette smoke-induced lung damage and cancer, and have demonstrated effectiveness in switching off the genes involved in many types of cancer. Studies have shown theaflavin supplementation significantly reduces levels of inflammatory cytokines such as TNF-alpha, Il-6, Il-8, and C-reactive protein and lowers rates of production of inflammation-generating transcription factor NF-kB, cytokine generating COX-2, and the adhesion molecule ICAM-1. Vitamin K2 has been shown to induce apoptosis in leukemia cells in vitro and inhibitory effects against myeloma and lymphoma, as well as being effective at reducing liver cancer in patients with hepatitis B or C (known risk factors for liver cancer), and also to be effective at reducing rate of re-occurrence of liver cancer in liver cancer patients in remission. Vit C and Vit K3 have been demonstrated to significantly delay cancer progression in a group of end stage prostate cancer patients.
Patients with advanced cancer have been found to be vitamin K deficient, and it is recommended to monitor levels and supplement when needed. Several studies found evidence of benefit of intravenous Vit C in treatment of cancer. A connection between cancer and fungus candida has been demonstrated, and many types of cancers have been successfully treated using sodium bicarbonate. Magnesium and Iodine have also been found beneficial in treating cancer and flax oil with cottage cheese, which addresses common digestive problems that can be related to cancer. Supplementation with chlorella has been found to result in beneficial effects when used in cancer patients or for other chronic conditions such as ulcerative colitis, hypertension, or fibromyalgia. Doctors have suggested that the mechanism by which chlorella improves treatment of such conditions is metals detoxification, which is the main mechanism of action of chlorella. People who drink two or more high fructose syrup sweetened soft drinks a week have a much higher (87%) risk of pancreatic cancer. The high levels of sugar in soft drinks may be increasing the level of insulin in the body, which the authors think contributes to pancreatic cancer cell growth.
Case #3: A 51 year-old male presented with stage-four squamous cell carcinoma located in the right pharyngeal-tonsil space. EG underwent conventional therapy with little to no success. Clinical exam revealed cavitational osteonecrotic lesion in the area of the lower right third molar. Soft tissue exam revealed swollen and inflamed pharyngeal arches, bilateral tonsilar inflammation and enlargement. Extraoral palpation revealed minor swelling of lymphatic nodes on the right side. Treatment goal was not to treat the cancer but to eradicate the infective state in the head and neck. EG was placed on a three month head and neck oxygen/ozone protocol developed by Dr. Mollica. This protocol was inclusive of direct and indirect infusion of 21 micograms/cc of oxygen/ozone into the afflicted areas. The afflicted areas showed osteonecrotic lesions, soft tissues, and lymphatic tissue. In addition to the oxygen/ozone therapy nutritional and drainage support was provided. Within a month after the completion of the protocol, EG was given an exam which included a PET scan. No trace of the cancer or any activity associated with the lesion was found, which was attributed to spontaneous remission.
- Documentation of the average level of mercury exposure from dental amalgam fillings, DAMS Intl, An Investigation of Factors Related to Levels of Mercury in Human Hair. J Pharmacol Exp Thera. 1975; 194(1): 171-181.
- Ozer EY, Rosenspire AJ, et al. Mercuric chloride damages cellular DNA by a non-apoptotic mechanism. Mutat Res. 2000 Oct 10; 470(1): 19-27.
- Ogura H, Takeuchi T, Morimoto K. A comparison of chromosome aberrations and micronucleus techniques for the assessment of the genotoxicity of mercury compounds in human blood lymphocytes. Mutat Res. 1996 Jun; 340(2-3): 175-82.
- Durham TR, Snow ET. Metal ions and carcinogenesis. EXS. 2006; 96: 97-130.
- Martin MB, Reiter R, Pham T, et al. Estrogen-like activity of metals in MCF-7 breast cancer cells. Endocrinology. 2003 Jun; 144(6): 2425-36.
- Darbre PD, Aluminium, antiperspirants and breast cancer. J Inorg Biochem. 2005 Sep; 99(9): 1912-9.
- Salnikow K, Kasprzak KS. Ascorbate depletion: a critical step in nickel carcinogenesis? Environmental Health Perspective. 2005 May; 113(5): 577-84.
- Perez-Gomez B, Aragones N, Gustavsson P, Plato N, Lopez-Abente G, Pollan M. Cutaneous melanoma in Swedish women: Occupational risks by anatomic site. Am J Ind Med. 2005 Oct; 48(4): 270-81.
- Ionescu JG, Novotny J, Stejskal VD, Latsch A, Blaurock-Busch E, Eisenmann-Klein M. Increased levels of transition metals in breast cancer tissue. Endocrinol Lett. 2006 Aug 5; 27(Suppl 1).
- Shukla VK, et al. Biliary heavy metal concentrations in carcinoma of the gall bladder: Case-control study. British Medical Journal. 1998; 317:1288-1289.
- Waldbrenner A, Runnebaum B. Heavy metals and fertility. J of Toxicology and Environmental Health. 1998; 54(8): 593-611.
- Gerhard I, Waibel S, Daniel V, Runnebaum B. Impact of heavy metals on hormonal and immunological factors in women with repeated miscarriages. Hum Reprod Update. 1998 May; 4(3): 301-309.
- Martin MB, Reiter R, et al. Estrogen-like activity of metals in MCF-7 breast cancer cells. Endocrinology. 2003 Jun; 144(6): 2425-36.
- Colborn T, Dumanoski D. Our Stolen Future, Ed. Myers JP. New York: Dutton Books, 1997.
- Drasch G, Schopfer J, Schrauzer GN. Selenium/cadmium ratios in human prostates: Indicators of prostate cancer risk of smokers and nonsmokers, and relevance to the cancer protective effects of selenium. Biol Trace Elem Res. 2005 Feb; 103(2): 103-7.
- Darbre PD. Aluminium, antiperspirants and breast cancer. J Inorg Biochem. 2005 Sep; 99(9): 1912-9.
- Salnikow K, Kasprzak KS. Ascorbate depletion: a critical step in nickel carcinogenesis? Environmental Health Perspective. 2005 May; 113(5): 577-84.
- Perez-Gomez B, Aragones N, et al. Cutaneous melanoma in Swedish women: Occupational risks by anatomic site. Am J Ind Med. 2005 Oct; 48(4): 270-81.
- Padayatty SJ, Riordan HD, Hewitt SM, Katz A,Hoffer LJ, Levine M. Intravenously administered vitamin C as cancer therapy: three cases. CMAJ. 2006 Mar 28; 174(7): 937-42.
- Padayatty, et al. Vitamin C pharmacokinetics: Implications for oral and intravenous use. Ann Intern Med. 2004 Apr 6; 140(7): 533.
- Gonzalez MJ, Miranda-Massari JR, et al. Orthomolecular oncology review: Ascorbic acid and cancer 25 years later. Integr Cancer Ther. 2005 Mar; 4(1): 32-44.
- Ionescu JG, Novotny J, Stejskal VD, Latsch A, Blaurock-Busch E, Eisenmann-Klein M. Increased levels of transition metals in breast cancer tissue. Neuro Endocrinol Lett. 2006 Aug 5; 27(1).
- 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.
- McFadden SA. Xenobiotic metabolism and adverse environmental response: Sulfur-dependent detox pathways. Toxicology. 1996; 111(1-3): 43-65.
- Langley-Evans SC, et al. SO2: A potent glutathione depleting agent. Comp Biochem Physiol Pharmocol Toxicol Endocrinol. 1996; 114(2): 89-98.
- Huggins HA, Levy TE. Uniformed Consent: The Hidden Dangers in Dental Care. Hampton Roads Publishing Company Inc., 1999.
- Ziff S, Ziff M. Infertility and Birth Defects: Is Mercury from Dental Fillings a Hidden Cause? Orlando, FL: Bio-Probe Inc., 1987.
- Khera, et al. Teratogenic and genetic effects of Mercury toxicity: The biochemistry of mercury in the environment. Teratology. 1979; 8: 293-304.
- Prati M, Gornati R, Boracchi P, et al. A comparative study of the toxicity of mercury dichloride and methylmercury, assayed by the frog embryo teratogenesis assay—xenopus (FETAX). Altern Lab Anim. 2002 Jan-Feb; 30(1): 23-32.
- Babich, et al. The mediation of mutagenicity and clastogenicity of heavy metals by physiochemical factors. Environ Res. 1985; 37: 253-286.
- Hansen K, et al. A survey of metal induced mutagenicity in vitro and in vivo. J Amer Coll Toxicol. 1984; 3: 381-430.
- Rodgers JS, Hocker JR, et al, Mercuric ion inhibition of eukaryotic transcription factor binding to DNA. Biochem Pharmacol. 2001 Jun 15; 61(12): 1543-50.
- Veltman JC, et al. Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland. Arch Biochem Biophys. 1986; 248(2): 467-78.
- Fowler BA, Woods JS, et al. Porphyrinurias induced by mercury and other metals. Toxicological Sciences. 2001; 197-198.
- Riedl AG, et al. P450 and hemeoxygenase enzymes in the basal ganglia and their roles in Parkinson’s disease. Adv Neurol. 1999; 80: 271-86.
- Ostman PO. Amalgam-associated oral lichenoid reactions: Clinical and histologic changes after removal of amalgam. Oral Surgery, Oral Medicine, and Endodontics. 1996; 81(4): 459-465.
- Ibbotson SH, et al. The relevance of amalgam replacement on oral lichenoid reactions. British Journal of Dermatology. 1996; 134(3): 420-3.
- Lindqvist B, et al. Effects of removing amalgam fillings from patients with diseases affecting the immune system. Med Sci Res. 24(5): 355-356, 1996.
- Berglund F. Case Reports Spanning 150 Years on the Adverse Effects of Dental Amalgam. Orlando, FL: Bio-Probe Inc., 1995.
- Nylander, et al. Mercury accumulation in tissues from dental staff and controls. Swedish Dental Journal. 1989; 13: 235-243.
- Colborn T, Ed. Chemically Induced Alterations in Functional Development. Princeton Scientific Press, 1992.
- Colborn, T. Developmental effects of endocrine-disrupting chemicals. Environ Heath Perspectives. 1993; 101(5): 1993.
- Doctors Data Lab. Cysteine metabolism and metal toxicity. Altern Med Rev. 1998; 3(4): 262-270.
- de Ceaurriz J, et al. Role of gamma-glutamyltraspeptidase and extracellular glutathione in dissipation of inorganic mercury. J Appl Toxicol. 1994; 14(3): 201.
- Aschner M, et al. Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury vapor. Brain Research. 1997; 8(1): 222-32.
- Aschner M, Rising L, Mullaney KJ. Differential sensitivity of neonatal rat astrocyte cultures to mercuric chloride (MC) and methylmercury (MeHg): Studies on K+ and amino acid transport and metallothionein(MT) induction. Neurotoxicology. 1996; 17(1): 107-16.
- O’Halloran TV. Transition metals in control of gene expression. Science. 1993; 261(5122): 715-25.
- Christensen MM, Ellermann-Eriksen S, Mogensen SC. Influence of mercury chloride on resistance to generalized infection with herpes simplex virus type 2 in mice. Toxicology. 1996, 114(1): 57-66.
- Ellermann-Eriksen S, et al. Effect of mercuric chloride on macrophage-mediated resistance mechanisms against infection. Toxicology. 1994; 93: 269-297.
- Christensen MM, et al. Comparison of interaction of meHgCl2 and HgCl2 with murine macrophages. Arch Toxicol. 1993; 67(3): 205-11.
- Ariza ME, Bijur GN, Williams MV. Lead and mercury mutagenesis: Role of H2O2, superoxide dismustase, and xanthine oxidase. Environ Mol Mutagen. 1998; 31(4): 352-61.
- Ariza ME, et al. Mercury mutagenesis. Biochem Mol Toxicol. 1999; 13(2): 107-12.
- Boffetta P, et al. Carciagenocity of mercury. Scand J Work Environ Health. 1993; 19(1): 1-7.
- Boeffetta P. Study of workers compensated for mercury intoxication. J Occup Med. 1994; 36(11): 1260-4.
- Zaichick Y, et al. Trace Elements and thyroid cancer. Analyst. 1995; 120(3).
- Langworth, et al. Effects of low exposure to inorganic mercury on the human immune system. Scand J Work Environ Health. 1993; 19(6): 405-413.
- Eggert-Kruse W, et al. Effect of heavy metals on in vitro interaction between human sperm and cervical mucus. Dtsch Med Wochenschr. 1992; 117(37): 1383-9.
- Ernst E, et al. Effect of mercury on human sperm motility. Toxicology. 1991; 68(6): 440-4.
- Daily A, et al. Declining sperm count: Evidence that Young’s syndrome is associated with mercury. BMJ. 1996; 313(7048): 44.
- Mohamed MK, et al. Effects of methyl mercury on testicular functions in monkeys. Toxicology. 1987; 60(1): 29-36.
- Ivanitskaia NF. Evaluation of effect of mercury on reproductive function of animals. Gig Sanit. 1991.
- Huggins HA. Proposed role of dental amalgam toxicity in leukemia and hemotopoietic dyscrasias. International J of Biosocial and Medical Research. 1989; 11: 84-93.
- Young WH, Greene WH. Origin of infections in acute non-lymphocytic leukemia. Annals of International Medicine. 1972; 77: 707-711.
- Kinjo Y, et al. Cancer mortality in patients exposed to methyl mercury through fish diet. J Epidemiol. 1996; 6(3): 134-8.
- Mathieson PW. Mercury: God of TH2 cells. Clinical Exp Immunol. 1995; 102(2): 229-30.
- Cohen EN, et al. Occupational disease in dentistry. JADA. 1980; 101(1): 21-31.
- Bjorklund G. Risk evaluation of the occupational environment in dental care. Tidsski Nor Laegeforen. 1991; 111(8): 948-50.
- Ahlbom A, et al. Dentists, dental nurses, and brain tumors. BMJ. 1986; 202(6521): 662.
- Nadarajah V, et al. Localized cellular inflammatory response to subcutaneously implanted dental mercury. J Toxicol Environ Health. 1996; 49(2): 113-25.
- Henningsson C, Hoffmann S, McGonigle L, Winter JS. Acute mercury poisoning mimicking pheochromocytoma in an adolescent. J Pediatr. 1993 Feb; 122(2): 252-3.
- Ma R, et al. Association between dental restorations and carcinoma of the tongue. European Journal of Cancer, Part B, Oral Oncology. 1995; 31B(4): 232-4.
- Acay, SC, Sousa OM, Felizzola CR. Evaluation of premalignancy in oral lichenplanus and oral lichenoid lesions using immunohistochemical expression of p53 and Ki67. Oral Oncology Supplement. 2005; 1(1): 155.
- Meleti, A. Ripasarti, et al. Lichenoid dysplasia and malignant transformation of oral lichen planus and oral lichenoid lesions. Oral Oncology Supplement. 2007; 2(1): 201.
- Improvement of nerve and immunological damages after amalgam removal. Amer J Probiotic Dentistry and Medicine. 1991.
- Yannai S, et al. Transformations of inorganic mercury by candida albicans. Applied Envir Microbiology. 1991; 7: 245-247.
- 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.
- Zamm AF. Removal of dental mercury: Often an effective treatment for very sensitive patients. J Orthomolecular Med. 1990; 5(53): 138-142.
- Myshkin AE, Khromova VS. Histidin as a mercurial poisoning inhibitor. Biochem Biophys Res Commun. 2000; 273(3): 816-9.
- Hamre HJ. Mercury from dental amalgam and chronic fatigue syndrome. CFIDS Chronicle. 1994 Fall: 44-47.
- Foster HD. The calcium-selenium-mercury connection in cancer and heart disease. Hypotheses. 1997; 48(4): 335-60.
- Whanger PD. Selenium in the treatment of heavy metal poisoning and chemical carcinogenesis. J Trace Elem Electrolytes Health Dis. 1992 Dec; 6(4): 209-21.
- Varga JM, et al. High incidence of cross stimulation by natural allergens of rat basophilic leukemia cells sensitized with IgE antibodies. Int Arch Allergy Immunol. 1995; 108(2): 196-9.
- Gainer JH, Activation of Rauscher leukemia virus by metals. J Natl Cancer Inst. 1973; 51(2): 609-13.
- Omura Y, et al. Role of mercury in resistant infections and recovery after Hg detox with cilantro. Acupuncture & Electro-Therapeutics Research. 1995; 20(3): 195-229.
- Omura Y. Mercury exposure from silver fillings. Acupuncture & Electrotherapy Research. 1996: 133.
- Woods JS, et al. Urinary profiles as biomarker of mercury exposure: Studies on dentists. J Toxicol Environ Health. 1993; 40(2-3): 235.
- Woods JS. Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity. Physiol Pharmocol. 1996; 74(2): 210-15.
- Martin MD, et al. Validity of urine samples for low-level mercury exposure assessment and relationship to porphyrin and creatinine excretion rates. J Pharmacol Exp Ther. 1996.
- Ahlbom A, et al. Dentists, dental nurses, and brain tumors. BMJ. 1986; 292.
- Perlingeiro RC, et al. Polymorphonuclear phagentosis in workers exposed to mercury vapor. Int J Immounopharmacology. 1994; 16(12): 1011-7.
- Bucio L et al. Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line. Res. 1999 Jan 25; 423(1-2): 65-72.
- Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspects of homocysteine neurotoxicity: Glutamate excitotoxicity, kinase hyperactivation and DNA damage. J Neurosci Res. 2002 Dec 1; 70(5): 694-702.
- Snyder RD, Lachmann PJ. Thiol involvement in the inhibition of DNA repairs by metals in mammalian cells. Source Mol Toxicol. 1989 Apr-Jun; 2(2): 117-28.
- Verschaeve L, et al. Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes. Muta Res. 1985; 157(2-3): 221-6.
- Verschaeve L. Genetic damage induced by low level mercury exposure. Environ Res. 1976; 12: 306-10.
- McKeever P, et al. Patterns of antigenic expression in human glioma cells. Crit Rev Neurobiology. 1991; 6: 119-147.
- Navas-Acien A, Pollan M, Gustavsson P, Plato N. Occupation, exposure to chemicals and risk of gliomas and meningiomas in Sweden. Am J Ind Med. 2002 Sep; 42(3): 214-27.
- Waring RH. Cysteine dioxygenase: Modulation of expression in human cell lines by cytokines and control of sulphate production. Toxicol In Vitro. 2002 Aug; 16(4): 481-3.
- Tanner CM, et al. Abnormal Liver Enzyme Metabolism in Parkinson’s. Neurology. 1991; 41(5): 89-92.
- Heafield MT, et al. Plasma cysteine and sulphate levels in patients with Motor neurone disease, Parkinson’s Disease, and Alzheimer’s Disease. Neurosci Lett. 1990; 110(1-2): 216-220.
- Pean A, et al. Pathways of cysteine metabolism in MND and ALS. J Neurol Sci. 1994; 124: 59-61.
- Steventon GB, et al. Xenobiotic metabolism in motor neuron disease. Neurology. 1990; 40: 1095-98.
- Gordon C, et al. Abnormal oxidation in systemic lupus erythrmatosus SLE. Lancet. 1992; 339: 8784, 25-6.
- Emory P, et al. Poor sulphoxidation in patients with rheumatoid arthritis. Ann Rheum Dis. 1992; 51(3): 318-20.
- Bradley H, et al. Sulfate metabolism is abnormal in patients with rheumatoid arthritis. Confirmation by in vivo biochemical findings. J Rheumatol. 1994 Jul; 21(7): 1192-6.
- Perry TL, et al. Hallevorden-Spatz disease: Cysteine accumulation and cysteine dioxygenase deficiency. Ann Neural. 1985; 18(4): 482-489.
- Freitas AJ, et al. Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain. Brain Research. 1996; 738(2): 257-64.
- Yallapragoda PR, et al. Inhibition of calcium transport by Hg salts in rat cerebellum and cerebral cortex. J Appl Toxicol. 1996; 164(4): 325-30.
- Chavez E, et al. Mitochondrial calcium release by Hg+2. J Biol Chem. 1988; 263(8): 3582.
- Sterzl I, Prochazkova J, Stejskal VDM, et al. Mercury and nickel allergy: Risk factors in fatigue and autoimmunity. Neuroendocrinology Letters. 1999; 20: 221-228.
- 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. www.nel.edu/pdf_/25_3/NEL250304A07_Prochazkova_.pdf
- Baranski B. Effect of mercury on the sexual cycle and prenatal and postnatal development of progeny. Med Pr. 1981; 32(4): 271-6.
- Hooper A, Mercury poisoning in dentistry. Wisconsin Medical J. 1980; 79.
- Shapiro IM, Cornblath DR, Sumner AJ. Neurophysiological and neuropsychological function in mercury-exposed dentists. Lancet. 1982; 1: 1147-1150.
- Uzzell BP and Oler J. Chronic low-level mercury exposure and neuropsychological functioning. J of Clin and Exper Neuropsych. 1986; 8: 581-93.
- Mayall FG, Hickman J, Knight LC, Singharo S. An amalgam tattoo of the soft palate: A case report with energy dispersive X-ray analysis. J Laryngol Otol. 1992; 106(9): 834-5.
- Pierson HF. Pharmacological perturbation of murine melanoma growth by copper chelates. Cancer Lett. 1985 Mar; 26(2): 221-33.
- Godfrey ME. Candida, dysbiosis, and amalgam. J Adv Med. 1996; 9(2).
- Romani L. Immunity to candida albicans: Th1,Th2 cells and beyond. Curr Opin Microbiol. 1999; 2(4): 363-7.
- Zamm AV. Candida albicans therapy: Dental mercury removal, an effective adjunct. J Orthmol Med. 1986; 4: 261-5.
- Stejskal J, Stejskal V. The role of metals in autoimmune diseases and the link to neuroendocrinology. Neuroendocrinology Letters. 1999; 20: 345-358.
- Panasiuk J, Peripheral blood lymphocyte transformation test in various skin diseases of allergic origin. Przegl Dermatol. 1980; 67(6): 823-9.
- van Benschoten MM, Acupoint energetics of mercury toxicity and amalgam removal with case studies. American Journal of Acupuncture. 1994; 22(3): 251-262.
- M.M. Van Benschoten and Associates. Available at: http://www.mmvbs.com. Accessed December 30, 2014.
- Dr. Clark Information Center. Available at: http://www.drclark.net. Accessed December 30, 2014.
- Gerson Institute. Available at: http://www.gerson.org/. Accessed December 30, 2014.
- Du Bois C, Lubecki J. The End of Cancer. Nelson’s Books, 2003.
- Klinghardt D, Mercury detoxification. Healing Cancer Naturally. Available at: http://www.healingcancernaturally.com/brain-cancer-cure-testimonials.html. Accessed December 30, 2014.
- Cure Zone: Cancer-Dental Risk. Available at: http://www.curezone.com/diseases/cancer/cancer_dental_risk.asp. Accessed December 30, 2014.
- Science and Environmental Health Network. Available at: http://www.sehn.org. Accessed December 30, 2014.
- van Wijngaarden E, Singer EA, Palapattu GS. Prostate-specific antigen levels in relation to cadmium exposure and zinc intake: Results from the 2001-2002 National Health and Nutrition Examination Survey. Prostate. 2008 Feb 1; 68(2): 122-8.
- Huff J, Lunn RM, Waalkes MP, Tomatis L, Infante PF. Cadmium-induced cancers in animals and in humans. Int J Occup Environ Health. 2007 Apr-Jun; 13(2): 202-12.
- Navarro Silvera SA, Rohan TE. Trace elements and cancer risk: A review of the epidemiologic evidence. Cancer Causes Control. 2007 Feb; 18(1): 7-27.
- Benbrahim-Tallaa L, Waalkes MP. Inorganic arsenic and human prostate cancer. Environmental Health Perspectives. 2008 Feb; 116(2): 158-64.
- Yu HN, Shen SR, Yin JJ. Effects of metal ions, catechins, and their interactions on prostate cancer. Rev Food Sci Nutr. 2007; 47(8): 711-9.
- Benbrahim-Tallaa MP. Inorganic arsenic and human prostate cancer. Environmental Health Perspectives. 2008 Feb; 116(2): 158-64.
- Huff J, Lunn RM, Waalkes MP, Tomatis L, Infante PF. Cadmium-induced cancers in animals and in humans. J Occup Environ Health. 2007 Apr-Jun; 13(2): 202-12.
- Navarro Silvera SA. Trace elements and cancer risk: A review of the epidemiologic evidence. Cancer Causes Control. 2007 Feb; 18(1): 7-27.
- Pereira M, et al. Soda drinkers have high pancreatic cancer risk. Cancer Epidemiology, Biomarkers & Prevention. 2010.
- Mercola, J. Prostate cancer treatment choices. 2009. Available at: http://articles.mercola.com/sites/articles/archive/2005/03/09/prostate-cancer-part-twelve.aspx. Accessed December 30, 2014.
- Yu HN, Shen SR, Yin JJ. Effects of metal ions, catechins, and their interactions on prostate cancer. Crit Rev Food Sci Nutr. 2007; 47(8): 711-9.
- Banerjee S, Manna S, Saha P, Panda CK, Das S. Black tea polyphenols suppress cell proliferation and induce apoptosis during benzo pyrene-induced lung cancer. Eur J Cancer Prev. 2005; 14(3): 215-21.
- Banerjee S, Manna S, Mukherjee S, et al. Black tea polyphenols restrict benzopyrene-induced mouse lung cancer progression through inhabitation of Cox-2 and induction of caspase-3 expression. Asian Pac J Cancer Prev. 2006; 7(4): 661-6.
- Beltz LA, Bayer DK, Moss AL, Simet IM. Mechanisms of cancer prevention by green tea and black tea polyphenols. Anticancer Agents, Med Chem. 2006; 6(5): 389-406.
- Kalra N, Set K, Prasad S, et al. Theaflavins induced apoptosis of LNCaP cells is mediated through induction of p53, down-regulation of NF-kappa B and mitogen-activated protein kinases pathways. Life Sci. 2007; 16: 80(23): 2137-46.
- Park AM, Dong Z. Signal transduction pathways: targets for green and black tea polyphenols. J Biochem Mol Biol. 2003 Jan 31; 36(1): 66-77.
- Eliaz I, Weil E, Wilk B. Integrative medicine and the role of modified citrus pectin/alginates in heavy metal chelation and detoxification—five case reports. Forsch Komplementärmed. 2007; 14: 358-364.
- Heyer NJ, Bittner AC, Echeverria D, Woods JS. A cascade analysis of the interaction of mercury and coproporphyrinogen oxidase (CPOX) polymorphism on the heme biosynthetic pathway and porphyrin production. Toxicol Lett. 2006 Feb 20; 161(2): 159-66.
- London SJ, Bowman JD, Sobel E, et al. Exposure to magnetic fields among electrical workers in relation to leukemia risk. Ind Med. 1994 Jul; 26(1): 47-60.
- Caplan LS, Schoenfeld ER, O’Leary ES, Leske MC. Breast cancer and electromagnetic fields—a review. Ann Epidemiol. 2000 Jan; 10(1): 31-44.
- Leffall L, et al. Environmental cancer risk: What we can do now? President’s Cancer Panel Report. 2008-2009.
- Malpas JS. Treatment options for multiple myeloma. NEJM. 2002.
- Cure Naturalli Cancro. Available at: http://www.curenaturalicancro.com/en/. Accessed December 30, 2014.
- Sircus M. Cancer articles. Available at: http://drsircus.com/cancer. Accessed December 30, 2014.
- Sircus M. Magnesium articles. Available at: http://drsircus.com/medicine/magnesium. Accessed December 30, 2014.
- Thought for Food. A mind-opening discussion on iodine with Dr. Mark Sircus podcast. 2007. Available at: http://phaelosopher.com/2007/08/01/an-mind-opening-discussion-on-iodine-with-dr-mark-sircus-podcast/. Accessed December 30, 2014.
- The Budwig Diet. Available at: http://www.cancertutor.com/Cancer/Budwig.html. Accessed December 30, 2014.
- 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. 2001 Feb-Mar.