A large U

Cancer Connection to Mercury, Toxic Metals, a= nd Dental Cavitations B Wi= ndham (Ed)

Medical labs, medical studies, and government agencies have documented that dental amalgam is the largest source of mercu= ry in most people who have several amalgam fillings (1). Fish, vaccinations, a= nd occupational exposure such as dental offices are other sources of significa= nt 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(2). Toxic metal levels were measure= d in 6-24 hours urinary samples of 100 randomly chosen patinets 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(571).

A large U.S. Centers for Disease Control epidemiological study, NHANES III, found that those with more amalgam fillings(more m= ercury exposure) have significantly higher levels of chronic health conditions(543= ). The conditions in which the number of dental amalgam su= rfaces were most highly correlated with disease incidence were MS, epilepsy, migraines, mental disorders, diseases of the nervous system, disorders of t= he thyroid gland, cancer, and infectious diseases (543).

Mercury and other toxic metals such as copper= and lead cause breaks in DNA (4,38,41,42,197,272,296) and also have synergistic effects = with x-rays(296) . Several toxic metals, including arsenic, cadmium, chromium, a= nd nickel, have been documented to be carcinogenic(= 5). Some of the mechanisms by which toxic metals such as mercury cause cancer h= ave been documented by many medical studies(5). Low non-= cytotoxic levels of mercury induce dose dependent binding of mercury to DNA and significantly increased cell mutations (= 142,4) and birth defects(197,38,105). In addition to effects on <= st1:stockticker>DNA, mercury also promotes cancer in other ways.= Mercury by its effect of weakening the immune system contributes to increased chron= ic diseases and cancer (91,180,228a,237,239,222,234,355,36= 9, 405,530,543,570, 35,38,40,etc.).

Nobel Prize winner Dr. Otto Warburg determine= d that cancer has only one prime cause (581). It is = the replacement of normal oxygen respiration of the body's cells by an anaerobic [i.e., oxygen-deficient] cell respiration. Porphy= rins are precursors to heme, the ox= ygen carrying component of blood. Merc= ury inhibits the conversion of specific porphyrins = to heme.&= nbsp; (84,35,201,539) Mercury has been documented to bind to oxygen carryi= ng sites in the blood, reducing a person’s available oxygen supply. (232= ,233,570,571). Mercury binds with hemoglobin, which is located inside the red blood cell and carries oxygen for transport to tissues. Mercury bound to hemoglobin results in less oxygen carrying capacity of the red blood cell a= nd therefore less oxygen will reach the 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 incre= ased hemoglobin level combined with symptoms of lack of oxygen (fatigue, weaknes= s, appearing pale, rapid heart rate, shortness of breath, etc) could indicate mercury toxicity. But this can confuse some doctors since the patient seems like they are anemic but in fact the blood counts seem fine (233).

= At the energetic-molecular level, the boundary between health and the state of abs= ence of health is marked by oxidosis, acidosis, and dysoxygenosis (dysox). (571,= 581) There is but one fundamental difference between a healthy cell and= an unwell cell: a healthy cell has a well preserved oxygen homeostasis. A heal= thy cell utilizes oxygen well, without incremental oxidative stress (oxidosis) and without accumulating organic acids (aci= dosis). In contrast, an unwell cell cannot utilize oxyge= n well and gets clogged up with Krebs cycle metabolites and other organic acids. At the bioenergetic cellular level, all inflammato= ry, autoimmune, and neurodegenerative disorders are caused by the oxygen disord= er (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(571,233). Other such disrupters are thioethers related to root canal teeth or cavitations and ot= her microbial toxins . Those factors also alter the local conditions that either inhibit or foster microbial growth, so facilitating biofilm formation. Such dynamics seem to play crucial roles in the pathogenesis of systemic disorde= rs rooted in the oral cavity. The crucial importance of oral toxicity in triggering, amplifying, and perpetua= ting 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 excre= tion of organic acids.

Mercury has been found to bind oxygen binding= sites in hemoglobin, thus reducing access to oxygen carried by the blood. (232,233,35,582) Oxyhemoglobin saturation levels in venous blood shoul= d 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(<= /span>232,35). After amalgam replacement the majo= rity of those with oxyhemoglobin levels equal to or = less than 45% had significant increases in oxyhemoglobin saturation levels, on average about 15%.&n= bsp; Heme is used for 2 main functions, in red blood cells and in product= ion of energy by enzymatic processes in the ATP cytochrome= oxidaze system. Mercury and other toxics have been documented to block these enzymat= ic processes, resulting in dumping porphyrin waste= s 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, the fractionated porphrin test, and indicate the level of toxic disrup= tion of the basic enzymatic ATP production process. The majority of the patients in the study had high levels of porphyrins in the urin= e, which decreased significantly after amalgam replacement. This has also been confirmed by ot= her studies(260,233).

Mercury from amalgam binds to the -SH (sulfhydryl) groups, resulting in inactivation of sulf= ur and blocking of enzyme functions such as cysteine <= span class=3DSpellE>dioxygenase(CDO), gamma‑ glutamyltraspeptidase(GGC) and sulfite oxidase, producing sulfur metabolites with extreme toxicity that the body is unable = to properly detoxify(33,111,114,405), along with a deficiency in sulfates requ= ired 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 (333). Mercury from ama= lgam thus has the potential to disturb all metabolic processes (33,35,60,111,114= ,180,181,194,333,405). 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 conditi= ons and cancer.

Mercury has a high affinity for and readily binds to selenium and to the = thiol or sulfhydryl (sulfur/hydrogen combinati= on) 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 extreme= ly common in the human body. It occurs as part of certain amino acids, which a= re building blocks of proteins. Since these amino acids are used to build cell= s, hormones, and enzymes, the occurrence of the thiol combination in the body is not only common but extremely important, as norm= al function is altered. There are several thiol si= tes 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 o= ther animals. When mercury attaches to the thiol sit= es, 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= 217;s adverse influence on thyrocytes can play a majo= r role in thyroid cancer etiology(144) . Among those with chronic imm= une system problems with related immune antibodies, the types showing the highe= st level of antibody reductions after amalgam removal incl= ude thyroglobulin= and microsomal thyroid antigens (91,369). 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 a= nd clinical cases have demonstrated that detoxification and nutritional suppor= t can be effective in treating multip= le myeloma (550) and other cancers(486,530,35,228a).

&= nbsp; Exposure to mercury vapor causes decreased zinc and methionine<= /span> availability, depresses rates of methylation, a= nd increased free radicals- all factors in increased susceptibility to cancer (14,34,38,43,143,144,180,237,239,251,256,283,530). Amalgam fillings have also b= een found to be positively associated with oral cancer (206,251,403). Mercury f= rom amalgam fillings has also been found to cause increase in white blood cells= and in some cases to result in leukemia (35,180). 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 (35,38,180,239). Among a group of patients testing positive as allergic to mercury, low level mercury exposure was found to ca= use adverse immune system response, including effects on vitro production of tu= mor necrosis factor TNF alfa and reductions in interleukin-1. (126,131,152)

Mercury has been found to cause decreased spe= rm volume and motility , increased sperm abnormalities and spontaneous abortio= ns, increased uterine fibroids/endometritis, and decreased fertility in animals (4,104,105,162) and in humans (9,10,23,31,37= ,105,146,159, 395,433,27,35,38). In&= nbsp; studies of women having miscarriages or birth defects, husban= ds were found to typically have low sperm counts and significantly more visual= ly abnormal sperm(393). It's now estimated that up to 85 per cent of the sperm produced by a healthy male is DNA-= damaged(433). &n= bsp; Abnormal sperm is also being blamed for a global increase in testicu= lar cancer, birth defects,= and other reproductive conditions.

There are extensive documented cases (many thousands) where removal of amalgam fillings led to cure or significant improvement of serious heal= th problems such as oral keratosis (pre cancer)(87,251), cancer (breast,leukemia,etc.) (35,38,94,180,228a,469,486,487,530). =

&n= bsp; Some studies have found increased risk of lung, kidney, brain, and CNS system cancers among dental workers (34,99,143,283). Other studies reviewed found increased rates of brain cancer related= to mercury exposure (193,383,328). Dr. Max Daunderer's ser= ial biopsies on malignant tumors in-patients that had amalgam fillings found toxic metals containe= d in amalgam in the tumor. The concentration is highest in the center of the tum= or (malignant melanoma, brain cancer, bladder, stomach, co= lon and tongue cancer). (570) An occupational study = found that Occupations with likely exposure to mercury or arsenic such as dental nurses displayed increased risk of melanoma (14).

&= nbsp; Some studies have also found persons with chronic exposure to electromagnetic fields(EMF) to have higher release of mercury from dental amalgam, higher l= evels of mercury exposure and excretion (28,251c) and higher likelihood of getting chronic conditions like ALS(526) and Alzheimer’s(251c) and cancer(= 546).

&= nbsp; Mercury causes significant destruction of stomach and intestine epithelial cells, resulting in damage&nb= sp; to stomach lining which along with mercury’s ability to bind to SH hydroxyl radical in cell membranes alters permeability(338,405,35,21c) and adversely alters bacterial populations in = the intestines- causing leaky gut syndrome with toxic, incompletely digested complexes in the blood(222,228b,35) and accumulation of heliobacter pylori, a suspected major factor in

s= tomach ulcers and stomach cancer(256) and candida albicans(404),

a= s well as poor nutrient absorption.=

From extensive clinical experience the spread= of cancer has been commonly found to be related to fungal/Candida incidence, a= nd treating Candida through blood alkalinity balance and reduction of toxic me= tals body level has been found to reduce the spread of cance= r(233a). Such treatments also increase oxyg= en supply to the cells. (580). An anaerobic en= vironment favors the development of y= east 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 i= n the body and promotes the proliferation of Candida. Mercury impairs the body’s ability to kill Candida albicans by impairment of the lytic activity of neutrophils and myeloperoxidase<= /span> in workers whose mercury excretion levels are within current safety limits(233,285,404).&= nbsp; Immune Th1 cells inhibit Candida by cytokine related activation of macrophages and neutrophils. Development of Th2 type immune res= ponses deactivate such defenses(404b,181). Mercury inhi= bits macrophage and neutrophil defense against Candi= da by its affects on Th1 and Th2 cytokine effects(181,= 285,404b). 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 ( 225,405 ) Candidiasis= is often observed= in immunocompromised individuals such as those with toxic metal exposures, especially those who are found by test to be immune reacti= ve to mercury or other toxic metals (60,235,405). Amalgam replacement cures or significantly improves Candida (404,222,35,etc.),

Nickel and beryllium are 2 o= ther metals commonly used in dentistry that are very carcinogenic, toxic, and ca= use DNA malformations (35,456,13= ). Nickel ceramic crowns, root canals= and cavitations have also been found to be a factor in some breast cancer and o= ther cancers and some have recovered after TDR, which includes amalgam replacement, replace= ment of metal crowns over amalgam, nickel crowns, extraction of root canaled teeth, and treatment of cavitations where nec= essary (35,200,228a,486,530). 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(13). Pr= oline hydroxylation is crucial for collagen and extracellula= r 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 n= ickel could be deleterious for lung cells and may lead to lung cancer.

Root canals and cavitations also facilitate c= ancer by effect on immune system. (570) &nb= sp; 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. (571) This is due in part to the progressive loss of vascularity in the jaw bones and associated structures. This allows the pathogenic anaerobic micro= bial 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 met= als, 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 cavi= tations. (571,etc.)

&= nbsp; Prostate cancer is the most commonly diagnosed cancer in men in the US<= span style=3D'font-family:Verdana'>. 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(490). Both breast cancer and prostate ca= ncer 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 fac= tors in prostate cancer, with environmental factors being the larger with exposu= res in early life facilitating later effects. Low-level developmental exposures= to substances that modulate endocrine activity can have life long impacts if t= he exposure occurs during window(s) of unique vulnerability.

Cadmium and arsenic are known human carcinogens and are linked to prostate & br= east cancer in epidemiologic and laboratory animal studies (490-494). Cadmium and arsenic have also been= found to be associated with lung cancer(491e,494c,etc.= ) Food, cigarette smoke, and well wat= er are 3 sources of cadmium exposure. Sel= enium (Se) in a large-scale human supplementation trial has been shown to significantly reduce the incidence of prostate cancer in elderly men. Becau= se Se is known to interact with cadmium (Cd), it h= as been suggested that its cancer protective action could be attributable in p= art to its interaction with cadmium(11). The excessive accumulation of Cd in the prostates o= f 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 have been found to cure or result in significant improvement= in the condition (490,491,486,530,531,11,35). =

&= nbsp; Dietary factors such as consumption level of red meat and environmental exposures to estrogenic chemicals have been found to increase the incidence of both pros= tate and breast cancer(490). Many occupational studie= s 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 severa= l organochlorine pesticides, a pyr= ethroid, and a fungicide each caused proliferation of androgen-dependent cancer cells (490). Another “environmental estrogen”, b= isphenol A (BPA-a component of epoxy resins, polycarbonate plastic, and dental seala= nts 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(490). =

&= nbsp; The toxic metals mercury, lead, cadmium, copper, cobalt, nickel, lead, aluminum, and tin have been found to have reproductive and endocrine system disrupting effects(10,12= ). The ability of metals to activate estro= gen receptor-alpha (ERalpha) was measured in the hu= man 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 van= adate stimulated cell proliferation; by d 6, 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 wa= s a 2- to 4-fold increase in chloramphenicol acetyltransferase activity after treatment with the m= etals in COS-1 cells transiently cotransfected with t= he wild-type receptor and an estrogen-responsive chloramp= henicol acetyltransferase reporter gene. The ability of= the metals to alter gene expression was blocked by an anti= estrogen, suggesting that the activity of these compounds is mediated by ERalpha(10,12). Aluminium in the form of alumini= um chloride or aluminium chlo= rhydrate, 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(12).

<= /span>

Cancer Treatments<= o:p>

As previously seen, th= ere are several estrongenic or carciagenic 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.

Vit K2, Vit D, zinc, and = green tea have all been found to be effective in preventing or treatment of prost= ate cancer and other types of cancer(501-503,493a). = Black tea theaflavins have been found to be effective= at prevention of cigarette smoke-induced lung damage and cancer(504), and have demonstrated = effectiveness in switching off the genes involved in many types of cancer(505). Studies h= ave shown theaflavin supplementation significantly reduces levels of inflammatory cytokines such as TNF-alpha, Il-6, Il-8, and C-reactive protein; and lowered rates of production of inflammation-generat= ing trasnscription factor NF-kB, cytokine generating COX-2, and the adhesion molecule ICAM-1(506). Vi= tamin K2 has been shown to induce apoptosis in leukemia cells in vitro and inhibi= tory 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(506). Apatone (Vit C & Vit K3= ) was demonstrated to significantly delay cancer progression in a group of end st= age prostate cancer patients.

Patients with advanced= cancer have been found to be vitamin K deficient and it is recommended to monitor levels and supplement where needed(506). Several studies found evidence of benefit of intravenous Vit C in treatment of cancer(15). A connection between cancer and fungus/candida has been demonstrated and many types of cancers have been successfully treated using sodium bicarbonate (551,552). Magnesium and Iodine have also been found beneficial in treating = cancer(552) and flax oil with cottage cheese which addresses common digestive problems = that can be related to cancer (553).

&= nbsp;

References<= o:p>

(1) Documentation of the average level= of mercury exposure from dental amalgam fillings, DAMS Intl,

&= nbsp; www.flcv.com/damspr1.html

(2) An Investigation of Factors Related to Levels of Mercury in Human Hair,

Environmental Quality Instit= ute, October 01, 2005,

www.greenpeace.org/raw/content/usa/press/reports/mercury-report= .pdf

www.greenpeace.org/usa/assets/binaries/addendum-to-mercury-report

(4) Lee IP,”Effects of Mercury on Spermatogenis= is”, J Pharmacol Exp Thera 1975, 194(1);171- 181; & Ben-Ozer EY, Rosenspire AJ, et al, Mercuric chloride damages cellu= lar DNA= by a non-apoptotic mechanism. Mutat Res. 2000 Oct 10;470= (1):19-27; & Ogura H, Takeuchi T, Morimoto K,&nbs= p; “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

(5) = Metal ions and carcinogenesis, Durham TR, Snow ET.,
EXS. 2006;(96):97-130; & (b) Estrogen-like activity of metals in MCF-7 breast cancer cells.Martin MB, Reiter R, Pham T= , Avellanet YR, Camara J, <= span class=3DSpellE>Lahm M, Pentecost E, Pratap K, Gilmore BA, Divekar S, Dag= ata RS, Bull JL, Stoica A,Endo= crinology. 2003 Jun;144(6):2425-36,&(c ) Aluminium, antiperspirants and breast cancer. Darbre PD., Division of Cell and Molecular Biology, School of Animal and Micro= bial Sciences, The <= span style=3D'font-size:10.0pt;line-height:108%;font-family:Verdana;mso-bidi-f= ont-family: Arial'>University of Reading, <= st1:address>P.O. Box 228, Whiteknights, Reading, RG6 6AJ, = UK. J Inorg Bioc= hem. 2005 Se p;99(9):1912-9,&(d) Ascorbate depletion: a critical step in nickel carcinogenesis? S= alnikow K, Kasprzak KS., Laboratory of Comparative Carcinogenesis, Building 538, Room 205 E., National Cancer Institute at Frederick/NIH, Frederic= k, MD 21702, USA., Environ Health= Perspect. 2005 May;113(5):= 577-84.& (e) Cutaneous melanoma in Swedish women: Occupa= tional risks by anatomic site. Perez-Gomez B, Aragones= N, Gustavsson P, Plato N, Lopez-Abe= nte G, Pollan M, Cancer and Environmental Epidemiol= ogy Section, National Center for Epidemiology, Carlos <= span style=3D'font-size:10.0pt;line-height:108%;font-family:Verdana;mso-bidi-fo= nt-family: Arial'>III Institute of Health, Madrid, Spain. Am J Ind Med. 2005 Oct;48(4):270-81, & (f) Increased levels of transition metals in breast cancer tissue.
Ionescu JG, Novotny J, Stejskal VD, Latsch A, Blaurock-Busch E, Eisen= mann-Klein M., Research Department of Spezialklinik Neukirchen, Neukirchen, Germany. Neuro = Endocrinol Lett. 2= 006 Aug 5;27(Suppl1). & (g) Bil= iary heavy metal concentrations in carcinoma of the gall bladder: case-control s= tudy
Shukla VK et al, Departments of Surgery and Com= munity Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi - 221 005, India, British Medical Journal 1998;317:1288-1289 http://www.melisa.= org/abstracts.php#1

(9)Gerhard = I, Monga B, Waldbrenner A, <= span class=3DSpellE>Runnebaum B “Heavy Metals and Fertility”, J of Toxicology and Enviro= nmental Health,Part A, 54(8):593-611, 1998; & (c) G= erhard I, Waibel S, Daniel V, Run= nebaum B “Impact of heavy metals on hormonal and immunological factors in women with repeated miscarriages”, Hum Reprod Update 1998 May;4(3):301‑309;

(10) Estrogen-like activity of metals in MCF= -7 breast cancer cells. Martin M= B, Reiter R, et al, Endocrinology. 2003 Jun;144(6):= 2425-36; & Dr.T<= /span>. Colborn, D.Dumanoski, JP Myers(Ed.), Our Stolen Future Dutton Books, NY, 1996;

(11) Selenium/cadmium ratios in human prostates: indicators of prostate cancer risk of smokers and nonsmokers, and relevance to the cancer protecti= ve effects of selenium. Drasch G, Schopfer J, Schrauzer GN., Biol Trace Elem Res. 2005 Feb;103(2):103-7.

(12) Aluminium, antiperspirants and breast c= ancer. Darbre PD., J Inorg= Biochem. 2005 Se p;99(9):1= 912-9.

(13) Ascorbate depletion: a critical step in nickel carcinogenesis? Salnikow K, Kasprzak KS., Environ Heal= th Perspect. 2005 May;113(5):= 577-84.

(14) Cutaneous melanoma in Swedish women: Occupational risks by anatomic site. Perez-Gomez B, Ar= agones N, et al, Am J Ind Med. 2005 Oct;48(4):270-81.
(15) Intravenously administered vitamin C as cancer therapy: three cases. <= span class=3DGramE>Padayatty SJ, Riordan HD, H= ewitt SM, Katz A, Hoffer LJ, Levine M., CMAJ. = 2006 Mar 28;174(7):937-42; & Vitamin C Pharmacokinetics: Implications for Or= al and Intravenous Use, Padayatty, et al. Ann Inte= rn Med. 2004 Apr 6;140(7):533-; & Orthomolecular oncology review: ascorbic acid and cancer 25 years later, Gonzalez MJ, Miranda-M= assari JR et al, Integr Cancer Th= er. 2005 Mar;4(1):32-44.

(16) Increased levels of transition metals in breast can= cer tissue. Ionescu JG, Novotny J, Stejskal VD, Latsch A, Blaurock-Busch E, Eisen= mann-Klein M, Neuro= Endocrinol Lett. 2006 Aug= 5;27(Suppl1)

(33) (a) Markovich et al, "Heavy metals (Hg,Cd<= /span>) inhibit the activity of the liver and kidney sulfate transporter Sat‑= 1", Toxicol = Appl Pharmacol, 1999,154(2):181‑7; & (b)2S.A.McFadden, “Xenobiotic metab= olism and adverse environmental response: sulfur-dependent d= etox pathways”,Toxicology, 1996, 111(1-3):43-6= 5; &(c) S.C. Langley-Evans e= t al, “SO2: a potent glutathion depleting agent”, Comp Biochem Physiol Pharmocol Toxicol <= span class=3DSpellE>Endocrinol, 114(2):89-98

(34) Pa= trickStörtebecker,Associate Professor of Neurology, Karolinska Institute, Stockholm= . Mercury Poisoning from Dental amalgam-A Hazard to the Human Brains, ISBN: 0-941011001-1

(35) (a)Hug= gins HA, Levy,TE, Uniformed Consent: the hidden d= angers in dental care, 1999, Hampton Roads Publishing Company Inc; & (c) Toxic Elemen= ts Research Foundation, Colorado Springs Colorado, “Survery of 1320 patients being treated for heavy metal toxicity”, 2001. 800-331-2303 www. peakenergy.com

(38) S.= Ziff and M.Ziff, Infertility and B= irth Defects: Is Mercury from Dental Fillings a Hidden Cause?, Bio-Probe, In= c. ISBN: 0-941011-03-8.1987

(41) Kh= era et al., Teratogenic and genetic effects of Mercury toxicit= y. The biochemistry of Mercury in the environment Nriagu<= /span>, J.O.Ed, Amsterdam, Elsevier, 503‑18,1979; & Teratology, 8: 293-304; &= ; Prati M, Gornati R, Boracchi P, Biganzoli E, = Fortaner S, Pietra R, Sabbioni E, Bernardini G.= 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):2= 3-32.

(42) Ba= bich et al ., The mediation of m= utagenicity and clas= togenicity of heavy metals by physiochemical factors.= Environ Res., 1985:37;253‑286; &= ; K.Hansen et al A survey of metal induced mutagenicity <= /span>in vitro and in vivo, J Amer = Coll Toxicol , 1984:3;381‑430; & Rodgers J= S, Hocker JR, et al,&nb= sp; Mercuric ion inhibition of eukaryotic transcription factor binding t= o DNA= . B= iochem Pharmacol. 2001 Jun 15;61(12):1543-50.

(43) M. J. McCabe, University of Rochester School of Medicine & Dentistry, 2002, Mechanisms of Immunomodulation by Metals, www2.envmed.rochester.edu/envmed/TOX= /faculty/mc= cabe.html;

(60) Melisa Medica Foundation,= http://www.melisa.org/candida.ph= p ; & VDM Stejskal et al, "MELISA: tool for the study of m= etal allergy", Toxicology in Vitro, 8(5):991-1000, 1994;<= /p>

(84) J.C.V= eltman et al, “Alterations of heme, cytochrome P= -450, and steroid metabolism by mercury in rat adrenal gland”, Arch Biochem Biophys, 1986, 24= 8(2):467-78; & Po= rphyrinurias Induced by Mercury and Other Metals, B.A. Fowler, J.S. Woods, et al, Toxicologic= al Sciences 61, 197-198 (2001), & A.= G.Riedl et al, Neurodegenerative Disease Research Center, King’s College, UK, “P450 and hemeoxygenase enzymes in the ba= sal ganglia and their role’s in Parkinson’s disease”, Adv Neurol, 1999; 80:271-86;

(87) P.O.Ostman et al, “Amalgam-associated oral lic= henoid reactions: Clinical & histologic changes aft= er removal of amalgam”, Oral Surgery, Oral Medicine= , and Endodonti= cs, 1996, 81(4):459-465; & S.H.Ibbotson<= /span> et al, “The relevance of amalgam replacement on oral lichenoid reactions”, British Journal of Dermatology, 134(3):420-3, 1996; (270 cases)

(91) B= .Lindqvist et al, "Effects of removing amalgam fillings from patients with diseas= es affecting the immune system", Med Sci Res = 24(5): 355-356, 1996.

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

(99) M. Nylander et al, Mercury accumulation in tissues from dental staff and controls”, Swedish De= ntal Journal, 13:235-243, 1989

(105) T.Colborn(Ed.),Chemically Induced Alterations in Functional Development, Princeton Scientific Press,1992; & ” Developm= ental Effects of Endocrine-Disrupting Chemicals",Enviro= n Heath Perspectives, V 101, No.5, Oct 1993

(111) (a) <= span class=3DSpellE>Quig D, Doctors Data Lab,"C= ysteine metabolism and metal toxicity", Altern Med Rev, 1998;3:4, p262‑270, & (b) J.de Ceaurriz et al, Role of gamma‑ glutamyltrasp= eptidase(GGC= ) and extracellular &= nbsp; glutathione in dissipation of inorganic mercury",J Appl Toxicol,1994, 14(3): 201

(114) M.Aschner et al, “Metallothionein induction in fetal r= at brain by in utero exposure to elemental mercury vapor”, Brain Research, 1997, dec 5, 778(1):222-32= ; & Aschner M, Rising L, Mull= aney KJ. Differential sensit= ivity of neonatal rat astrocyte cultures to mercuric chloride (MC) and methylmercury (MeHg): studies on K+ and amino acid transport and metallothio= nein (MT) induction. Neurotoxicology. 1996 Spring;17(1):107-16. & T.V. O’Halloran, “Transition metals in control= of gene expression”, Science, 1993, 261(5122):715-25;<= /p>

(131) Christensen MM, Ellermann-Eriksen S, Mogensen SC. Influence of mercury chloride on r= esistance to generalized infection with herpes simplex virus type 2 in mice. Toxicology 1996, 114(1): 57-66; & S.Ellermann-E= riksen et al, "Effect of mercuric chloride on macrophage-mediated resistance mechanisms against infection", Toxicology, 93:269-297,1994; &M.M.Christensen et al, Institute of Medical Microbiol= ogy, “Comparison of interaction of meHgCl2 and HgCl2 with murine macrophages”, Arch Toxicol, 1993, 67(3):2= 05-11;

(142) Ariza M= E; Bijur GN; Williams MV. Lead and mercury mutagenesis= : role of H2O2, superoxide

= dismustase, a= nd xanthine oxidase. Environ Mol Mutagen 1998;31(4):352‑61; & M.E. Ariza et al,

&= nbsp; “Mercury mutagenesis”, Biochem Mol Toxicol, 1999, 13(2):107-12; = &nb= sp;

(143) P.Boffetta et al, "Carciage= nocity of mercury", Scand J Work Environ Health, 1993,19<= /span>(1):1-7, & “Study of workers compensated for mercury = intoxication”,J Occup Med, 1994,36(11):1260-4; & J Occup Med, 36(11):1260-64, 1994;

(144) .Y Zaichick et al,”Trace Elements and thyroid cancer",Analyst, 120(3),1995.

(152) Langworth et al, “Effects of low exposure to inorganic mercury on the human immune system”, Scand J Work Environ Health, 19(6): 405-413.1993;

(159) W.Eggert-Kruse et al, “Effect of heavy metals on in vitro interaction between human sperm and cervical mucus”, Dtsch Med Wochenschr , 1992, 117(37):1383-9(German); E.Ernst et al, “Effect of mercury on human sperm motility”, Toxicol 1991, 68(6):440-4; & A= .Daily et al, “Declining sperm count: evidence that Young’s syndrome is associated with mercury”, BMJ, 1996, 313(7048): 44;=

(162) M.K.Mohamed et al, “Effects of methyl mercury on testicular functions in monkeys”.Toxicol,= 1987, 60(1):29-36= ;

& N.F. I= vanitskaia,” Evaluation of effect of mercury on reproductive function of animals”, Gig Sani= t, 1991, 12: 48-51;

(180) Pinto OF et al, J Intl Acad Prev Med, Vol 3, No.2, 1976; & Huggins HA, Proposed r= ole of dental amalgam toxicity in leukemia and hemotopoietic<= /span> dyscrasias.&nb= sp; International J of Biosocial and Medical Research, 1989, 11:84-93; & S= chimpff SC, Young WH, Greene WH, Origin of infections in acute nonlymphocytic leukemia. Annals of Internati= onal Medicine 1972, 77:707-711; & Y.Kinjo et al, “Cancer morta= lity in patients exposed to methyl mercury through fish diet”, J Epidemiol, 1996, 6(3):134-8..

(181) P.W= . Mathieson, “Mercury: god of TH2 cells”,1995, Clinical Exp Immunol.,102(2):229-30<= /span>

(193) E.N.Cohen et al, “Occupational disease in dentistry”, Amer. Dent Assoc, 1980, 101(1): 21-31; & = G.Bjorklund, “Risk evaluation of t= he occupational environment in dental care”, Tidssk= i Nor Laegeforen, 1991, 111(8): 948-50; & A.Ahlbom et al, :Dentists,= dental nurses, and brain tumors”, Br Med J, 1986, 202(6521):662. =

(200) V.Nadarajah et al, “Localized cellular inflammatory response to subcutaneously impla= nted dental mercury”, = J Toxicol Environ Health, 1996, 49(2):113-25; Kulacz & Levy , "The Roots of Disease". Xlibris= Corporation at 1-888-795-= 4274 www.xlibri= s.com; & B.E. Haley, Dental Lab, www.altcorp.com

(201) Henningsson C, Hoffmann S, McGonigle L, Winter JS. A= cute mercury poisoning mimicking pheochromocytoma&n= bsp; in an adolescent. J Pediatr 1993 Feb;122(2):252‑3

(206) R. Ma et al, “Association between d= ental restorations and carcinoma of the tongue”, European Journal of Cancer= . Part B, Oral Oncology, 1995; 31B(4): 232-4.R.

(222) M. Daunderer, <= u>Handbuch der Amalgamvergiftu= ng, Ecomed Verlag, Landsberg 1998, ISBN 3‑609‑71750‑5 = (in German); & “Improvement of Nerve and Immunological Damages after Amalgam Removal”, Amer. J. Of Probiotic Dentistry and Medicine, Jan 1991;

(225) S. = Yannai et al, “Transformations of inorganic mer= cury by candida&nbs= p; albicans ”, Applied Envir Microbiology,1991, 7:245-247; & &= nbsp; Ridley WP, Dizikes L, Cheh A, Wood JM. Recent studies on= biomethylation and demethylation= of toxic = elements. Environ Health Perspect 1977 Aug;19:43‑6

(228) (a)A.F.Zamm, “Removal of dental mercury: often an effective treatment for very sensitive patients”, J Orthomolecular Med, 1990, 5(53):138-142. (2= 2 patients), & (b)Dr. T. Rau, Paracelsus Alergy Clinic, Lustmuhle, Switzerla= nd, Allergies: Causes, Clarification, Treatment; Explore, 8(4),1996, www.explorepub.com/articles/bio‑therapy.html ;

(232) H.A. Huggins study funded by Adolph Coors Foundation, Denver, Study of blood chemistry changes related to the presence or absence of amalgam in 30 patie= nts,

(233)(a) Surviving The Toxic Crisis = by William R. Kellas , An= drea S. Dworkin , Comprehensive Health, 1996; & (b) Histidin as a mercurial poisoning inhibitor. Myshkin AE, Khromova VS. Biochem Biophys Res Commun. 2000 273(3):816-9;

(235) H.J.Hamre, Mercury from Dental Amalgam and Chronic Fatigue Syndrome”, The CFIDS Chronicle= , Fall 1994, p44-47.

(237) H.D.Foster, The calcium-selenium-mercury connection in cancer and heart disease”, Hypotheses, 1997, 48(4):335-60; & Whanger PD. Selen= ium in the treatment of heavy metal poisoning and chemical carcinogenesis.<= span style=3D'mso-spacerun:yes'> J Trace Elem Electrolytes Health Dis. 1992 Dec;6(4):209-21. <= o:p>

(239) J.M.Varga 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; & J.H.Gainer, “Activation of Rauscher leukemia virus by metals”, J Natl Cancer Inst, 1973, 51(2).609-13.

(251) (a) Y.Omura e= t al, Heart Disease Research Foundation, NY,NY, “Role of mercury in resistant infections and recovery after Hg detox with cilantro”, Acupuncture & Electro-Therapeutics Research, 20(3):195-229, 1995; &(b) “Mercury expo= sure from silver fillings”, Acupuncture & Electrotherapy Res, 1996, 133- & The mercury connection to oral cancers, DAMS, www.flcv.com/olp.html<= /span>

(256) D.B.Alymbaevae= t al, Med Tr Prom Ekol, 6:13-15, 1995 (Russian)

(260) J.S. = Woods et al, “Urinary porphyrin profiles as biomarker of mercury exposure: studies on dentists”, J Toxicol Environ H= ealth, 40(2-3):1993, p235-; & “Altered porphyrin metabolites as a bioma= rker of mercury exposure and toxicity”, Physiol Pharmocol, 1996,74(2):210-15, & Canadian J Physiology and Pharmacology, Feb 1996; &= M.D.Martin et al, “Validity of urine samples for low-level mercury exposure assessment and relationship to porphyrin and creatinine excretion= rates”, J Pharmacol Exp Ther, Apr 1996;

(271) , “Alternative treatment of Multiple Schlerosis, Tumor, or Cancer”, Institute for Naturopathic Medicine 1997 (40 MS cases), = http://home,t‑online.de/home/Institut_f._Naturheilverfahren/pa= tinf.htm" = &nb= sp;

(283) A.Ahlbom et al, “Dentists, dental nurses, and brain tumors”, British Medical Journal, Vol292, March 8, 1986, p262.

(285) R.C.Perlingeiro et al, “Po= lymorphonuclear phagentosis in workers expo= sed to mercury vapor”, Int J Immounopharmacology= ”, 16(12):1011-7,1994; & Hum Exp Toxicol 1995, 14(3):281-6;

(296) L.Bucio= et al, Uptake, cellular distribution and DNA= damage pro= duced by mercuric chloride in a human fetal = ; hepatic cell line. Mutat Res 1999 Jan 25;423(= 1‑2):65‑72; & (b) Ho PI, Ortiz D, Rogers E, Shea TB. = Multiple &= nbsp; aspects of homocysteine neurotoxic= ity: glutamate excitotoxicity, = kinase hyperactivation and DNA= damage. J Neuro= sci Res. 2002 Dec 1;70(5):694-702; &(c) Snyder R= D; Lachmann PJ; <= /span>Thiol involvement in the inhibition of DNA= repair by = metals in mammalian = cells. Source Mol To= xicol, 1989 &n= bsp; Apr‑Jun, 2:2, 117‑28 ; & L.Verschaeve et al, “Comparative in vitro cytogenetic studies in mercury-exposed hu= man lymphocytes”, Muta R= es, 1985, 157(2-3):221-6; & L.Verschaeve,= “Genetic damage induced by low level mercury exposure”, Envir Res,12:306-10,197= 6.

(328) P.McKeever et al, “Patterns of antigenic expres= sion 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.

(330) (a) Wilkinson LJ, Waring RH. Cysteine dioxygenase: modulation of expression in human cell l= ines by cytokines and control of sulphate production= . Toxicol In Vitro. 2002 Aug= ;16(4):481-3;; & (b) C.M. Tanner et al,“Abnormal Liv= er Enzyme Metabolism in Parkinson’s”,Neurolog= y, 1991, 41(5): = Suppl 2, 89-92; & &nb= sp; M.T.Heafield et al, "Plasma cysteine and sulphate lev= els in patients with Motor neurone disease, Parkinson's Disease, and Alzheimer’s Disease", Neurosci= Lett, 1990, 110(1‑2), 216,20; & A= .Pean et al, "Pathways of cysteine metabolism in= MND= /ALS= ", J <= span class=3DSpellE>neurol Sci, 1994, 124, Suppl:59‑61; & Stevent= on GB, et al; Xenobiotic metabolism in motor neuron disease, The Lancet, <= st1:date Year=3D"1988" Day=3D"17" Month=3D"9" ls=3D"trans">Sept 17 1988, p 644-47;= & Neurology 1990, 40:1095= -98.

(331) C.Gordon et al, “Abnormal = sulphur oxidation in systemic lupus erythrmatosus(SLE= )”, Lancet, = 1992,339:8784,25-6; & P.Emory et al, “Poor sulphoxidation in patients with rheumatoid arthitis”, Ann Rheum = Dis,&nb= sp; 1992, 51:3,318-20; &am= p; 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; & T.L. Perry et al, “= Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase defieciency”, Ann Neural, 1985, 18(4):482-489.<= o:p>

(333) A.J.Freitas et al, “Effects of Hg2+ and CH3Hg+ = on Ca2+ fluxes in the rat brain”, = Brain Research, 1996, 738(2): 257-64; & P.R.Yallapragoda= et al,“Inhibition of calcium transport by= Hg salts” in rat cerebellum and cerebral cortex”, J Appl toxicol, 1996, 164(4= ): 325-30; & E.Chavez et al, “Mitochondrial cal= cium release by Hg+2",J Biol Chem, 1988, 263:8, 3582-;

(369) Sterzl I, Prochazkova J, Stejskal VDM et al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity. N= euroendocrinology Letters 1999; 20:221-228; & Prochazkova= J, Sterzl I, Kucerova H, Bartova J, Stejskal VD; The beneficial effect of amalgam replacement on health in patien= ts with autoimmunity. Neuro Endocrinol = Lett. 2004 Jun;25(3):211-8. www.nel= .edu/pdf_/25_3/NEL250304A07_Prochazkova_.pdf

(395) Baranski B. Environmental Health Perspectives 1993; 1= 01(suppl 2): 85-90; & (b)Baranski B.&n= bsp; Effect of = mercury on the sexual cycle and prenatal and postnatal development of progeny. Med Pr 1981; 32(4): 271-6; &a= mp;(c) Hooper A, Mercury poisoning in Dentistry, Wisconsin Medical J, Aug 1980, vol 79; & (d) Shapiro IM, Co= rnblath DR, Sumner AJ. Neurophysiological and neuropsychological function in mercury-exposed dentists. The Lancet 1982; 1:1147-1150; &a= mp;(e) Uzzell BP and Oler = J. Chronic low-le= vel mercury exposure and neuropsychological = functioning. J of Clin and Exper Neuropsych 1986; 8:= 581-93;

(403) Mayall FG; Hickman J; Knight LC; Singharo S. "An amalgam ta= ttoo of the soft palate: a case report with &nbs= p; energy dispersive X-ray analysis. J = Laryngol Otol, 1992 Sep, = 106:9, 834-5; & Pierson HF.

"Pharm= acological perturbation of murine melanoma growth by coppe= r chelates.Cancer Lett, 198= 5 Mar, =

26:2, 221-3= 3.

(404) M. E. Godfrey, Candida, Dysbiosis and Amalgam. J. Adv. Med. vol 9 no 2 (1996); &

Romani L, Immunit= y to Candida Albicans: Th1,Th2 cells and beyond. Curr Opin Microbiol 1999, 2(4):363-7; & Alfred V. <= span class=3DSpellE>Zamm. C= ANDIDA ALBICANS THERAPY: Dental mercury removal, an effective adjunct. J. Orthmol. Med. v1#4 pp261-5 (1986)

(405) Stejskal J, Stejskal V. The role of metals in autoimmune diseases and the link to

neuroendocrinology Neuroendocrin= ology Letters, 2= 0:345‑358, 1999. www.melisa.org/knowledge/education14.html

(456) Panasiuk J , Peripheral blood lymphocyte transformation test in various skin diseases of allergic origin. Przegl Dermatol 1980;67(6)= :823‑9 [Article in Polish] = ; (nickel & lupus)

(469) M.M. van Bens= choten, ““Acupoint Ene= rgetics of Mercury Toxicity and Amalgam Removal with Case Studies,”” American Journal of Acupuncture, Vol. 22, No. 3, 1994, pp. 251-262; & M.M. Van Bens= choten and Associates, Reseda, Calif. Clinic; http://www.mmvbs.com/

(486) Dr. <= span class=3DSpellE>Hulda Clark, The Cure for All Cancers, 1998, www.drclark.net; = ;& Gerson <= /span>

Clinics, www.gerson= .org ; & Charlott= e Du Bois and John Lubecki,= The End of Cancer, Nelson’s Books, 2003; & Mercury detoxification, Healing Cancer Naturally, Dr. D. Kling= hardt, www.healingcancernaturally.com/brain-cancer-cure-testimonials.html<= /a> &

The Canc= er Homepage, www= .curezone.com/diseases/cancer/cancer_dental_risk.asp =

(487) Dr. Hulda Clark, The Cure of HIV/AIDS, New Century Press, = 1993; &

Dr. Hulda<= /span> Clark, The Cure for All Diseases, New Century Press, 2000, www.consumerhealth.org/articles/display.cfm?ID=3D19990303133500=

(490) Prostate cancer, Ted Schettler= , MD, Science Director, Science and Environmental Health Network, and Chair, Science Work Group, CHE, http://www.protectingourhealth.org/newscience/prostate/2= 003-04peerreviewprostate.htm

(491) DOH, Agency for Toxics Substances and Disease Registry 1997; Waalkes 2000); & (c) Prostate-specific antigen levels in relation to cadmium exposure and zinc intake: results from the 2001-2002 National Health and Nutrition Examination Survey. van Wijngaard= en E, Singer EA, Palapattu GS. Prostate. 2008 Feb 1;68(2):122-8; & (d) Cadmium-induced cancers in animals and in humans. Huff J, Lu= nn RM, Wa= alkes MP, <= /span>Tomatis L, Infante PF. Int J Occup Environ Health. 2007 Apr-Jun;13(2):202-12; &(e) Trace elements and cancer risk: a review of the epidemiolog= ic evidence. Navarro Silvera SA, Rohan TE. C= ancer Causes Control. 2007 Feb= ;18(1):7-27

(492) Inorganic arsenic and h= uman prostate cancer. Be= nbrahim-Tallaa L, <= /span>Waalkes MP. Environ Health Perspect. 2008 Feb;116(2):= 158-64

(501) European Prospective Investigation into Cancer = and Nutrition (EPIC), <= /span>American Journal of Clinical Nutrition. 87(4):985-92 ; & NutraIngredients.com April 9, 2008 =

(493) Effects of metal ions, = catechins, and their interactions on prostate cancer.= Yu HN, Shen SR, Yin JJ. Crit Rev Food Sci N= utr. 2007;47(8):711-9; & (b)In= organic arsenic and human prostate cancer. Benbrahim-Tallaa L, Waalkes MP. Environ Health Perspect. 2008 Feb;1= 16(2):158-64

(494) (= a) Cadmium-induced cancers = in animals and in humans. Hu= ff J, Lunn RM, Waalkes MP, Tomatis L<= span style=3D'font-size:10.0pt;font-family:Verdana;font-weight:normal;mso-bidi-f= ont-weight: bold;font-style:normal;mso-bidi-font-style:italic'>, Infante PF. Int J = Occup Environ Health. 2007 Apr-Jun;13(2):202-12, & (b) Trace elements and cancer risk: a review of the epidemiolo= gic evidence. Navarro Silvera SA, Rohan TE= . Cancer Causes Control. 2007 Feb;18(1):7-27; & (c) Prostate-specific antigen levels in relation to cadmium exposure and zinc intake: results from the 2001-2002 National Health and Nutrition Examination Survey. van Wijngaarden E, Singer EA, Palapattu GS. Prostate.= 2008 Feb 1;68(2):122-8.<= /o:p>

(502) Vitamin D from Sunshine, = = &nb= sp; http://articles.mercola.com/sites/articles/arc= hive/2005/03/09/prostate-cancer-part-twelve.aspx; & http://articl= es.mercola.com/sites/articles/archive/2007/08/24/lack-of-sunshine-causes-60= 0-000-cancers-a-year.aspx?PageIndex=3D2

(503) Effects of metal ions, catechins, and t= heir interactions on prostate cancer. Yu HN, Shen SR, Yin JJ. Crit R= ev Food Sci Nutr. 2007;47(8):711-9.

(504) Banerj= ee S, Manna S, Saha P, Panda CK, Das S. Black tea polyphenols suppress cell proliferation and induce apoptosis during benzo(a)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 thr= ough inhabitation of Cox-2 and induction of caspase-3 expression. Asian Pac J Cancer Prev. 2006, 7(4):661-6; & Banerjee S, Maity P, Mukherjee S et al, Black tea prevents cigarette smoke-induced apoptosis and lung damage, J Inflamm (Lond.) 2007: 43.

(505) Beltz<= /span> LA, Bayer DK, Moss AL, Simet IM. Mechanisms of cancer prevention by green tea and black tea polyph= enols. Anticancer Agents, Med Chem. 2006<= span class=3DGramE>, 6(5):3= 89-406; & Kalra N, Set K, Prasad S, et al, Theaflavins induced apo= ptosis of LNCaP cells is mediated through induction of= p53, down-regulation of NF-kappa B and mitogen-activ= ated 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.

= (506) Life Extension Foundation, Life Extension Jan 2009

(530) Cancer case histories followed by doctors, www.whale.to/d/cancer.html

(531) Integrative Medicine and the Role of Modified Citrus Pectin/Alginates in Heavy MetIntegrative Medicine and the Role of Modified Citr= us Pectin/Alginates in Heavy Metal Chelation and Detoxification – Five Case Reports; Eliaz, I.,Weil, E., Wilk, B. ; Forsc= h Komplementärmed 2007;14:358-364; = ; http://content.karger.com/ProdukteDB/prod= ukte.asp?Aktion=3DJournalFreeSample&ProduktNr=3D224242

(539) A cascade analysis of the interaction of mercury and cop= roporphyrinogen oxidase (CPOX) polymorphism on the heme biosynt= hetic pathway and porphyrin production.= H= eyer NJ, Bittner AC, Echeverria D<= /span>, Woods JS. Toxicol Lett. 2006 Feb 20;161(2):1= 59-66. Epub 2005 Oct 7.

(543) U.S. Centers for Disease Control, National Center for Health Statistics, NHANES= III study(thousands of people&#= 8217;s health monitored), www.flcv.co= m/NHanes3.html

& http://www.m= ercola.com/article/mercury/no_mercury.htm

(546) Rob Edwards and Duncan Graham-Rowe.&nbs= p; "Electrical connection" New Scientist 6= March 2002; & Dr. Mae-Wan Ho, National Radiological Protection Board (NRPB), “Electromagnetic Fields Double Leukemia Risks” 2002; & Richard Doll et al, Cancer Studies Unit, Oxford Univ., March 2002; & London SJ; Bowman JD; Sobel E; Thomas DC; Garabrant DH; Pearce N; Bernstein L; Peters JM. Exposure to magnetic = fields among electrical workers in relation to leukemia risk in Los Angeles County. Am J Ind Med 1994 Jul;26(1):47-= 60; & Caplan LS; Schoenfel= d ER; O'Leary ES; Leske MC. Breast cancer and electromagnetic fields--a review. Ann Epidemiol= 2000 Jan;10(1):31-44;

(550) J. S.= Malpas, M.D., Treatment Options for Multiple Myeloma, New England Journal of Medicine, December 12th, 2002; & Riccardi et al, British Journal of Cancer 2000;82:1254-60.

(551) Cancer Treatment, Dr. T. Simoncini, http://www.curenaturalicancro.c= om/

(552) International Medical Veritas Assoc., ht= tp://www.life-enthusiast.com/index/Articles/Sircus & http://www.winningcancer.com/ &

Dr. Mark Sircus, http://www.magnesiumforlife.co= m/ & http://ww= w.beating-cancer-gently.com/nl118.html

& Iodine Treatment= , http://phaelosopher.wordpress.= com/2007/08/01/an-mind-opening-discussion-on-iodine-with-dr-mark-sircus-pod= cast/

(553) Budwig Flax Oil & Cottage Cheese Cancer Treatment,

http://www.cancertut= or.com/Cancer/Budwig.html & http://www.cancure.org/budw= ig_diet.htm

(570) Reversing Cancer: A Journey from Cance= r to Cure, Dr. Gerald H. Smith, ICNR, 2006

(571) “Of metalicized mouths, mycotoxicosis, and oxygen”, Townsend Letter for Doctors and Patients, June,= 2005 by Philip Mollica, Robert Harris

http://www.findarticles.com/p/articles/mi_m0ISW/is_263/ai_n13784466/= pg_1

(580) <= /span>Cancer as a Fungal Disease, Tullio Simon= cini, MD, www.cancerisafungus.com/

(581) The Prime Cause and Prevent= ion of Cancer (1969)--Dr Otto Warburg (Nobel prize winner)

(582) R= ising Ocean Temperatures, Toxic Metal Pollution Have Oysters In Hot Water, American Physiological Society, Comparative Physiology 2006, www.sciencedaily.com/releases/2006/10/061012185131.htm

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 oste= onecrotic lesion in the area of the lower right third molar. Soft tissue exam revealed swollen and inflamed pharyngeal arches, bilateral tons= ilar inflammation and enlargement. Extraoral palpati= on 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 3 month head and neck oxygen/ozone protocol developed by Dr. Mollica. This protocol was inc= lusive of direct and indirect infusion of 21 micograms= /cc of oxygen/ozone into the afflicted areas. The afflicted ar= eas being the 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 t= he protocol EG was given an exam which included a PET scan. No trace of the ca= ncer or any activity associated with the lesion was found. A= ttributed to spontaneous remission.