Mer ury from Amalgam Fillings is a Common Cause of MS, ALS, PD,SLE, RA, MCS, AD, et .

Bernard Windham (Ed.)

Contents1 Mer ury from amalgam �llings is a ommon ause of MS, ALS, PD, SLE, RA, MCS, AD,et . 11.1 Introdu tion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11.2 Do umentation of High Common Exposures and A umulation of Mer ury in the Brainand Motor Neurons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41.3 Mer ury Toxi ity: Summary of Neurologi al E�e ts . . . . . . . . . . . . . . . . . . . 51.4 Mer ury Related Neurologi al Damage: Me hanisms of Causality . . . . . . . . . . . . 61.5 Endo rine System and Metaboli Enzymati System Impairments . . . . . . . . . . . . 91.6 Autoimmunity, Neurologi al and Immune Diseases, and Mer ury . . . . . . . . . . . . 111.7 Re overy from Chroni Neurologi al and Immune Related Diseases After AmalgamRemoval and Mer ury Detoxi� ation . . . . . . . . . . . . . . . . . . . . . . . . . . . 121.8 Referen es . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141 Mer ury from amalgam �llings is a ommon ause of MS, ALS,PD, SLE, RA, MCS, AD, et .Mer ury from Amalgam Fillings is a Common Cause of MS, ALS, PD, SLE, RA, MCS, AD, et .Bernard Windham (Ed.), Chemi al Engineer/Biostatisti ian1.1 Introdu tionProper fun tioning of the human body and mind depends on intera tions of the brain and CNS usingneuronal signaling me hanisms with elaborate metaboli and enzymati pro esses and respirationthat o urs at the ellular level in the various organs and parts of the body, as ontrolled by lowlevels of hormones from the endo rine system. It will be shown that toxi substan es, su h as mer urythat the body is hroni ally exposed to, a umulate in the brain, pituitary gland, CNS, liver, kidneys,et . and an damage, inhibit, and ause imbalan es at virtually any stage of these various pro essesat very low levels of exposure, whi h an have major neurologi al, immunologi al, and metaboli e�e ts on an individual. Multiple S lerosis (MS) is aused by the erosion of myelin, a substan ewhi h helps the brain send messages to the body. Metal parti les entering the body an bind tothis myelin. For those who are hypersensitive, this myelin-metal bond omes under atta k from theimmune system. This is alled autoimmunity1. In su h ases, the progression of MS an be haltedby removing the sour e of the metal (369, 303b, 35).Mer ury is known to be one of the most toxi substan es ommonly en ountered and to be alongwith lead and arseni the toxi substan es adversely a�e ting the largest numbers of people (276).Dental amalgam is do umented by medi al studies and medi al lab tests to be the largest sour e ofboth inorgani and methyl mer ury2 in most people who have several mer ury amalgam �llings (599).Ba teria, yeasts, and Vitamin B12 methylate inorgani mer ury to methyl mer ury in the mouth andintestines (599, 510) and mer ury inhibits fun tional methylation in the body, a ne essary pro ess(509).1Internet: \http://www. v. om/autoimmD.html".2Informativo: \Dental Amalgam Mer ury Solutions".1

The main fa tors determining whether hroni onditions are indu ed by metals appear to beexposure and geneti sus eptibility3, whi h determines individuals immune sensitivity and ability todetoxify metals (405). Very low levels of exposure have been found to seriously a�e t relativelylarge groups of individuals who are immune sensitive to toxi metals, or have an inability to detoxifymetals due to su h as de� ient sulfoxidation or metallothionein fun tion or other inhibited enzymati pro esses related to detoxi� ation or ex retion of metals.A large epidemiologi al study of 35,000 Ameri ans by the National Institute of Health, the nation'sprin ipal health statisti s agen y, found that there was a signi� ant orrelation between having agreater than average number of dental amalgam surfa es and having the a hroni ondition su has epilepsy, MS, or migraine heada hes. Fewer of those with this ondition have zero �llings thanthose of the general population while signi� antly more of those with the ondition have 17 or moresurfa es than in the general population (543). MS lusters in areas with high metals emissions fromfa ilities su h as metal smelters have been do umented (184).As far ba k as 1996 it was shown that the lesions produ ed in the myelin sheath of axons in asesof multiple s lerosis were related to ex itatory re eptors on the primary ells involved alled oligo-dendroglia. The loss of myelin sheath on the nerve �bers hara teristi of the disease are due to thedeath of these oligodendroglial ells at the site of the lesions ( alled plaques). Further, these studieshave shown that the death of these important ells is as a result of ex essive exposure to ex itotoxinsat the site of the lesions (576, 598). Most of these ex itotoxins are se reted from mi roglial immune ells in the entral nervous system. This not only destroys these myelin-produ ing ells it also breaksdown the blood-brain barrier (BBB), allowing ex itotoxins in the blood stream to enter the site ofdamage. Some ommon exposures that ause su h proliferation of su h ex itotoxins resulting in MSare mer ury and aspartame, with additional e�e ts from MSG and methanol. Mer ury and othertoxi metals inhibit astro yte fun tion in the brain and CNS (119), ausing in reased glutamate and al ium related neurotoxi ity (119, 333, 416, 496) whi h are fa tors in neural degeneration in MS andALS. There is eviden e that astro yte damage/malfun tion is a major fa tor in MS (544). Mer uryand in reased glutamate a tivate free radi al forming pro esses like xanthine oxidase whi h produ eoxygen radi als and oxidative neurologi al damage (142, 13). Nitri oxide related toxi ty ausedby peroxynitrite formed by the rea tion of NO with superoxide anions, whi h results in nitration oftyrosine residues in neuro�laments and manganese Superoxide Dimustase (SOD) has been found to ause inhibition of the mito hondrial respiratory hain, inhibition of the glutamate transporter, andglutamate-indu ed neurotoxi ity involved in ALS (524, 521).It is now known the ause for the destru tion of the myelin in the lesions is overa tivation ofthe mi roglia in the region of the myelin (598). An enzyme that onverts glutamine to glutamate alled glutaminase in reases tremendously, thereby greatly in reasing ex itotoxi ity. Any dietaryex itotoxin an a tivate the mi roglia, thereby greatly aggravating the injury. This in ludes theaspartate in aspartame and MSG whi h is in many pro essed foods. The methanol in diet drinksadds to this toxi ity as well. Now, the se ret to treatment appears to be alming down in ammationof the mi roglia.Mer ury and admium inhibit magnesium and zin levels as well as inhibiting glu ose transferare other me hanisms by whi h mer ury and toxi metals are fa tors in metaboli syndrome andinsulin resistan e/diabetes (43, 198, 338, 597). Redu ed levels of magnesium and zin are relatedto metaboli syndrome, insulin resistan e, and brain in ammation and are prote tive against these onditions (595, 43).A ording to neurologist Dr. RL Blaylo k (598), the good news is that there are supplementsand nutrients that alm the mi roglia-the most potent are: silymarin, ur umin and ibuprophen.Phosphatidyl holine helps re-myelinate the nerve sheaths that are damaged, as does B12, B6, B1,3Informativo: \Sus eptibility Fa tors in Mer ury Toxi ity: Immune Rea tivity, Detoxi� ation System Fun tion,Enzymati Blo kages, Synergisti Exposures". 2

vitamin D, folate, vitamin C, natural vitamin E (mixed to opherols) and L- arnitine (576). Astudy demonstrated prote tive e�e ts of methyl obalamin, a vitamin B12 analog, against glutamate-indu ed neurotoxi ity (508), and similarly for iron in those who are iron de� ient DHA plays a majorrole in repairing the myelin sheath. Vitamin D may even prevent MS, but it a ts as an immunemodulator, preventing further damage - the dose is 2000 IU a day. Magnesium, as magnesiummalate, is needed in a dose of 500 mg 2X a day. They must avoid all ex itotoxins, even natural onesin foods-su h as soy, red meats, nuts, mushrooms and tomatoes. Avoid all uoride and espe iallyall va inations sin e these either inhibit antioxidant enzymes or triggers harmful immune rea tions.It has also been found that the antibioti mino y line powerfully shuts down the mi roglia. Dr.Blaylo k tried this treatment on a patient who just ame down with fulmanant MS. He was on�nedto a wheel hair. He was pla ed on mino y line and now, just a few weeks later, he is walking.The various neurologi al, immune, and metaboli related diseases dis ussed together here arediagnosed and labeled lini ally based primarily on symptoms, along with tests for some underlying onditions found ommon in ea h disease. But ea h individual will be seen to have their own unique ombination of neurologi al, endo rine, and enzymati imbalan es along with autoimmunities thatresult in the fun tional problems that lead to symptoms that are diagnosed as multiple s lerosis(MS) or Amyotrophi Lateral S lerosis (ALS) or Alzheimer's Disease (AD), or Parkinson's Disease(PD), or Systemi Lupus Erythematosus (SLE), rheumatoid arthritis (RA), hroni fatigue syndrome(CFS), or oral li hen planus (OLP), et .(100) However, a lot of ommonality among these fa tors hasbeen do umented, both within spe i� diseases and among the various diseases dis ussed here. InMS, an autoimmune T- ell atta k on CNS myelin sheath results in demyelinated plaques (405, et .).A tivated T- ells, plasma ells, and ma rophages have been found in the demyelinated areas. ALSis a systemi motor neuron disease that a�e ts the orti ospinal and orti obulbar tra ts, ventralhorn motor neurons, and motor ranial nerve nu lei (405, et .). Approximately 10 per ent of ALS ases are of the familial type that has been linked to a mutation of the opper/zin super oxidedismustase gene (Cu/Zn SOD). The majority of ALS ases are of the sporadi type. There are manytoxi substan es as well as some ommon drugs (336) that have been found to be major fa tors inprodu ing the fun tional onditions that result in these diseases. However mer ury appears to bethe most ommonly impli ated of these, and in parti ular mer ury from amalgam �llings - as willbe do umented here. For the majority of ases there are now tests to identify the various fa torsinvolved in these types of diseases; and on e an individual's underlying ausative fa tors have beenidenti�ed, high su ess rates at ure or signi� ant improvement are being a hieved.Toxi metals su h as mer ury, lead, admium, et . have been do umented to be neurotoxi ,immunotoxi , reprodu tive/developmental toxins that a ording to U.S. Government agen ies auseadverse health e�e ts and learning disabilities to millions in the U.S. ea h year, espe ially hildren andthe elderly (2, 125, 441, 505, 601, 600, 503). Exposure of humans and animals to toxi metals su has mer ury, admium, lead, opper, aluminum, arseni , hromium, manganese, et . is widespreadand in many areas in reasing. The U.S. Center for Disease Control (276) ranks toxi metals as thenumber one environmental health threat to hildren. A ording to an EPA/ATSDR assessment, thetoxi metals mer ury, lead, and arseni are the top 3 toxi s having the most adverse health e�e tson the publi based on toxi ity and urrent exposure levels in the U.S., with admium, ni kel and hromium also highly listed.While there is onsiderable ommonality to the health e�e ts ommonly aused by these toxi metals, and e�e ts are umulative and synergisti 4 in many ases, this paper will on entrate on thehealth e�e ts of elemental mer ury from amalgam �llings. The reason is that the publi appearsto be generally unaware that onsiderable s ienti� eviden e supports that mer ury is the metal ausing the most widespread adverse health e�e ts to the publi , and amalgam �llings have beenwell do umented to be the number one sour e of exposure of mer ury to most people, with exposure4Informativo: \Sus eptibility Fa tors in Mer ury Toxi ity: Immune Rea tivity, Detoxi� ation System Fun tion,Enzymati Blo kages, Synergisti Exposures". 3

levels often ex eeding Government health guidelines and levels do umented to ause adverse healthe�e ts. Mu h of the dire t hroni exposure to toxi metals for persons with the autoimmune diseasesdis ussed here appears to be from use of metals in dental work. The most ommon dental metals thathave been do umented to be ausing widespread adverse health e�e ts are mer ury, ni kel, palladium,gold, and opper. Although hroni exposure learly is a�e ting a mu h larger population, ni kel hasbeen found to be a major fa tor in many ases of MS and lupus, with palladium having very similare�e ts to ni kel. Likewise hroni exposures to manganese and opper have been impli ated in some ases of Parkinson's disease. Another group of toxi substan e substan es with widespread exposurethat have been demonstrated to generate rea tive oxygen spe ies and have positive orrelationsto some of the diseases dis ussed here are the organo hlorine pesti ides. Toxi metals appear tobe only one of the fa tors involved in hroni autoimmune onditions. Pathogens su h as viruses,my oplasma, ba teria and parasites have been found to usually be present and a fa tor to deal within treating those with hroni degenerative onditions and weakened immune systems su h as MS(448e, 468, 470, 485, 303) and other autoimmune onditions.1.2 Do umentation of High Common Exposures and A umulation of Mer ury inthe Brain and Motor NeuronsAmalgam �llings are the largest sour e of mer ury in most people with daily exposures do umentedto ommonly be above government health guidelines (14, 49, 79, 99, 183, 506, 500, 217). This isdue to ontinuous vaporization of mer ury from amalgam in the mouth, along with galvani urrentsfrom mixed metals in the mouth that deposit the mer ury in the gums and oral avity (605). Due tothe high daily mer ury exposure and ex retion into home and business sewers of those with amalgam,dental amalgam is also the largest sour e of the high levels of mer ury found in all sewers and sewersludge, and thus a ording to government studies a signi� ant sour e of mer ury in rivers, lakes,bays, �sh, and rops (603). People also get signi� ant exposure from va inations, �sh, and dentaloÆ e vapor (600).When amalgam was pla ed into teeth of monkeys and rats, within one year mer ury was foundto have a umulated in the brain, trigeminal ganglia, spinal ganglia, kidneys, liver, lungs, hormoneglands, and lymph glands (22, 303). People also ommonly get exposures to mer ury and other toxi metals su h as lead, arseni , ni kel, and aluminum from food, water, and other sour es (601). Allof these are highly neurotoxi and are do umented to ause neurologi al damage whi h an result in hroni neurologi al onditions over time, as well as ADHD, mood, and behavioral disorders (601,303).Mer ury is one of the most toxi substan es in existen e and is known to bioa umulate in thebody of people and animals that have hroni exposure (600). Mer ury exposure is umulative and omes primarily from 4 main sour es: silver (mer ury) dental �llings, food (mainly �sh), va inations,and o upational exposure. Whereas mer ury exposure from �sh is primarily methyl mer ury andmer ury from va inations is thimerosal (ethyl mer ury), mer ury from o upational exposure anddental �llings is primarily from elemental mer ury vapor. Developmental and neurologi al onditionso ur at lower levels of exposure from mer ury vapor than from inorgani mer ury or methyl mer ury(606). Mer ury in amalgam �llings, be ause of its relatively high vapor pressure ompared to its PELsafety limit and galvani a tion with other metals in the mouth, has been found to be ontinuouslyvaporized and released into the body, and has been found to be the dire tly orrelated to the numberof amalgam surfa es and the largest sour e of mer ury in the majority of people (14, 49, 183, 199,209, 79, 99, 500), typi ally between 60 and 90% of the total. The level of daily exposure of those withseveral amalgam �llings ommonly ex eeds the U.S. EPA health guideline for daily mer ury exposureof 0.1 �g/kg body weight/day, and the oral mer ury level ommonly ex eeds the mer ury MRL ofthe U.S.ATSDR of 0.2 �g/ ubi meter of air (217, 500). When amalgam �llings are repla ed, levels4

of mer ury in the blood, urine, and fe es typi ally rise temporarily but de line between 60 to 85%within 6 to 9 months (79, 600.).Mer ury has been found to a umulate preferentially in the brain, major organs, hormone glands,and primary motor fun tion related areas involved in ALS - su h as the brain stem, erebellum,rhomben ephalon, dorsal root ganglia, and anterior horn motor neurons, whi h enervate the skeletalmus les (22, 14, 99, 163, 291, 327, 329, 442, 48, 604). Mer ury, with exposure either to vaporor organi mer ury tends to a umulate in the glial ells in a similar pattern, and the pattern ofdeposition is the same as that seen from morphologi al hanges (327g, 287, 305). Though mer uryvapor and organi mer ury readily ross the blood-brain barrier, mer ury has been found to be takenup into neurons of the brain and CNS without having to ross the blood-brain barrier, sin e mer uryhas been found to be taken up and transported along nerve axons as well through al ium and sodium hannels and along the olfa tory path (329, 288, 333, 34).1.3 Mer ury Toxi ity: Summary of Neurologi al E�e tsMer ury has been found to a umulate in the erebellum and other brain areas, produ ing rea tiveoxygen spe ies (ROS), in luding superoxide that ause damage to those parts of the brain (194, 13).Mer ury was also found to ause a redu tion in antioxidant fun tion su h as superoxide dimustase(SOD) and glutathione peroxide (GPx) that tries to ounter-balan e the ROS (13, 56a). Mer ury,with exposure either to vapor or organi mer ury tends to a umulate in the glial ells in a similarpattern, and the pattern of deposition is the same as that seen from morphologi al hanges (327g,287a). Mer ury (espe ially mer ury vapor or organi mer ury) penetrates and damages the bloodbrain barrier allowing penetration of the barrier by other substan es that are neurotoxi (along withredu ed amino a id uptake to brain) (22, 38, 85, 604, 162, 301, 311/262). Su h damage to the bloodbrain barrier's fun tion has been found to be a major fa tor in hroni neurologi al diseases su h asMS (286, 289, 291, 302, 324, 326, 478).Programmed ell death (apoptosis) is do umented to be a major fa tor in degenerative neurologi al onditions like MS, ALS, Alzheimer's, Parkinson's, et . Some of the fa tors do umented to beinvolved in apoptosis of neurons and immune ells in lude indu ement of the in ammatory ytokineTumor Ne rosis Fa tor-alpha (TNFa) (126), rea tive oxygen spe ies and oxidative stress (13, 43a,56a, 296b, 495), redu ed glutathione levels (56, 126a, 111a), liver enzyme e�e ts and inhibition ofprotein kinase C and yto hrome P450 (43, 84, 260), nitri oxide and peroxynitrite toxi ity (43a, 521,524), ex itotoxi ity and lipid peroxidation (490, 496), ex ess free ysteine levels (56d, 111a, 33, 330),ex ess glutamate toxi ity (13b, 416), ex ess dopamine toxi ity (56d, 13a), beta-amyloid generation(462, 56a), in reased al ium in ux toxi ity (296b, 333, 416, 432, 462 , 507) and DNA fragmentation(296, 42, 114, 142) and mito hondrial membrane dysfun tion (56de, 416).TNFa (tumor ne rosis fa tor-alpha) is a ytokine that ontrols a wide range of immune ell re-sponse in mammals, in luding ell death (apoptosis). This pro ess is involved in in ammatory anddegenerative neurologi al onditions like ALS, MS, Parkinson's, rheumatoid arthritis, et . Cell sig-naling me hanisms like sphingolipids are part of the ontrol me hanism for the TNFa apoptosisme hanism (126a). Gluthathione is an amino a id that is a normal ellular me hanism for on-trolling apoptosis. When glutathione is depleted in the brain, rea tive oxidative spe ies in reased,and CNS and ell signaling me hinsisms are disrupted by toxi exposures su h as mer ury, neuronal ell apoptosis results and neurologi al damage. Mer ury has been shown to indu e TNFa, depleteglutathione, and in rease glutamate, dopamine, and al ium related toxi ity, ausing in ammatorye�e ts and ellular apoptosis in neuronal and immune ells (126b, 126 ). Mer ury's bio hemi aldamage at the ellular level in lude DNA damage, inhibition of DNA and RNA synthesis (42, 114,142, 197, 296, 392); alteration of protein stru ture (33, 111, 114, 194, 252, 442); alteration of thetransport and signaling fun tions of al ium (333, 43b, 254, 416d, 462, 507); inhibition of glu ose5

transport (338, 254), and of enzyme fun tion and other essential nutrients (96, 198, 254, 263, 264,33, 330, 331, 338, 339, 347, 441, 442); indu tion of free radi al formation (13a, 43b, 54, 405, 424),depletion of ellular glutathione (ne essary for detoxi� ation pro esses) (56, 111, 126, 424), inhibi-tion of glutathione peroxidase enzyme (13a, 442), inhibits glutamate uptake (119, 416d), indu esperoxynitrite and lipid peroxidation damage (521b), auses abnormal migration of neurons in the erebral ortex (149), immune system damage (111, 194, 226, 252, 272, 316, 325, 355); indu ementof in ammatory ytokines (126, 152, 181) and autoimmunity (181, 226, 272, 314, 369, 405, 507, 100,et .)MS patients have been found to have mu h higher levels of mer ury in erebrospinal uid omparedto ontrols (163, 291, 35, 139). German studies in luding studies at German universities have foundthat MS patients usually have high levels of mer ury body burden, with one study �nding 300%higher than ontrols (271, 302). Most re overed after mer ury detox, with some requiring additionaltreatment for viruses and intestinal dysbiosis.Very high levels of mer ury are also found in brainmemory areas su h as the erebral ortex and hippo ampus of patients with diseases with memoryrelated symptoms (158, 34, 207, et .). Studies have found mer ury related neurologi al e�e ts to beindistinguishable from those of MS (207, 212, 222, 244, 271, 289, 291, 302, 183, 184, 303, 324, 326,406).Mer ury has been shown to be a fa tor that an ause rheumatoid arthritis by a tivating lo alizedCD4+ T- ells whi h trigger produ tion of immune ma rophages and immunoglobulin (Ig) produ ing ells in joints (405, 513, 514).1.4 Mer ury Related Neurologi al Damage: Me hanisms of CausalityExposure to inorgani mer ury has signi� ant e�e ts on blood parameters and liver fun tion. Stud-ies have found that in a dose dependent manner, mer ury exposure auses redu tions in oxygen onsumption and availability, perfusion ow, biliary se retion, hepati ATP on entration, and y-to hrome P450 liver ontent (260), while in reasing blood hemolysis produ ts and tissue al ium ontent and indu ing heme oxygenase, porphyria, platelet aggregation through interfering with thesodium pump.Mer ury vapor and methyl mer ury penetrate and damage the blood brain barrier (311, 22, 85,105, 162, 600/262), also fa ilitating other toxi substan es penetration of the BBB. Damage to theblood brain barrier's fun tion has been found to be a major fa tor in hroni neurologi al diseasesdis ussed here. Mer ury also auses high levels of oxidative stress and rea tive oxygen spe ies (ROS)(13), whi h have been impli ated as major fa tors in neurologi al disorders in luding stroke, ALS(501) PD (502), Alzheimer's (503), CFS (504), Lupus (113, 234, 331, 602). Studies have foundmer ury related neurologi al e�e ts to be indistinguishable from those of MS (163, 207, 271, 244,289, 291, 302, 303, 184, 324, 326).Metals like mer ury bind to SH-groups (sulphydryl) in sulfur ompounds like amino a ids andproteins, hanging the stru ture of the ompound that it is atta hed to. This often results in theimmune systems T- ells not re ognizing them as appropriate nutrients and atta king them (181, 226,314, 507). Su h binding and autoimmune damage has been do umented in the fat-ri h proteins ofthe myelin sheaths and ollagen (405), whi h are a�e ted in MS. Metals by binding to SH radi alsin proteins and other su h groups an ause autoimmunity by modifying proteins whi h via T- ellsa tivate B- ells that target the altered proteins indu ing autoimmunity as well as ausing aberrantMHC II expression on altered target ells (425de, 343). Studies have also found mer ury and lead ause autoantibodies to neuronal proteins, neuro�laments, and myelin basi protein (MBP) (269ag,405, 478, 515, 516). Mer ury and admium also have been found to interfere with zin binding toMBP (517b) whi h a�e ts MS symptoms sin e zin stabilizes the asso iation of MBP with brainmyelin (517a). MS has also been found to ommonly be related to in ammatory a tivity in the6

CNS su h as that aused by the rea tive oxygen spe ies and ytokine generation aused by mer uryand other toxi metals (405, 478, 515, 516). Antioxidants like lipoi a id whi h ountera t su h freeradi al a tivity have been found to alleviate symptoms and de rease demyalination (494, 572). Agroup of metal exposed MS patients with amalgam �llings were found to have lower levels of redblood ells, hemoglobin, hemo rit, thyroxine, T- ells, and CD8+ suppressor immune ells than agroup of MS patients with amalgam repla ed, and more exa erbations of MS than those without(102a). Immune and autoimmune me hanisms are thus seen to be a major fa tor in neurotoxi ity ofmetals.Na(+), K(+)-ATPase is a transmembrane protein that transports sodium and potassium ionsa ross ell membranes during an a tivity y le that uses the energy released by ATP hydrolysis.Mer ury is do umented to inhibit Na(+), K(+)-ATPase fun tion at very low levels of exposure(288ab). Studies have found that in Ms ases there was an elevation in plasma serum digoxinand a redu tion in serum magnesium and RBC membrane Na(+)-K+ ATPase a tivity (263). Thea tivity of all serum free-radi al s avenging enzymes, on entration of glutathione, alpha to opherol,iron binding apa ity, and eruloplasmin de reased signi� antly in Ms, while the on entration ofserum lipid peroxidation produ ts and nitri oxide in reased. The inhibition of Na+-K+ ATPase an ontribute to in rease in intra ellular al ium and de rease in magnesium, whi h an resultin 1) defe tive neurotransmitter transport me hanism, 2) neuronal degeneration and apoptosis, 3)mito hondrial dysfun tion, 4) defe tive golgi body fun tion and protein pro essing dysfun tion. It isdo umented in this paper that mer ury is a ause of most of these onditions seen in MS (13a, 111,288, 442, 521b, 43, 56, 263et .)Autoimmunity has also been found to be a fa tor in hroni degenerative autoimmune onditionssu h as MS, ALS, et ., with geneti sus eptibility a major fa tor in who is a�e ted. One geneti fa torin Hg indu ed autoimmunity is major histo ompatibility omplex (MHC) linked. Both immune elltype Th1 and Th2 ytokine responses are involved in autoimmunity (425 ). One geneti di�eren efound in animals and humans is ellular retention di�eren es for metals related to the ability toex rete mer ury (426). For example it has been found that individuals with geneti blood fa tortype APOE-4 do not ex rete mer ury readily and bioa umulate mer ury, resulting in sus eptibilityto hroni autoimmune onditions su h as Alzheimer's, Parkinson's, et . as early as age 40 (437),whereas those with type APOE-2 readily ex rete mer ury and are less sus eptible (437, 35). Thosewith type APOE-3 are intermediate to the other 2 types. The in iden e of autoimmune onditionshas in reased to the extent this is now one of the leading auses of death among women (450). Alsowhen a ondition has been initiated and exposure levels de line, autoimmune antibodies also de linein animals or humans (233, 234d, 369, 60, 118, 303, 368, 405)Cal ium plays a major role in the extreme neurotoxi ity of mer ury and methyl mer ury. Bothinhibit ellular al ium ATPase and al ium uptake by brain mi rosomes at very low levels of exposure(333). Protein Kinase C (PKC) regulates intra ellular and extra ellular signals a ross neuronalmembranes, and both forms of mer ury inhibit PKC at mi romolar levels, as well as inhibitingphorbal ester binding (43). They also blo k or inhibit al ium L- hannel urrents in the brain inan irreversible and on entration dependent manner. Metalli mer ury is mu h more potent thanmethyl mer ury in these a tions, with 50 % inhibition in animal studies at 13 ppb (333).A dire t me hanism involving mer ury's inhibition of ellular enzymati pro esses by bindingwith the hydroxyl radi al (SH) in amino a ids appears to be a major part of the onne tion toallergi /immune rea tive onditions. The binding of mer ury from amalgam to the -SH groups oftenresults in ina tivation of sulfur and blo king of enzyme fun tion, produ ing sulfur metabolites withextreme toxi ity that the body is unable to properly detoxify (33, 114). Sulfur is essential in enzymes,hormones, nerve tissue, and red blood ells. These exist in almost every enzymati pro ess in thebody. Blo ked or inhibited sulfur oxidation at the ellular level has been found in most with manyof the hroni degenerative diseases, in luding Parkinson's, Alzheimer's, ALS, lupus, rheumatoidarthritis, CFS, FMS, MCS, autism, et .(33, 234, 330, 331, 501-505, 602)7

Some studies of patients with major neurologi al or degenerative diseases have found eviden eamalgam �llings may play a major role in development of onditions su h as su h as, MS (102, 163,170, 184, 212, 285, 291, 302, 303, 324, 326), ALS (92, 97, 325, 501), RA (600), AD (66, 67, 158, 166,204, 207, 221, 238, 242, 244, 258, 296, 300, 303, 503), SLE (234, 60, 405), PD (56, 84, 98, 169, 218,248, 250, 258, 303, 502), and many other onditions (600, 303). Mer ury indu ed lipid peroxidationhas been found to be a major fa tor in mer ury's neurotoxi ity, along with leading to de reasedlevels of glutathione peroxidation and superoxide dismustase (SOD) (13). Only a few mi rograms ofmer ury severely disturb ellular fun tion (33, 56, 226).Mer ury exposure auses high levels of oxidative stress/rea tive oxygen spe ies (ROS) (13), whi hhas been found to be a major fa tor in neurologi al disease (56, 501-505). Mer ury and quinones form onjugates with thiol ompounds su h as glutathione and ysteine and ause depletion of glutathione,whi h is ne essary to mitigate rea tive damage. Su h ongugates are found to be highest in the brainsubstantia nigra with similar ongugates formed with L-Dopa and dopamine in Parkinson's disease(56, 502). Mer ury depletion of GSH and damage to ellular mito hrondria and the in reased lipidperxodation in protein and DNA oxidation in the brain appear to be a major fa tor in Parkinson'sdisease (33). A Canadian study found those with 15 or more amalgam �llings to have more than250% greater risk of MS than ontrols, and likewise higher risk for those who have had amalgam�llings more than 15 years, and another study also found higher mr ury body burden in those withmore �llings and in reased risk of MS with more �llings (324). Another study (169) found blood andurine mer ury levels to be very strongly related to Parkinson's with odds ratios of approx. 20.Exposure to mer ury results in metalloprotein ompounds that have geneti e�e ts, having bothstru tural and atalyti e�e ts on gene expression (114). Some of the pro esses a�e ted by su hmetalloprotein ontrol of genes in lude ellular respiration, metabolism, enzymati pro esses, metal-spe i� homeostasis, and adrenal stress response systems. Signi� ant physiologi al hanges o urwhen metal ion on entrations ex eed threshold levels. Su h metalloprotein formation also appearsto ause a hange in antigeni ity and autoimmune rea tions in signi� ant numbers of people (114,60, 342, 405). Mu h mer ury in saliva and the brain is also organi , the most neurotoxi form (506,51, 220, 272), sin e mouth ba teria and other organisms in the body methylate inorgani mer ury toorgani mer ury (506, 51, 254). Dental amalgam has been found to be the largest sour e of methylmer ury in most with mer ury amalgam �llings (506, et .).Spatial and temporal hanges in intra ellular al ium on entrations are riti al for ontrollingneurotransmitter release in neurons (432). Mer ury alters al ium homeostasis and al ium levels inthe brain and a�e ts neurotransmitter release through its e�e ts on al ium levels (270 , 333, 372,43). Low levels of toxi metals have been found to inhibit dihydroteridine redu tase, whi h a�e ts theneural system fun tion by inhibiting neurotransmitters through its e�e t on phenylalanine, tyrosineand tryptophan transport into neurons (257, 258). This was found to ause severe impaired aminesynthesis and hypokinesis. Tetrahydro-biopterin, whi h is essential in produ tion of neurotransmit-ters, is signi� antly de reased in patients with Alzheimer's, Parkinson', and MS. Su h patients haveabnormal inhibition of neurotransmitter produ tion.Mer ury at extremely low levels also interferes with formation of tubulin produ ing neuro�brillarytangles in the brain, similar to those observed in Alzheimer's patients with high levels of mer uryin the brain (207, 303). Mer ury and the indu ed neuro�brillary tangles also appear to produ e afun tional zin de� ien y in the of AD su�erers (242), as well as ausing redu ed lithium levels whi his another fa tor in su h diseases. The low Zn levels result in de� ient CuZnSuperoxide dismutase(CuZnSOD), whi h in turn leads to in reased levels of superoxide (463). Lithium prote ts brain ellsagainst ex ess glutamate indu ed ex itability and al ium in ux (280). Also mer ury binds with ell membranes interfering with sodium and potassium enzyme fun tions, ausing ex ess membranepermeability, espe ially in terms of the blood-brain barrier (159, 207, 311℄. Less than 1ppm mer uryin the blood stream an impair the blood-brain barrier. Mer ury was also found to a umulatein the mito hondria and interfere with their vital fun tions, and to inhibit yto hrome C enzymes8

whi h a�e t energy supply to the brain. Persons with extra Apo-E4 gene opies appear espe iallysus eptible to this damage (207, 221)Mer ury blo ks the immune fun tion of magnesium and zin (198, 427, 43, 38), whose de� ien- ies are known to ause signi� ant neurologi al e�e ts (461, 463, 430). The low Zn levels result inde� ient CuZnSuperoxide dismustase (CuZnSOD), whi h in turn leads to in reased levels of super-oxide due to toxi metal exposure. This is in addition to mer ury's e�e t on metallothionein and opper homeostasis as previously dis ussed (477). Copper is an essential tra e metal whi h playsa fundamental role in the bio hemistry of the nervous system (489, 495463, 464). Several hroni neurologi al onditions involving opper metaboli disorders are well do umented like Wilson's Dis-ease and Menkes Disease. Mutations in the opper/zin enzyme superoxide dismustase (SOD) havebeen shown to be a major fa tor in the motor neuron degeneration in onditions like familial ALS.Exposures to toxi metals su h as mer ury and admium have been found to ause su h e�e ts, andsimilar e�e ts on Cu/Zn SOD have been found to be a fa tor in other onditions su h as autism,Alzheimer's, Parkinson's, and ALS (489, 495, 464, 469, 111, 501-504). This ondition an result inzin de� ient SOD and oxidative damage involving nitri oxide, peroxynitrite, and lipid peroxidation(495, 496, 489), whi h have been found to a�e t glutamate mediated ex itability and apoptosis ofnerve ells and e�e ts on mito hondria (495, 496, 119) These e�e ts an be redu ed by zin supple-mentation (464, 495, 430), as well as supplementation with antioxidants and nitri oxide-suppressingagents and peroxynitrite s avengers su h as Vit C, Vit E, lipoi a id, Coenzyme Q10, arnosine,gingko biloba, N-a etyl ysteine, et . (444, 464, 494, 495, 469, 470, 572). Some of the antioxidantssu h as ginkgo bilabo were also found to have prote tive e�e ts through in reasing atalase and SODa tion, while redu ing lipid peroxidations (494a) Ceruloplasmin in plasma an be similarly a�e tedby opper metabolism dysfun tion, like SOD fun tion, and is often a fa tor in neurodegeneration(489).Ex ess zin from produ ts su h as GSK Superpolygrip (before reformulated) an also ause demye-lating onditions with e�e ts similar to MS, Demyelinating Syndrome, and Chroni In ammatoryDemyelinating Polyneuropathy (CIDP) (530)Mer ury and other toxi metals inhibit astro yte fun tion in the brain and CNS (119, 131), ausing in reased glutamate and al ium related neurotoxi ity (119, 152, 333, 226a, 496) whi h areresponsible for mu h of the Fibromyalgia symptoms and a fa tor in neural degeneration in MS andALS. There is some eviden e that astro yte damage/malfun tion is the main fa tor in MS (544).This is also a fa tor in onditions su h as CFS, Parkinson's, and ALS (346, 416, 496). Animalstudies have on�rmed that in reased levels of glutamate (or aspartate, another amino a id ex itoryneurotransmitter) ause in reased sensitivity to pain, as well as higher body temperature - bothfound in CFS/Fibromyalgia. Mer ury and in reased glutamate a tivate free radi al forming pro esseslike xanthine oxidase whi h produ e oxygen radi als and oxidative neurologi al damage (346, 142,13). Medi al studies and do tors treating Fibromyalgia have found that supplements whi h ausea de rease in glutamate or prote t against its e�e ts have a positive e�e t on Fibromyalgia andother hroni neurologi al onditions. Some that have been found to be e�e tive in lude CoQ10(444), ginkgo biloba and py nogenol (494a), NAC (54, 494a), Vit B6, methyl obalamine (B12),L- arnitine, holine, ginseng, vitamins C and E, ni otine, and omega 3 fatty a ids (�sh and axseedoil) (417, 495e).1.5 Endo rine System and Metaboli Enzymati System ImpairmentsMer ury has been well do umented to be an endo rine system-disrupting hemi al a�e ting hormonalpro esses (85, 146, 149, 199, 312, 604) and enzyme produ tion pro esses (33, 111, 194) at very lowlevels. The pituitary gland, in whi h mer ury has been do umented to a umulate, ontrols manyof the body's endo rine system fun tions and se retes hormones involved in ontrol of most bodily9

pro esses. The hypothalamus regulates body temperature and many metaboli pro esses. Su hhormonal se retions are a�e ted at levels of mer ury exposure mu h lower than the a ute toxi itye�e ts normally tested for (146, 199). Some of the ommon e�e ts of mer ury on the endo rine systemin lude inhibiting human growth hormone, ausing hormonal imbalan es that a�e t the reprodu tivesystem and body temperature regulation, and ausing hormonal imbalan es resulting in imbalan esin metabolism of important minerals su h as al ium (333, 21, 25, 35, 280). Cal ium ux is inhibitedin synopti plasma membranes of the erebellum and erebrum ortex. A permanent in rease in ytosoli al ium levels appears to be asso iated with various pathologi al onditions whi h resultin ell death (333). All of the e�e ts on hormonal regulation of the various bodily pro esses add toand reinfor e the imbalan es aused in the metaboli enzymati pro esses.All body fun tions depend on ellular enzymati and respiratory pro esses that use Nutrientsdelivered by the blood, detoxify toxi substan es, and eliminate waste produ ts through the ellularrespiratory pro ess ba k through the lymph and blood to the lungs, kidneys, or liver for ex retion.Proteins are onverted by enzymati pro esses to amino a ids su h as ysteine, ystine, glutami a id,methionine, et . for ellular metaboli pro esses and to organi ompounds su h as glutathione whi his ne essary to detoxify toxi substan es su h as mer ury (13, 111, 194). Imbalan es or blo kages inany of several of these enzymati pro esses have been do umented to ause major neurologi al andimmune damage that appears to be involved in most of the diseases being dis ussed here.Mer ury vapor of those with hroni exposure is ontinuously released into the blood streamthrough the lungs and distributed to ells throughout the body, where it reates metal-protein om-pounds and rea tive oxidative spe ies (ROS) su h as superoxide, whi h must be detoxi�ed. Cysteineand glutathione, whi h are produ ed and inter hanged as required through enzymati pro esses, arene essary for detoxi� ation. Blo kages or impairments aused by mer ury or other toxi substan esor pro esses an then result in ellular toxi ity and damage to vital organs su h as the brain, CNS,liver, or kidneys.Clini al tests of patients with motor neurone disease (MND), ALS, PD, AD, SLE, and RA havefound that the patients generally have damaged enzymati pro esses resulting in elevated plasma ysteine to sulphate ratios, with the average being 500% higher than ontrols (330, 331), and ingeneral are poor sulphur oxidizers (33, 331). High levels of free ysteine have been found to re-sult in major neurologi al damage to the brain, CNS, and ellular pro esses (194, 330, 331). Thetwo main enzymati pro esses that down regulate ysteine to taurine, sulfates, and glutathione are ysteine dioxygenese (CDO) and gamma-glutamyl ysteine synthetase (GGCS). Impairment in CDO an result in high ysteine levels, high ysteine to sulfate ratio, low taurine levels, and neurologi aldamage (194, 330, 331). GGCS onverts ysteine to glutathione, whi h has been demonstrated tobe ne essary to detoxi� ation of toxi substan es like mer ury (111). If this enzymati pro ess isblo ked, inhibited, or overloaded by hroni high toxi ity levels or autoimmune rea tions, there is in-suÆ ient glutathione and toxi damage o urs due to immune inability to pro ess the metal-organi ompounds and the ROS reated by exposure to mer ury or other toxi substan es (111, 33, 60, 56).Another enzymati pro ess ne essary for proper ellular metabolism is sul�te oxidase (SO) whi h isinvolved in onversion of toxi sulfur forms su h as sul�tes, sulfur dioxide (SO2), hydrogen sul�de(H2S), et . to nontoxi sulfates (33). SO an be blo ked or inhibited by mer ury or other toxi exposures, resulting in more of these very toxi sulfur ompounds. SO is ommonly found to betotally blo ked or inhibited in patients with MND, PD, AD, SLE, RA, et .(330, 331). Glutathioneperoxidase (GPx) is another enzymati pro ess in this loop that is often a�e ted, as well as the pro- ess involved in onverting Vitamin B6 through the essential oenzyme pyrodoxal 5-phosphate (P5P)in the synthesis of neurotransmitters. Impairment in this pro ess results in brain neurotransmitterimbalan es. Individual patients with any of these diseases who ommonly have been shown to havehigh ratio of ysteine to sulfate an thus have several di�erent individual enzymati blo kages orimbalan es that result in su h high ratios, and di�erent levels of neurologi al, immune, and ellulardamage due to high ysteine levels or low glutathione levels. Autoimmune rea tions have also been10

found to be ommonly involved in su h blo kages or imbalan es, parti ularly for those with the majordiseases being onsidered here. This aspe t will thus be further dis ussed.1.6 Autoimmunity, Neurologi al and Immune Diseases, and Mer uryMer ury has been do umented to ause autoimmune disease (45, 91, 234, 269, 270, 291, 328, 405)and many resear hers have on luded that autoimmunity is a fa tor in the major hroni neurologi aldiseases su h as MS, ALS, PD, SLE, RA, et . Mer ury and other toxi metals also form inorgani ompounds with OH, NH2, CL, in addition to the SH radi al and thus inhibits many ellular enzymepro esses, oenzymes, hormones, and blood ells (405, 600). Mer ury has been found to impair onversion of thyroid T4 hormone to the a tive T3 form as well as ausing autoimmune thyroiditis ommon to su h patients (369, 382). In general, immune a tivation from toxi metals su h as mer uryresulting in ytokine release and abnormalities of the hypothalamus-pituitary-adrenal (HPA) axis an ause hanges in the brain, fatigue, and severe psy hologi al symptoms (342, 369, 379-382, 385, 405,118) su h as profound fatigue, mus osketal pain, sleep disturban es, gastrointestinal and neurologi alproblems as are seen in CFS, �bromyalgia, and autoimmune thyroidititis. Su h hypersensitivity hasbeen found most ommon in those with geneti predisposition to heavy metal sensitivity (60, 342, 369,382, 405), su h as found more frequently in patients with human lympho yte antigens (HLA-DRA)(381-383). A signi� ant portions of the population appear to fall in this ategory.The enzymati pro esses blo ked by su h toxi substan es as mer ury also result in hroni forma-tion of metal-protein ompounds (HLA antigens or antigen-presenting ma rophages) that the body'simmune system (T-lympho ytes) does not re ognize, resulting in autoimmune rea tions (114, 342,405). The metals bind to SH-groups on proteins whi h an then be re ognized as \foreign" andatta ked by immune lympho ytes. Su h has been extensively do umented by studies su h as thedo umentation of the autoimmune fun tion test MELISA, a sophisti ated immune/autoimmune testwhi h was developed to test for su h rea tions (60, 405).Very low doses and short term exposures of inorgani Hg (20-200 mug/kg) exa erbates lupusand a elerates mortality in mi e. low dose Hg exposure in reases the severity and prevalen e ofexperimental autoimmune myo arditis indu ed by other fa tors. A strong signi� ant orrelation wasfound between o upational exposure to mer ury or pesti ides to lupus (SLE), with dental personalhaving a very high risk fa tor (113 ). In a study of small-s ale gold mining using mer ury, there wasa positive intera tion between Hg autoimmunity and malaria. These results suggest a new model forHg immunotoxi ity, as a o-fa tor in autoimmune disease, in reasing the risks and severity of lini aldisease in the presen e of other triggering events, either geneti or a quired (234f).Autoimmune rea tions to inorgani and methyl mer ury have been found to be relatively indepen-dent, o urring in over 10% of ontrols. In the population of over 3,000 patients tested by MELISA,the following per entages tested positive for lympho yte rea tivity: ni kel-34%, inorgani mer ury-22%, phenyl mer ury-15%, methyl mer ury-8%, gold-10%, palladium-10%, admium-11%, silver-1%.Groups with autoimmune symptoms su h as oral li hen planus, CFS, MS, autoimmune thyroidi-tis, et . generally have high per entages with lympho yte rea tivity to metals (60, 342, 369, 405).Among a population of patients being tested for autoimmune problems, 94% of su h patients hadsigni� ant immune rea tions to inorgani mer ury (MELISA test, 60, 342, 369, 405) and 72% hadimmune rea tions to low on entrations of HgCl2 (<0.5 �g/ml). Of a population of 86 patients withCFS symptoms who had amalgam �llings repla ed, 78% reported signi� ant health improvement ina relatively short time period after repla ent, and MELISA test s ores had a signi� ant redu tionin lympho yte rea tivity ompared to pre-repla ement (369). Similar results were experien ed forthose with MS, lupus, and autoimmune thyroiditis (369). The MELISA test has proved su essful indiagnosing and treating environmentally aused autoimmune diseases su h as MS, SLE, oral li henplanus, CFS, et . (60, 313, 342, 369, 405). A high per entage of patients subje tively diagnosed with11

CNS and systemi symptoms suggestive of mer ury intoxi ation have been found to have immunerea tivity to inorgani mer ury (MELISA test, 118), and likewise for MRI positive patients for braindamage. Controls without CNS problems did not have su h positive orrelations. Ni kel, palladium,and gold have also been found to indu e autoimmunity in geneti ally predisposed or highly exposedindividuals (60, 118, 313, 314, 234, 369, 130). Tests have found a signi� ant portion of people (over10%) to be in this ategory and thus more a�e ted by exposure to amalgam than others. On e ompromised by a toxi substan e that depletes the immune prote tors and auses autoimmunity,the immune system is more sus eptible to being sensitized to other toxi hemi als, a fa tor in mul-tiple hemi al sensitivity (MCS). Mer ury also auses a redu tion in thyroid produ tion (50) and ana umulation in the thyroid of radiation. Among those with hroni immune system problems withrelated immune antibodies, the types showing the highest level of antibody redu tions after amalgamremoval in lude glomerular basal membrane, thyroglobulin, and mi rosomal thyroid antigens (91).Mer ury and toxi metals blo k enzymes required to digest milk asein and wheat gluten, resultingin in reased IgA and IgG to gluten and IgA to asein, as well as dumping morphine like substan es inthe blood that are neurotoxi and psy hoti , as a major fa tor in s hizophrenia, autism, ADHD, andMS (24-26). A me hanism in MS o urs due to a redu tion in immune system a tivity. Spe i� ally,it is the redu tion in the number of the suppressor T- ells within the immune system that allowsCD4 helper T- ells to do damage (102a, 181, 226, 314, 405, 507, 513, 514, 20). Thus, during an a uterelapse the overall number of T- ells is redu ed, the normal balan e of helper and suppressor T- ells isdisrupted, and helper T- ells tend to predominate. This is most pronoun ed during an a ute relapse,but a similar situation o urs although perhaps to a lesser extent, in hroni progressive MS. A doubleblind study using a potent opiate antagonist, naltrexone (NAL), produ ed signi� ant redu tion inneurologi al symptomology among the 56% most responsive to opioid e�e ts in a population ofautism patients (18, 19). The behavioral improvements was a ompanied by alterations in thedistribution of the major lympho yte subsets, with a signi� ant in rease in the T-helper-indu ersand a signi� ant redu tion of the T- ytotoxi -suppressors and a normalization of the CD4/CD8 ratio.Low dose naltrexone (LDN) has been found to ommonly be e�e tive in redu ing MS symptoms andexerbations, apparently due its opioid suppressive e�e ts (20).1.7 Re overy from Chroni Neurologi al and Immune Related Diseases After Amal-gam Removal and Mer ury Detoxi� ationThere are extensive do umented ases (many thousands) where removal of amalgam �llings led to ure of serious health problems su h as MS (369, 35, 94, 95, 102, 163, 170, 212, 222, 271, 291, 302,468, 470, 34, 229, 406, 485, 523), SLE (369, 12, 35, 113, 222, 229, 233, 323, 60), Chroni FatigueSyndrome (8, 35, 60, 212, 293, 229, 222, 232, 233, 271, 317, 323, 342, 369, 376, 382, 440, 470, 523),mus ular/joint pain/Fibromyalgia (35, 222, 293, 317, 322, 369, 440, 468, 470, 523, 94), depression (94,107, 222, 271, 294, 212, 229, 233, 285e, 317, 322, 376, 453, 465, 468, 485, 523, 35, 40), RheumatoidArthritis (35, 95, 103, 212, 222, 271, 322, 358, 470, 523), autoimmune thyroiditis (369, 382, 91),OralLi henPlanus (60, 75, 78, 82, 86, 87, 90, 94, 101, 133, 168, 313), ALS (97, 229, 405, 406, 468-470,485, 35), Parkinson's/ mus le tremor (222, 248, 229, 271, 470, 212, 94, 98, 35), Alzheimer's (204,35), and many other hroni onditions (600). In several of the studies, over 75% of those with MSand having amalgams repla ed re overed or had signi� ant improvement (369, 212(a), (b), (e), 302,222, 35). Some of the studies reported similar su ess rates for SLE and autoimmune thyroiditis,but with lower number of ases treated. There is onsensus that dental amalgam is the main auseof oral li hen planus and most re over after amalgam repla ement.In one study all 6 of those tested for autoimmunity by the MELISA blood lympho yte immunerea tivity test were found to be immune rea tive to mer ury, and all had signi� ant improvementin their ondition after amalgam repla ement, as well as redu tion in immune rea tivity (369). Out12

of 15 patients with lupus (SLE), 73% had signi� ant improvement in health, and out of 8 withautoimmune thyroiditis 75% had signi� ant improvement after amalgam repla ement. The patientswho did not have signi� ant improvement were found to have immune rea tivity to ni kel whi h didnot improve after amalgam repla ement as the amalgam was not the sour e of the ni kel exposure(369).Clini al studies have found that pat h testing is not a good predi tor of su ess of amalgamremoval, as a high per entage of those testing negative also re overed from hroni onditions afterrepla ement of �llings (86, 87, 90). Follow up tests for autoimmune rea tion to inorgani mer uryafter amalgam repla ement have found that in most patients tested, the immune rea tion as well asmost symptoms disappear over time (60, 313, 405, et .).The level of mer ury in the gums is often 1200 ppm near a gold ap on an amalgam �lling (30,35, 48, 194). These levels are among the highest levels ever measured in tissues of living organisms,ex eeding the highest levels found in hroni ally exposed hloralkali workers, those who died frommer ury in Minamata, or animals that died from mer ury poisoning. The FDA/EPA a tion level forwarnings of dangerous levels in �sh or food is 1 ppm.Tests and TreatmentIn a large German study of MS patients after amalgam revision, extra tion resulted in 85% re overyrate versus only 16% for �lling repla ement alone (302, 222). Another large lini in Colorado haslikewise found that more seriously a�e ted ases often require more than simple repla ement forsu essful treatment (35). Other lini s have found that re overy from serious autoimmune diseases,dementia, or an er may require more aggressive mer ury removal te hniques than simple �llingrepla ement due to body burden. This appears to be due to migration of mer ury into roots & gumsthat is not eliminated by simple �lling repla ement. Also toxi metals, formaldehyde, and other toxi substan es have been do umented to a umulate in the jaw bone and tissue near teeth with multiplemetals, as well as in po kets from extra ted teeth and form avitations (areas of toxi materials anddiseased bone). Su h avitations and toxi ba teria a umulating from root- analed teeth sometimesmust be leaned out before signi� ant re overy an o ur (200, 35, 302, 222, 207, et .). There is adire t onne tion between the teeth and gums with the brain and CNS by both travel along nerve�bers and through the ranio-vertebral venous system for either toxi substan es su h as mer ury orfor ba teria (34, 325, 207, et .), The following proto ol is perhaps the most used proto ol for treatingthese onditions and has had onsiderable su ess:Huggins Total Dental Revision Proto ol (35)(a) history questionnaire and panel of tests.(b) repla e amalgam �llings starting with �lling with highest negative urrent or highest negativequadrant, with supportive vitamin/mineral supplements. extra t all root analed teeth using proper �nish proto ol.(d) test and treat avitations and amalgam tattoos where relevant(e) supportive supplementation, periodi monitoring tests, evaluate need for further treatment(not usually needed).note: after treatment of many ases of hroni autoimmune onditions su h as MS, ALS, Parkin-son's, Alzheimer's, CFS, Lupus, Rheumatoid Arthritis, et ., it has been observed that often mer uryalong with root anal toxi ity or avitation toxi ity are major fa tors in these onditions, and mostwith these onditions improve after TDR if proto ol is followed arefully (35, 200, 600). Other mea-sures in addition to TDR that have been found to help in treatment of MS in lini al experien e areavoidan e of milk produ ts, get lots of sunlight, supplementation of al ium AEP (448) and alphalipoi a id (448b). Progesterone reme has been found to promote regrowth of myelin sheaths inanimals (448 ). 13

Tests suggested by Huggins/Levy (35) for evaluation and treatment of mer ury toxi ity:(a) hair element test (386) (low hair mer ury level does not indi ate low body level) (more than3 essential minerals out of normal range indi ates likely metals toxi ity)(b) CBC blood test with di�erential and platelet ount blood serum pro�le(d) urinary mer ury (for person with average exposure with amalgam �llings, average mer urylevel is 3 to 4 ppm; lower test level than this likely means person is poor ex retor and a umulatingmer ury, often mer ury toxi (35)(e) fra tionated porphyrin (note test results sensitive to light, temperature, shaking)(f) individual tooth ele tri urrents (repla e high negative urrent teeth �rst)(g) patient questionnaire on exposure and symptom historyBased on the known me hanisms of damage found in these onditions, the authors of the study(463) suggest that supplementation with 100 mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and400 IU vit D and E, 100 & mgr; g Se, 180 mg EPA nd 120 mg DHA per day between 14 and 16 yearsof age may prevent MS, and redu e futher damage for those with the ondition.An Oregon resear her, Dr. R. Swank, found a signi� ant orrelation between MS and dietaryfat (274). He developed a low fat diet, with animal meat mostly repla ed by �sh or �sh oil (withEPA/DHA) and olive oil. Studies found the Swank diet e�e tive at redu ing the e�e ts of MS.European studies have on�rmed his �ndings regarding onne tion of MS to high fat animal diets,and e�e tiveness of the Swank diet. Studies have also found de� ien y in essential fatty a idsto be asso iated with demyelination, again onsistent with the Swank �ndings. Studies have alsofound prote tive e�e ts of diets high in vegetable protein, dietary �ber, ereal �ber, vit C, vit D,thiamin, ribo avin, al ium, potassium, and magnesium. A study found in reased vit D helpful inredu ing MS e�e ts. Additionally ur umin and A etyl-L-Carnitine were found by studies to beneuroprote tive. Both redu e in ammation/ oxidative stress. Extra ts of green tea (EGCG) andbla k tea (thea avins) also have been found to be highly e�e tive at redu ing in ammatory e�e ts(274). A study omparing alternative treatment of MS to onventional treatment found the majorityusing alterntive treatments were satis�ed with their treatment, and mu h lower adverse health e�e tsfrom alternative treatments ompared to onvention treatments (273). Amalgam repla ement wasone of the alternatives used by some.More information on auses, prevention, and treatment of autoimmune onditions an be foundat the following review5 (100). Information on test and treatment options and do tors and dentistswith experien e at dealing with toxi metal related onditions an be obtained from DAMS6 (800-311-6265) or the dental and medi al asso iation IAOMT (www.iaomt.org/7).1.8 Referen es(2) U.S. Environmental Prote tion Agen y (EPA), 1999, \Integrated Risk Information System", Na-tional Center for Environmental Assessment, Cin innati, Ohio, http://www.epa.gov/n ea/iris.htm;& United States Environmental Prote tion Agen y, OÆ e of Water, November 2000, The NationalListing of Fish andWildlife Advisories: Summary of 1999 Data, EPA-823-F-00-20, www.epa.gov/ost/�sh/advisories/general.html8(12) Dimaval S ienti� monograph, sixth Ed., Jan 1997, Dr Johann Rupre ht, Heyl Corporation5Internet: \http://www. v. om/autoimmD.html".6Internet: \http://www. v. om/dams.html".7Internet: \http://www.iaomt.org/".8Internet: \http://www.epa.gov/ost/�sh/advisories/general.html".14

(13) (a) S.Hussain et al, \Mer uri hloride-indu ed rea tive oxygen spe ies and its e�e t onantioxidant enzymes in di�erent regions of rat brain", J Environ S i Health B 1997 May; 32(3):395-409; & P.Bulat, \A tivity of Gpx and SOD in workers o upationally exposed to mer ury", Ar hO up Environ Health, 1998, Sept, 71 Suppl:S37-9; & Stohs SJ, Bag hi D. Oxidative me hanisms inthe toxi ity of metal ions. Free Radi Biol Med 1995; 18(2): 321-36; & D.Jay, \Glutathione inhibitsSOD a tivity of Hg", Ar h Inst ardiol Mex, 1998, 68(6):457-61 & El-Demerdash FM. E�e ts ofselenium and mer ury on the enzymati a tivities and lipid peroxidation in brain, liver, and bloodof rats. J Environ S i Health B. 2001 Jul; 36(4):489-99. & (b) S.Tan et al, \Oxidative stress indu esprogrammed ell death in neuronal ells", J Neuro hem, 1998, 71(1):95-105; & Matsuda T, TakumaK, Lee E, et al. Apoptosis of astroglial ells [Arti le in Japanese℄ Nippon Yakurigaku Zasshi. 1998O t; 112 Suppl 1:24P-; & Lee YW, Ha MS, Kim YK. Role of rea tive oxygen spe ies and glutathionein inorgani mer ury-indu ed injury in human glioma ells. Neuro hem Res. 2001 Nov; 26(11):1187-93; & ( ) Ho PI, Ortiz D, Rogers E, Shea TB. Multiple aspe ts of homo ysteine neurotoxi ity:glutamate ex itotoxi ity, kinase hypera tivation and DNA damage. J Neuros i Res. 2002 De 1;70(5):694-702.(14) (a) M.Nylander et al, \Mer ury on entrations in the human brain and kidneys and exposurefrom amalgam �llings", Swed Dent J 1987; 11:179-187, & (b) D.W.Eggleston et al, Correlation ofdental amalgam with mer ury in brain tissue. J Prosthet Dent, 1987, 58(6), 704-7; & J.A.Weiner etal, \The relationship between mer ury on entration in human organs and predi tor variables", S iTot Environ, 138(1-3):101-115, 1993(18) S ifo R, Mar hetti B, et al. Opioid-immune intera tions in autism: behavioral and immuno-logi al assessment during a double-blind treatment with naltexone. Ann Ist Super Sanita 1996; 32(3):351-9.(19) Eedy DJ, Burrows D, Dli�ord T, Fay A. Elevated T ell subpopulations in dental students. Jprosthet Dent 1990; 63(5):593-6; & Yonk LJ et al, CD+4 helper T- ell depression in autism. ImmunolLett, 1990, 25(4):341-5.(20) LDN for MS Trials/Experien e www.ldnresear htrust.org/default.asp?page id=779(21) Goyer RA Toxi e�e ts of metals. Cassarett and Doull's toxi ology{The basi s ien e ofpoisons, ed3, New York, Ma Millan Publ.Co 1986, pp582-609(22) (a) Gali N, Feren i Z et al, Dental amalgam mer ury exposure in rats. Biometals. 1999Sep; 12(3):227-31; & Arvidson B, Arvidsson J, Johansson K., Mer ury deposits in neurons of thetrigeminal ganglia after insertion of dental amalgam in rats. Biometals. 1994 Jul; 7(3):261-3; &(b) Dans her G, Horsted-Bindslev P, Rungby J. Tra es of mer ury in organs from primates withamalgam �llings. Exp Mol Pathol. 1990 Jun; 52(3):291-9; & L.Hahn et al, \Distribution of mer uryreleased from amalgam �llings into monkey tissues", FASEB J., 1990, 4:5536(24) J.R. Cade et al, Autism and s hizophrenia linked to malfun tioning enzyme for milk proteindigestion. Autism, Mar 1999. http://news.u .edu/1999/03/15/autism/10; & Autism and S hizophre-nia: Intestinal Disorders, Cade R et al. Nutritional Neuros ien e, Mar h 2000. www.feingold.org/Resear h/ ade.html11& www.paleodiet. om/autism/12; & \Beta- asomorphin indu es Fos-like immunorea tivity in dis- rete brain regions relevant to s hizophrenia and autism" Autism Mar h 1999 vol 3(1) 67-83; Sun,ZJ, Cade JR, et al & A Peptide Found in S hizophrenia and Autism Causes Behavioral Changesin Rats, J.R. Cade, Z. Sun, Univ of Florida, USA, Autism, Vol. 3, No. 1, 85-95 (1999) DOI:10.1177/1362361399003001007 1999 The National Autisti So iety, SAGE Publi ations http://aut.sagepub. om/ gi/ ontent/abstra t/3/1/8513;& Opiate hypothesis in infantile autism? Therapeuti trials with naltrexone, Leboyer M, et al.,9Internet: \http://www.ldnresear htrust.org/default.asp?page id=77".10Internet: \http://news.u .edu/1999/03/15/autism/".11Internet: \http://www.feingold.org/Resear h/ ade.html".12Internet: \http://www.paleodiet. om/autism/".13Internet: \http://aut.sagepub. om/ gi/ ontent/abstra t/3/1/85".15

En ephale 1993 Mar-Apr; 19(2):95-102; & Food allergy and infantile autism. Lu arelli S, et al.,Panminerva Med 1995 Sep; 37(3):137-41; www.feingold.org/Resear h/autism.html14 & Appli ation ofthe Exorphin Hypothesis to Attention De� it Hypera tivity Disorder: A Theoreti al Framework byRonald Hoggan A Thesis Submitted To The Fa ulty Of Graduate Studies In Partial Ful�lment OfThe Requirements For The Degree Of Master Of Arts, Graduate Division Of Edu ational Resear h,Calgary, April, 1998 University of Calgary(25) Rei helt KL. Bio hemistry and psy holphisiology of autisti syndromes. Tidsskr Nor Laege-foren 1994, 114(12):1432-4; & Rei helt KL et al, Biologi ally a tive peptide- ontaining fra tions ins hizophrenia and hildhood autism. Adv Bio hem Psy hopharmo ol 1981; 28: 627-43; Lu arelli S,Cardi E, et al, Food allergy and infantile autism. Panminerva Med 1995; 37(3):137-41; & Shel L,Autisti disorder and the endogenous opioid system. Med Hypotheses 1997, 48(5): 413-4.(26) The mer ury/ asein/gluten fa tor e�e t on opioid peptides as a me hanism in ausing autism,s hizophrenia, ADHD, MS, and other neurologi al onditions, BWindham (Ed), www. v. om/hgopioid.html15;& (b) IgA antibodies against gliadin and gluten in multiple s lerosis, Rei helt KL16, Jensen D.17 A taNeurol S and. 2004 O t; 110(4):239-41; & ( ) Gluten sensitivity in Japanese patients with adult-onset erebellar ataxia, Ihara M, Makino F, et al; Intern Med. 2006; 45(3):135-40; & (d) Multiple s lerosisand o ult gluten sensitivity, Pengiran Tengah CD, Lo k RJ, Unsworth DJ, Wills AJ. Neurology.2004 Jun 22; 62(12):2326-7.(28) F.S hmidt et al, \Mer ury in urine of employees exposed to magneti �elds", Tidsskr NorLaegeforen, 1997, 117(2): 199-202; & Sheppard AR and EisenbudM., Biologi al E�e ts of ele tri and magneti �elds of extremely low frequen y. New York university press. 1977; & Ortendahl T W,Hogstedt P, Holland RP, \Mer ury vapor release from dental amalgam in vitro aused by magneti �elds generated by CRT's", Swed Dent J 1991 p 31 Abstra t 22.(30) Till et al., Zahnarztl. Welt/reform, 1978:87; 1130-1134; & S.Olssonl, \Release of elementsdue to ele tro hemi al orrosion of dental amalgam" J of Dental Resear h, 1994, 73:33-43(33) (a) Markovi h et al, \Heavy metals (Hg, Cd) inhibit the a tivity of the liver and kidney sulfatetransporter Sat-1", Toxi ol Appl Pharma ol, 1999, 154(2):181-7; & (b) S.A. M Fadden, \Xenobioti metabolism and adverse environmental response: sulfur-dependent detox pathways", Toxi ology,1996, 111(1-3):43-65; & ( ) S.C. Langley-Evans et al, \SO2: a potent glutathion depleting agent",Comp Bio hem Physiol Pharmo ol Toxi ol Endo rinol, 114(2):89-98; & (d) Alberti A, Pirrone P, EliaM, Waring RH, Romano C. Sulphation de� it in \low-fun tioning" autisti hildren. Biol Psy hiatry1999, 46(3):420-4.(34) Patri kSt�ortebe ker, Asso iate Professor of Neurology, Karolinska Institute, Sto kholm. Mer- ury Poisoning from Dental amalgam-A Hazard to the Human Brains, ISBN: 0-941011001-1 & JCanadian Dental Asso , 33(6): 300-; & Henriksson J, Tjalve H. Uptake of inorgani mer ury in theolfa tory bulbs via olfa tory pathways in rats. Environ Res. 1998 May; 77(2):130-40.(35) (a) Huggins HA, Levy, TE, Solving the MS Mystery: Help, hope and re overy, 2002; & (b)Huggins HA, Levy, TE, Uniformed Consent: the hidden dangers in dental are, 1999, HamptonRoads Publishing Company In ; & ( ) Hal Huggins, Its All in Your Head, 1993; & (d) Center forProgressive Medi ine, & www.hugginsappliedhealing. om/ms.php18(38) S.Zi� and M.Zi�, Infertility and Birth Defe ts: Is Mer ury from Dental Fillings a HiddenCause?, Bio-Probe, In . ISBN: 0-941011-03-8.1987, www.bioprobe. om(42) Rodgers JS, Ho ker JR, et al, Mer uri ion inhibition of eukaryoti trans ription fa tor14Internet: \http://www.feingold.org/Resear h/autism.html".15Internet: \http://www. v. om/hgopioid.html".16\. . . gaia/ohttp://www.n bi.nlm.nih.gov/sites/entrez?Db=pubmed&amp;Cmd=Sear h&amp;Term=%22Rei helt%20KL%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed ResultsPanel.Pubmed Dis overyPanel.Pubmed RVAbstra tPlus".17Internet: \http://www.n bi.nlm.nih.gov/sites/entrez?Db=pubmed&amp;Cmd=Sear h&amp;Term=%22Jensen%20D%22%5BAuthor%5D&amp;itool=EntrezSystem2.PEntrez.Pubmed.Pubmed ResultsPanel.Pubmed Dis overyPanel.Pubmed RVAbstra tPlus".18Internet: \http://www.hugginsappliedhealing. om/ms.php".16

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Physi ians and Surgeons, Summer, 2004; & Sodium-mediated axonal degeneration in in ammatorydemyelinating disease. Be htold DA, Smith KJ., J Neurol S i. 2005 Jun 15; 233(1-2):27-35(577) Joa himMutter et al, Alzheimer Disease: Mer ury as pathogeneti fa tor and apolipoproteinE as a moderator, Neuroendo rinol Lett 2004; 25(5):331-339; & (b) Mutter J, Das hner F, et al,Amalgam risk assessment with overage of referen es up to 2005℄, Gesundheitswesen. 2005 Mar;67(3):204-16.(595) High fru tose onsumption ombined with low dietary magnesium intake may in rease thein iden e of the metaboli syndrome by indu ing in ammation. Magnes Res. 2006 De ; 19(4):237-43. Rayssiguier Y, Gueux E, et al; & (b) Dietary magnesium and �ber intakes and in ammatoryand metaboli indi ators in middle-aged subje ts from a population-based ohort. Am J Clin Nutr.2006 Nov; 84(5):1062-9 Bo S, Durazzo M, Pagano G. et al; & ( ) Hypomagnesemia, oxidative stress,in ammation, and metaboli syndrome. Diabetes Metab Res Rev. 2006 Nov-De ; 22(6):471-6.Guerrero-Romero F, Rodr��guez-Mor�an(596) E�e ts of antidiabeti and antihyperlipidemi agents on C-rea tive protein. Mayo Clin Pro .2008 Mar; 83(3):333-42, Dandona P; & Role of advan ed gly ation end produ ts in hypertension andatheros lerosis: therapeuti impli ations. Cell Bio hem Biophys. 2007; 49(1):48-63, Vasdev S, GillV, Singal P.(597) E�e ts of mer uri hloride on glu ose transport in 3T3-L1 adipo ytes. Toxi ol In Vitro.2005 Mar; 19(2):207-14. Barnes DM, Kir her EA; & E�e ts of inorgani HgCl2 on adipogenesis.Toxi ol S i. 2003 O t; 75(2):368-77. Epub 2003 Jul 25, Barnes DM, Hanlon PR, Kir her EA; & (b)Heavy metal-indu ed inhibition of a tive transport in the rat small intestine in vitro. Intera tionwith other ions. Comp Bio hem Physiol C. 1986; 84(2):363-8, Iturri SJ, Pe~na A; & Intera tion ofthe sugar arrier of intestinal brush-border membranes with HgCl2. Bio him Biophys A ta. 1980May 8; 598(1):100-14, Klip A, Grinstein S, Biber J, Semenza G.(598) Over oming Depression, Dr. Russell Blaylo k, The Blaylo k Wellness Report, Vol 5, No. 3,Mar h 2008, & Food Additives, What you eat an kill you, Vol 4, No. 10, www.blaylo kreport. om/51(599) Do umentation that dental amalgam is the largest sour e of both organi and inorgani mer ury in most people who have several amalgam �llings, DAMS FS, www. v. om/damspr1.html52(600) Annotated bibliography: Exposure levels and health e�e ts related to mer ury/dental amal-gam and results of amalgam repla ement, 2004; B Windham (Ed.), (over 4000 medi al study refer-en es do umenting me hanism of ausality of 40 hroni onditions and over 60,000 lini al ases ofre overy or signi� ant improvement of these onditions after amalgam repla ement-do umented bydo tors) www. v. om/amalg6.html53(601) Cognitive and Behavioral E�e ts of Toxi Metal Exposures, 2002; B. Windham (Ed), (over150 medi al study referen es) www. v. om/tmlbn.html54(602) The me hanisms by whi h mer ury auses hroni immune and in amatory ondtions,B.Windham (Ed.), 2002, www. v. om/immunere.html55(603) The environmental e�e ts of mer ury from amalgam a�e t everyone. B. Windham (Ed.)(Gov't studies) www. v. om/damspr2f.html5651Internet: \http://www.blaylo kreport. om/".52Informativo: \Dental Amalgam Mer ury Solutions".53Informativo: \Mer ury Exposure Levels from Amalgam Dental Fillings; Do umentation of Me hanisms byWhi hMer ury Causes over 30 Chroni Health Conditions; Results of Repla ement of Amalgam Fillings; and O upationalE�e ts on Dental Sta�".54Informativo: \E�e ts of Toxi Metals on Learning Ability and Behavior".55Informativo: \Immune Rea tive Conditions: The Mer ury Conne tion to E zema, Psoriasis, Lupus, Asthma,S leroderma, Rheumatoid Arthritis, and Allergies".56Internet: \http://www. v. om/damspr2f.html". 38

(604) \Health, Hormonal, and Reprodu tive E�e ts of Endo rine Disrupting Chemi als" (in lud-ing mer ury), Annotated Bibliography, 2002, B.Windham, www. v. om/endohg.html57 www. v. om/endo rin.html58(605) Me hanisms of mer ury release from amalgam dental �llings: vaporization, oral galvanism,and e�e ts of Ele tromagneti �elds, www. v. om/galv.html59(606) Developmental and neurologi al e�e ts of mer ury vapor, B.Windham (Ed) www. v. om/damspr13.html60Note: et . when it is used in a list of referen es means that Author knows of several more referen essupporting the statement, in #600 for example, but doesn't think them ne essary here.

57Internet: \http://www. v. om/endohg.html".58Internet: \http://www. v. om/endo rin.html".59Informativo: \Oral galvanism and Ele tromagneti Fields (EMF)".60Internet: \http://www. v. om/damspr13.html". 39