Jump to content
RemedySpot.com

Re: correlation between all things (my longest post ever!)

Rate this topic


Guest guest

Recommended Posts

Well, I have been meaning to getting around to studying flax seed, which is

not real easy to study. Anyhow, I found this great posting I thought I would

share concerning the cause of many diseases and how mercury is killing us:

Heidi N

================BEGIN

QUOTE===================================================

And most Yeasts proliferate in the presence of mercury, and altered pH (a

great debate!), which accompanies abnormal composition of bacterial flora - and

actually drives down the iron levels - because the yeasts have a way of not

using iron! Also, I found that historically, flax seed oil has been used to

remove mercury from the body, and this is where " you come in. "

When I got this far in my little investigation, I did a search for " mercury

flaxseed " and the following was at the top of the list! I made all of that

text blue, so you can keep track of what it says, and whatever I might add. You

can find this web page at http://www.talkinternational.com/science/als.htm

" Daily mercury exposures to those with _Amalgam_

(http://curezone.com/c/?http://curezone.com/faq/c.asp?a=3,76) dental fillings

commonly exceed the

Government health guideline for mercury, due to mercury's negative vapor

pressure

and galvanic action with other metals in the mouth(500). People also commonly

get exposures to mercury and other toxic metals such as lead, arsenic,

nickel, and aluminum from food, water, and other sources(501). All of these are

highly neurotoxic and are documented to cause neurological damage which can

result in chronic neurological conditions over time.

Mercury has been found to accumulate preferentially in the primary motor

function related areas involved in ALS- such as the brain stem, cerebellum,

rhombencephalon, dorsal root ganglia, and anterior horn motor neurons, which

enervate the skeletal muscles(48,291,327,329,442,500). Many studies of patients

with major neurological or degenerative diseases have found evidence amalgam

fillings play a major role in development of conditions such as such as ALS

(48,92,97,207,229b,325,416,423,442,468,470,35).

Here's what it does! A direct mechanism involving mercury's inhibition of

cellular enzymatic processes by binding with the hydroxyl radical(SH) in amino

acids appears to be the noticeable effects that pertain to a major part of

the connection to allergic/immune reactive conditions such as autism,

schizophrenia, eczema, psoriasis, and allergies(500), as well as to autoimmune

conditions such as ALS, Lupus, Alzheimer's(AD), Scleroderma, Chronic

Fatigue(CFS),

and Fibromyalgia(FM), etc . For example the patient has a lot of intestinal

distress with all types of milk products, simply because, mercury has been

found to strongly inhibit the activity of dipeptyl peptidase (DPP IV) which is

required in the digestion of the milk protein casein(411,412) as well as of

xanthine oxidase(439) Additional cellular level enzymatic effects of mercury's

binding with proteins include blockage of sulfur oxidation processes

(33,114,194,412), enzymatic processes involving vitamins B6 and B12(418),

effects on

the cytochrome-C energy processes (43,84,232,338c,35), along with mercury's

adverse effects on cellular mineral levels of calcium, magnesium, copper,zinc,

and lithium (43,96,119,198,333, 386,427,432,489,500). And along with these

blockages of cellular enzymatic processes, mercury has been found to cause

additional neurological and immune system effects in many through

immune/autoimmune reactions (60,313,314,375,405) A recent study gives a

comprehensive review

of studies finding a connection between ALS, toxic metals, and

autoimmunity(405).

Oxidative stress and reactive oxygen species(ROS) have been implicated as

major factors in neurological disorders including ALS, motor neuron

disease(MND), CFS, FM, Parkinson's(PD), Multiple Schlerosis(MS), and

Alzheimer's(AD)

(13,56,84,98,145,169,207b,424,442-444,453, 462,496). Mercury forms conjugates

with thiol compounds such as glutathione and cysteine and causes depletion of

glutathione, which is necessary to mitigate reactive damage. One study found

that insertion of amalgam fillings or nickel dental materials causes a

supression of the number of T-lympocytes(270), and impairs the T-4/T-8 ratio.

Low

T4/T8 ratio has been found to be a factor in autoimmune conditions. Mercury

induced lipid peroxidation has been found to be a major factor in mercury's

neurotoxicity, along with leading to decreased levels of glutathione

peroxidation and superoxide dismustase(SOD)(13,254,489,494-496).

Metalloprotein(MT) are

involved in metals transport and detoxification(114,442,464) What do you

think would happen if the MT's were all knocked out? Mercury inhibits sulfur

ligands in MT and in the case of intestinal cell membranes inactivates MT that

normally bind cuprous ions(477), thus allowing buildup of copper to toxic

levels in many and malfunction of the Zn/Cu SOD function. Exposure to mercury

results in changes in metalloprotein compounds that have genetic effects,

having

both structural and catalytic effects on gene _expression

(114,241,296,442,464,477,495). Some of the processes affected by such MT

control of genes

include cellular respiration, metabolism, enzymatic processes, metal-specific

homeostasis, and adrenal stress response systems. Significant physiological

changes occur when metal ion concentrations exceed threshold levels. Such MT

formation also appears to have a relation to autoimmune reactions in

significant

numbers of people (114,60,313, 342,369,442,464). Of a population of over 3000

tested by the immune lymphocyte reactivity test(MELISA,60,275), 22% tested

positive for inorganic mercury and 8% for methyl mercury, but much higher

percentages tested positive for autoimmune condition patients. In the MELISA

laboratory, 12 out of 13 ALS patients tested showed positive immune reactivity

lymphocyte responses to metals in vitro [87], indicating metals reactivity a

likely major factor in their condition. A recent study assessed the possible

causes of high ALS rates in Guam and similar areas and the recent decline in

this

conditions. One of the studies conclusions was that a likely major factor

for the high ALS rates in Guam and similar areas in the past was chronic

dietary deficiency since birth in Ca, Mg and Zn induced excessive absorption of

divalent metal cations such as mercury which accelerates oxidant-mediated

neuronal degenerations in a genetically susceptible population(466).

Mercury blocks the immune function of magnesium and zinc (198,427,43,38),

(And what effect to you think that might produce?) whose deficiencies are known

to cause significant neurological effects(461,463,430). The low Zn levels

result in deficient CuZnSuperoxide dismustase (CuZnSOD), which in turn leads to

increased levels of superoxide due to toxic metal exposure. This is in

addition to mercury's effect on metallothionein and copper homeostasis as

previously discussed(477). Copper is an essential trace metal which plays a

fundamental role in the biochemistry of the nervous system(489,495463,,464).

Several

chronic neurological conditions involving copper metabolic disorders are well

documented like 's Disease and Menkes Disease. Mutations in the

copper/zinc enzyme superoxide dismustase(SOD) have been shown to be a major

factor

in the motor neuron degeneration in conditions like familial ALS. Exposures to

toxic metals such as mercury and cadmium have been found to cause such

effects, and similar effects on Cu/Zn SOD have been found to be a factor in

other

conditions such as autism, Alzheimer's, Parkinson's, and non-familial ALS

(489,495,464,469,111). This condition can result in zinc deficient SOD and

oxidative damage involving nitric oxide, peroxynitrite, and lipid

peroxidation(495,496,489), which have been found to affect glutamate mediated

excitability

and apoptosis of nerve cells and effects on mitochondria (495,496,119) These

effects can be reduced by zinc supplementation(464,495,430), as well as

supplementation with antioxidants and nitric oxide-suppressing agents and

peroxynitrite scavengers such as Vit C, Vit E, lipoic acid, Coenzyme Q10,

carnosine,

gingko biloba, N-acetylcysteine, etc.(444,464,494,495,469,470). Ceruloplasmin

in plasma can be similarly affected by copper metabolism disfunction, like SOD

function, and is often a factor in neurodegeneration(489).

Calcium plays a major role in the extreme neurotoxicity of mercury and

methyl mercury. Both inhibit cellular calcium ATPase and calcium uptake by

brain

microsomes at very low levels of exposure (270,288,329,333,432,56,). Protein

Kinase C (PKC) regulates intracellular and extra cellular signals across

neuronal membranes, and both forms of mercury inhibit PKC at micromolar levels,

as

well as inhibiting phorbal ester binding(43,432). They also block or inhibit

calcium L-channel currents in the brain in an irreversable and concentration

dependent manner. Mecury vapor or inorganic mercury exposure affects the

posterior cingulate cortex and causes major neurological effects with

sufficient

exposure(428,453). Some of the resulting conditions include stomatitis,

tremor, ADD, erythism, etc. Metallic mercury is much more potent than methyl

mercury in such actions, with 50 % inhibitation in animal studies at 13

ppb(333,329).

Mercury exposure also degrades the immune system resulting in more

susceptability to viral, bacterial, or parasitic effects along with candida

albicans

which are often present in those with chronic conditions and require treatment

(404,468,470,485,500). Four such commonly found in ALS patients are

mycoplasma AND echo-7 enterovirus(468,470), candida albicans(404), and

parasites(485). Mercury from amalgam interferes with production of cytokines

that activate

macrophage and neutraphils, disabling early control of viruses or other

pathogens and leading to enhanced infection(131,251).

Spatial and temporal changes in intracellular calcium concentrations are

critical for controlling gene _expression and neurotransmitter release in

neurons(432,438). Mercury alters calcium homeostasis and calcium levles in the

brain and affects gene _expression and neurotransmitter release through its

effects on calcium, etc. Mercury inhibits sodium and potassium (N,K)ATPase in

dose

dependent manner and inhibits dopamine and noreprenephrine uptake by

synaptosomes and nerve implulse transfer(288,270,56,43,35). Mercury also

interrupts

the cytochrome oxidase system, blocking the ATP energy function (35,43,84),

chronic flatigue syndrom, lowering immune growth factor IGF-I levels and

impairing astrocyte function(119,131). Astrocytes are common cells in the CNS

involved in the feeding and detox of nerve cells. Increases in inflamatory

cytokines such as caused by toxic metals trigger increased free radical

activity

and damage to astrocyte and astrocyte function(152). IGF-I protects against

brain and neuronal pathologies like ALS, MS, and Fibromyalgia by protecting the

astrocytes from this destructive process.

Mercury lymphocyte reactivity and effects on glutamate in the CNS induce

_CFS_ (http://curezone.com/c/?http://curezone.com/faq/c.asp?a=4,111,676) type

symptoms including profound tiredness, musculoskeletal pain, sleep

disturbances, gastrointestinal and neurological problems along with other CFS

symptoms

and Fibromyalgia(342,346,369,375,496). Mercury has been found to be a common

cause of Fibromyalgia(293,346,369) , which based on a Swedish survey occurs in

about 12% of women over 35 and 5.5% of men(368). Glutamate is the most

abundant amino acid in the body and in the CNS acts as excitory neurotransmitter

(346,386,412,496,119), which also causes inflow of calcium. Astrocytes, a type

of cell in the brain and CNS with the task of keeping clean the area around

nerve cells, have a function of neutralizing excess glutamate by transforming

it to glutamic acid. If astrocytes are not able to rapidly neutralize excess

glutamate, most obviously because of the mercury's influence, then a buildup

of glutamate and calcium occurs, causing swelling and neurotoxic

effects(119,131,152,333,496). Mercury and other toxic metals inhibit astrocyte

function

in the brain and CNS(119,131), causing increased glutamate and calcium

related neurotoxicity(119,152,333,226a,496) which are responsible for much of

the

Fibromyalgia symptoms and a factor in neural degeneration in MS and ALS. This

is also a factor in conditions such as CFS, Parkinson's, and

ALS(346,416,496). Animal studies have confirmed that increased levels of

glutamate(or

aspartate, another amino acid excitory neurotransmitter) cause increased

sensitivity

to pain , as well as higher body temperature- both found in

CFS/Fibromyalgia. Mercury and increased glutamate activate free radical forming

processes

like xanthine oxidase which produce oxygen radicals and oxidative neurological

damage(346,142,13). Medical studies and doctors treating Fibromyalgia have

found that supplements which cause a decrease in glutamate or protect against

its effects have a positive effect on Fibromyalgia and other chronic neurologic

conditions. Some that have been found to be effective include CoQ10 (444),

ginkgo biloba and pycnogenol(494a), NAC(54,494a), Vit B6, methyl

cobalamine(B12), L-carnitine, choline, ginseng, vitamins C and E, nicotine, and

omega 3

fatty acids(fish and flaxseed oil) (417,495e).

Another neurological effect of mercury that occurs at very low levels is

inhibition of nerve growth factors, for which deficiencies result in nerve

degeneration. Only a few micrograms of mercury severely disturb cellular

function

and inhibits nerve growth (175,147,226,255,305,149). Prenatal or neonatal

exposures have been found to have life long effects on nerve function and

susceptability to toxic effects. Prenatal mercury vapor expsoure that results

in

levels of only 4 parts per billion in newborn rat brains was found to cause

decreases in nerve growth factor and other effects(305). This is a level that

is

common in the population with several amalgam fillings or other

exposures(500). Insulin-like-growth factor I (IGF-I) are positively correlated

with

growth hormone levels and have been found to be the best easily measured marker

for levels of growth hormone, but males have been found more responsive to this

factor than women(497). IGF-I controls the survival of spinal motor neruons

affected in ALS during development as well as later in life(497,498). IGF-I

and insulin levels have been found to be reduced in ALS pateients with

evidence this is a factor in ALS(497,498). Several clinical trials have found

IGF-I

treatment is effective at reducing the damage and slowing the progression of

ALS and Alzheimer's with no medically important adverse effects(498). It has

also been found that in chronically ill patients the levels of pituitary and

thyroid hormones that control many bodily processes are low, and that

supplenting both thyrotropin-releasing hormone and growth control hormone is

more

effective at increasing all of these hormone levels in the patient(499).

Tick-borne encephalitis, such as Lyme Diseaese, has been found to cause ALS

in a significant portion of untreated acute cases(471). Lyme disease is

widespread in the U.S.

Large numbers of patients diagnosed with ALS have been found to have

treatable tick-borne encephaltis, and many have recovered after treatment.

Extremely toxic anerobic bacteria from _root canals_

(http://curezone.com/c/?http://curezone.com/dental/root_canal.asp) or

cavitations formed at

incompletely healed tooth extraction sites have also been found to be common

factors

in fibromyalgia and other chronic neurological conditions such as

Parkinson's and ALS, with condensing osteitis which must be removed with a

surgical

burr along with 1 mm of bone around it(35,437,500). Have you had any teeth

extracted in the last year or so? Cavitations have been found in 80% of sites

from

wisdom tooth extractions tested and 50% of molar extraction sites

tested(35,437). The incidence is likely somewhat less in the general

population.

Medical studies and doctors treating fibromylagia have found that supplements

which

cause a decrease in glutamate or protect against its effects have a positive

effect on fibromyalgia and other chronic neurologic conditions like ALS.

Some that have been found to be effective include Vit B6, methyl

cobalamine(B12), L-carnitine, choline, ginseng, Ginkgo biloba,vitamins C and E,

CoQ10,

nicotine, and omega 3 fatty acids(fish and flaxseed oil) (417,468).

Clinical tests of patients with ALS, MND, Parkinson's, Alzheimer's,

Lupus(SLE), and rheumatoid arthritis have found that the patients generally

have

elevated plasma cysteine to sulphate ratios, with the average being 500% higher

than controls(330,331,56,84), and in general being poor sulphur oxidizers.

This means that these patients have blocked enzymatic processes for converting

the basic cellular fuel cysteine to sulfates and glutathione, and thus

insufficient sulfates available to carry out necessary bodily processes.

Mercury has

been shown to diminish and block sulphur oxidation and thus reducing

glutathione levels which is the part of this process involved in detoxifying

and

excretion of toxics like mercury(33). Glutathione is produced through the

sulphur oxidation side of this process. Low levels of available glutathione

have

been shown to increase mercury retention and increase toxic effects(111), while

high levels of free cysteine have been demonstrated to make toxicity due to

inorganic mercury more severe(333,194,56,33e). The deficiency in conjugation

and detoxification of sulfur based toxins in the liver results in toxic

metabolites and progressive nerve damage over time (331). Mercury has also been

found to play a part in inducing intolerance and neuronal problems through

blockage of the P-450 enzymatic process(84,33e). Patients with some of these

conditions have found that bathing in _Epsom Salts_

(http://curezone.com/c/?http://curezone.com/forums/m.asp?f=73 & i=116) (magnesium

sulfate) offers temporary

relief for some of their symptoms by providing sulfates that avoid the

blocked metabolic pathway. A test that some doctors treating conditions like

ALS

usually prescribe to measure the cysteine to sulfate ratio and other

information useful in diagnosis and treatment is the Great Smokies Diagnostic

Labs

comprehensive liver detox test(386). The test results come with some

recommendations for treatment. A hair test for toxic metals is also usually

ordered to

determine toxic exposures that might be involved(386). A more definitive test

such as MELISA for immune reactivity to toxics is available by sending blood

to a European lab(87). Other labs also have other useful tests such as Immune

Reactivity Biocompatability Tests(445), ELISA or organic acid panels or amino

acid panels(386). Treatment using IV glutathione, vitaminC, and minerals has

been found to be very effective in the stabilizing and ammelioration of some

of these chronic neurological conditions by neurologist such as Perlmutter

in Florida(469).

In one subtype of ALS, damaged, blocked, or faulty enzymatic superoxide

dimutase (SOD) processes appear to be a major factor in cell apoptosis involved

in the codition(443). Mercury is known to damage or inhibit SOD

actitivity(441,33,111).

Total dental revision(TDR) which includes replacing amalgam fillings,

extracting root canaled teeth, and treating cavitations has been found to offer

significant health improvements to many with ALS and other autoimmune

conditions(35,293,437). Root canals and cavitations have been found to harbor

anerobic

bacteria which give off toxins of extreme toxicity which block enzymatic

processes at the cellular level causing degenerative processes according to the

medical labs that do the tests(437,35), similar to mercury's effects but in

some cases even more toxic . IGF-1 treatments have also been found to

alleviate some of the symptoms of ALS(424). Medical studies and doctors

treating

fibromylagia have found that supplements which cause a decrease in glutamate or

protect against its effects have a positive effect on fibromyalgia. Some that

have been found to be effective in treating metals related autoimmune

conditions include Vit B6, CoenzymeQ10, methyl cobalamine(B12), L-carnitine,

choline, ginseng, Ginkgo biloba, vitamins C and E, nicotine, and omega 3 fatty

acids(fish and flaxseed oil) (417,444,468).

One dentist with severe symptoms similar to ALS improved after treatment for

mercury poisoning(246), and others treated for mercury poisoning or using

TDR have also recovered or significantly improved

(97,229,423,405,406,468-470,485,35).The Edelson Clinic in Atlanta which treats

ALS patients reports

similar experience(406), and the Perlmutter Clinic has also had success with

treatment of ALS and other degenerative neurological coditions(469).

While there are many studies documenting effectiveness of chemical chelators

like DMSA and DMPS at reducing metals levels and alleviating adverse effects

for most conditions, and many thousands of clinical case results(500,501);

there is also some evidence from animal studies that these chelators can

result in higher levels of mercury in the motor neurons in the short term which

might be a problem for ALS patients(). Thus other detox options might be

preferable for ALS patients until enough clinical evidence is available

treating

ALS patients with them with mercury toxicity. Another chelator used for clogged

arteries, EDTA, forms toxic compounds with mercury and can damage brain

function(307). Use of EDTA may need to be restricted in those with high Hg

levels. N-acetylcysteine(NAC) has been found to be effective at increasing

cellular

glutathione levels and chelating mercury(54). Experienced doctors have also

found additional zinc to be useful when chelating mercury(222) as well as

counteracting mercury's oxidative damage(43). Zinc induces metallothionein

which

protects against oxidative damage and increases protective enzyme activities

and glutathione which tend to inhibit lipid peroxidation and suppress

mercury toxicity(430,464). Also lipoic acid,LA, has been found to dramatically

increase excretion of inorganic mercury(over 12 fold), but to cause decreased

excretion of organic mercury(494d) and copper. Lipoic acid has a protective

effect regarding lead or inorganic mercury toxicity through its antioxidant

properties(494), but should not be used with high copper until copper levels

are

reduced. LA and NAC (N-acetylcysteine) also increase glutathione levels and

protect against superoxide radical/ peroxynitrite damage, so thus have an

additional neuroprotective effect(494ab,54). Zinc is a mercury and copper

antagonist and can be used to lower copper levels and protect against mercury

damage.

Lipoic acid has been found to have protective effects against cerebral

ischemic-reperfusion, excitotoxic amino acid(glutamate) brain injury,

mitochondrial dysfunction, diabetic neuropathy(494). Other antioxidants such as

carnosine(495a), Coenzyme Q10,Vitamins C & E, gingko biloba, and pycnogenol

have also

been found protective against degenerative neurological conditions(494,495e,

444).

________________________

References

(13) S.Hussain et al, " Mercuric chloride-induced reactive oxygen species and

its effect on antioxidant enzymes in different regions of rat brain " ,J

Environ Sci Health B 1997 May;32(3):395-409; & S.Tan et al, " Oxidative stress

induces programmed cell death in nueronal cells " , J Neurochem, 1998,

71(1):95-105. & J.S. Bains et al, " Neurodegenerative disorders in humans and

role of

glutathione in oxidative stress mediated neuronal death " , Brain Res Rev, 199,

25(3):335-58; & Stohs SJ, Bagchi D. Oxidative mechanisms in the toxicity of

metal ions. Free Radic Biol Med 1995; 18(2): 321-36.

(33) S.C. Langley- et al, " SO2: a potent glutathion depleting agent " ,

Comp Biochem Physiol Pharmocol Toxicol Endocrinol, 114(2):89-98; & (b)P.E.

Emory et al, " Increased Prevalence of poor sulphuoxidation in patients with

Rheumatoid Arthritis " , Ann Rheum Dis, 1992, 51(3): 318-20; & © Markovich et

al,

" Heavy metals (Hg,Cd) inhibit the activity of the liver and kidney sulfate

transporter Sat-1 " , Toxicol Appl Pharmacol, 1999,154(2):181-7; &

(d)2S.A.McFadden, " Xenobiotic metabolism and adverse environmental response:

sulfur-

dependent detox pathways " ,Toxicology, 1996, 111(1-3):43-65;

(35) Huggins HA, Levy,TE, Uniformed Consent: the hidden dangers in dental

care, 1999, Hampton Roads Publishing Company Inc; & Hal Huggins, Its All in

Your Head, 1993; & Center for Progressive Medicine, 1999, http://www.hugnet.com

(43) Knapp LT; Klann E. Superoxide-induced stimulation of protein kinase C

via thiol modification and modulation of zinc content. J Biol Chem 2000 May

22; & B.Rajanna et al, " Modulation of protein kinase C by heavy metals " ,

Toxicol Lett, 1995, 81(2-3):197-203: & A.Badou et al, " HgCl2-induced IL-4 gene

_expression in T cells involves a protein kinase C-dependent calcium influx

through L-type calcium channels " , & D.B.Veprintsev, 1996, Institute for

Biological

Instrumentation, Russian Academy of Sciences, Pb2+ and Hg2+ binding to

alpha-lactalbumin " .Biochem Mol Biol Int 1996 Aug;39(6):1255-65

(48) K.Arvidson, " Corrosion studies of dental gold alloy in contact with

amalgam " , Swed. Dent. J 68: 135-139,1984; & Skinner, EW, The _Science_

(http://curezone.com/c/?http://curezone.com/forums/f.asp?f=443) of Dental

Materials,

4th Ed.revised, W.B.Saunders Co., Philadelphia, p284-285,1957.

(54) M.E. Lund et al, " Treatment of acute MeHg poisoning by NAC " , J Toxicol

Clin Toxicol, 1984, 22(1):31-49; & Livardjani F; Ledig M; Kopp P; Dahlet M;

Leroy M; Jaeger A. Lung and blood superoxide dismustase activity in mercury

vapor exposed rats: effect of N-acetylcysteine treatment. Toxicology 1991 Mar

11;66(3):289-95. & G.Ferrari et al, Dept. Of Pathology, Columbia Univ., J

Neurosci,1995, 15(4):2857-66; & RR. Ratan et al, Dept. of Neurology, s

Hopkins Univ., J Neurosci, 1994, 14(7): 4385-92;

(56) X.M.Shen et al, Neurolbehavioral effects of NAC conjugates of dopamine:

possible relevance for Parkinson'sDisease " , Chem Res Toxicol, 1996,

9(7):1117-26; & Chem Res Toxicol, 1998, 11(7):824-37; & A. et al, " Direct

evidence for glutathione as mediator of apoptsosis in neuronal cells " , Biomed

Pharmacother, 1998; 52(9):349-55; & J.P.Spencer et al, " Cysteine & GSH in PD " ,

mechinsms involving ROS " , J Neurochem, 1998, 71(5):2112-22: &

P.Jenner, " Oxidative mechanisms in PD " , Mov Disord, 1998; 13(Supp1):24- 34; & D.

Offen et al,

" Use of thiols in treatment of PD " , Exp Neurol, 1996,141(1):32-9; & A.D.Owen

et al, Ann NY Acad Sci, 1996, 786:217-33; & JJ Heales et al, Neurochem Res,

1996, 21(1):35-39.

(84) J.C.Veltman et al, " Alterations of heme, cytochrome P-450, and steroid

metabolism by mercury in rat adrenal gland " , Arch Biochem Biophys, 1986,

248(2):467-78; & A.G.Riedl et al, Neurodegenerative Disease Research Center,

King's College,UK, " P450 and hemeoxygenase enzymes in the basal ganglia and

their

role's in Parkinson's disease " , Adv Neurol, 1999; 80:271-86; & Alfred V.

Zamm. Dental Mercury: A Factor that Aggravates and Induces Xenobiotic

Intolerance. J. Orthmol. Med. v6#2 pp67-77 (1991).

(87) Stejskal V. Immunological effects of amalgam components: MELISA--a new

test for the diagnosis of mercury allergy. Proceedings of the International

Symposium Status Quo and Perspectives of Amalgam and other Dental Materials;

April 29-May 14, 1994; Otzenhausen, Germany. http://www.melisa.org

(92) L. Tandon et al, " Elemental imbalance studies by INAA on ALS patients " ,

J Radioanal Nuclear Chem 195(1):13-19,1995; & Y.Mano et al, " Mercury in the

hair of ALS patients " , Rinsho Shinkeigaku, 1989, 29(7): 844-848; & Mano et

al, 1990, Rinsho Shinkeigaku 30: 1275-1277; & Khare et al, 1990, " Trace element

imbalances in ALS " , Neurotoxicology, 1990,11:521-532..

(96) A.F.Goldberg et al, " Effect of Amalgam restorations on whole body

potassium and bone mineral content in older men " ,Gen Dent, 1996, 44(3): 246-8;

&

K.Schirrmacher,1998, " Effects of lead, mercury, and methyl mercury on gap

junctions and [Ca2+]I in bone cells " , Calcif Tissue Int 1998 Aug;63(2):134-9.

(97) Redhe O, Pleva J, " Recovery from ALS after removal of dental amalgam

fillings " , Int J Risk & Safety in Med 4:229-236, 1994; & Vanacore N, Corsi L,

Fabrizio E, Bonifati V, Meco G, " Relationship between exposure to environmental

toxins and motor neuron disease: a case report " , Med Lav 1995 Nov-Dec;

86(6):522-33.

(98) A.Seidler et al, Possible environmental factors for Parkinson's

disease " ,Neurology 46(5): 1275- 1284, 1996; & Vroom FO, Greer M, " Mercury vapor

intoxication " , 95: 305-318, 1972; & Ohlson et al, " Parkinson's Disease and

Occupational Exposure to Mercury " , Scand J. Of Work Environment Health, Vol7,

No.4:

252-256, 1981; L.G.

(111)T.W.son et al, " Billiary secretion of glutathione-metal

complexes " , Fundam Appl Toxicol, 1985, 5(5):816-31; & D.Quig, Doctors Data

Lab, " Cysteine metabolism and metal toxicity " , Altern Med Rev, 1998;3:4,

p262-270, & J.de

Ceaurriz et al, Role of gamma- glutamyltraspeptidase(GGC) and extracellular

glutathione in disopition of inorganic mercury " ,J Appl Toxicol,1994, 14(3):

201-; & W.O. Berndt et al, " Renal glutathione and mercury uptake " , Fundam Appl

Toxicol, 1985, 5(5):832-9; & R.K. Zulups et al, J Toxicol Environ Health,

1995, 44(4): 385-99; & Pocernich CB, Cardin AL, Racine CL, Lauderback CM, Allan

Butterfield D. Glutathione elevation and its protective role in

acrolein-induced protein

damage in synaptosomal membranes: relevance to brain lipid peroxidation in

neurodegenerative disease. Neurochem Int 2001 Aug;39(2):141-9;

(114) M.Aschner et al, " Metallothionein induction in fetal rat brain by in

utero exposure to elemental mercury

vapor " , Brain Research, 1997, dec 5, 778(1):222-32; & T.V. O'Halloran,

" Transition metals in control

Of gene _expression " , Science, 1993, 261(5122):715-25; & Matts RL, Schatz

JR, Hurst R, Kagen R. Toxic heavy metal ions inhibit reduction of disulfide

bonds. J Biol Chem 1991; 266(19): 12695-702; Boot JH. Effects of SH-blocking

compounds on the energy metabolism in isolated rat hepatocytes. Cell Struct

Funct 1995; 20(3): 233-8.

(119) L.Ronnback et al, " Chronic encephalopaties induced by low doses of

mercury or lead " , Br J Ind Med 49: 233-240, 1992; & H.Langauer-Lewowicka, "

Changes in the nervous system due to occupational metallic mercury poisoning "

Neurol Neurochir Pol 1997 Sep-Oct;31(5):905-13; & Kim P, Choi BH. " Selective

inhibition of glutamate uptake by mercury in cultured mouse astrocytes " , Yonsei

Med J 1995; 36(3): 299-305; & s N. In vitro evidence for the role of

glutatmate in the CNS toxicity of mercury. Toxicology 1992, 76(3):245-56.

(131) M.Kubicka-Muranyi et al, " Systemic autoimmune disease induced by

mercuric chloride " , Int Arch Allergy Immunol;1996, 109(1):11-20 &

M.M.Christensen

et al, Institute of Medical Microbiology, " Comparision of interaction of

meHgCl2 and HgCl2 with murine macrophages " , Arch Toxicol, 1993, 67(3):205-11; &

Christensen MM, Ellermann-sen S, Mogensen SC. Influence of mercury

chloride on resistance to generalized infection with herpes simplex virus type

2

in mice. Toxicology 1996, 114(1): 57-66; & S.Ellermann-sen et al, " Effect

of mercuric chloride on macrophage-mediated resistance mechinisms against

infection " , Toxicology, 93:269-297,1994;

(142) Ariza ME; Bijur GN; MV. Lead and mercury mutagenesis: role of

H2O2, superoxide dismutase, and xanthine oxidase. Environ Mol Mutagen

1998;31(4):352-61; & M.E. Ariza et al, " Mercury mutagenisis " , Biochem Mol

Toxicol,

1999, 13(2):107-12; & M.E.Ariza et al, " Mutagenic effect of mercury " , InVivo

8(4):559-63,1994;

145) J.M.Gorell et al, " Occupational exposure to mercury, manganese, copper,

lead, and therisk of Parkinson's disease " , Neurotoxicology, 1999,

20(2-3):239-47

(147) .M.Wood, " Mechanisms for the Neurotoxicity of Mercury " , in

Organotransitional Metal Chemistry, Plenum Publishing Corp, N.Y, N.Y, 1987. &

R.P. Sharma

et al, " Metals and Neurotoxic Effects " , J of Comp

Pathology, Vol 91, 1981.

(149) F. Monnet-Tschudi et al, " Comparison of the developmental effects of 2

mercury compounds on glial cells and neurons in the rat telencephalon " ,

Brain Research, 1996, 741: 52-59

(152) Pons S, -Aleman I. Insulin-like growth factor-I stimulates

dephosphorylation of ikappa B through the serine phosphatase calcineurin. J

Biol

Chem 2000 Dec 8;275(49):38620-5; & 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; J Biol Chem 2000 Dec 8;275(49):38620-5.

(169) C.H.Ngim et al, Neuroepidemiology, " Epidemiologic study on the

association between body burden mercury level and idiopathic Parkinson's

disease " ,

1989, 8(3):128-41.

(175) Soderstrom S, Fredriksson A, Dencker L, Ebendal T, " The effect of

mercury vapor on cholinergic neurons in the fetal brain, Brain Research &

Developmental Brain Res, 1995, 85:96-108; & Toxicol Lett 1995; 75(1-3):

133-44.; &

L.Larkfors et al, " Methyl mercury induced alterations in the nerve growth

factor level in the developing brain " , Res Dev Res,62(2),1991,287- .

(194) Lu SC, FASEB J, 1999, 13(10):1169-83, " Regulation of hepatic

glutathione synthesis: current concepts and

controversies " ; & R.B. Parsons, J Hepatol, 1998, 29(4):595-602; & R.K.Zalups

et al, " Nephrotoxicity of inorganic mercury co-administered with L-cysteine " ,

Toxicology, 1996, 109(1): 15-29. & T.L. et al, " Hallevorden-Spatz

Disease: cysteine accumulation and cysteine dioxygenase defieciency " , Ann

Neural,

1985, 18(4):482-489.

(198) E.S. West et al, Textbook of Biochemistry, MacMillan Co, 1957,p853; &

B.R.G.sson et al, " Ferotoxicity of inorganic mercury: distribution and

effects of nutrient uptake by placenta and fetus " , Biol Res Preg Perinatal.

5(3):102-109,1984; & sson et al, Neurotoxicol. Teratol., 18:129-134;

(207) Haley, B. Kasarskis, EJ; et al. GTP-binding proteins in amyotrophic

lateral sclerosis cerebrospinal fluid. Ann Neurol, 1995; & " Mercury Vapor

Inhaltion Inhibits Binding of GTP . Neurotoxicology 1997, 18(2)::315-24

(222) M. Daunderer, Handbuch der Amalgamvergiftung, 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 (amalgam replacement & DMPS, over 5,000 cases)

(226) B.J. Shenker et al, Dept. Of Pathology,Univ. Of Penn. School of Dental

Med., " Immunotoxic effects of mercuric compounds on human lymphocytes and

monocytes:Alterations in cell viability " Immunopharmacologicol Immunotoxical,

1992, 14(3):555-77; & M.A. et al, " Mercuric chloride induces apoptosis in

human T lymphocytes " , Toxicol Appl Pharmacol, 153(2):250-7 1998; & Rossi

AD,Viviani B, Vahter M. Inorganic mercury modifies Ca2+ signals, triggers

apoptosis, and potentiates NMDA toxicity in cerebral granule neurons. Cell

Death and

Differentiation 1997; 4(4):317-24. & Goering PL, D, Rojko JL, Lucas

AD. Mercuric chloride-induced apoptosis is dependent on protein synthesis.

Toxicol Lett 1999; 105(3): 183-95;

(229) M.,editor, Defense Against Mystery Syndromes " , Chek Printing Co.,

&

March, 1994(case histories documented); & Kantarjian A, " A syndrome

clininically resembling amyotrophic lateral sclerosis following chronic

mercurialism " , Neurology 11:639-644 (1961)

(241) R.Schoeny, U.S.EPA, " Use of genetic toxicology data in U.S. EPA risk

assessment: the mercury study " , Environ Health Perspect, 1996, 104, Supp 3:

663-73

(246) K.Iyer et al, " Mercury Poisoning in a dentist " , Arch Neurol,1976,

33:788-790.

(251) Y.Omura et al, Heart Disease Research Foundation, NY,NY, " Role of

mercury in resistant infections and recovery after Hg detox with cilantro " ,

Acupuncture & Electro-Theraputics Research, 20(3):195-229, 1995; & " Mercury

exposure from silver fillings " , Acupunture & Electrotherapy Res, 1996, 133-

(254) al-Saleh I, Shinwari N. Urinary mercury levels in females: influence

of dental amalgam fillings. Biometals 1997; 10(4): 315-23; & Zabinski Z;

Dabrowski Z; Moszczynski P; Rutowski J. The activity of erythrocyte enzymes and

basic indices of peripheral blood erythrocytes from workers chronically exposed

to mercury vapors. Toxicol Ind Health 2000 Feb;16(2):58-64.

(255) D.C. Rice, " Evidence of delayed neurotoxicity produced by methyl

mercury developmental exposure " , Neurotoxicology, Fall 1996, 17(3-4), p583-96;

(270) D.W.Eggleston, " Effect of dental amalgam and nickel alloys on

T-lympocytes " ,J Prosthet Dent. 51(5):617-623, 1984; & D.W.Eggleston et al, J

Prosthet

Dent, 1987,58(6),704-7; & J of the American Medical Assoc., Sept 96.

(288)Rajanna B, Hobson M, L, Ware L, Chetty CS. Effects of cadmium

and mercury on Na(+)-K(+)ATPase and uptake of 3H-dopamine in rat brain

synaptosomes. Arch Int Physiol Biochim 1990, 98(5):291-6; & M.Hobson &

B.Rajanna,

" Influence of mercury on uptake of dopamine and norepinephrine " , Toxicol

Letters, Dep 1985, 27:2-3:7-14; & McKay SJ, Reynolds JN, Racz WJ. Effects of

mercury

compounds on the spontaneous and potassium-evoked release of [3H]dopamine

from mouse striatial slices. Can J Physiol Pharmacol 1986, 64(12):1507-14; &

Scheuhammer AM; Cherian MG. Effects of heavy metal cations, sulfhydryl reagents

and other chemical agents on striatal D2 dopamine receptors. Biochem

Pharmacol 1985 Oct 1;34(19):3405-13 ; RN; Bowler K. Rat brain

(Na+-K+)ATPase:

modulation of its ouabain-sensitive K+-PNPPase activity by thimerosal. Int J

Biochem 1983;15(1):5-7; & Anner BM, Moosmayer M. Mercury inhibits Na-K-ATPase

primarily at the cytoplasmic side. Am J Physiol 1992; 262(5 Pt2):F84308

(291) H.A.Huggins & TE Levy, " cerebrospinal fluid protein changes in MS

after Dental amalgam removal " , Alternative Med Rev, Aug 1998, 3(4):295-300.

(293) H.Huggins,Burton Goldberg, & Editors of Alternative Medicine

Digest,Chronic Fatigue Fibromyalgia & Environmental Illness, Future Medicine

Publishing, Inc, 1998, p197-;

(296) L.Bucio et al, Uptake, cellular distribution and DNA damage produced

by mercuric chloride in a human fetal hepatic cell line. Mutat Res 1999 Jan

25;423(1-2):65-72; & L.Verschaeve et al, " Comparative in vitro cytogenetic

studies in mercury-exposed human lymphocytes " , Muta Res, 1985, 157(2-3):221-6;

&

L.Verschaeve, " Genetic damage induced by low level mercury exposure " , Envir

Res,12:306-10,1976.

(305) S. Soederstroem et al, " The effect of mercury vapor on chloinergic

neurons in the fetal brain " ,Developmental Brain Research,85(1):96-108.1995; &

E.M. Abdulla et al, " Comparison of neurite outgrowth with neurofilament

protein levels In neuroblastoma cells following mercuric oxide exposure " , Clin

Exp

Pharmocol Physiol, 1995, 22(5): 362-3.

(307) Duhr EF, Pendergrass JC, Slevin JT, Haley BE: HgEDTA complex inhibits

GTP interactions with the E-site of brain beta-tubulin. Toxicology & Applied

Pharmacology 1993; 122 (2): 273-80.

(313) V.D.M.Stejskal et al, " Mercury-specific Lymphocytes: an indication of

mercury allergy in man " , J. Of Clinical Immunology, 1996, Vol 16(1);31-40.

(314) M.Goldman et al,1991, " Chemically induced autoimmunity ... " ,Immunology

Today,12:223-; & K. Warfyinge et al, " Systemic autoimmunity due to mercury

vapor exposure in genetically susceptible mice " , Toxicol Appl Pharmacol, 1995,

132(2):299-309; & L.M. Bagentose et al, " Mercury induced autoimmunity in

humans " , Immunol Res, 1999,20(1): 67-78; & " Mercury-induced autoimmunity " , Clin

Exp

Immunol, 1998, 114(1):9-12;

(325) B. Arvidson(Sweden), Inorganic mercury is transported from muscular

nerve terminals to spinal and brainstem motorneurons. Muscle Nerve, 1992,

15(10);1089-94, & JD. Heavy metals and trace elements in amyotrophic

lateral sclerosis. Neurol Clin 1987 Feb;5(1):43-60; & M. Su et al, Selective

involvement of large motor neurons in the spinal cord of rats treated with

methylmercury. J Neurol Sci,1998, 156(1):12-7;

(327) G. Danscher et al, Environ Res, " Localization of mercury in the CNS " ,

1986, 41:29-43; & Exp Mol Pathol, 1990, 52: 291-299; & " Ultrastructural

localization of mercury after expsoure to mercury vapor " , Prog Histochem

Cytochem,

1991, 23:249-255; & R.Pamphlett et al, " Entry of low doses of mercury vapor

into the nervous system " , Neurotoxicology, 1998, 19(1):39-47; & Pamphlett et

al, " Oxidative damage to nucleic acids in motor neurons containing Hg " , J

Neurol Sci,1998,159(2):121-6. (rats & primates); & Pamphlett R, Waley P, " Motor

Neuron Uptake of Low Dose Inorganic Mercury " , J. Neurological Sciences 135:

63-67 (1996) ;

Schionning JD, Danscher G, " Autometallographic inorganic mercury correlates

with degenerative changes in dorsal root ganglia of rats intoxicated with

organic mercury " , APMIS 1999 Mar;107(3):303-10

(329) B. Arvidson et al, Acta Neurol Scand, " Retograde axonal transport of

mercury in primary sensory neurons " 1990,82:324-237 & Neurosci Letters, 1990,

115:29-32; & S.M. Candura et al, " Effects of mercuryic chloride and methyly

mercury on cholinergic neuromusular transmission " , Pharmacol Toxicol 1997;

80(5): 218-24; & Castoldi AF et al, " Interaction of mercury compounds with

muscarinic receptor subtypes in the rat brain " , Neurotoxicology 1996; 17(3-4):

735-41; & Arvidson B; Arvidsson J; Johansson K, " Mercury Deposits in Neurons of

the Trigeminal Ganglia After Insertion of Dental Amalgam in Rats " , Biometals;

7 (3) p261-263 1994

(330) C.M. Tanner et al, " Abnormal Liver Enzyme Metablolism in

Parkinson's " ,Neurology, 1991, 41(5): Suppl 2, 89-92; & M.Watanabe et al, Amino

Acids, 1998,

15(2): 143-50 & M.T.Heafield et al, " Plasma cysteine and sulphate levels in

patients with Motor neurone disease, Parkinson's Disease, and Alzheimer's

Disease " , Neurosci Lett, 1990, 110(1-2), 216,20; & A.Pean et al, " Pathways of

cysteine metabolism in MND/ALS " , J neurol Sci, 1994, 124, Suppl:59-61;

(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, 1992,

51:3,318-20; &

P.Emory et al, Br J Rheumotol, 1992, 31:7,449-51; & ton GB, et al;

Xenobiotic metabolism in motor neuron disease, The Lancet, Sept 17 1988, p

644-47; & Neurology 1990,

40:1095-98.

(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

calcium release by Hg+2 " ,J Biol Chem, 1988, 263:8, 3582-; A. Szucs et al,

Cell Mol Neurobiol, 1997,17(3): 273-8; & D.Busselberg, 1995, " Calcium channels

as target sites of heavy metals " ,Toxicol Lett, Dec;82-83:255-61; & Cell Mol

Neurobiol 1994 Dec;14(6):675-87.

(338) (a)W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I

Inst of Tech., Haifa, Israel, " In vitro effect of mercury on enzyme activities

and its accumulation in the first-trimester human placenta " , Environ Res,

1992, 57(1):96-106; & " In vitro exposure to mercury and cadmium alters term

human placental membrane fluidity " , Pharmacol, 1992, 116(1): 17-23; &

(b)J.Urbach

et al, Dept. of Obstetrics & Gynecology, Rambam Medical Center, Haifa,

Israel, " Effect of inorganic mercury on in vitro placental nutrient transfer

and

oxygen consumption " , Reprod Toxicol, 1992,6(1):69-75; & © Karp W, Gale TF et

al, Effect of mercuric acetate on selected enzymes of maternal and fetal

hamsters " Environmental Research, 36:351-358; & W.B. Karp et al, " Correlation

of

human placental enzymatic activity with tracemetal concentration in placenta " ,

Environ Res. 13:470- 477,1977; & (d) Boot JH. Effects of SH-blocking

compounds on the energy metabolism and glucose uptake in isolated rat

hepatocytes.

Cell Struct Funct 1995 Jun;20(3):233-8.

(342) V.Stejskal, " MELISA: A New Technology for Diagnosing and Monitoring of

Metal Sensitivity " , Proceedings: 33rd Annual Meeting of American Acadamy of

Environmental Medicine, Nov. 1998, Baltimore, land.

(346) Clauw DJ, " The pathogenesis of chronic pain and fatigue syndroms:

fibromyalgia " Med Hypothesis, 1995, 44:369-78; & Hanson S, Fibromyalgia,

glutamate, and mercury. Heavy Metal Bulletin, Issue 4, 1999, p5,6.

(368) Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A

et al. Metal- specific memory lymphoctes: biomarkers of sensitivity in man.

Neuroendocrinology Letters, 1999.

(369) Sterzl I, Prochazkova J, Stejskal VDM et al, Mercury and nickel

allergy: risk facotrs in fatigue and autoimmunity. Neuroendocrinology Letters

1999;

20:221-228.

(375) Stejskal VDM, Danersund A, Lindvall A. Metal-specific memory

lympocytes: biomarkers of sensitivity in man. Neuroendocrinology Letters 1999;

&

Stejskal V, Hudecek R, Mayer W, " Metal-specific lymphocytes: risk factors in

CFS

and other related diseases " , Neuroendocrinology Letters, 20: 289-298, 1999

(386) Doctors Data Lab ,http://www.doctorsdata.com , inquiries@doctors

data.com, &

Great Smokies Diagnostic Lab, http://www.gsdl.com; & MetaMatrix Lab,

http://www.metamatrix.com &

Biospectron/LMI, Lennart Månsson International ABlmi.analyslab@... .

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

(1996); & Romani L, Immunity to Candida Albicans: Th1,Th2 cells and beyond.

Curr Opin Microbiol 1999, 2(4):363-7

(405) Stejskal, Vera Stejskal. The role of metals in autoimmune

diseases and the link to neuroendocrinology Neuroendocrinology Letters,

20:345-358,

1999.

http://www.melisa.org

(406) The Edelson Clinic, Atlanta, Ga. (http://www.edelsoncenter.com) (see

the testimonials)

(411) Puschel G, Mentlein R, Heymann E, 'Isolation and characterization of

dipeptyl peptidase IV from human placenta', Eur J Biochem 1982

Aug;126(2):359-65; & Kar NC, Pearson _cm._

(http://curezone.com/c/?http://curezone.com/conversions.asp) Dipeptyl

Peptidases in human muscle disease. Clin Chim Acta 1978;

82(1-2): 185-92; & Seroussi K, Autism and Pervasive Developmental Disorders

, 1998, p174,etc.

(412) Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V, Plasma excitatory

amino acids in autism. Invest Clin 1996,37(2): 113-28; & Rolf LH, Haarman FY,

Grotemeyer KH, Kehrer H. Serotonin and amino acid content in platelets of

autistic children. Acta Psychiatr Scand 1993, 87(5): 312-6; & Naruse H, Hayashi

T, Takesada M, Yamazaki K. Metabolic changes in aromatic amino acids and

monoamines in infantile autism and a new related treatment, No To Hattatsu,

1989,

21(2):181-9; & Carlsson ML. Is infantile autism a hypoglutamatergic

disorder? J Neural Transm 1998, 105(4-5): 525-35.

(416) Rothstein JD, LJ, Kuncl RW. Decreased glutamte transport by the

brain and spinal cord in ALS. New Engl J Med 1992, 326: 1464-8.

(417) Folkers K et al, Biochemical evidence for a deficiency of vitamin B6

in subjects reacting to MSL-Glutamate. Biochem Biophys Res Comm 1981, 100:

972; & Felipo V et al, L-carnatine increases the affinity of glutamate for

quisqualate receptors and prevents glutamate neurotoxicity. Neurochemical

Research

1994, 19(3): 373-377; & Akaike A et al, Protective effects of a vitamin-B12

analog(methylcobalamin, against glutamate cytotoxicity in cultured cortical

neurons. European J of Pharmacology 1993, 241(1):1-6 .

(418) Srikantaiah MV; Radhakrishnan AN. Studies on the metabolism of vitamin

B6 in the small intestine. Purification and properties of monkey intestinal

pyridoxal kinase. Indian J Biochem 1970 Sep;7(3):151-6.

(423) C.R. et al, " Mercury intoxication simulating ALS " , JAMA, 1983,

250(5):642-5; & T.Barber, " Inorganic mercury intoxification similar to ALS " , J

of Occup Med, 1978, 20:667-9; &

Schwarz S, Husstedt I, Bertram HP, Kuchelmeister K. Amyotrophic lateral

sclerosis after accidental injection of mercury. J Neurol Neurosurg Psychiatry.

1996 Jun;60(6):698; & Sienko DG, BR. Amyotrophic lateral sclerosis. A

case-control study following detection of a cluster in a small Wisconsin

communit Arch Neurol 1990 Jan;47(1):38-41; & Felmus MT, Patten BM, Swanke L;

Antecedent events in amyotrophic lateral sclerosis

Neurology 1976 Feb;26(2):167-72; & Patten BM, Mallette LE. Motor neuron

disease: retrospective study of associated abnormalities. Dis Nerv Syst 1976

Jun;37(6):318-21.

(424) Cephalon, Inc. , http://www.cephalon.com/

(427) Chetty CS, McBride V, Sands S, Rajanna B. Effects in vitro on rat

brain Mg(++)-ATPase. Arch Int Physiol Biochem 1990, 98(5):261-7; & M.Burk et

al,

Magnesium, 4(5-6): 325-332, 1985 ?

(428) O'Carroll RE, Masterton G, Goodwin GM. The neuropsychiatric sequelae

of mercury poisoning. The Mad Hatter's disease revisited. Br J Psychiatry

1995, 167(1): 95-8; & PUBLIC HEALTH REPORTS, PUBLIC HEALTH BULLETIN #263. March

28, 1941. Mercurialism and its control in the felt hat industry.

(430) Fukino H, Hirai M, Hsueh YM, Yamane Y. Effect of zinc pretreatment on

mercuric chloride-induced lipid peroxidation in the rat kidney. Toxicol Appl

Pharmacol 1984, 73(3): 395-401.

(432) Sutton KG, McRory JE, Guthrie H, Snutch TP. P/Q-type calcium channels

mediate the activity-dependent feedback of syntaxin-1A. Nature 1999,

401(6755):800-4;

(437) Affinity Labeling Technology, Inc.(Dental Lab), oral toxicity testing

technology and tests,

see research web pages on amalgam toxicity, root canals, cavitaions.

http://www.altcorp.com ; &

G. Mienig, _root canal_

(http://curezone.com/c/?http://curezone.com/dental/root_canal.asp) Coverup,

1997.

(438) Moreno-Fuenmayor H, Borjas L, Arrieta A, Valera V, Plasma excitatory

amino acids in autism. Invest Clin 1996,37(2): 113-28; & Rolf LH, Haarman FY,

Grotemeyer KH, Kehrer H. Serotonin and amino acid content in platelets of

autistic children. Acta Psychiatr Scand 1993, 87(5): 312-6; & Naruse H, Hayashi

T, Takesada M, Yamazaki K. Metabolic changes in aromatic amino acids and

monoamines in infantile autism and a new related treatment, No To Hattatsu,

1989,

21(2):181-9; & Carlsson ML. Is infantile autsim a hypoglutamatergic disorer?

J Neural Transm 1998, 105(4-5): 525-35.

(439) Part 1, mercuric chloride intoxication. Bull Environ Contam Toxicol

1978; 20(6): 729-35 Mondal MS, Mitra S. Inhibition of bovine xanthine oxidase

activity by Hg2+ and other metal ions. J Inorg Biochem 1996; 62(4): 271-9; &

Sastry KV, Gupta PK. In vitro inhibition of digestive enzymes by heavy metals

and their reversal by chelating agents:

(441) P.Bulat, " Activity of Gpx and SOD in workers occupationally exposed to

mercury " , Arch Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; & D.Jay,

" Glutathione inhibits SOD activity of Hg " , Arch Inst cardiol Mex,

1998,68(6):457-61.

(442) Olanow CW, Arendash GW. Metals and free radicals in neurodegeneration.

Curr Opin Neurol 1994, 7(6):548- 58; & Kasarskis EJ(MD), Metallothionein in

ALS Motor Neurons(IRB #91-22026), FEDRIP DATABASE, NATIONAL TECHNICAL

INFORMATION SERVICE(NTIS), ID: FEDRIP/1999/07802766.

(443) Troy CM, Shelanski ML. Down-regulation of copper/zinc superoxide

dismutase causes apototic dealth in PC12 neuronal cells. Proc. National Acad

Sci,

USA, 1994, 91(14):6384-7; & Rothstein JD, Dristol LA, Hosier B, Brown RH,

Kunci RW. Chronic inhibition of superoxide dismutase produces apoptotic death

of

spinal neurons. Proc Nat Acad Sci,USA, 1994, 91(10):4155-9.

(444) Beal MF. Coenzyme Q10 administration and its potential for treatment

of neurodegenerative diseases. Biofactors 1999, 9(2-4):262-6; & DiMauro S,

Moses LG; CoQ10 Use Leads To Dramatic Improvements In Patients With Muscular

Disorder, Neurology, April 2001; & s RT, Yang L, Browne S, Baik M, Beal

MF. Coenzyme Q10 administration increases brain mitochondrial concentrations

and exerts neuroprotective effects. Proc Natl Acad Sci U S A 1998 Jul

21;95(15):8892-7; & Schulz JB, s RT, Henshaw DR, Beal MF.

Neuroprotective

strategies for treatment of lesions produced by mitochondrial toxins:

implications for neurodegenerative diseases. Neuroscience 1996

Apr;71(4):1043-8; &

Idebenone - Monograph. A potent antioxidant and stimulator of nerve growth

factor.

Altern Med Rev 2001 Feb;6(1):83-86; & Nagano S, Ogawa Y, Yanaghara T, Sakoda

S. Benefit of a combined treatment with trientine and ascorbate in familial

amyotrophic lateral sclerosis model mice. Neurosci Lett 1999, 265(3):159-62;

(445) Clifford Lab, Dental Materials Biocompatability Testing, Colorada

Springs, Colo.; & Peak Energuy Performance, inc., Dental Materials

Biocompatibility Testing, http://www.peakenergy.com

(466) Chen KM, Department of Neurology, Guam Memorial Hospital;

Disappearance of ALS from Guam: implications for exogenous causes, 2000.

(453) Blumer W, " Mercury toxicity and dental amalgam fillings " , Journal of

Advancement in Medicine, v.11, n.3, Fall 1998, p.219

(461) Rasmussen HH, Mortensen PB, Jensen IW. Depression and magnesium

deficiency. Int J Psychiatry Med

1989;19(1):57-63: & Bekaroglu M, Aslan Y, Gedik Y, Karahan C. Relationships

between serum free fatty

acids and zinc with ADHD. J Child Psychol Psychiatry 1996; 37(2):225-7; &

Maes M, Vandoolaeghe E, Neels H, Demedts P, Wauters, A, Meltzer HY, Altamura C,

Desnyder R. Lower serum zinc in major depression is a sensitive marker of

treatment resistance and of the immune/inflammatory response in that illness.

Biol Psychiatry 1997;42(5):349-358.

(462) Olivieri G; Brack C; Muller-Spahn F; Stahelin HB; Herrmann M; Renard

P; Brockhaus M; Hock C. Mercury induces cell cytotoxicity and oxidative stress

and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y

neuroblastoma cells. J Neurochem 2000 Jan;74(1):231-6.

(463) S. The possible role of gradual accumulation of copper,

cadmium, lead and iron

depletion of zinc, magnesium, selenium, vitamins B2, B6, D, and E and

essential fatty acids in multiple sclerosis. Med Hypotheses 2000

Sep;55(3):239-41.

(464) Walsh, WJ, Health Research Institute, Autism and Metal Metabolism,

http://www.hriptc.org/autism.htm, Oct 20, 2000; & Walsh WJ, Pfeiffer Treatment

Center, Metal-Metabolism and Human Functioning,

2000,http://www.hriptc.org/mhfres.htm;

(464) Walsh, WJ, Health Research Institute, Autism and Metal Metabolism,

http://www.hriptc.org/autism.htm, Oct 20, 2000; & Walsh WJ, Pfeiffer Treatment

Center, Metal-Metabolism and Human Functioning,

2000,http://www.hriptc.org/mhfres.htm

(468) M.M. Van Benschoten and Associates, Reseda, Calif. Clinic;

http://www.mmvbs.com/

(469)BrainRecovery.com, the book, by Perlmutter MD; Perlmutter Health

Center, Naples, Florida, http://www.perlhealth.com/about.htm

(470) Dr. Garth Nicholson, Institute for Molecular Medicine, Huntington

Beach, Calif., www.immed.org

(471) Umanekii KG, Dekonenko EP. Structure of progressive forms of

tick-borne encephalitis. Zh Nevropatol Psikhiatr Im S S Korsakova

1983;83(8):1173-9.

[article in Russian]; & B HEMMER, F X GLOCKER, R KAISER. Generalised motor

neuron disease as an unusual manifestation of Borrelia burgdorferi infection. J

Neurol Neurosurg Psychiatry 1997;63:257-258; & Fredrikson S, Link H.

CNS-borreliosis selectively affecting central motor neurons. Acta Neurol Scand

1988;78:181-184[Medline]; & Halperin JJ, Kaplan GP, Brazinsky S, et al.

Immunologic

reactivity against Borrelia burgdorferi in patients with motor neuron

disease. Arch Neurol 1990;47:586-594

(477) Lars Landner and Lennart Lindestrom. Swedish Environmental Research

Group(MFG), Copper in society and the Environment, 2nd revised edition. 1999.

(485) _Hulda _ (http://curezone.com/c/?http://curezone.com/clark/) ,

_The Cure For All Diseases_

(http://curezone.com/c/?http://curezone.com/clark/) , 2000, www.drclark.net

(U.S. CDC confirms parasites common in those with

chronic immune conditions)

(489) Waggoner DJ, Bartnikas TB, Gitlin JD. The role of copper in

neurodegenerative disease. Neurobiol Dis 1999 Aug;6(4):221-30; & (B) Torsdottir

G,

sson J, Gudmundsson G, Snaedal J, Johannesson T. Copper, ceruloplasmin

and

superoxide dismustase (SOD) in amyotrophic lateral sclerosis. Pharmacol

Toxicol 2000 Sep;87(3):126-30; & © Estevez AG,Beckman JS et al, Induction of

nitric oxide-dependent apoptosis in motor neurons by zinc-deficient superoxide

dismustase. Science 1999 Dec 24;286(5449):2498-500; & (d) Cookson MR, Shaw PJ.

Oxidative stress and motor neurons disease. Brain Pathol 1999 Jan;9(1):165-86.

(494) (a)Kobayashi MS, Han D, Packer L. Antioxidants and herbal extracts

protect HT-4 neuronal cells against glutamate-induced cytotoxicity. Free Radic

Res 2000 Feb;32(2):115-24(PMID: 10653482); & Packer L, Tritschler HJ, Wessel

K. Neuroprotection by the metabolic antioxidant alpha-lipoic acid. Free Radic

Biol Med 1997;22(1-2):359-78(PMID: 8958163); & (b)Whiteman M, Tritschler H,

Halliwell B. Protection against peroxynitrite-dependent tyrosine nitration and

alpha 1-antiproteinase inactivation by oxidized and reduced lipoic acid.

FEBS Lett 1996 Jan 22;379(1):74-6(PMID: 8566234); & © " Decreased phagocytosis

of

myelin by macrophages with ALA. Journal of Neuroimmunology 1998, 92:67- 75;

& (d) & Z.Gregus et al, " Effect of lipoic acid on biliary excretion of

glutathione and metals " , Toxicol APPl Pharmacol, 1992, 114(1):88-96;

(495) Kang JH, Eum WS. Enhanced oxidative damage by the familial amyotrophic

lateral sclerosis-associated Cu,Zn-superoxide dismustase mutants. Biochem

Biophys Acta 2000 Dec 15;1524(2-3):162-70; & (B) JH, Eum WS. Enhanced oxidative

damage by the familial amyotrophic lateral sclerosis- associated

Cu,Zn-superoxide dismustase mutants. Biochem Biophys Acta 2000 Dec 15;

1524(2-3):

162-70; & © Liu H, Zhu H, Eggers DK, Nersissian AM, Faull KF, Goto JJ, Ai J,

-Loehr J, Gralla EB, Valentine JS. Copper(2+) binding to the surface

residue

cysteine 111 of His46Arg human copper-zinc superoxide dismustase, a familial

amyotrophic lateral sclerosis mutant. Biochemistry 2000 Jul

18;39(28):8125-32; & (d) Wong PC, Gitlin JD; et al, Copper chaperone for

superoxide dismustase

is essential to activate mammalian Cu/Zn superoxide dismustase. Proc Natl

Acad Sci U S A 2000 Mar 14;97(6):2886-91; & (e)Kruman II, Pedersen WA, Springer

JE, Mattson MP. ALS-linked Cu/Zn-SOD mutation increases vulnerability of

motor neurons to excitotoxicity by a mechanism involving increased oxidative

stress and perturbed calcium homeostasis. Exp Neurol 1999 Nov;160(1):28-39

(496) Doble A. The role of excitotoxicity in neurodegenerative disease:

implications for therapy. Pharmacol There 1999 Mar;81(3):163-221; & Urushitani

M,

Shimohama S. N-methyl-D-aspartate receptor-mediated mitochondrial Ca(2+)

overload in acute excitotoxic motor neuron death: a mechanism distinct from

chronic neurotoxicity after Ca(2+) influx. J Neurosci Res 2001 Mar

1;63(5):377-87; & Cookson MR, Shaw PJ. Oxidative stress and motor neurons

disease. Brain

Pathol 1999 Jan;9(1):165-86.

(497) -Aleman I, Barrios V, Berciano J. The peripheral insulin-like

growth factor system in amyotrophic lateral sclerosis and in multiple

sclerosis. Neurology 1998 Mar;50(3):772-6 ; & Dall R, Sonksen PH et al; The

effect of

four weeks of supraphysiological growth hormone administration on the

insulin-like growth factor axis In women and men. GH-2000 Study Group. J Clin

Endocrinol Metab 2000 Nov;85(11):4193-200

(498) Lai EC, Rudnicki SA. Effect of recombinant human insulin-like growth

factor-I on progression of ALS. A placebo-controlled study. Neurology 1997

Dec;49(6):1621-30; & Yuen EC, Mobley WC. Therapeutic applications of

neurotrophic factors in disorders of motor neurons and peripheral nerves. Mol

Med Today

1995 Sep;1(6):278-86; & Dore S, Kar S, Quirion R. Rediscovering an old

friend, IGF-I: potential use in the treatment of neurodegenerative diseases.

Trends Neurosci 1997 Aug;20(8):326-31; & Couratier P, Vallat JM. Therapeutic

effects of neurotrophic factors in ALS; Rev Neurol (Paris). 2000

Dec;156(12):1075-7. French.

(499) Van den Berghe G, Bowers C et al, Neuroendocrinology of prolonged

critical illness: effects of

exogenous thyrotropin-releasing hormone and its combination with growth

hormone secretagogues.

J Clin Endocrinol Metab 1998 Feb;83(2):309-19.

(500) B. Windham, Annotated bibliography: Exposure levels and health effects

related to mercury/dental amalgam and results of amalgam replacement, 2001;

(over 1000 medical study references documenting mechanism of causality of 40

chronic conditions and over 60,000 clinical cases of recovery or significant

improvement of these conditions after amalgam replacement-documented by

doctors) www.home.earthlink.net/~berniew1/amalg6.html

(501) B. Windham, Cognitive and Behavioral Effects of Toxic Metal Exposures,

2001; (over 150 medical study references)

www.home.earthlink.net/~berniew1/tmlbn.html

==================END QUOTE==================================================

**************************************See AOL's top rated recipes

(http://food.aol.com/top-rated-recipes?NCID=aoltop00030000000004)

Link to comment
Share on other sites

Join the conversation

You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
×
×
  • Create New...