Mercury
from Amalgam Fillings is a Common Cause of
MS, ALS, PD, SLE, RA, MCS,AD,
etc.
Bernard
Windham (Ed.), Chemical Engineer/Biostatistician
I.
Introduction
Proper functioning of the human
body and mind depends on interactions of the brain and CNS using neuronal
signaling mechanisms with elaborate
metabolic and enzymatic processes and respiration that occurs at the cellular
level in the various organs and parts of the body, as controlled by low levels
of hormones from the endocrine
system. It will be shown that toxic
substances, such as mercury that the body is chronically exposed to, accumulate
in the brain, pituitary gland, CNS, liver, kidneys, etc. and can damage,
inhibit, and cause imbalances at virtually any stage of these various processes
at very low levels of exposure, which can have major neurological,
immunological, and metabolic effects on an individual. Multiple Sclerosis(MS)
is caused by the erosion of myelin, a substance which helps the brain send
messages to the body. Metal particles entering the body can bind to this
myelin. For those who are hypersensitive, this myelin-metal bond comes under
attack from the immune system. This is called autoimmunity. In such cases, the
progression of MS can be halted by removing the source of the metal(369,35).
Mercury is known to be one of the most
toxic substances commonly
encountered and to be
along with lead the toxic substances adversely
affecting the largest numbers of people(276). Dental amalgam
is documented
by medical studies and medical
lab tests to be the
largest source of both inorganic and methyl mercury in
most people who
have several mercury amalgam fillings(599).
The
main factors determining whether chronic conditions are induced
by metals appear to be exposure and genetic susceptibility,
which
determines individuals immune sensitivity and ability to
detoxify metals
(405). Very low levels of exposure have been
found to seriously affect
relatively large groups of individuals who are immune
sensitive to toxic
metals, or have an inability to detoxify metals due to such as deficient
sulfoxidation or metallothionein function or other inhibited
enzymatic
processes related to detoxification or excretion of metals.
A large epidemiological study of 35,000 Americans
by the National Institute of Health, the nation's principal health statistics
agency, found that there was a significant correlation between having a greater
than average number of dental amalgam surfaces and having the a chronic
condition such as epilepsy, MS, or migraine headaches. Fewer of those with this
condition have zero fillings than those of the general population while significantly
more of those with the condition have 17 or more surfaces than in the general population(543). MS
clusters in areas with high metals emissions from facilities such as metal
smelters have been documented(184).
As far back as 1996 it was shown that the lesions
produced in the myelin sheath of axons in cases of multiple sclerosis were
related to excitatory receptors on the primary cells involved called oligodendroglia. The loss of myelin sheath on the nerve fibers characteristic of the
disease are due to the death of these oligodendroglial cells at the site
of the lesions (called plaques). Further, these studies have shown that the
death of these important cells is as a result of excessive exposure to
excitotoxins at the site of the lesions(576,598). Most of these excitotoxins are secreted from
microglial immune cells in the central nervous system. This not only destroys
these myelin-producing cells it also breaks down the blood-brain barrier (BBB),
allowing excitotoxins in the blood stream to enter the site of damage. Some common exposures that cause
such proliferation of such excitotoxins resulting in MS are mercury and
aspartame, with additional effects from MSG and methanol. Mercury and other toxic metals inhibit astrocyte
function in the brain and CNS(119), causing increased
glutamate and calcium related neurotoxicity (119,333,416,496) which are factors
in neural degeneration in MS and ALS. There is evidence that astrocyte
damage/malfunction is a major factor in
MS(544). Mercury and increased
glutamate activate free radical forming processes like xanthine oxidase which
produce oxygen radicals and oxidative neurological damage(142,13). Nitric oxide related toxicty caused by
peroxynitrite formed by the reaction of NO with superoxide anions, which
results in nitration of tyrosine residues in neurofilaments and manganese
Superoxide Dimustase(SOD) has been found to cause inhibition of the
mitochondrial respiratory chain, inhibition of the glutamate transporter, and
glutamate-induced neurotoxicity involved in ALS(524,521).
It is now
known the cause for the destruction of the myelin in the lesions is
overactivation of the microglia in the region of the myelin(598).
An enzyme that converts glutamine to glutamate called glutaminase increases
tremendously, thereby greatly increasing excitotoxicity. Any dietary
excitotoxin can activate the microglia, thereby greatly aggravating the injury.
This includes the aspartate in aspartame and MSG which is in many processed
foods. The methanol in diet drinks adds to this toxicity as well. Now, the
secret to treatment appears to be calming down inflammation of the microglia.
Mercury and cadmium
inhibiting magnesium and zinc levels as well as inhibiting glucose transfer are
other mechanisms by which mercury and toxic metals are factors in metabolic
syndrome and insulin resistance/diabetes (43,198,338,597). Reduced levels of
magnesium and zinc are related to metabolic syndrome, insulin resistance, and
brain inflammation and are protective against these conditions(595,43).
According to neurologist Dr. RL Blaylock(598), the
good news is that there are supplements and nutrients that calm the
microglia-the most potent are: silymarin, curcumin and ibuprophen.
Phosphatidylcholine helps re-myelinate the nerve sheaths that are damaged, as
does B12, B6, B1, vitamin D, folate, vitamin C, natural vitamin E (mixed
tocopherols) and L-carnitine (576) . DHA plays a major role in repairing the
myelin sheath. Vitamin D may even prevent MS, but it acts as an immune
modulator, preventing further damage - the dose is 2000 IU a day. Magnesium, as
magnesium malate, is needed in a dose of 500 mg 2X a day. They must avoid all
excitotoxins, even natural ones in foods-such as soy, red meats, nuts, mushrooms
and tomatoes. Avoid all fluoride and especially all vaccinations since these
either inhibit antioxidant enzymes or triggers harmful immune reactions.
It has also been found that the antibiotic
minocycline powerfully shuts down the microglia. Dr. Blaylock tried this
treatment on a patient who just came down with fulmanant MS. He was confined to
a wheelchair. He was placed on minocycline and now, just a few weeks later, he
is walking.
The various neurological, immune, and metabolic related diseases
discussed together here are diagnosed and labeled clinically based primarily on
symptoms, along with tests for some underlying conditions found common in each
disease. But each individual will be
seen to have their own unique combination of neurological, endocrine, and
enzymatic imbalances along with autoimmunities that result in the functional
problems that lead to symptoms that are diagnosed as multiple sclerosis(MS) or Amyotrophic
Lateral Sclerosis(ALS) or Alzheimer’s Disease(AD), or Parkinson’s Disease(PD),
or Systemic Lupus Erythematosus(SLE), rheumatoid arthritis(RA), chronic fatigue
syndrome(CFS), or oral lichen planus(OLP), etc. However, a lot of commonality among these
factors has been documented, both within specific diseases and among the
various diseases discussed here. In
MS, an autoimmune T-cell attack on CNS myelin sheath results in demyelinated
plaques (405,etc.). Activated T-cells,
plasma cells, and macrophages have been found in the demyelinated areas. ALS is
a systemic motor neuron disease that affects the corticospinal and
corticobulbar tracts, ventral horn motor neurons, and motor cranial nerve
nuclei(405,etc.). Approximately 10 percent of ALS cases are of the familial
type that has been linked to a mutation of the copper/zinc super oxide
dismustase gene(Cu/Zn SOD). The majority
of ALS cases are of the sporadic type.
There are many toxic substances as well as some common drugs(336) that
have been found to be major factors in producing the functional conditions that
result in these diseases. However
mercury appears to be the most commonly implicated of these, and in particular
mercury from amalgam fillings- as will be documented here. For the majority of cases there are now
tests to identify the various factors involved in these types of diseases; and
once an individual’s underlying causative factors have been identified, high
success rates at cure or significant improvement are being achieved.
Toxic metals such as mercury, lead,
cadmium, etc. have been documented to be neurotoxic, immunotoxic,
reproductive/developmental toxins that according to U.S. Government agencies
cause adverse health effects and learning disabilities to millions in the U.S.
each year, especially children and the elderly(2,125,441,505,601,600,503). Exposure of humans and animals to toxic
metals such as mercury, cadmium, lead, copper, aluminum, arsenic, chromium,
manganese, etc. is widespread and in many areas increasing. The U.S. Center for Disease Control(276)
ranks toxic metals as the number one environmental health threat to
children. According to an EPA/ATSDR
assessment, the toxic metals mercury, lead,
and arsenic are the top 3 toxics having the most adverse health effects
on the public based on toxicity and current exposure levels in the U.S., with
cadmium, nickel and chromium also highly listed.
While there is considerable commonality to
the health effects commonly caused by these toxic metals, and effects are cumulative
and synergistic in many cases, this paper will concentrate on the health
effects of elemental mercury from amalgam fillings. The reason is that the public appears to be
generally unaware that considerable scientific evidence supports that mercury
is the metal causing the most widespread adverse health effects to the public,
and amalgam fillings have been well documented to be the number one source of
exposure of mercury to most people, with exposure levels often exceeding
Government health guidelines and levels documented to cause adverse health
effects. Much of the direct chronic
exposure to toxic metals for persons with the autoimmune diseases discussed
here appears to be from use of metals in dental work. The most common dental metals that have been
documented to be causing widespread adverse health effects are mercury, nickel,
palladium, gold, and copper. Although
chronic exposure clearly is affecting a much larger population, nickel has been
found to be a major factor in many cases of MS and lupus, with palladium having
very similar effects to nickel. Likewise chronic exposures to manganese and
copper have been implicated in some cases of Parkinson’s disease. Another group of toxic substance substances
with widespread exposure that have been demonstrated to generate reactive
oxygen species and have positive correlations to some of the diseases discussed
here are the organochlorine pesticides.
Toxic metals appear to be only one of the factors involved in chronic
autoimmune conditions. Pathogens such as
viruses, mycoplasma, bacteria and parasites have been found to usually be
present and a factor to deal with in treating those with chronic degenerative
conditions and weakened immune systems such as MS(448e,468,470,485) and other
autoimmune conditions.
II.
Documentation of High Common Exposures and Accumulation of Mercury in the Brain
and Motor Neurons
Amalgam fillings are the largest source of mercury
in most people with daily exposures documented to commonly be above government
health guidelines (14,49,79,99,183,506,500,217). This is due to continuous vaporization of mercury
from amalgam in the mouth, along with galvanic currents from mixed metals in
the mouth that deposit the mercury in the gums and oral cavity(605). Due to the high daily mercury exposure and excretion
into home and business sewers of those with amalgam, dental amalgam is also the
largest source of the high levels of mercury found in all sewers and sewer
sludge, and thus according to government studies a significant source of
mercury in rivers, lakes, bays, fish, and crops(603). People also get significant exposure from
vaccinations, fish, and dental office vapor(600).
When amalgam was placed into teeth of monkeys and
rats, within one year mercury was found to have accumulated in the brain,
trigeminal ganglia, spinal ganglia, kidneys, liver, lungs, hormone glands, and
lymph glands(22).
People also commonly get
exposures to mercury and other toxic metals such as lead, arsenic,
nickel, and aluminum from food, water, and other sources(601). All of these are highly neurotoxic and are
documented to cause neurological damage
which can result in chronic neurological conditions over time, as well as ADHD,
mood, and behavioral disorders(601).
Mercury is
one of the most toxic substances in existence and is known to bioaccumulate in
the body of people and animals that have chronic exposure(600). Mercury exposure is cumulative and comes
primarily from 4 main sources: silver(mercury) dental fillings, food(mainly
fish), vaccinations, and occupational exposure. Whereas mercury exposure from fish
is primarily methyl mercury and mercury from vaccinations is thimerosal(ethyl
mercury), mercury from occupational
exposure and dental fillings is primarily from elemental mercury vapor.
Developmental and neurological conditions occur at lower levels of exposure
from mercury vapor than from inorganic mercury or methyl mercury(606). Mercury in amalgam fillings, because of its relatively high vapor pressure
compared to its PEL safety limit and galvanic action with other metals in the
mouth, has been found to be continuously vaporized and released into the body, and has been found to
be the directly correlated to the number of amalgam surfaces and the largest
source of mercury in the majority of people (14,49,183,199,209,79,99,500),
typically between 60 and 90% of the total.
The level of daily exposure of those with several amalgam fillings
commonly exceeds the U.S. EPA health guideline for daily mercury exposure
of 0.1 ug/kg body weight/day, and the
oral mercury level commonly exceeds the
mercury MRL of the U.S.ATSDR of 0.2 ug/ cubic meter of air(217,500). When amalgam fillings are replaced, levels
of mercury in the blood, urine, and feces typically rise temporarily but
decline between 60 to 85% within 6 to 9 months (79,600.).
Mercury has been found to accumulate preferentially in the brain, major
organs, hormone glands, and 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(22,14,99,163,291,327,329,442,48,604). Mercury, with exposure either to vapor or
organic mercury tends to accumulate in the glial cells in a similar pattern,
and the pattern of deposition is the same as that seen from morphological
changes(327g,287,305). Though mercury
vapor and organic mercury readily cross the blood-brain barrier, mercury has
been found to be taken up into neurons of the brain and CNS without having to
cross the blood-brain barrier, since mercury has been found to be taken up and
transported along nerve axons as well through calcium and sodium channels and
along the olfactory path(329, 288,333,34).
III.
Mercury Toxicity: Summary of Neurological Effects
Mercury has
been found to accumulate in the cerebellum and other brain areas, producing
reactive oxygen species(ROS), including superoxide that cause damage to those
parts of the brain(194,13). Mercury was
also found to cause a reduction in antioxidant function such as superoxide
dimustase(SOD) and glutathione peroxide(GPx) that tries to counter-balance the
ROS(13,56a). Mercury, with exposure
either to vapor or organic mercury tends to accumulate in the glial cells in a
similar pattern, and the pattern of deposition is the same as that seen from
morphological changes (327g,287a).
Mercury(especially mercury vapor or organic mercury) penetrates and damages the blood brain
barrier allowing penetration of the barrier by other substances that are
neurotoxic (along with reduced amino
acid uptake to brain) (22,38,85,604,162,301,311/262). Such damage to the blood brain barrier’s
function has been found to be a major factor in chronic neurological diseases
such as MS(286,289,291,302, 324,326,478).
Programmed cell
death(apoptosis) is documented to be a major factor in degenerative
neurological conditions like MS, ALS, Alzheimer’s, Parkinson’s, etc. Some of the factors documented to be involved
in apoptosis of neurons and immune cells include inducement of the inflammatory
cytokine Tumor Necrosis Factor-alpha(TNFa) (126), reactive oxygen species and
oxidative stress(13,43a,56a,296b,495), reduced glutathione
levels(56,126a,111a), liver enzyme effects and inhibition of protein kinase C
and cytochrome P450(43,84,260), nitric oxide and peroxynitrite toxicity (43a,521,524),
excitotoxicity and lipid peroxidation(490,496), excess free cysteine levels
(56d,111a,33,330),excess glutamate toxicity(13b, 416), excess dopamine toxicity
(56d,13a), beta-amyloid generation(462,56a), increased calcium influx toxicity
(296b,333,416,432,462c,507) and DNA fragmentation(296,42,114,142) and
mitochondrial membrane dysfunction (56de, 416).
TNFa(tumor necrosis
factor-alpha) is a cytokine that controls a wide range of immune cell response
in mammals, including cell death(apoptosis).
This process is involved in inflammatory and degenerative neurological
conditions like ALS, MS, Parkinson’s, rheumatoid arthritis, etc. Cell signaling mechanisms like sphingolipids
are part of the control mechanism for the TNFa apoptosis mechanism(126a). Gluthathione is an amino acid that is a normal cellular mechanism for controlling
apoptosis. When glutathione is depleted
in the brain, reactive oxidative species increased, and CNS and cell signaling
mechinsisms are disrupted by toxic exposures such as mercury, neuronal cell
apoptosis results and neurological damage.
Mercury has been shown to induce TNFa, deplete glutathione, and increase
glutamate, dopamine, and calcium related toxicity, causing inflammatory effects and cellular
apoptosis in neuronal and immune cells(126b,126c). Mercury’s biochemical damage at the cellular
level include DNA damage, inhibition of DNA and RNA synthesis
(42,114,142,197,296,392); alteration of
protein structure (33,111,114,194,252,442);
alteration of the transport and signaling functions of
calcium(333,43b,254,416d,462,507); inhibition of glucose transport(338,254),
and of enzyme function and other essential nutrients
(96,198,254,263,264,33,330,331,338,339,347, 441,442); induction of free radical formation
(13a,43b,54,405,424), depletion of cellular glutathione (necessary for
detoxification processes) (56,111,126,424), inhibition of glutathione
peroxidase enzyme(13a,442), inhibits glutamate uptake(119,416d), induces
peroxynitrite and lipid peroxidation damage(521b), causes abnormal migration of
neurons in the cerebral cortex(149),
immune system damage (111,194, 226,252, 272,316,325,355); inducement of inflammatory
cytokines(126,152,181) and autoimmunity (181,226,272,314,369,405,507,etc.)
MS patients have been found to have much higher
levels of mercury in cerebrospinal fluid compared to controls (163,291,35,139). German studies including studies at German
universities have found that MS patients usually have high levels of mercury
body burden, with one study finding 300% higher than controls(271,302). Most recovered after mercury detox, with some
requiring additional treatment for viruses and intestinal dysbiosis.Very high
levels of mercury are also found in brain memory areas such as the cerebral
cortex and hippocampus of patients with diseases with memory related symptoms
(158,34, 207,etc.). Studies have found
mercury related neurological effects to be indistinguishable from those of MS
(207,212,222,244,271,289, 291,302,183,184,324,326,406).
Mercury has been shown to be a factor
that can cause rheumatoid arthritis by activating localized CD4+ T-cells which
trigger production of immune macrophages and immunoglobulin(Ig) producing cells
in joints (405,513,514).
IV.
Mercury Related Neurological Damage: Mechanisms of Causality
Exposure to inorganic
mercury has significant effects on blood parameters and liver function. Studies
have found that in a dose dependent manner, mercury exposure causes reductions
in oxygen consumption and availability, perfusion flow, biliary secretion,
hepatic ATP concentration, and
cytochrome P450 liver content(260), while increasing blood hemolysis products
and tissue calcium content and inducing heme oxygenase, porphyria, platelet
aggregation through interfering with the sodium pump.
Mercury vapor and methyl mercury
penetrate and damage the blood brain barrier (311,22,85,105,162,600/262),
also facilitating other toxic substances penetration of the BBB. Damage to the blood brain barrier's function
has been found to be a major factor in chronic neurological diseases discussed
here. Mercury also causes high levels
of oxidative stress and reactive oxygen species(ROS)(13), which have been
implicated as major factors in neurological disorders including stroke,
ALS(501) PD(502), Alzheimer’s(503), CFS(504), Lupus(113,234,331,602). Studies
have found mercury related neurological effects to be indistinguishable from
those of MS (163,207,271,244,289,291,302,184,324,326).
Metals like
mercury bind to SH-groups(sulphydryl) in sulfur compounds like amino acids and
proteins, changing the structure of the compound that it is attached to. This often results in the immune systems
T-cells not recognizing them as appropriate nutrients and attacking them(181,226,314,507).
Such binding and autoimmune damage has been documented in the fat-rich
proteins of the myelin sheaths and collagen(405), which are affected
in MS. Metals by binding to SH radicals
in proteins and other such groups can cause autoimmunity by modifying proteins
which via T-cells activate B-cells that target the altered proteins inducing
autoimmunity as well as causing aberrant MHC II expression on altered target
cells(425de,343). Studies have also
found mercury and lead cause autoantibodies to neuronal proteins,
neurofilaments, and myelin basic protein(MBP) (269ag,405,478,515,516). Mercury and cadmium also have been found to interfere
with zinc binding to MBP(517b) which affects MS symptoms since zinc stabilizes
the association of MBP with brain myelin(517a).
MS has also been found to commonly be related to inflammatory activity
in the CNS such as that caused by the reactive oxygen species and cytokine
generation caused by mercury and other toxic metals (405,478,515,516).
Antioxidants like lipoic acid which counteract such free radical activity have
been found to alleviate symptoms and decrease demyalination(494,572). A group of metal exposed MS patients with
amalgam fillings were found to have lower levels of red blood cells, hemoglobin,
hemocrit, thyroxine, T-cells, and CD8+ suppressor immune cells than a group of
MS patients with amalgam replaced, and more exacerbations of MS than those
without(102a). Immune and autoimmune
mechanisms are thus seen to be a major
factor in neurotoxicity of metals.
Na(+),K(+)-ATPase is a
transmembrane protein that transports sodium and potassium ions across cell
membranes during an activity cycle that uses the energy released by ATP
hydrolysis. Mercury is documented to
inhibit Na(+),K(+)-ATPase function at very low levels of exposure(288ab).
Studies have found that in Ms cases there was an elevation in plasma serum
digoxin and a reduction in serum magnesium and RBC membrane Na(+)-K+
ATPase activity (263). The activity of all serum free-radical
scavenging enzymes, concentration of glutathione, alpha tocopherol, iron
binding capacity, and ceruloplasmin decreased significantly in Ms, while the
concentration of serum lipid peroxidation products and nitric oxide
increased. The inhibition of Na+-K+ ATPase can contribute to
increase in intracellular calcium and decrease in magnesium, which can result
in 1) defective neurotransmitter transport mechanism, 2) neuronal degeneration
and apoptosis, 3) mitochondrial dysfunction, 4) defective golgi body function
and protein processing dysfunction. It is documented in
this paper that mercury is a cause of most of these conditions seen in MS
(13a,111,288,442,521b,43,56,263etc.)
Autoimmunity has also been found to be a factor in
chronic degenerative autoimmune conditions such as MS,ALS, etc., with genetic
susceptibility a major factor in who is affected. One genetic factor in Hg induced
autoimmunity is major histocompatibility complex(MHC) linked. Both immune cell type Th1 and Th2 cytokine
responses are involved in autoimmunity(425c).
One genetic difference found in animals and humans is cellular retention
differences for metals related to the ability to excrete mercury(426). For example it has been found that
individuals with genetic blood factor type APOE-4 do not excrete mercury
readily and bioaccumulate mercury, resulting in susceptibility to chronic
autoimmune conditions such as Alzheimer’s, Parkinson’s, etc. as early as age
40(437), whereas those with type APOE-2 readily excrete mercury and are less
susceptible (437,35). Those with type APOE-3 are intermediate to
the other 2 types. The incidence of
autoimmune conditions has increased to the extent this is now one of the
leading causes of death among women(450).
Also when a condition has been initiated and exposure levels decline,
autoimmune antibodies also decline in animals or humans(233,234d,369,60,118,368,405)
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(333). 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). They
also block or inhibit calcium L-channel currents in the brain in an irreversible
and concentration dependent manner.
Metallic mercury is much more potent than methyl mercury in these
actions, with 50 % inhibition in animal studies at 13 ppb(333).
A direct mechanism involving
mercury’s inhibition of cellular enzymatic processes by binding with the
hydroxyl radical(SH) in amino acids appears to be a major part of the
connection to allergic/immune reactive conditions. The binding of mercury from
amalgam to the -SH groups often results in inactivation of
sulfur and blocking of enzyme function, producing sulfur metabolites with
extreme toxicity that the body is unable to properly detoxify(33,114). Sulfur is essential in enzymes, hormones,
nerve tissue, and red blood cells. These
exist in almost every enzymatic process in the body. Blocked or inhibited sulfur oxidation at the
cellular level has been found in most with many of the chronic degenerative
diseases, including Parkinson’s, Alzheimer’s, ALS, lupus, rheumatoid arthritis,
CFS,FMS,MCS, autism, etc.(33,234,330,331,501-505,602)
Some studies of patients with
major neurological or degenerative diseases have found evidence amalgam
fillings may play a major role in development of conditions such as such as ,
MS(102,163,170,184,212,285,291,302,324,326), ALS(92,97,325,501), RA(600),
AD(66,67,158,166,204,207,221,238,242,244,258,296,300,503), SLE
(234,60,405), PD(56,84,98,169,218,248,250, 258,502) , and many other
conditions(600). 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). Only a few
micrograms of mercury severely disturb cellular function (33,56,226).
Mercury
exposure causes high levels of oxidative stress/reactive oxygen
species(ROS)(13), which has been found to be a major factor in neurological
disease(56,501-505). Mercury and
quinones form conjugates with thiol compounds such as glutathione and cysteine
and cause depletion of glutathione, which is necessary to mitigate reactive
damage. Such congugates are found to be
highest in the brain substantia nigra with similar congugates formed with
L-Dopa and dopamine in Parkinson’s disease(56,502). Mercury depletion of GSH and damage to
cellular mitochrondria and the increased lipid perxodation in protein and DNA
oxidation in the brain appear to be a major factor in Parkinson’s disease(33).
A Canadian study found those with 15 or more amalgam fillings to have more than
250% greater risk of MS than controls, and likewise higher risk for those who
have had amalgam fillings more than 15 years, and another study also found
higher mrcury body burden in those with more fillings and increased risk of MS
with more fillings(324). Another study(169) found blood and urine mercury
levels to be very strongly related to Parkinson's with odds ratios of approx.
20.
Exposure to mercury results in metalloprotein
compounds that have
genetic effects, having both structural and catalytic effects
on gene
expression(114). Some
of the processes affected by such metalloprotein
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 metalloprotein formation also appears to
cause a change in antigenicity and autoimmune reactions
in significant
numbers of people(114,60,342,405). Much mercury in saliva and
the brain is also organic, the most neurotoxic form(506,51,220,272),
since
mouth bacteria and other organisms in the body methylate
inorganic
mercury to organic mercury(506,51,254). Dental amalgam has
been found
to be the largest source of methyl mercury in most
with mercury amalgam
fillings(506,etc.).
Spatial and temporal changes in
intracellular calcium concentrations are critical for controlling neurotransmitter
release in neurons(432). Mercury alters calcium homeostasis
and calcium levels in the brain and affects neurotransmitter release through
its effects on calcium levels(270c,333,372,43).
Low levels of toxic metals have been found to inhibit dihydroteridine
reductase, which affects the neural system function by inhibiting
neurotransmitters through its effect on phenylalanine, tyrosine and tryptophan
transport into neurons(257,258). This
was found to cause severe impaired amine synthesis and hypokinesis. Tetrahydro‑biopterin,
which is essential in production of
neurotransmitters, is significantly decreased in patients with
Alzheimer's, Parkinson', and MS. Such
patients have abnormal inhibition of neurotransmitter production..
Mercury at extremely low levels also
interferes with formation of tubulin producing neurofibrillary tangles in the
brain, similar to those observed in Alzheimer’s patients with high levels of
mercury in the brain (207). Mercury and the induced neurofibrillary tangles
also appear to produce a functional zinc deficiency in the of AD sufferers(242), as well as causing
reduced
lithium
levels which is another factor in such diseases. The low Zn levels result in
deficient CuZnSuperoxide
dismutase (CuZnSOD), which in turn leads to increased levels of
superoxide(463). Lithium protects brain
cells against excess glutamate induced excitability and calcium influx(280).
Also mercury binds with cell membranes interfering with sodium and potassium
enzyme functions, causing excess membrane permeability, especially in terms of the
blood‑brain barrier (159,207,311].
Less than 1ppm mercury in the blood stream can impair the blood‑
brain barrier. Mercury was also found to
accumulate in the mitochondria and interfere with their vital functions, and to
inhibit cytochrome C enzymes which affect energy supply to the brain. Persons with extra Apo‑E4 gene copies
appear especially susceptible to this damage(207,221)
Mercury blocks the immune function of magnesium and zinc (198,427,43,38), 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 Wilson’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 ALS (489,495,464,469,111,501-504). 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. (444,464,494,495,469,470,572). Some of the antioxidants such as ginkgo
bilabo were also found to have protective effects through increasing catalase
and SOD action, while reducing lipid peroxidations(494a) Ceruloplasmin in plasma can be similarly affected by copper metabolism dysfunction,
like SOD function, and is often a factor in neurodegeneration (489).
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. There
is some evidence that astrocyte damage/malfunction is the main factor in MS(544). 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 neurological 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).
V.
Endocrine System and Metabolic Enzymatic System Impairments
Mercury has been well
documented to be an endocrine system-disrupting chemical(affecting hormonal
processes(85,146,149,199,312,604) and enzyme production processes(33,111,194)
at very low levels. The pituitary gland, in which mercury has been
documented to accumulate, controls many of the body’s endocrine system
functions and secretes hormones involved in control of most bodily
processes. The hypothalamus regulates
body temperature and many metabolic processes.
Such hormonal secretions are affected at levels of mercury exposure much
lower than the acute toxicity effects normally tested for (146,199). Some of the common effects of mercury on the
endocrine system include inhibiting human growth hormone, causing hormonal
imbalances that affect the reproductive system and body temperature regulation,
and causing hormonal imbalances resulting in imbalances in metabolism of
important minerals such as calcium(333,21,25,35,280).
Calcium
flux is inhibited in synoptic plasma membranes of the cerebellum and cerebrum
cortex. A permanent increase in
cytosolic calcium levels appears to be associated with various pathological
conditions which result in cell death(333).
All of the effects on hormonal regulation of the various bodily
processes add to and reinforce the imbalances caused in the metabolic enzymatic
processes.
All
body functions depend on cellular enzymatic and respiratory processes that
use Nutrients delivered by the blood,
detoxify toxic substances, and eliminate waste products through the cellular
respiratory process back through the lymph and blood to the lungs, kidneys, or
liver for excretion. Proteins are converted by enzymatic processes to amino
acids such as cysteine, cystine, glutamic acid, methionine, etc. for cellular
metabolic processes and to organic compounds such as glutathione which is
necessary to detoxify toxic substances such as mercury(13,111,194). Imbalances or blockages in any of several of
these enzymatic processes have been documented to cause major neurological and
immune damage that appears to be involved in most of the diseases being
discussed here.
Mercury vapor of those with chronic exposure is continuously released
into the blood stream through the lungs and distributed to cells throughout the
body, where it creates metal-protein compounds and reactive oxidative
species(ROS) such as superoxide, which must be detoxified. Cysteine and glutathione, which are produced
and interchanged as required through enzymatic processes, are necessary for
detoxification. Blockages or impairments caused by mercury or other toxic
substances or processes can then result in cellular toxicity and damage to
vital organs such as the brain, CNS, liver, or kidneys.
Clinical
tests of patients with motor neurone disease( MND),ALS, PD, AD, SLE, and RA
have found that the patients generally have damaged enzymatic processes
resulting in elevated plasma cysteine to sulphate ratios, with the average
being 500% higher than controls (330,331),
and in general are poor sulphur oxidizers (33,331).
High levels of free cysteine have been found to result in major
neurological damage to the brain, CNS, and cellular processes(194,330,331). The two main enzymatic processes that down
regulate cysteine to taurine, sulfates, and glutathione are cysteine
dioxygenese(CDO) and gamma-glutamylcysteine synthetase(GGCS). Impairment in CDO can result in high cysteine
levels, high cysteine to sulfate ratio, low taurine levels, and neurological
damage(194,330,331). GGCS converts
cysteine to glutathione , which has been demonstrated to be necessary to
detoxification of toxic substances like mercury(111). If this enzymatic process is blocked,
inhibited, or overloaded by chronic high toxicity levels or autoimmune reactions,
there is insufficient glutathione and toxic damage occurs due to immune
inability to process the metal-organic compounds and the ROS created by
exposure to mercury or other toxic substances(111,33,60,56). Another enzymatic process necessary for
proper cellular metabolism is sulfite oxidase(SO) which is involved in
conversion of toxic sulfur forms such as sulfites, sulfur dioxide(SO2),
hydrogen sulfide(H2S), etc. to nontoxic sulfates(33). SO can be blocked or inhibited by mercury or
other toxic exposures, resulting in more of these very toxic sulfur compounds.
SO is commonly found to be totally blocked or inhibited in patients with
MND,PD,AD,SLE,RA, etc.(330,331).
Glutathione peroxidase(GPx) is another enzymatic process in this loop
that is often affected, as well as the process involved in converting Vitamin
B6 through the essential coenzyme pyrodoxal 5-phosphate(P5P) in the synthesis
of neurotransmitters. Impairment in this
process results in brain neurotransmitter imbalances. Individual patients with any of these
diseases who commonly have been shown to have high ratio of cysteine to sulfate
can thus have several different individual enzymatic blockages or imbalances
that result in such high ratios, and different levels of neurological, immune,
and cellular damage due to high cysteine levels or low glutathione levels. Autoimmune reactions have also been found to
be commonly involved in such blockages or imbalances, particularly for those
with the major diseases being considered here.
This aspect will thus be further discussed.
V.
Autoimmunity, Neurological and Immune Diseases, and Mercury
Mercury has been documented to cause autoimmune disease (45,91,234,269,270,291,
328,405) and many researchers have concluded that
autoimmunity is a factor in the major chronic neurological diseases such as MS,
ALS, PD, SLE,RA,etc.. Mercury and other toxic metals also form inorganic
compounds with OH, NH2, CL, in addition to the SH radical and thus inhibits
many cellular enzyme processes, coenzymes, hormones, and blood
cells(405,600). Mercury has been found
to impair conversion of thyroid T4 hormone to the active T3 form as well as
causing autoimmune thyroiditis common to such patients(369,382). In general, immune activation from toxic
metals such as mercury resulting in cytokine release and abnormalities of the
hypothalamus‑pituitary‑adrenal(HPA) axis
can cause changes in the brain, fatigue, and severe psychological symptoms (342,369,379‑382,385,405,118)
such as profound fatigue, muscosketal pain, sleep disturbances,
gastrointestinal and neurological problems as are seen in CFS, fibromyalgia,
and autoimmune thyroidititis. Such hypersensitivity has been found most common
in those with genetic predisposition to heavy metal sensitivity(60,342,369,382,405),
such as found more frequently in patients with human lymphocyte antigens (HLA‑DRA)
(381-383). A significant portions of the
population appear to fall in this category.
The enzymatic
processes blocked by such toxic substances as mercury
also result in chronic formation of metal‑protein
compounds (HLA antigens
or antigen-presenting
macrophages) that the body’s immune
system(T-
lymphocytes) does not recognize, resulting in autoimmune
reactions
(114,342,405). The metals bind to
SH-groups on proteins which can then be
recognized as “foreign” and
attacked by immune lymphocytes. Such
has
been extensively documented
by studies such as the documentation of the
autoimmune function test MELISA,
a sophisticated immune/autoimmune test
which was developed to test
for such reactions(60,405).
Very low doses and short term
exposures of inorganic Hg (20-200 mug/kg) exacerbates lupus and
accelerates mortality in mice. low dose Hg exposure increases the severity and prevalence
of experimental autoimmune myocarditis induced by other factors. A strong significant correlation was found
between occupational exposure to mercury or pesticides to lupus (SLE) with
dental personal having a very high risk factor(113c). In a study of small-scale gold mining using
mercury, there was a
positive interaction between Hg autoimmunity and malaria. These
results suggest a new model for Hg immunotoxicity, as a co-factor in autoimmune
disease, increasing the risks and severity of clinical disease in the presence
of other triggering events, either genetic or acquired(234f).
Autoimmune reactions to inorganic and methyl mercury have been found to
be relatively independent, occurring in over 10% of controls. In the population
of over 3,000 patients tested by MELISA, the following percentages tested
positive for lymphocyte reactivity:
nickel-34%, inorganic mercury-22%, phenyl
mercury-15%, methyl mercury-8%, gold-10%, palladium-10%, cadmium-11%,
silver-1%. Groups with autoimmune symptoms such as oral lichen planus, CFS, MS,
autoimmune thyroiditis, etc. generally have high percentages with lymphocyte
reactivity to metals(60,342,369,405). Among a population of patients being tested
for autoimmune problems, 94% of such patients had significant immune reactions
to inorganic mercury(MELISA test,60,342,369,405) and 72% had immune reactions
to low concentrations of HgCl2(<0.5 ug/ml). Of a population of 86 patients
with CFS symptoms who had amalgam fillings replaced, 78% reported significant
health improvement in a relatively short time period after replacent, and
MELISA test scores had a significant reduction in lymphocyte reactivity
compared to pre- replacement(369). Similar
results were experienced for those with MS, lupus, and autoimmune thyroiditis(369). The
MELISA test has proved successful in
diagnosing and treating environmentally caused autoimmune diseases such as MS,
SLE, oral lichen planus, CFS,etc. (60,313,342,369,405). A high percentage of patients subjectively
diagnosed with CNS and systemic symptoms suggestive of mercury intoxication
have been found to have immune reactivity to inorganic mercury(MELISA
test,118), and likewise for MRI positive patients for brain damage. Controls without CNS problems did not have
such positive correlations. Nickel,
palladium, and gold have also been found to induce autoimmunity in genetically
predisposed or highly exposed individuals (60,118,313,314,234,369,130). Tests have found a significant portion of
people(over 10%) to be in this category and thus more affected by exposure to amalgam
than others. Once compromised by a
toxic substance that depletes the immune protectors and causes autoimmunity,
the immune system is more susceptible to being sensitized to other toxic
chemicals, a factor in multiple chemical sensitivity(MCS). Mercury also causes a reduction in thyroid
production(50) and an accumulation in the thyroid of radiation. Among those with chronic immune system
problems with related immune antibodies, the types showing the highest level of
antibody reductions after amalgam removal include glomerular basal membrane,
thyroglobulin, and microsomal thyroid antigens(91).
Mercury and toxic metals block enzymes required to digest milk casein and wheat gluten, resulting in dumping morphine like substances in the blood that are neurotoxic and psychotic, as a major factor in schizophrenia, autism, ADHD, and MS (24-26). A mechanism in MS occurs due to a reduction in immune system activity. Specifically, it is the reduction in the number of the suppressor T-cells within the immune system that allows CD4 helper T-cells to do damage (102a,181,226, 314,405,507,513,514,20). Thus, during an acute relapse the overall number of T-cells is reduced, the normal balance of helper and suppressor T-cells is disrupted, and helper T-cells tend to predominate. This is most pronounced during an acute relapse, but a similar situation occurs although perhaps to a lesser extent, in chronic progressive MS. A double blind study using a potent opiate antagonist, naltrexone (NAL), produced significant reduction in neurological symptomology among the 56% most responsive to opioid effects in a population of autism patients(18,19). The behavioral improvements was accompanied by alterations in the distribution of the major lymphocyte subsets, with a significant increase in the T-helper-inducers and a significant reduction of the T-cytotoxic-suppressors and a normalization of the CD4/CD8 ratio. Low dose naltrexone (LDN) has been found to commonly be effective in reducing MS symptoms and exerbations, apparently due its opioid suppressive effects(20).
VI. Recovery from Chronic Neurological and
Immune Related Diseases After Amalgam Removal and Mercury Detoxification
There
are extensive documented cases (many thousands) where removal of amalgam fillings led to cure of serious
health problems such 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), Chronic Fatigue Syndrome
(8,35,60,212,293,229,222,232, 233,271,317,323,342,369, 376,382,440,470,523), muscular/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), Rheumatoid Arthritis(35,95,103,212, 222,271, 322,358,470, 523), autoimmune
thyroiditis (369,382,91), OralLichenPlanus(60,75,78,82,86, 87,90,94,101,133, 168,313), ALS(97,229,405,406,468-470,485,35), Parkinson’s/
muscle tremor (222,248,229,271,470,212,94,98,35), Alzheimer’s’s(204,35), and many other chronic
conditions(600). In several of the
studies, over 75% of those with MS and having amalgams replaced recovered or
had significant improvement( 369,212(a),(b),(e),302,222,35). Some of the studies reported similar success
rates for SLE and autoimmune thyroiditis, but with lower number of cases
treated. There is consensus that dental
amalgam is the main cause of oral lichen planus and most recover after amalgam
replacement.
In one study all 6 of those tested for
autoimmunity by the MELISA blood lymphocyte immune reactivity test were found
to be immune reactive to mercury, and all had significant improvement in their
condition after amalgam replacement, as well as reduction in immune
reactivity(369). Out of 15 patients with lupus (SLE), 73% had significant
improvement in health, and out of 8 with autoimmune thyroiditis 75% had
significant improvement after amalgam replacement. The patients who did not have significant
improvement were found to have immune reactivity to nickel which did not improve
after amalgam replacement as the amalgam was not the source of the nickel exposure(369).
Clinical studies have found that patch testing is not a good predictor
of success of amalgam removal, as a high
percentage of those testing negative also recovered from chronic conditions
after replacement of fillings(86,87,90).
Follow up tests for autoimmune reaction to inorganic mercury after
amalgam replacement have found that in most patients tested, the immune
reaction as well as most symptoms disappear over time (60,313,405,etc.).
The
level of mercury in the gums is often 1200 ppm near a gold cap on an amalgam
filling(30,35,48,194). These levels are among the highest levels ever measured
in tissues of living organisms, exceeding the highest levels found in
chronically exposed chloralkali workers, those who died from mercury in Minamata, or animals that died from
mercury poisoning. The FDA/EPA action
level for warnings of dangerous levels in fish or food is 1 ppm.
Tests and Treatment
In a
large German study of MS patients after amalgam revision, extraction resulted
in 85% recovery rate versus only 16% for filling replacement alone
(302,222). Another large clinic in
Colorado has likewise found that more seriously affected cases often require
more than simple replacement for successful treatment(35). Other clinics have found that recovery from
serious autoimmune diseases, dementia, or cancer may require more aggressive
mercury removal techniques than simple filling replacement due to body burden.
This appears to be due to migration of mercury into roots & gums that is
not eliminated by simple filling replacement.
Also toxic metals, formaldehyde, and other toxic substances have been
documented to accumulate in the jaw bone and tissue near teeth with multiple
metals, as well as in pockets from extracted teeth and form cavitations(areas
of toxic materials and diseased bone). Such cavitations and toxic bacteria
accumulating from root-canaled teeth sometimes must be cleaned out before
significant recovery can occur(200,35,302,222,207,etc.). There is a direct connection between the
teeth and gums with the brain and CNS by both travel along nerve fibers and
through the cranio-vertebral venous system for either toxic substances such as
mercury or for bacteria(34,325,207,etc.), The following protocol is perhaps the
most used protocol for treating these conditions and has had considerable
success:
Huggins
Total Dental Revision Protocol(35)
(a)
history questionnaire and panel of tests.
(b)
replace amalgam fillings starting with filling with
highest negative current or highest negative quadrant, with supportive
vitamin/mineral supplements.
©
extract all root canaled teeth using proper finish protocol.
(d)
test and treat cavitations and amalgam tattoos where
relevant
(e)
supportive supplementation, periodic monitoring tests,
evaluate need for further treatment(not usually needed).
note: after treatment of many cases of
chronic autoimmune conditions such as MS, ALS, Parkinson’s, Alzheimer’s, CFS,
Lupus, Rheumatoid Arthritis, etc., it has been observed that often mercury
along with root canal toxicity or cavitation toxicity are major factors in
these conditions, and most with these conditions improve after TDR if protocol
is followed carefully(35,200,600).
Other measures in addition to TDR that have been found to help in
treatment of MS in clinical experience are avoidance of milk products, get lots
of sunlight, supplementation of calcium AEP(448) and alpha lipoic
acid(448b). Progesterone creme has been
found to promote regrowth of myelin sheaths in animals(448c).
Tests suggested by Huggins/Levy(35) for
evaluation and treatment of mercury toxicity:
(a)
hair element test(386) (low hair mercury level does not indicate
low body level)(more than 3 essential minerals out of normal range indicates likely
metals toxicity)
(b)
CBC blood test with differential and platelet count
©
blood serum profile
(d)
urinary mercury (for person with average exposure with
amalgam fillings, average mercury level is 3 to 4 ppm;
lower test level
than this likely means person is poor excretor and accumulating mercury, often
mercury toxic(35)
(e) fractionated porphyrin(note test results sensitive to
light, temperature, shaking)
(f)
individual tooth electric currents(replace high
negative current teeth first)
(g)
patient questionnaire on exposure and symptom history
Based on the known mechanisms of damage found in
these conditions, the authors of the study(463) suggest that supplementation with 100
mg MG, 25 mg vit B6, 10 mg vit B2, 15 mg Zn and 400 IU vit D and E, 100
&mgr;g Se, 180 mg EPA nd 120 mg DHA per day between 14 and 16 years of age
may prevent MS, and reduce futher damage for those with the condition.
References
(2)U.S. Environmental Protection
Agency(EPA), 1999, "Integrated Risk Information System, National Center for Environmental Assessment,
Cincinnati, Ohio, http://www.epa.gov/ncea/iris.htm; & United States Environmental Protection Agency,
Office of Water, November 2000, The National Listing of Fish and
Wildlife Advisories: Summary of 1999
Data, EPA‑823‑F‑00‑20, http://www.epa.gov/ost/fish/advisories/general.html
(12) Dimaval Scientific monograph,
sixth Ed., Jan 1997, Dr Johann Ruprecht, Heyl Corporation
(13)(a) 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; & P.Bulat,
“Activity of Gpx and SOD in workers occupationally exposed to mercury”, Arch
Occup Environ Health, 1998, Sept, 71 Suppl:S37-9; &
Stohs SJ, Bagchi D. Oxidative
mechanisms in the toxicity of metal ions.
Free Radic Biol Med 1995; 18(2): 321-36 ; & D.Jay, “Glutathione
inhibits SOD activity of Hg”, Arch Inst cardiol Mex, 1998,68(6):457-61 & El-Demerdash FM. Effects of selenium and mercury on the enzymatic activities and
lipid peroxidation in brain, liver, and blood of rats. J Environ Sci Health B. 2001 Jul;36(4):489-99.
&(b) S.Tan et al,
“Oxidative stress induces programmed cell death in neuronal cells”, J
Neurochem, 1998, 71(1):95-105; & Matsuda T, Takuma K, Lee E, et
al. Apoptosis of astroglial cells [Article in Japanese] Nippon Yakurigaku
Zasshi. 1998 Oct;112 Suppl 1:24P-; & & Lee
YW, Ha MS, Kim YK.. Role of reactive
oxygen species and glutathione in inorganic mercury-induced injury in human
glioma cells. Neurochem Res. 2001
Nov;26(11):1187-93; & (c)Ho PI, Ortiz D, Rogers E, Shea
TB. Multiple aspects
of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation
and DNA damage. J
Neurosci Res. 2002 Dec 1;70(5):694-702.
(14) (a) M.Nylander et al, "Mercury concentrations in the human
brain and kidneys and exposure from amalgam fillings", Swed Dent J 1987;
11:179-187, & (b) D.W.Eggleston et
al, Correlation of dental amalgam with mercury in brain tissue. J Prosthet
Dent, 1987,58(6),704-7; & J.A.Weiner et al,“The
relationship between mercury concentration in human organs and predictor
variables", Sci Tot Environ, 138(1-3):101-115,1993
(18)
Scifo R, Marchetti B, et al.
Opioid-immune interactions in autism: behavioral and immunological
assessment during a double-blind treatment with naltexone. Ann Ist Super Sanita
1996; 32(3): 351-9.
(19) Eedy DJ, Burrows D, Dlifford
T, Fay A. Elevated T
cell subpopulations in dental students.
J prosthet Dent 1990; 63(5):593-6;
& & Yonk
LJ et al, CD+4 helper T-cell depression in autism. Immunol Lett, 1990, 25(4):341-5.
(20) LDN for MS Trials/Experience http://www.ldnresearchtrust.org/default.asp?page_id=77
(21) Goyer RA Toxic effects of
metals. Cassarett and Doull's toxicology‑‑The
basic science of poisons , ed3, New York , MacMillan Publ.Co
1986, pp582‑609
(22) (a) Galic
N, Ferencic Z et al, Dental amalgam
mercury exposure in rats.
Biometals. 1999 Sep;12(3):227-31; &
Arvidson B, Arvidsson J, Johansson K,. Mercury deposits in neurons of
the trigeminal ganglia after insertion of dental amalgam in rats. Biometals. 1994 Jul;7(3):261-3; &
(b)Danscher G, Horsted-Bindslev P, Rungby J. Traces of mercury in organs from
primates with amalgam fillings. Exp
Mol Pathol. 1990 Jun;52(3):291-9; & L.Hahn et al, Distribution of mercury
released from amalgam fillings into
monkey tissues”, FASEB J.,1990, 4:5536
(24) J.R. Cade et al, Autism and
schizophrenia linked to malfunctioning enzyme for milk protein digestion. Autism, Mar 1999. http://news.ufl.edu/1999/03/15/autism/ ;& Autism and
Schizophrenia: Intestinal Disorders, Cade R et al. Nutritional Neuroscience, March 2000. http://www.feingold.org/Research/cade.html & http://www.paleodiet.com/autism/
; &
"Beta-casomorphin induces Fos-like immunoreactivity in discrete brain
regions relevant to schizophrenia and autism" Autism March 1999 vol 3(1)
67-83; Sun, ZJ, Cade JR, et al & A
Peptide Found in Schizophrenia and Autism Causes Behavioral Changes in 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 Autistic Society, SAGE
Publications http://aut.sagepub.com/cgi/content/abstract/3/1/85 ; & Opiate
hypothesis in infantile autism? Therapeutic trials with naltrexone,
Leboyer M, et al., Encephale
1993 Mar-Apr;19(2):95-102; & Food allergy and infantile autism.
Lucarelli S, et al., Panminerva Med
1995 Sep;37(3):137-41; http://www.feingold.org/Research/autism.html
& Application of the
Exorphin Hypothesis to Attention Deficit Hyperactivity Disorder: A Theoretical Framework by Ronald
Hoggan A Thesis Submitted To The
Faculty Of Graduate Studies In Partial Fulfilment Of The Requirements For The Degree Of Master Of Arts, Graduate Division Of Educational
Research,Calgary, April, 1998 University
of Calgary
(25)
Reichelt KL. Biochemistry
and psycholphisiology of autistic syndromes. Tidsskr Nor
Laegeforen 1994, 114(12):1432-4; & Reichelt KL et al, Biologically active
peptide-containing fractions in schizophrenia and childhood autism. Adv Biochem
Psychopharmocol 1981; 28: 627-43; Lucarelli S, Cardi E, et al, Food allergy and
infantile autism. Panminerva Med 1995; 37(3):137-41; & Shel L,
Autistic disorder and the endogenous opioid system. Med Hypotheses 1997, 48(5): 413-4.
(26)The mercury/casein/gluten
factor effect on opioid peptides as a mechanism in causing autism,
schizophrenia, ADHD, MS, and other neurological conditions, B Windham (Ed), www.flcv.com/hgopioid.html
(28) F.Schmidt et al, “Mercury in
urine of employees exposed to magnetic fields”, Tidsskr Nor Laegeforen, 1997,
117(2): 199-202; & Sheppard AR and EisenbudM., Biological
Effects of electric and magnetic
fields of extremely low
frequency. New York university press.
1977; & Ortendahl T W, Hogstedt P,
Holland RP, "Mercury vapor release from dental amalgam in vitro caused by
magnetic fields generated by CRT's", Swed Dent J 1991 p 31 Abstract 22.
(30)
Till et al.,Zahnarztl. Welt/reform, 1978:87;1130‑1134; & S.Olssonl, "Release of
elements due to electrochemical corrosion of
dental amalgam" J of Dental Research, 1994, 73:33‑43
(33) (a) 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;
& (b)2S.A.McFadden, “Xenobiotic metabolism and adverse environmental
response: sulfur-dependent detox pathways”,Toxicology, 1996, 111(1-3):43-65;
&(c) S.C. Langley-Evans et al, “SO2:
a potent glutathion depleting agent”, Comp Biochem Physiol Pharmocol Toxicol
Endocrinol, 114(2):89-98; & (d)Alberti A, Pirrone P, Elia M,
Waring RH, Romano C. Sulphation deficit
in “low-functioning” autistic children. Biol Psychiatry 1999, 46(3):420-4.
(34) PatrickStörtebecker,Associate
Professor of Neurology, Karolinska Institute, Stockholm. Mercury Poisoning
from Dental amalgam-A Hazard to the Human Brains, ISBN: 0-941011001-1 & J Canadian Dental Assoc,
33(6): 300-; & Henriksson
J, Tjalve H. Uptake of inorganic mercury in the
olfactory bulbs via olfactory pathways in rats. Environ Res. 1998
May;77(2):130-40.
(35) (a) Huggins HA, Levy,TE, Solving the MS Mystery: Help, hope and
recovery, 2002; & (b) Huggins HA, Levy,TE, Uniformed Consent: the
hidden dangers in dental care, 1999, Hampton Roads Publishing Company
Inc; & (c)Hal Huggins, Its All in Your Head,
1993; & (d) Center for Progressive Medicine, & http://www.hugginsappliedhealing.com/ms.php
(38)S.Ziff and M.Ziff, Infertility
and Birth Defects: Is Mercury from Dental Fillings a Hidden Cause? , Bio‑Probe, Inc. ISBN: 0‑941011‑03‑8.1987, www.bioprobe.com
(42) Rodgers JS, Hocker JR, et al, Mercuric ion
inhibition of eukaryotic transcription factor
binding to DNA. Biochem
Pharmacol. 2001 Jun 15;61(12):1543-50; & K.Hansen et
al A survey of metal induced mutagenicity
in vitro and in vivo, J Amer Coll Toxicol , 1984:3;381‑430;
(43) (a)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; & P.Jenner,“Oxidative mechanisms in PD”, Mov Disord, 1998; 13(Supp1):24-34;&(b) Rajanna B et al, “Modulation of protein kinase C by heavy metals”, Toxicol Lett, 1995, 81(2-3):197-203: & Badou A et al, “HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels”J Biol Chem. 1997 Dec 19;272(51):32411-8., & D.B.Veprintsev, 1996, Institute for Biological Instrumentation, Russian Academy of Sciences, Pb2+ and Hg2+ binding to alpha‑lactalbumin”.Biochem Mol Biol Int 1996 ;39(6): 1255‑65; & M. J. McCabe, University of Rochester School of Medicine & Dentistry, 2002, Mechanisms of Immunomodulation by Metals, www.envmed.rochester.edu