Amyotrophic Lateral Sclerosis(ALS): Lou Gehrig’s Disease - the Mercury
Connection Bernard
Windham (Ed.)
I. Introduction.
ALS is a progressive systemic motor neuron disease that affects
the corticospinal and corticobulbar tracts, ventral horn motor neurons, and motor
cranial nerve nuclei (405). Senile plaques (amyloid
beta) and neurofibrillary tangles accumulate and cause cellular damage in key
areas of brain (52). Supplementation
that boost Acetylcholine slows progress of the disease (52). Oxidative stress, Glutamate Toxicity, Inflammation,
and Mitochondrial Dysfunction and Excitotoxicity are factors in ALS that cause
brain damage (52). Loss of sex hormones may also contribute (52). [(All of
these factors have been found to be caused by mercury and toxic metals (33,52,108,113,114)
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. Based on studies of
groups of monozygous twins, animal studies, and ALS patient case studies, the
majority of ALS cases do not appear to be genetic but rather have primarily
environmental related causes often affecting genetically susceptible
individuals (405,416,423,471,520,93,94,95,97,200,303,580,35, etc.}
[Mutation of the FUS gene or TPD-43 gene has been shown to be one
of the major factors in familial and some sporadic ALS (527).
A
significant 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) (405). In a
mouse study of the ALS model transgenic mice, concentrations of Cu, Zn and
Fe were significantly elevated in muscle tissue of the SOD1 transgenic mice. In
a study of amalgam filling effect on women, Hg, Ag, Al and Ba metal levels
increased in women who had dental amalgam fillings for long periods and Hg had
a positive correlation with SOD-1. SOD-1 may be a possible biomarker for
assessing chronic Hg toxicity(405d). Significant elevation in mercury or other
toxic metal concentration in muscle tissue from SOD1-G93a transgenic individuals
appear to facilitate the development of ALS, making transgenic individuals more
susceptible to mercury and metal exposures and imbalances (405bc,118).
Resveratrol was found to be protective against such effects(405c). Susceptibility
factors like these are a major factor in the accumulation and toxicity of
mercury and toxic metals and the of getting neurological conditions such as ALS,
AD, PD, MS, etc. (www.myflcv.com/suscept.html).
(Inherited defects or differences in the body’s ability to detoxify
can contribute to heavy metal accumulation and toxicity. Deficiencies of
certain minerals, vitamins, and amino acids reduce the body’s ability to
excrete toxins following exposure. Those with the genetic
allele ApoE4 protein in the blood have been found to detoxify metals poorly and
to be much more genetically susceptible to chronic neurological conditions than
those with types ApoE2 or E3. Researchers
have shown that genetic carriers of the brain protein APO E2 are protected
against Alzheimer's disease (AD) whereas genetic carriers of the APO E4
genotype are at enhanced risk factor for developing AD and other degenerative
neurological conditions. (113, www.myflcv.com/suscept.html);
(Glutathione
is produced by methylation that’s responsible for brain neurotransmitter
production, immune function, and detoxification. DNA
methylation and other epigenetic factors are important in the pathogenesis of
late-onset Alzheimer's disease (LOAD) Methylenetetrahydrofolate reductase (MTHFR)
gene mutations occur in most elderly patients with memory loss (118e,108). MTHFR is critical for production of
S-adenosyl-l-methionine (SAMe), the principal methyl donor. A common mutation (1364T/T) of the cystathionine-γ-lyase
(CTH) gene affects the enzyme that converts cystathionine to cysteine in
the transsulfuration pathway causing plasma elevation of total homocysteine
(tHcy) or hyperhomocysteinemia-a strong and independent risk factor for
cognitive loss and AD. Other causes of hyperhomocysteinemia include aging,
nutritional factors, and deficiencies of B vitamins.)]
ALS is
not a unique disease with a single cause or factor, but instead is a result of
damage to motor neurons and the support system that they depend on by a variety
of factors. Spinal and bulbar-onset subtypes of the disease appear to be
biochemically different and have differences in mechanisms of causality (416f).
Some of the mechanisms of neural damage found in ALS include increased free
radical generation/oxidative damage, impaired electron transport, disrupted
calcium channel function, reactive astrogliosis and dysfunctional transporters
for L-glutamate, neurotoxicity, oxidative damage to mitochondrial DNA/
inhibition of the mitochondrial respiratory chain, autoimmunity, and
generalized disruption of metabolism of neuroexciotoxic amino acids like
glutamate, aspartate, NAAG. The mechanisms by which exposure to mercury and
other neurotoxic substances cause all of this will be documented.
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 excrete and detoxify
metals (405,342,60,181,303,314,330,464). 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. Those
with the genetic allele ApoE4 protein in the blood have been found to detox
metals poorly and to be much more susceptible to chronic neurological conditions
than those with types ApoE2 or E3(437,577). There are also other similar
factors. Other susceptibility factors that have major effects on
accumulation and toxicity of mercury and toxic metals and thus on timing of getting
chronic neurological conditions are the type of Apolipoprotein allele of the individual,
along with the mutation of mercury
protective superoxide dismutase SOD1 gene
and mutation the the MTHFR gene(see www.myflcv.com/suscept.html)
(In a study of amalgam filling
effect on women, Hg, Ag, Al and Ba metal levels increased in women who had
dental amalgam fillings for long periods and Hg had a positive correlation with
SOD-1. SOD-1 may be a possible biomarker for assessing chronic Hg toxicity(118d).
Significant elevation in mercury or other toxic metal concentration in muscle
tissue from SOD1-G93a transgenic individuals appear to facilitate the development
of ALS and other neurological conditions, making transgenic individuals more
susceptible to mercury and metal exposures and imbalances and being affected at
earlier ages in individuals with chronic exposure such as dental amalgams(118bc,33).
Resveratrol was found to be protective against such effects(118c)). (Inherited
defects or differences in the body’s ability to detoxify can contribute to
heavy metal accumulation and toxicity. Deficiencies of certain minerals,
vitamins, and amino acids reduce the body’s ability to excrete toxins following
exposure. Those with the genetic allele ApoE4 protein in the blood have
been found to detoxify metals poorly and to be much more genetically
susceptible to chronic neurological conditions than those with types ApoE2 or
E3. Researchers
have shown that genetic carriers of the brain protein APO E2 are protected
against Alzheimer's disease (AD) whereas genetic carriers of the APO E4
genotype are at enhanced risk factor for developing AD and other degenerative
neurological conditions. (112, www.myflcv.com/suscept.html);
(Glutathione
is produced by methylation that’s responsible for brain neurotransmitter
production, immune function, and detoxification. DNA
methylation and other epigenetic factors are important in the pathogenesis of
late-onset Alzheimer's disease (LOAD) Methylenetetrahydrofolate reductase (MTHFR)
gene mutations occur in most elderly patients with memory loss (118e,108). MTHFR is critical for production of
S-adenosyl-l-methionine (SAMe), the principal methyl donor. A common mutation (1364T/T) of the cystathionine-γ-lyase
(CTH) gene affects the enzyme that converts cystathionine to cysteine in
the transsulfuration pathway causing plasma elevation of total homocysteine
(tHcy) or hyperhomocysteinemia-a strong and independent risk factor for
cognitive loss and AD. Other causes of hyperhomocysteinemia include aging,
nutritional factors, and deficiencies of B vitamins.). People are exposed to a large number of toxic
metals and toxins. Interactions among components of a mixture may change
toxicokinetics and toxicodynamics, resulting in additive or synergistic neurological
effects (18). Mercury, lead, arsenic, and cadmium induce Fe, Cu, and Zn
dyshomeiostatis which can result in AD, PD, etc.(18c)
Some of
the toxic exposures which have been found to be a factor in ALS like symptoms
other than mercury include lead(94), pyretherins (93), agricultural chemicals(95),
Lyme disease (471,580), monosodium glutamate (MSG,580), failed root
canaled teeth(35,200,437), post-poliomyelitis(580),
pesticides/formaldehyde(95e), and smoking(95acd). All have been demonstrated to
cause some of the mechanisms of damage listed above seen in ALS and since such
exposures are common as is exposure to mercury, such exposures appear to
synergistically cause the types of damage seen in ALS. A study of approx.
1000 men and women who died of ALS found that male programmers and laboratory
technicians and female machine assemblers may be at increased risk of death
from ALS(95f).
This
paper will demonstrate that mercury is the most common of toxic substances
which are documented to accumulate through chronic exposure in the neurons
affected by ALS and which have been documented to cause all of the conditions
and symptoms seen in ALS. It will also be noted that chronic infections such as
mycoplasma,echo-7 enterovirus, and candida albicans
also usually affect those with chronic immune deficiencies such as ALS patients
and need to be dealt with in treatment. Some studies have also found persons
with chronic exposure to electromagnetic fields(EMF) or
Wi-fi to have higher levels of mercury exposure and excretion(28) and higher
likelihood of getting chronic conditions like ALS(526).
II. Documentation
of High Common Exposures and Accumulation of Mercury in Motor Neurons
Amalgam
dental fillings are the largest
source of mercury in most people with daily exposures documented to
commonly be above government health guidelines (49,79,183,506,577,589,599,600).
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 (589,600). The mercury vapor from amalgam
is lipid soluble and enters the blood through the lungs as well as through
capillaries of the gums. Since the vapor and inorganic mercury are also
converted to organic (methyl) mercury in the intestines, there is exposure from
all 3 types of mercury (589,600). Both mercury vapor and methyl mercury readily
cross the blood brain barrier where they accumulate and cause neurological
damage. Mercury has been found in autopsy studies to accumulate in the brain of
those with chronic exposures, and levels are directly proportional to the
number of amalgam filling surfaces (85,270). 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 (20). 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.
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(20,291,327,329,442,48).
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). 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.
III. Effects of
Exposure to Mercury and Toxic Metals
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 such as eczema, psoriasis,
rheumatoid arthritis, Lupus, Scleroderma, allergies, autism, schizophrenia,
(114c,181,303,330,331,411,412,152b, 439,602,601), as well as to autoimmune
conditions such as ALS, Alzheimer’s(AD), Chronic
Fatigue(CFS), Fibromyalgia(FM), etc.(405,342,60,181,303,314b,513,580,etc.)
. For example 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 (30,114c,194,330,331,412), enzymatic
processes involving vitamins B6(417) 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
(43b,96,198,333, 338,386,427,430,432,461,489,507). Lithium (other than high
levels) is neuroprotective(280,590). Along with these blockages of cellular
enzymatic processes, mercury has been found to cause additional neurological
and immune system effects in many by causing immune/ autoimmune reactions
(60,152c,181,288c,314,342,405,513). Recent studies gives
a comprehensive review of studies finding a connection between ALS, toxic
metals, and autoimmunity (405,580). Studies have found the presence of
antibiodies in ALS patients that interact with motor neurons, inhibiting the
sprouting of axons. Immune complexes have also been found in the spinal cords
of ALS patients (580). T cells, activated microglia, and IgG within the spinal
cord may be a primary event that leads to lesions and tissue destruction.
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 Sclerosis(MS), and
Alzheimer’s(AD) (13,43,56,84,145,169,207b,424,442-444,453, 462,491,496,577).
Mercury forms conjugates with thiol compounds such as glutathione and cysteine
and causes depletion of glutathione (56), which is necessary to mitigate
reactive damage. One study found that insertion of amalgam fillings or nickel
dental materials causes a suppression of the number of T-lymphocytes(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)(13,254,490,494-496).
Only a few micrograms of mercury severely disturb cellular function and
inhibits nerve growth (305,147,175,226,255). Metalloprotein(MT)
have a major role in regulation of cellular copper and zinc metabolism, metals
transport and detoxification, free radical scavenging, and protection against
inflammation (114,442,464,602). Mercury inhibits sulfur ligands in MT and in
the case of intestinal cell membranes inactivates MT that normally bind cuprous
ions(477,114), thus allowing buildup of copper to toxic
levels in many and malfunction of the Zn/Cu SOD function (495,13a, 443).
Mercury also causes displacement of zinc in MT and SOD, which has been shown to
be a factor in neurotoxicity and neuronal diseases(405,495,517).
Exposure to mercury results in changes in metalloprotein compounds that have
genetic effects, having both structural and catalytic effects on gene expression(114,241,296,442,464,477,495,517). 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,
342,369, 442,464). Of a population of over 3000 tested by the immune lymphocyte
reactivity test(MELISA,60,342), 22% tested positive
for inorganic mercury and 8% for methyl mercury, but much higher percentages tested
positive among autoimmune condition patients. In the MELISA laboratory, 12 out
of 13 ALS patients tested showed positive immune reactivity lymphocyte
responses to metals in vitro [60c], 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 condition.
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 reduced 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).
The Veterans Administration concluded that higher levels of veterans of Gulf
War I than normal contracted ALS (580). These veterans were subjected to large
exposures of toxic metals in vaccines and other toxic exposures and there is
evidence that aluminum hydroxide in vaccines can cause symptoms seen in ALS(582).
Programmed
cell death(apoptosis) is documented to be a major factor in degenerative
neurological conditions like ALS, Alzheimer’s, MS, 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,491,495), 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(490,491,496,593), excess free cysteine
levels (56d,111a,30,330),excess glutamate toxicity( 416,593,13b), excess dopamine
toxicity (56d,13a), beta-amyloid generation(462,56a), increased calcium influx
toxicity (296b,333,416,432,462c,507) and DNA fragmentation(296,41,114,142) and
mitochondrial membrane dysfunction (56de, 416).
Chronic neurological
conditions such as ALS appear to be primarily caused by chronic or acute brain
inflammation. The brain is very sensitive to inflammation. Disturbances in
metabolic networks: e.g., immuno-inflammatory processes, insulin-glucose
homeostasis, adipokine synthesis and secretion, intra-cellular signaling cascades,
and mitochondrial respiration have been shown to be major factors in chronic
neurological conditions (592,593,598,580, etc.). Inflammatory chemicals such as
mercury, aluminum, and other toxic metals as well as other excitotoxins
including MSG and aspartame cause high levels of free radicals, lipid
peroxidation, inflammatory cytokines, and oxidative stress in the brain and
cardiovascular systems (13,491,582,593,595-598)
In
amyotrophic lateral sclerosis (ALS) non-neuronal cells play key roles in
disease etiology and loss of motoneurons via noncell-autonomous mechanisms.
Reactive astrogliosis and dysfunctional transporters for L-glutamate are common
hallmarks of ALS pathology(416d). Oxidative and excitotoxic insults exert
differential effects on spinal motoneurons and astrocytic glutamate
transporters in the progression of ALS. Excitotoxicity in ALS affects both
motor neurons and astrocytes, favouring their local interactive degeneration(593). 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).
Mercury and increased glutamate in the plasma activate free radical forming
processes like xanthine oxidase which produce oxygen radicals and oxidative neurological
damage(142,416,13). 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). A
recent study has linked some cases of sporadic ALS with the failure to edit key
residues in ionotropic glutamate receptors, resulting in excessive influx of
calcium ions into motor neurones which in turn triggers cell death. The study
suggests that edited AMPA glutamate (GluR2) receptor subunits serve as
gatekeepers for motor neurone survival. (525)
These inflammatory processes damage cell structures including DNA,
mitochondria, and cell membranes. They also activate microglia cells in the
brain, which control brain inflammation and immunity. Once activated, the
microglia secrete large amounts of neurotoxic substances such as glutamate, an
excitotoxin, which adds to inflammation and stimulates the area of the brain
associated with anxiety(593,598). Inflammation also
disrupts brain neurotransmitters resulting in reduced levels of serotonin,
dopamine, and norepinephrine. Some of the main causes of such disturbances that
have been documented include vaccines, mercury, aluminum, other toxic metals,
MSG, aspartame, etc. (582,593,598,600,etc.) High
levels of aluminum exposure along with low levels of other minerals such as
calcium and magnesium have been documented to cause neurological degeneration
and appear to be the cause of high ALS and Parkinson’s in the past in Guam
(518). There is evidence that aluminum hydroxide in vaccines can cause symptoms
such as those seen in ALS(582). Aluminum has been
found to be a factor in some Alzheimer’s and Parkinson’s cases.
Programmed
cell death (apoptosis) is documented to be a major factor in degenerative
neurological conditions like ALS, Alzheimer’s, MS, Parkinson’s, etc. Some of
the factors documented to be involved in apoptosis of neurons and immune cells
include mitochondrial membrane dysfunction (56bc, 416). Mitochondrial DNA
mutations or dysfunction is fairly common, found in at least 1 in every 200 people(275), and toxicity effects affect this population
more than those with less susceptibility to mitochondrial
dysfunction. Mercury depletion of GSH and damage to cellular
mitochrondria and the increased lipid peroxidation in protein and DNA oxidation
in the brain appear to be a major factor in conditions such as ALS, Parkinson’s
disease, autism, etc. (30,56,416,442).
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 (43,196,338,580,597). Reduced
levels of magnesium and zinc are related to metabolic syndrome, insulin
resistance, and brain inflammation and are protective against these conditions(595,43).
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). glutathione 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 mechanisms 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 (41,114,142,197,296,
392); alteration of protein structure (30,111,114,194,252,442); alteration of
the transport and signaling functions of calcium (333,43b,254,416d,462 ,507);
inhibitation of glucose transport(338,254,580), and of enzyme function and
transport of other essential nutrients (96,198,254,263,264,33,330,331, 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(119,416), 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);
inhibits functional methylation(504), inducement of inflammatory
cytokines(126,152,181) and autoimmunity(226,272,369,405,etc.)
Exposure to mercury vapor
and methyl mercury is well documented to commonly cause conditions involving
tremor, with populations exposed to mercury experiencing tremor levels on
average proportional to exposure level (250,565). However
bacteria, yeasts, and Vitamin B12 methylate inorganic mercury to methyl mercury
in the mouth and intestines (599,505) and mercury inhibits functional
methylation in the body, a necessary process (504).
Mercury
exposure causes high levels of oxidative stress/ reactive oxygen species(ROS)(13,491), which has been found to be a major
factor in apoptosis and neurological disease (56,250,441,442,443,13) including
dopamine or glutamate related apoptosis(288c).
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
conjugates are found to be highest in the brain substantia nigra with similar
conjugates formed with L-Dopa and dopamine in Parkinson’s disease(56).
Mercury depletion of GSH and damage to cellular mitochondria and the increased
lipid peroxidation in protein and DNA oxidation in the brain appear to be a
major factor in Parkinson’s disease(33,56,442)
and a factor in other neurological conditions.
Mercury blocks the immune
function of magnesium and zinc (198,427,38), whose deficiencies are known to
cause significant neurological effects(461,463,430,601).
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 (477,489,495,463,464). 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(580). Exposures to
toxic metals such as mercury and cadmium have been found to cause such
effects(13a,495,517,etc.) 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 (489,490,495,464,469,111). This
condition can result in zinc deficient SOD and oxidative damage involving
nitric oxide, peroxynitrite, and lipid peroxidation(490,491,495,496,489,521,524),
which have been found to affect glutamate mediated excitability and apoptosis
of nerve cells and effects on mitochondria (119c,412,416,495,496, 502,519,524).
These effects can be reduced by zinc supplementation
(464,495,517,430), 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-acetyl cysteine,melatonin, etc.(444,449,464,494,495,469,
470,521,524,572). In a study involving over 1 million participants, a 23
percent reduction in the risk of the disease was found among those who used
vitamin E supplements for two to four years and a 36 percent reduction
occurred among those who used the supplements for five years or more compared
to those who did not supplement with the vitamin. For those whose
vitamin E from diet was among the top 25 percent of participants, a 21 percent
lower adjusted risk of ALS was noted(449a). This effect increased with greater
dietary vitamin E intake among women, with those in the top 25 percent having a
43 percent lower risk than that experienced by those whose intake was
lowest. Vitamin E has attracted significant attention from ALS
researchers as a result of its antioxidant properties. Vitamin E protects cell
membranes against a process known as lipid peroxidation (Cameron A et al,
2002). Lipid peroxidation is the breakdown of the cell membrane,
and appears to play a role in degenerative diseases such as ALS. Another
study in humans indicated that vitamin E can help prevent ALS because of its
antioxidant properties (449b).
Ceruloplasmin in plasma can
be similarly affected by copper metabolism dysfunction, like SOD function, and
is often a factor in neurodegeneration(489).
Motor neuron
dysfunction and loss in amyotrophic lateral sclerosis (ALS) have been
attributed to several different mechanisms, including increased intracellular
calcium (333,496,507), glutamate dysregulation and excitotoxicity(119c,412,416,491,496,502),
oxidative stress and free radical damage(13,43,56,442,491), nitric oxide
related toxicity caused by peroxynitrite(524,521), mitochondrial
damage/dysfunction(519), neurofilament aggregation and dysfunction of transport
mechanisms(507), and autoimmunity(313,314,369,405,513). These alterations and
effects are not mutually exclusive but rather are synergistic, and increased
calcium and altered calcium homeostasis appears to be a common denominator. Mercury
forms strong bonds with the-SH groups of proteins causing alteration of the
transport of calcium (333,43,96,254,329,432,496) and causes mitochondrial
release of calcium (21,35,43,329,333,432,496,519). This results in a rapid and
sustained elevation in intracellular levels of calcium (333,496). 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 micro molar levels, as well as
inhibiting phorbal ester binding(43,432). They also
block or inhibit calcium L-channel currents in the brain in an irreversible and
concentration dependent manner. Mercury vapor or inorganic mercury exposure
affects the posterior cingulate cortex and causes major neurological effects
with sufficient exposure (428,453). Metallic mercury is much more potent than
methyl mercury in such actions, with 50 % inhibition in animal studies at 13 ppb(333,329). Mercury is seen to be a factor in all of these
known mechanisms of neural degeneration seen n ALS and other motor neuron conditions.
Spatial and temporal
changes in intracellular calcium concentrations are critical for controlling
gene expression and neurotransmitter release in neurons(432,496,43,114).
Mercury alters calcium homeostasis and calcium levels 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 impulse transfer(288,270,56,43,35). Mercury also
interrupts the cytochrome oxidase system, blocking the ATP energy function
(35,43,84), lowering immune growth factor IGF-I levels and impairing astrocyte function(119,152,416d,497). Astrocytes are common cells in
the CNS involved in the feeding and detox of nerve cells. Increases in
inflammatory cytokines such as caused by toxic metals trigger increased free
radical activity and damage to astrocyte and astrocyte function(152,416d).
IGF-I protects against brain and neuronal pathologies like ALS, MS, and
Fibromyalgia by protecting the astrocytes from this destructive process.
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 ALS cases there was a reduction in
serum magnesium and RBC membrane Na(+)-K+ ATPase
activity and an elevation in plasma serum digoxin(263,260d). The activity of
all serum free-radical scavenging enzymes, concentration of glutathione, alpha
tocopherol, iron binding capacity, and ceruloplasmin decreased significantly in
ALS, 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 ALS
(13a,111,288,442,521b,43,56,263etc.)
Mercury
exposure also degrades the immune system resulting in more susceptibility to
viral, bacterial, or parasitic effects along with candida albicans which are
often present in those with chronic conditions and require treatment
(404,468,470,485,600). Four such commonly found in ALS patients are mycoplasma
AND echo-7 enterovirus(468,470), candida albicans
(404), and parasites(485). One clinic found that over 85% of patients with ALS
tested have mycoplasma infection, often M. Pneumoniae(470),
but in Gulf War veterans mostly a manmade variety used in bioterrorism agents-
M. fermentans. Mercury from amalgam interferes with production of cytokines
that activate macrophage and neutrophils, disabling early control of viruses or
other pathogens and leading to enhanced infection(131).
While the others are also being commonly found, mycoplasma has been found in
85% of ALS patients by clinics treating such conditions(470).
Mycoplasma appears to be a cofactor with mercury in the majority of cases and
shifts the immune T cell balance toward inflammatory cytokines(470b). Treatment
of these chronic infections are required and documented to cause improvement in
such patients(470).
Mercury lymphocyte
reactivity and effects on amino acids such as glutamate in the CNS induce CFS
type symptoms including profound tiredness, musculoskeletal pain, sleep
disturbances, gastrointestinal and neurological problems along with other CFS symptoms
and Fibromyalgia (346,342,369,416,496,513,119b,152,314).
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(342). ALS patients have been found to have a
generalized deficiency in metabolism of the neuroexcitotoxic amino acids like
glutamate, aspartate, NAAG, etc.(416).
The brain has elaborate protective mechanisms for regulating
neurotransmitters such as glutamate, which is the most abundant of all
neurotransmitters. When these protective regulatory mechanisms are damaged or
affected, chronic neurological conditions such as ALS can result
(593). Glutamate is the most abundant amino acid in the body and in the
CNS acts as excitory neurotransmitter (346,412,416,438,496,119c), 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, then a buildup
of glutamate and calcium occurs, causing swelling and neurotoxic effects
(119,152,333,416,496, 524). Mercury and other toxic metals inhibit astrocyte
function in the brain and CNS (119,152,416), 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(346,416,496,524,600). 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 radicals forming processes like xanthine
oxidase which produce oxygen radicals and oxidative neurological damage(346,142,13). 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).
In addition to the
documentation showing the mechanisms by which mercury causes the conditions and
symptoms seen in ALS and other neurodegenerative diseases, many studies of
patients with major neurological or degenerative diseases have found direct
evidence mercury and amalgam fillings play a major role in development of
conditions such as such as ALS
(92,97,207,229b,305,325,327,416,423,442,468,470,520,35). Such supplements
including N-acetylcysteine(NAC), Vitamins E and C,
zinc, and creatinine have been found to offer significant protection against
cell apoptosis and neurodegeneration in neurological conditions such as
ALS(13c,56a,517,524,564,494).
Medical studies and doctors
treating chronic conditions like 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). A study
demonstrated protective effects of methylcobalamin, a vitamin B12 analog,
against glutamate-induced neurotoxicity(503), and
similarly for iron in those who are iron deficient .
In a study of the brains of
persons dying of ALS, spherical and crescent-shaped introneuronal inclusions(SCI) were distributed in association with each
other among the parahippocampal gyrus, dentate gyrus of the hippocampus and amygdala,
but not any non-motor-associated brain regions(522). The occurrence of SCI in
both the second and third layers of the parahippocampal gyrus and amygdala was
significantly correlated to the presence of dementia in ALS cases. Mercury has
been found to accumulate in these areas of the brain and to cause adverse
behavioral effects in animal studies and humans(66,287,305).
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 susceptibility to
toxic effects. Prenatal mercury vapor exposure 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(600). There is also evidence that fetal or infant
exposure causes delayed neurotoxicity evidenced in serious effect at middle age(255). 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 neurons 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 patients 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 supplementing both thyrotropin-releasing hormone
and growth control hormone is more effective at increasing all of these hormone
levels in the patient(499).
Extremely toxic anaerobic
bacteria from root canals 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(35,200, 437, 600). Cavitations have been
found in 80% of sites from wisdom tooth extractions tested and 50% of molar
extraction sites tested(35,200,437). The incidence is
likely somewhat less in the general population. 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 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).
As seen
here, mercury is a well-documented
neurotoxin implicated in a wide range of neurological or psychiatric disorders
including autism spectrum disorders, Alzheimer's disease, Parkinson's disease,
epilepsy, depression, mood disorders and tremor (281, etc.).
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(30). 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 (333,194,56,33b). 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(84,33b). Patients with
some of these conditions have found that bathing in Epsom Salts (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 amelioration 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 dimustase
(SOD) processes appear to be a major factor in cell apoptosis involved in the
condition (443,495). Mercury is known to damage or inhibit SOD activity (13,33,111)
and a common mutated form of the SOD1 gene results in low levels of glutathione
protection and greatly increased mercury toxicity(118).
IV. Prevention and
Treatment of ALS
Tick-borne encephalitis,
such as Lyme Disease, has been found to cause ALS symptoms in a significant
portion of untreated acute cases(471). Lyme disease is
widespread in the U.S. Large numbers of patients diagnosed with ALS and other
neurological conditions have been found to have treatable tick-borne
encephalitis, and many have recovered after treatment. Anyone diagnosed with
degenerative neurological symptoms should investigate the possibility of lyme
disease or post-polio encephalitis. Spirochete infection was found in
about 90% of ALS patients and not in most healthy people (52), with a strong
statistical relation to ALS. Early intervention against infection may prevent
or delay ALS development (52).
Since
elevated plasma cysteine has been reported in some ALS patients, sulfite and
cysteine toxicity may be involved in other cases of ALS. Patients with ALS with
nonmutant-SOD should be tested for sulfite toxicity, cysteine, glutamate and
GSH levels, and whether they have low levels of GSH metabolism enzymes. During
the time when strict dietary and supplement measures normalized a patient's
whole blood GSH, blood cysteine, and urine sulfite, the patient did not
experience additional physical decline (330b).
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 (35,200,293,437). Root canals and cavitations have been found to
harbor anaerobic 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 (437,200,35), 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 Fibromyalgia
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), SAMe, L-carnitine, choline,
ginseng, Ginkgo biloba, vitamins C and E, nicotine, and omega 3 fatty acids(fish and flaxseed oil)(417,444,468,580).
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
(97,229,405,406,437,468-470,485,575,35).The Edelson Clinic in Atlanta which
treats ALS patients reports similar experience(406), and the Perlmutter Clinic
has also had some success with treatment of ALS and other degenerative
neurological conditions(469). A 49-year-old male
patient suffering from muscle weakness and fasciculations, progressive muscular
atrophy, a variant of ALS, was diagnosed after extensive examinations ruling
out other diseases. Due to supposed mercury exposure from residual amalgam, the patient's teeth were restored (575) The patient received sodium 2,3-dimercaptopropanesulfate
(DMPS; overall 86 × 250 mg in 3 years) in combination with α-lipoic acid and
followed by selenium. In addition, he took vitamins and micronutrients and kept
a vegetarian diet. The excretion of metals was monitored in the urine. The
success of the therapy was followed by scoring muscle weakness and
fasciculations and finally by electromyography (EMG) of the affected muscles.
First improvements occurred after the dental restorations. Two months after
starting therapy with DMPS, the mercury level in the urine was increased (248.4 µg/g creatinine). After
1.5 years, EMG confirmed the absence of typical signs of ALS. In the course of
3 years, the patient recovered completely(575).
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(600,601); 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(600). 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-acetyl cysteine(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(572d) and copper. Lipoic acid has a protective effect regarding lead or
inorganic mercury toxicity through its antioxidant properties (572), but should not be used with high copper until copper
levels are reduced. LA and NAC (N-acetyl cysteine) also increase glutathione
levels and protect against superoxide radical/ peroxynitrite damage, so thus
have an additional neuroprotective effect(494ab,521,572c,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).
Antioxidants
such as carnosine(495a), Coenzyme Q10, Vitamins B& C & E & D,
gingko biloba, superoxide dismutase (SOD), N-acetyl-cysteine (NAC), Alpha
Lipoic Acid, and pycnogenol have also been found protective against degenerative
neurological conditions(494,495e, 444,449,580). Other
supplements found to be protective against neuronal degenerative conditions
include Acetyl-L-Carnitine, EFAs (DHA/EPA), DHEA,
CoQ10, magnesium, Vit B1 & B5, hydergine, and octacosanol
(580). Such supplements only offer limited protection and reductions in
progression of ALS without other measures that deal with underlying mechanisms
of causality. In a study involving over 1 million participants, a 23
percent reduction in the risk of the disease was found among those who used
vitamin E supplements for two to four years and a 36 percent reduction
occurred among those who used the supplements for five years or more compared
to those who did not supplement with the vitamin (449).
Other
supplements that appear useful in conditions involving neurotoxicity or muscle
function degeneration include creatine (502,580)and
lithium(590). In the motor cortex of the ALS group the N-acetylaspartate
(NAA)/creatine (Cr(t)) metabolite ratio was lower than in our control group,
indicating NAA loss. Upon creatine supplementation we observed in the that
creatine supplementation causes an increase in the diminished NAA levels in ALS
motor cortex as well as an increase of choline levels in both ALS and control
motor cortices. This indicates an improvement in function of the pathological
ALS skeletal muscles related to changes of mitochondrial respiratory chain
which appears to affect motor neuron survival. In another study by the NAS,
lithium carbonate at 150 mg twice daily significantly reduced the degeneration
of ALS patients (590). A recent study demonstrated that combined
treatment with lithium and valproic acid elicits synergistic neuroprotective
effects against glutamate excitotoxicity in cultured brain neurons. Combined lithium and valproate treatment delays disease onset,
reduces neurological deficits and prolongs survival in an amyotrophic lateral
sclerosis mouse model (590c). Methylcobalamin and SAMe have also been found to
provide some protection against neurotoxicity (580).
Lithium has
been found to be brain protective in ALZ and reduces some of the factors in neurological
conditions (52,108,280,590). Lithium oratate; Enbrel (TNF-a blocker) was found
to be beneficial in some and is undergoing clinical trials (52). Comparison of ALZ patients to healthy
controls found lower levels of G-CSF (growth factor) in ALZ patients (52). Injections
of G-CSF in trials helped some and is being further studied. Brain-derived neurotrophic factor (BDNF)
injections in rodents showed promise and is in clinical trials); Tumeric Forte
with Coconut oil/MCT Oil(40); Piracetam(levetiracetam)
has been found to be beneficial in cognitive decline of older individuals (52). Nutritional Support (52): Vit
B12(methylcobalamin), zinc, Ginseng, Ginkgo Biloba, OQ10, Acetyl-L-Carnitine,
Lipoic Acid, Protein and Fish Oil, Creatine, NAC, Green Tea (EGCG), Pycogenol; HBOT
or ozone therapy or hydrogen peroxide IV (58)
Electromagnetic
Fields (EMF) & Wi-fi(117) & www.myflcv.com/EMFeff.html; & www.myflcv.com/wifiSMhe.html)
Many of the factors/causes of ALS are similar
to Alzheimer’s (108,99,33). See the causes/treatments in Alzheimer’s section of
www.myflcv.com/conditins.html, especially the ones referencing 99 or 108 and
The ICT Protocol, which also can be used in ALS.
Two experimental
treatment for ALS that has shown some effectiveness at reducing disease
progression is recombinant human insulin-like growth factor and Orap (Pimozide)
(580).
References
(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; & (d) The role for oxidative stress in neurodegenerative diseases, [Article in
Japanese], Shibata N, Kobayashi M. Brain Nerve. 2008
Feb;60(2):157-70
(18) Kuriane N, et al; The effect of different
workplace nanoparticles on the immune systems of employees. J Nanopart Res. 2017;19(9):320; & (b) Environmental pollutants as risk factors
for neurodegenerative disorders: Alzheimer and Parkinson diseases.Chin-Chan M et al; Front
Cell Neurosci. 2015
Apr 10;9:124; & (c) Neurotoxicity of Metal Mixtures. Andrade et al; Adv Neurobiol. 2017;18:227-265.
(20)
(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
(21) R.A.Goyer,”Toxic
effects of metals”in: Caserett and Doull’s Toxicology-
TheBasic Science of Poisons, McGraw-Hill Inc., N.Y., 1993; & Goodman,
Gillman, The Pharmacological Basis of Therapeutics, Mac Millan Publishing Company,
N.Y. 1985.
(30) (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)S.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.
(33) B. Windham, DAMS, Mercury or metals exposure and health
effects, www.myflcv.com & Dental Amalgam
Mercury Page, www.myflcv.com/dams.html
(over 5000 peer-reviewed studies cited)
(34) 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)
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,
ALS http://www.hugginsappliedhealing.com/als.php
(40) Dr. Bruce
West, Doctor’s A-Z Phytoceutical Guide; & Health Alert, 2017-2018, http://www.healthalert.com/Articles.aspx
& Health Alert Store, http://www.healthalertstore.com/Default.asp;
&(c) )National
Health and Nutrition Examination Survey, 2015 (26,000 adults)
(42) Dr. Frank Shallenberger, Second Opinion, Journal
of Natural Health, 2016-2018, https://www.secondopinionnewsletter.com/Home.htm
& Advanced Bionutritionals
(41)
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/envmed/TOX/faculty/mccabe.html; & Buzard
GS, Kasprzak KS. Possible roles of nitric oxide and redox cell signaling in
metal-induced toxicity and carcinogenesis: a review. Environ Pathol
Toxicol Oncol. 2000;19(3):179-99
(48) K.Arvidson,”Corrosion studies of dental gold alloy in
contact with amalgam”, Swed. Dent. J 68: 135-139,1984; & Skinner, EW, The
Science of Dental Materials, 4th Ed.revised,
W.B.Saunders Co., Philadelphia, p284-285,1957.
(49)
Kingman A, Albertini T, Brown LJ. National Institute of Dental Research,
“Mercury concentrations in urine and blood associated with amalgam exposure in
the U.S. military population”, J Dent Res.
1998 Mar;77(3):461-71.
(52) Life
Extension, Disease Prevention and Treatment, Fifth Edition, 2013.
(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, Johns Hopkins Univ., J Neurosci, 1994, 14(7):
4385-92;
(56)(a)
A.Nicole et al, “Direct evidence for glutathione as mediator of apoptosis in
neuronal cells”, Biomed Pharmacother, 1998; 52(9):349-55; & J.P.Spencer et
al, “Cysteine & GSH in PD”, mechanisms involving ROS”, J Neurochem, 1998,
71(5):2112-22: & & J.S. Bains et al, “Neurodegenerative disorders in
humans and role of glutathione in oxidative stress mediated neuronal death”,
Brain Res Rev, 1997, 25(3):335-58;&
Medina S, Martinez M,
Hernanz A, Antioxidants inhibit the human cortical neuron apoptosis induced by
hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid
peptide 1-42.. Free Radic Res. 2002
Nov;36(11):1179-84. &(b) Pocernich CB, et al. 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; & D. Offen et al, “Use of thiols
in treatment of PD”, Exp Neurol, 1996,141(1):32-9; & (c) Pearce RK, Owen A,
Daniel S, Jenner P, Marsden CD. Alterations in the distribution of
glutathione in the substantia nigra in Parkinson's disease. J Neural
Transm. 1997;104(6-7):661-77; & A.D.Owen et al, Ann NY Acad Sci, 1996,
786:217-33; & JJ Heales et al, Neurochem Res, 1996, 21(1):35-39; &
& X.M.Shen et al, Neurobehavioral 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; & (d) Li H, Shen XM, Dryhurst G.
Brain mitochondria catalyze the oxidation of
7-(2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1,4-benzothiazine-3-carboxyli c acid
(DHBT-1) to intermediates that irreversibly inhibit complex I and scavenge
glutathione: potential relevance to the pathogenesis of Parkinson's disease. J
Neurochem. 1998 Nov;71(5):2049-62; & (e) Araragi S, Sato M. et
al, Mercuric chloride induces apoptosis via a mitochondrial-dependent pathway
in human leukemia cells. Toxicology. 2003 Feb 14;184(1):1-9.
(58) (a) Hydrogen Peroxide: Medical Miricle, Dr.
W.C. Douglas, 1995; & (b) The One Minute Cure, Madison Cavanaugh, 2008;
&(c ) True Power of Hydrogen Peroxide, Mary Wright, & (d)
Anti-Inflammatory Oxygen Therapy, Dr. Mark Sircus, 2015, https://drsircus.com/general/anti-inflammatory-oxygen-therapy/; &(e)
Dr. David Williams, The Many Benefits of Hydrogen Peroxide, http://www.educate-yourself.org/cancer/benefitsofhydrogenperozide17jul03.shtml; &
(f)
(60) V.D.M.Stejskal,
Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden LYMPHOCYTE
IMMUNO STIMULATION ASSAY MELISA”
& 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. VDM Stejskal et al, "MELISA: tool for the study of
metal allergy", Toxicology in Vitro, 8(5):991-1000, 1994;
& Metal-specific lymphocytes: biomarkers of sensitivity in
man.Stejskal VD, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A, Mayer
W, Bieger W, Lindh U.Neuroendocrinology Letters 1998 www.melisa.org
(79) L.Bjorkman et al, "Mercury in Saliva and Feces after
Removal of Amalgam Fillings", Toxicology and Applied Pharmacology, 1997,
144(1), p156-62
(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).
(85)
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; & M.Nylander et al, "Mercury
concentrations in the human brain and kidneys and exposure from amalgam
fillings", Swed Dent J 1987; 11:179-187; & D.W.Eggleston et al,
Correlation of dental amalgam with mercury in brain tissue. J Prosthet Dent,
1987,58(6),704-7.
(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; & Carpenter DO. Effects
of metals on the nervous system of humans and animals. Int J Occup Med Environ
Health 2001;14(3):209-18.
(93) Vaccari
A, Ruiu S, Mocci I, Saba P,Bernard B. Brodie. Selected
pyrethroid insecticides stimulate glutamate uptake in brain synaptic vesicles.
Neuroreport 1998 Oct 26;9(15):3519 23; Gassner B, Wuthrich A, Scholtysik
G, Solioz M; The pyrethroids permethrin and cyhalothrin are potent inhibitors
of the mitochondrial complex I. J Pharmacol Exp Ther 1997
May;281(2):855 60; Narahashi T. Nerve membrane Na+ channels as targets of
insecticides. Trends Pharmacol Sci 1992 Jun;13(6):236 41; Zhao X, Dai S, Chen
G. Inhibition of glutamate uptake in rat brain synaptosome by pyrethroids.
Chung Hua Yu Fang I Hsueh Tsa Chih 1995 Mar;29(2):89 91; Eldefrawi AT,
Eldefrawi ME. Receptors for gamma aminobutyric acid and
voltage dependent chloride channels as targets for drugs and toxicants.
FASEB J 1987 Oct;1(4):262 71; D. Zuccari Bissacot and I. Vassilieff. HPLC
Determination of Flumethrin, Deltamethrin, Cypermethrin, and Cyhalothrin
Residues in the Milk and Blood or Lactating Dairy Cows. Journal of Analytical
Toxicology, Volume 21, Number 5, September 1997, pp. 397 –402.; Gassner B,
Wuthrich A, Lis J, Scholtysik G, Solioz M. Topical application of synthetic
pyrethroids to cattle as a source of persistent environmental contamination.J
Environ Sci Health B 1997 Sep;32(5):729 39; Patient Information
Network,Exposure Survey of patients with ALS,
http://members.aol.com/alspinpoint/results.html; & & McGuire,
Longstreth et al, Occupational exposures and amyotrophic lateral
sclerosis; Am J Epidemiol 1997 Jun 15;145(12):1076-88 & Baker,
1996.
(94)(a) Kamel
F, Umbach DM, Hu H, Sandler DP; Lead Exposure and Amyotrophic Lateral
Sclerosis. Epidemiology 2002 May;13(3):311-319; & (b)Conradi S, Ronnevi LO,
Vesterberg O. Abnormal tissue distribution of lead in amyotrophic lateral
sclerosis. J Neurol Sci 1976 Oct;29(2-4):259-65; & (c)Epidemiologic
correlates of sporadic amyotrophic lateral sclerosis, Armon C, Kurland
LT, Daube JR, O'Brien PC. Neurology. 1991 Jul;41(7):1077-84, &
(d) Association between blood lead and the
risk of amyotrophic lateral sclerosis. Fang F, Kwee LC, Allen KD, et al; Am J
Epidemiol. 2010 May 15;171(10):1126-33
(95)(a) Smoking and risk of amyotrophic lateral
sclerosis: a pooled analysis of 5 prospective cohorts. Wang H, O'Reilly EJ,
Ascherio A, et al, Arch Neurol. 2011 Feb;68(2):207-13. (b) McGuire V,
Longstreth WT Jr, van Belle G. Occupational exposures and amyotrophic lateral
sclerosis. A population-based case-control study. Am J Epidemiol 1997 Jun
15;145(12):1076-88.; & (c)Nelson LM, McGuire V, Longstreth WT Jr,
Matkin C. Population-based case-control study of amyotrophic lateral sclerosis
in western Washington State. I. Cigarette smoking and alcohol consumption. Am J
Epidemiol 2000 Jan 15;151(2):156-63 ; & (d)
An evidence-based medicine approach to the evaluation of the role of exogenous
risk factors in sporadic amyotrophic lateral sclerosis, Armon
C. Neuroepidemiology. 2003 Jul-Aug;22(4):217-28; & (e) Exposure
to chemicals and metals and risk of amyotrophic lateral sclerosis: a systematic
review. Sutedja NA, Veldink JH, Fischer K, et al, Amyotrophic Lateral
Scler. 2009 Oct-Dec;10(5-6):302-9, & (f) Prospective study of chemical
exposures and amyotrophic lateral sclerosis. Weisskopf MG, Morozova N, et
al, J Neurol Neurosurg Psychiatry. 2009 May;80(5):558-61; & (g)Environmental-induced
oxidative stress in neurodegenerative disorders and aging. Migliore L, Coppedè F. Mutat Res. 2009 Mar
31;674(1-2):73-84. Epub 2008 Oct 5.
(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; & (b) 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 and from asthma after removal of dental amalgam
fillings", Int J Risk & Safety in Med 1994; 4:229-236,
& Adams CR, Ziegler DK, Lin JT., “Mercury intoxication simulating
ALS”, JAMA, 1983, 250(5):642-5; & ALS and mercury intoxication: A
relationship?
References and further reading may be available for this article. To view
references and further reading you must purchase this article.
Julien Praline et
al, Clin Neurol Neurosurg. 2007 Dec;109(10):880-3. Epub 2007 Aug 23
(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.
99. Dr. Richard Gerhauser, Natural Health Response , https://naturalhealthresponse.com/author/rgerhauser/ & (b) Secrets
of Underground Medicine, 2018; &(c) Dr. Woodrow Montes, A.S.U., While
Science Sleeps, a Sweetener Kills,
108. (a) The Complete Guide
to Reversing Alzheimer’s, Dr, Glen Rothfeld, & (b) 81 Natural Cures for Cancer,
Alzheimer’s, Diabetes, etc. Dr.
Rothfeld, & (c) Dr. Rothfelds Health Secrets for Men, & (d) The End of
Alzheimer’s: A Program to Prevent and Reverse Cognitive Decline; Dr. Dale Bredesen(UCLA), Aug 2017
(111) (a)
Quig D, Doctors Data Lab,"Cysteine metabolism and metal toxicity",
Altern Med Rev, 1998;3:4, p262 270, & (b) J.de Ceaurriz et al, Role of
gamma glutamyltraspeptidase(GGC) and extracellular glutathione in
dissipation 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; & Zalups RK, Barfuss
DW. Accumulation and handling of inorganic mercury in the kidney after
coadministration with glutathione, J Toxicol Environ Health, 1995, 44(4):
385-99; & T.W.Clarkson et al, "Billiary
secretion of glutathione metal complexes", Fundam Appl Toxicol, 1985,
5(5):816 31;
(112)
Copper-2 Ingestion, Plus Increased Meat Eating Leading to Increased Copper
Absorption, Are Major Factors Behind the Current Epidemic of Alzheimer's
Disease. Brewer GJ; Nutrients. 2015 Dec 2;7(12):10053-64; & (b) Copper-2
Hypothesis for Causation of the Current Alzheimer's Disease Epidemic Together
with Dietary Changes That Enhance the Epidemic. Brewer G J et al; Chem Res
Toxicol. 2017 Mar
20;30(3):763-768.
(113) Alzheimer disease: mercury as
pathogenetic factor and apolipoprotein E as a moderator. Neuro
Endocrinol Lett. 2004 Oct;25(5):331-9. Mutter
J, Walach H, et al;
(114) (a)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; & Baauweegers HG, Troost D.
Localization of metallothionein in the mammilian central nervous system.. Biol Signals 1994, 3:181-7. &(b) T.V.
O’Halloran, “Transition metals in control Of gene
expression”, Science, 1993, 261(5122):715-25; &(c) 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.;
(118) J Stejskal, V Stejskal. The role of metals in autoimmune diseases
and the link to neuroendocrinology Neuroendocrinology Letters, 20:345 358,
1999. http://www.melisa.org; http://www.melisa.org & (a) Analysis of SOD1 mutations in a Chinese
population with amyotrophic lateral sclerosis: a case-control study and
literature review. Wei Q et al; Sci Rep. 2017 Mar 14;7; & (b) Longitudinal assessment of metal concentrations
and copper isotope ratios in the G93A SOD1 mouse model of amyotrophic lateral
sclerosis. Enge TG et al; Metallomics. 2017 Feb
22;9(2):161-174; & (c) Resveratrol treatment reduces the vulnerability of
SH-SY5Y cells and cortical neurons overexpressing SOD1-G93A
to Thimerosal toxicity through SIRT1/DREAM/PDYN pathway. Laudati G et al; Neurotoxicology. 2018 Nov 29;71:6-15; & (d) Increased Zn/Glutathione Levels and Higher
Superoxide Dismutase-1 Activity as Biomarkers of Oxidative Stress in Women with
Long-Term Dental Amalgam Fillings: Correlation between Mercury/Aluminium
Levels (in Hair) and Antioxidant Systems in Plasma. Cabana-Munoz ME et al; PLoS One. 2015 Jun 15;10(6); & (e) Epigenetic Factors in Late-Onset Alzheimer's Disease: MTHFR and CTH Gene
Polymorphisms, Metabolic Transsulfuration and Methylation Pathways, and B
Vitamins. Roman GC et al; Int
J Mol Sci. 2019 Jan 14;20(2).
(119)(a) 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; &(b) Kim P, Choi BH. “Selective
inhibition of glutamate uptake by mercury in cultured mouse astrocytes”, Yonsei
Med J 1995; 36(3): 299-305; &(b) Brookes N. In vitro evidence for the role
of glutatmate in the CNS toxicity of mercury. Toxicology 1992, 76(3):245-56;
& (c)Albrecht J, Matyja E. Glutamate: a potential mediator of inorganic
mercury toxicity. Metab Brain Dis 1996; 11:175-84; & (d) Heavy
metals modulate glutamatergic system in human platelets; & (e)
Borges VC, Santos FW, Rocha
JB, Nogueira CW. Neurochem Res. 2007 Jun;32(6):953-8; &
(f) Exploration of the direct metabolic effects of mercury II chloride on
the kidney of Sprague-Dawley rats using high-resolution magic angle spinning 1H
NMR spectroscopy of intact tissue and pattern recognition; Wang
Y, Bollard ME, Nicholson JK, Holmes E. J Pharm Biomed
Anal. 2006 Feb 13;40(2):375-81; & Mercury compounds disrupt neuronal
glutamate transport in cultured mouse cerebellar granule cells; Fonfría
E, Vilaró MT, Babot Z, Rodríguez-Farré E, Suñol C. J
Neurosci Res. 2005 Feb 15;79(4):545-53
(126)(a) Singh I, Pahan K, Khan M, Singh AK.
Cytokine-mediated induction of ceramide production is redox-sensitive.
Implications to proinflammatory cytokine-mediated apoptosis in demyelinating
diseases. J Biol Chem. 1998 Aug 7;273(32):20354-62; & Pahan K, Raymond JR,
Singh I. Inhibition of phosphatidylinositol 3-kinase induces nitric-oxide
synthase in lipopolysaccharide- or cytokine-stimulated C6 glial cells. J. Biol.
Chem. 274: 7528-7536, 1999; & Xu J, Yeh CH, et al, Involvement of de novo
ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced
cerebral endothelial cell death. J Biol Chem. 1998 Jun 26;273(26):16521-6;
& Dbaibo GS, El-Assaad W, et al, Ceramide generation by two distinct
pathways in tumor necrosis factor alpha-induced cell death. FEBS Lett. 2001 Aug
10;503(1):7-12; & Liu B, Hannun YA.et al, Glutathione regulation of neutral
sphingomyelinase in tumor necrosis factor-alpha-induced cell death.J
Biol Chem. 1998 May 1;273(18):11313-20; & (b)Noda M, Wataha JC, et al,
Sublethal, 2-week exposures of dental material components alter TNF-alpha
secretion of THP-1 monocytes. Dent Mater. 2003 Mar;19(2):101-5;
& Kim SH, Johnson VJ, Sharma RP. Mercury inhibits nitric oxide production
but activates proinflammatory cytokine expression in murine macrophage:
differential modulation of NF-kappaB and p38 MAPK signaling pathways. Nitric
Oxide. 2002 Aug;7(1):67-74; & Dastych J, Metcalfe DD et
al, Murine mast cells exposed to mercuric chloride release
granule-associated N-acetyl-beta-D-hexosaminidase and secrete IL-4 and
TNF-alpha. J Allergy Clin Immunol. 1999 Jun;103(6):1108-14;
& (c) Tortarolo M, Veglianese P, et al,
Persistent activation of p38 mitogen-activated protein kinase in a mouse model
of familial amyotrophic lateral sclerosis correlates with disease progression.. Mol Cell Neurosci. 2003 Jun;23(2):180-92.
(131) Christensen MM, Ellermann-Eriksen S,
Mogensen SC. Influence of mercury chloride on resistance to generalized infection
with herpes simplex virus type 2 in mice. Toxicology 1996, 114(1): 57-66;
(142) Ariza ME; Bijur GN; Williams 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 the risk 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)
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; & Walum E
et al, Use of primary cultures to sutdy astrocytic regulatory functions. Clin
Exp Pharmoacol Physiol 1995, 22:284-7; & J
Biol Chem 2000 Dec 8;275(49):38620-5; & (b)Kerkhoff H, Troost D, Louwerse
ES. Inflammatory cells in the peripheral nervous system in motor neuron
disease. Acta Neuropathol 1993; 85:560-5; & (c)Appel Sh, Smith RG.
Autoimmunity as an etiological factor in amyotrophic lateral sclerosis. Adv
Neurol 1995; 68:47-57.
(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)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- ; &
(181) Mathieson
PW, “Mercury: god of TH2 cells”,1995, Clinical Exp Immunol.,102(2):229-30;
& (b) Heo Y, Parsons PJ, Lawrence DA, Lead differentially modifies cytokine
production in vitro and in vivo. Toxicol Appl Pharmacol, 1996; 138:149-57;
& (c) Murdoch RD, Pepys J; Enhancement of antibody and IgE production by
mercury and platinum salts. Int Arch Allergy Appl Immunol 1986 80: 405-11;
(183)
World Health Organization(WHO),1991, Environmental
Health criteria 118, Inorgtanic Mercury, WHO, Geneva; & Envir. H. Crit. 101,
Methyl Mercury;1990.
(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.
(198)
Cd2+ and Hg2+ affect glucose release and cAMP-dependent transduction pathway in
isolated eel hepatocytes. Aquat Toxicol. 2003 Jan
10;62(1):55-65, Fabbri E, Caselli F, Piano A, Sartor G, Capuzzo A. &
Fluctuation of trace elements during methylmercury toxication and chelation
therapy. Hum Exp Toxicol. 1994 Dec;13(12):815-23, Bapu C, Purohit RC,
Sood PP; & E.S. West et al, Textbook of Biochemistry, MacMillan Co, 1957,p853;& B.R.G.Danielsson 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; & Danielsson et al,
Neurotoxicol. Teratol., 18:129-134;
(200)
Kulacz & Levy , "The Roots of Disease".
Xlibris Corporation at 1-888-795-4274 www.xlibris.com; & B.E. Haley,
www.altcorp.com; & G. Mienig, Root Canal Coverup, 1997.; & Dr. T. Rau,
Paracelsus Allergy Clinic, Lustmuhle, Switzerland,1996 www.flcv.com/damspr11.html
(207)
Boyd Haley, Univ. Of Kentucky, "The Toxic Effects of Mercury on CNS Proteins:
Similarity to Observations in Alzheimer's Disease", IAOMT Symposium paper,
March 1997 & (b)"Mercury Vapor Inhaltion Inhibits Binding of GTP
... Similarity to Lesions in Alzheimers Diseased Brains",
Neurotoxicology, 18:315 June 1997; & (c) Met Ions Biol
Syst,1997,34:461 78 (* web page & dental lab:cavitations,root
canals-www.altcorp.com/) &(d) Palkiewicz P, Zwiers H, Lorscheider FL;
ADP Ribosylation of Brain Neuronal Proteins Is Altered by In Vitro and In
Vivo Exposure to Inorganic Mercury, Journal of Neurochemistry.
62(5):2049 2052, 1994 May
(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.Miller et al, “Mercuric
chloride induces apoptosis in human T lymphocytes”, Toxicol Appl Pharmacol,
153(2):250 7 1998; &(b) 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, Thomas D, Rojko JL, Lucas AD. Mercuric
chloride-induced apoptosis is dependent on protein synthesis. Toxicol Lett
1999; 105(3): 183-95;
(229) M.Davis,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.
(250) Sorensen
FW, Larsen JO, Eide R, Schionning JD. Neuron loss in cerebellar cortex of rats
exposed to mercury vapor: a stereological study. Acta Neuropathol (Berl). 2000
Jul;100(1):95-100; & Shikata E, Mochizuki Y, Oishi M, Takasu
T. [A case of chronic inorganic mercury poisoning with progressive
intentional tremor and remarkably prolonged latency of P300] Rinsho
Shinkeigaku. 1998 Dec;38(12):1064-6.
& Yamanaga H, “Quantitative analysis of
tremor in Minamata disease”, Tokhoku J Exp Med, 1983 Sep, 141:1, 13 22
(252) B.J.Shenker et al, Dept. of Pathology, Univ. of Pennsylvania,
“Immunotoxic effects of mercuric compounds on human lymphoctes and monocytes:
Alterations in cellular glutathione content”, Immunopharmacol Immunotoxicol
1993, 15(2-3):273-90.
(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; & Weiss B, Clarkson TW, Simon
W. Silent latency periods in methylmercury poisoning and in
neurodegenerative disease. Environ Health Perspect. 2002 Oct;110 Suppl
5:851-4.
(260)
Woods JS et al, Altered porphyrin metabolites as a biomarker of mercury
exposure and toxicity”, Physiol Pharmocol, 1996,74(2):210-15, & Strubelt O,
Kremer J, et al, Comparative studies on the toxicity of mercury, cadmium, and
copper toward the isolated perfused rat liver. J Toxicol Environ Health. 1996
Feb 23;47(3):267-83; & Kaliman PA, Nikitchenko IV, Sokol OA,
Strel'chenko EV. Regulation of heme oxygenase activity in rat liver during
oxidative stress induced by cobalt chloride and mercury
chloride. Biochemistry (Mosc). 2001 Jan;66(1):77-82.; & (d) Kumar SV,
Maitra S, Bhattacharya S. In vitro binding of inorganic mercury to the
plasma membrane of rat platelet affects Na+-K+-Atpase activity and platelet
aggregation. Biometals. 2002 Mar;15(1):51-7.
(263) Kumar
AR, Kurup PA. Inhibition of membrane Na+-K+ ATPase activity: a common pathway
in central nervous system disorders. J Assoc Physicians India. 2002 Mar;50:400-6
(264) B.R.
Danielsson et al, “ ”Behavioral effects of prenatal
metallic mercury inhalation exposure in rats”, Neurotoxicol Teratol, 1993,
15(6): 391-6;& A. Fredriksson et al,”Prenatal exposure to metallic mercury
vapour and methylmercury produce interactive behavioral changes in adult rats”,
Neurotoxicol Teratol, 1996, 18(2): 129-34
(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, Correlation of dental amalgam with mercury in brain tissue, J Prosthet Dent,
1987,58(6),704-7;
(272) BJ
Shenker,“Low-level MeHg exposure causes human T-cells to undergo apoptosis:
evidence of mitochondrial disfunction”, Environ Res, 1998, 77(2):149-159; &
O.Insug et al, “Mercuric compounds inhibit human monocyte function by inducing
apoptosis: evidence for formation of reactive oxygen species(ROS), development
of mitochondrial membrane permeability, and loss of reductive reserve”,
Toxicology, 1997, 124(3):211-24;
(275) American Journal of Human
Genetics, www.tinyurl.com/68s7j2, Aug 2008
(280) S.Nonaka et al, Nat. Inst. of
Mental Health, Bethesda Md., “Lithium treatment protects neurons in
CNS from glutamate induced excitibility and calcium
influx”, Neurobiology, Vol 95(5):2642-2647, Mar 3, 1998; & Chuang D. Et al, National
Institute of Mental Health, Science News, Nov 11, 2000, 158:309; & Science
News, 3-14-98, p164; & Moore G.J.et al,
Lancet Oct 7, 2000; & Science News, 10-31-98, p276; & (b) Combined lithium and valproate treatment delays disease onset,
reduces neurological deficits and prolongs survival in an amyotrophic lateral
sclerosis mouse model; Feng HL, Leng Y, et al. Neuroscience. 2008 Aug 26;155(3):567-72.
(281) Mercury-induced toxicity of rat
cortical neurons is mediated through N-Methyl-D-Aspartate receptors. Xu F et
al; Mol Brain. 2012 Sep 14;5:30; & Uptake of environmental toxicants by the locus ceruleus: a
potential trigger for neurodegenerative, demyelinating and psychiatric disorders.
Pamphlett R; Med Hypotheses. 2014, Jan;82(1):97-104
(287) Warfvinge K, Mercury distribution in the
neonatal and adult cerebellum after mercury vapor exposure of pregnant squirrel
monkeys, Environ Res 2000, 83(2): 93-101;
(288)
(a)Hisatome I, Kurata Y, et al; Block of sodium channels by divalent
mercury: role of specific cysteinyl residues in the P-loop region.Biophys
J. 2000 Sep;79(3):1336-45; & Bhattacharya S, Sen S et al, Specific
binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane
and signal transduction. Biometals. 1997 Jul;10(3):157-62; &
Anner BM, Moosmayer M, Imesch E. Mercury blocks Na-K-ATPase by a
ligand-dependent and reversible mechanism. Am J Physiol. 1992 May;262(5 Pt 2):F830-6. & Anner BM, Moosmayer M. Mercury inhibits
Na-K-ATPase primarily at the cytoplasmic side. Am J Physiol 1992; 262(5 Pt2):F84308; & Wagner CA, Waldegger S,et al;
Heavy metals inhibit Pi-induced currents through human brush-border NaPi-3
cotransporter in Xenopus oocytes.. Am J Physiol. 1996 Oct;271(4 Pt 2):F926-30; & Lewis 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
&
(b) Rajanna B, Hobson M, Harris 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 Biochem 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 ;& K.R.Hoyt et al, “Mechanisms of
dopamine-induced cell death and differences from glutamate Induced cell death”,
Exp Neurol 1997, 143(2):269-81; & & (c)Offen D, et al, Antibodies
from ALS patients inhibit dopamine release mediated by L-type calcium channels.
Neurology 1998 Oct;51(4):1100-3.
(291) H.A.
Huggins, Solving the MS Mystery,
2002, & http://www.hugginsappliedhealing.com/ms.php ; &
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-; &
CFS, www.hugginsappliedhealing.com/fatigue.php & Depression, www.hugginsappliedhealing.com/emotional.php
(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; & &
(b) 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; &(c) & Snyder RD; Lachmann PJ; Thiol
involvement in the inhibition of DNA repair by metals in mammalian cells.
Source Mol Toxicol, 1989 Apr Jun, 2:2, 117 28 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.
(303) Heavy Metals and Chronic Diseases , Dr. Dietrich Klinghardt, M.D., PhD, http://www.neuraltherapy.com/a_metals_disease.asp
(305) 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.;
& (b)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: &(c) Leong CC, Syed NI, Lorscheider FL. Retrograde
degeneration of neurite membrane structural integrity of nerve growth cones
following in vitro exposure to mercury. Neuroreport 2001 Mar
26;12(4):733-7
(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)
Alexianu ME, Kozovska M, Appel SH. Immune reactivity in a mouse model of
familial ALS correlates with disease progression. Neurology 2001 Oct 9;57(7):1282-9
(314) M.Kubicka-Muranyi
et al, “Systemic autoimmune disease induced by mercuric chloride”, Int Arch
Allergy Immunol;1996, 109(1):11-20 & 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;& (b)L.M. Bagenstose 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;
(315) B.Engin-Deniz et al,”Die queckssilberkonzentration im
spichel zehnjariger kinder in korrelation zur anzahl und Grobe iher
amalgamfullungen”, Zeitschrift fur Stomatologie,1992, 89:471-179;
(316)B.J.Shenker et al,
Dept. Of Pathology, Univ. Of Pennsylvania School of Dental Medicine,
“Immunotoxic effects of mercuric compounds on human lymphocytes and monocytes:
Alterations in B-cell function and viability” Immunopharmacol Immunotoxicol,
1993, 15(1):87-112; & J.R.Daum,”Immunotoxicology of mercury and cadmium on
B-lymphocytes”, Int J Immunopharmacol, 1993, 15(3):383-94; & Johansson U,
et al, "The genotype determines the B cell response in mercury-treated
mice", Int Arch Allergy Immunol, 116(4):295-305, (Aug 1998)
(325) B. Arvidson(Sweden), Inorganic mercury is transported from
muscular nerve terminals to spinal and brainstem motorneurons. Muscle Nerve,
1992, 15(10);1089-94, & Mitchell 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) (a)G.
Danscher et al, Environ Res, “Localization of mercury in the CNS”, 1986, 41:29-43;
&(b) Danscher G; Horsted Bindslev P; Rungby J. Traces of mercury
in organs from primates with amalgam fillings. Exp Mol Pathol
1990;52(3):291 9; & (c) ”Ultrastructural localization of mercury
after exposure to mercury vapor”, Prog Histochem Cytochem, 1991, 23:249-255;
&(d) Pamphlett R,Coote P , “Entry of low doses of mercury vapor into the
nervous system”, Neurotoxicology, 1998, 19(1):39-47; & (e) Pamphlett et al,
“Oxidative damage to nucleic acids in motor neurons containing Hg”, J Neurol
Sci,1998,159(2):121-6. (rats & primates); & (f) Pamphlett R, Waley P,
"Motor Neuron Uptake of Low Dose Inorganic Mercury", J. Neurological
Sciences 135: 63 67 (1996); &(g) 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)
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; &(b) Arvidson B. Inorganic mercury is transported from
muscular nerve terminasl to spinal and brainstem motorneurons. Muscle Nerve
1992, 15:1089-94; & Arvidson B,et al, Acta Neurol Scand, “Retograde axonal
transport of mercury in primary sensory neurons” 1990,82:324-237 & Neurosci
Letters, 1990, 115:29-32; & (c)S.M. Candura et al, “Effects of mercuryic
chloride and methyly mercury on cholinergic neuromusular transmission”,
Pharmacol Toxicol 1997; 80(5): 218-24; & (d)Castoldi AF et al, “Interaction
of mercury compounds with muscarinic receptor subtypes in the rat brain”,
Neurotoxicology 1996; 17(3-4): 735-41;
(330) Wilkinson LJ, Waring RH. Cysteine
dioxygenase: modulation of expression in human cell lines by cytokines and
control of sulphate production. Toxicol In Vitro. 2002
Aug;16(4):481-3; & (b) 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; & Steventon GB, et al; Xenobiotic
metabolism in motor neuron disease, The Lancet, Sept 17 1988, p 644-47; &
Neurology 1990, 40:1095-98; & Cysteine, sulfite, and glutamate toxicity:
a cause of ALS? Woolsey PB. J Altern Complement Med. 2008
Nov;14(9):1159-64
(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; & Bradley H,et
al, Sulfate metabolism is abnormal in patients with rheumatoid arthritis.
Confirmation by in vivo biochemical findings. J Rheumatol. 1994
Jul;21(7):1192-6; & T.L. Perry et al, “Hallevorden-Spatz Disease:
cysteine accumulation and cysteine dioxygenase defieciency”, Ann Neural, 1985,
18(4):482-489.
(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,Effects of inorganic mercury and
methylmercury on the ionic currents of cultured rat hippocampal neurons. 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; & Rossi AD, et al, Modifications of Ca2+ signaling
by inorganic mercury in PC12 cells. FASEB J 1993, 7:1507-14.
(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.
(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.
(342) Metal-specific lymphocyte reactivity
is downregulated after dental metal replacement. Yaqob A, Danersund A, Stejskal
VD, Lindvall A, Hudecek R, Lindh U., Neuro Endocrinol Lett. 2006
Feb-Apr;27(1-2):189-97; & 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; (patients with
fatigue)
(369) Sterzl I, Prochazkova J, Stejskal VDM et
al, Mercury and nickel allergy: risk factors in fatigue and autoimmunity.
Neuroendocrinology Letters 1999; 20:221-228; & Prochazkova J, Sterzl
I, Kucerova H, Bartova J, Stejskal VD; The beneficial effect of
amalgam replacement on health in patients with autoimmunity. Neuro
Endocrinol Lett. 2004 Jun;25(3):211-8. http://www.melisa.org/pdf/Mercury-and-autoimmunity.pdf
(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@swipnet.se .
(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) J
Stejskal, V Stejskal. The role of metals in autoimmune diseases and the link to
neuroendocrinology Neuroendocrinology Letters, 20:345 358, 1999. http://www.melisa.org; http://www.melisa.org & (a) Analysis of SOD1 mutations in a Chinese
population with amyotrophic lateral sclerosis: a case-control study and
literature review. Wei Q et al; Sci Rep. 2017 Mar 14;7; & (b) Longitudinal assessment of metal concentrations
and copper isotope ratios in the G93A SOD1 mouse model of amyotrophic lateral
sclerosis. Enge TG et al; Metallomics. 2017 Feb
22;9(2):161-174; & (d) Increased Zn/Glutathione Levels and Higher Superoxide Dismutase-1
Activity as Biomarkers of Oxidative Stress in Women with Long-Term Dental
Amalgam Fillings: Correlation between Mercury/Aluminium Levels (in Hair) and Antioxidant Systems
in Plasma. Cabana-Munoz ME et al; PLoS One. 2015 Jun 15;10(6).
(406) The Edelson Clinic, Atlanta, Ga. (www.edelsoncenter.com/ALS/als_an.htm)
(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. 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.; &
Shibuya-Saruta H, Kasahara Y, Hashimoto Y. Human serum dipeptidyl peptidase IV
(DPPIV) and its unique properties. J Clin Lab Anal. 1996;10(6):435-40;
& Blais A, Morvan-Baleynaud J, Friedlander G, Le Grimellec C. Primary
culture of rabbit proximal tubules as a cellular model to study nephrotoxicity
of xenobiotics.Kidney Int. 1993 Jul;44(1):13-8
(412) Moreno-Fuenmayor
H, Borjas L, Arrieta A, Valera V, Plasma excitatory amino acids in autism.
Invest Clin 1996,37(2):113-28;& Carlsson ML. Is
infantile autsim a hypoglutamatergic disorer? J Neural Transm 1998, 105(4-5):
525-35. & (b)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; & (c)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;
(416)(a) Plaitakis
A, Constantakakis E. Altered metabolism of excitatory amino acids,
N-acetyl-aspartate and – acetyl-aspartyl-glutamate in amyotrophic lateral
sclerosis. Brain Res Bull 1993;30(3-4):381-6 &(b)Rothstein JD, Martin
LJ, Kuncl RW. Decreased glutamate transport by the brain and spinal cord in
ALS. New Engl J Med 1992, 326: 1464-8:& (c) Leigh
Pn. Pathologic mechanisms in ALS and other motor neuron diseases. In: Calne
DB(Ed.), Neurodegenerative Diseases, WB Saunder Co., 1997, p473-88; &
P.Froissard et al, Universite de Caen, “Role of glutathione metabolism in the
glutamate-induced programmed cell death of neuronal cells” Eur J Pharmacol,
1997, 236(1): 93-99; & (d) Oxidative and excitotoxic
insults exert differential effects on spinal motoneurons and astrocytic
glutamate transporters: Implications for the role of astrogliosis in
amyotrophic lateral sclerosis. Zagami CJ, Beart PM, Wallis N, Nagley
P, O'Shea RD. Glia. 2009 Jan 15;57(2):119-35; & Focal degeneration of astrocytes resulting from
excitotoxicity in amyotrophic lateral sclerosis; Rossi D, Brambilla
L, Valori CF, Roncoroni C, Crugnola A, Yokota
T, Bredesen DE, Volterra A. Cell Death Differ. 2008 Nov;15(11):1691-700. Epub 2008 Jul 11 ;& Kim P, Choi BH. “Selective inhibition of
glutamate uptake by mercury in cultured mouse astrocytes”, Yonsei Med J 1995;
36(3): 299-305; & Brookes N. In vitro evidence for the role of glutatmate
in the CNS toxicity of mercury. Toxicology 1992, 76(3):245-56; & Albrecht
J, Matyja E. Glutamate: a potential mediator of inorganic mercury toxicity.
Metab Brain Dis 1996; 11:175-84; &(e) Tirosh O, Sen CK, Roy S, Packer
L. Cellular and mitochondrial changes in glutamate-induced HT4 neuronal cell
death Neuroscience. 2000;97(3):531-41; &(f) Plasma glutamate and glycine levels in patients with amyotrophic
lateral sclerosis; Andreadou E, Vassilopoulos D et al. In Vivo. 2008
Jan-Feb;22(1):137-41
(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) T.Barber,
“Inorganic mercury intoxification similar to ALS”, J of Occup Med, 1978,
20:667-9; & Brown IA. Chronic mercurialism-a cause of the clinical syndrome
of ALS. Arch Neurol Psychiatry 1954, 72:674-9; & Schwarz
S, Husstedt I. ALS after accidental injection of mercury. J Neurol Neurosurg
Psychiatry 1996, 60:698; & 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;
&(b)Bara M, Guiet-Bara A, Durlach J. Comparison of the effects of
taurine and magnesium on electrical characteristics of artificial and natural
membranes. V. Study on the human amnion of the antagonism between magnesium,
taurine and polluting metals. [ French] Magnesium. 1985;4(5-6):325-32.
(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; 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.
(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), see research web pages on amalgam
toxicity, root canals, cavitaions. http://www.myflcv.com/damspr11.html)
(438) Amer. Colleg of Medical Genetics Working
Group on ApoE and Alzheimer’s Disease, JAMA, 1995, 274: 1627-29; &(b)
Godfrey ME, Wojcik DP, Krone CA. Apolipoprotein E genotyping as a potential
biomarker for mercury neurotoxicity. J Alzheimers Dis. 2003 Jun;5(3):189-95;
& Mercury toxicity presenting as chronic fatigue, memory impairment
and depression: diagnosis, treatment, susceptibility, and outcomes in a New
Zealand general practice setting (1994-2006), Wojcik DP, Godfrey ME, Christie
D, Haley BE. Northland Environmental Health Clinic, Neuro Endocrinol Lett.
2006 Aug;27(4):415-23.
(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: Bull
Environ Contam Toxicol. 1978 Dec;20(6):729-35: & Gupta PK, Sastry KV.
Effect of mercuric chloride on enzyme activities in the digestive system and
chemical composition of liver and muscles of the catfish. Ecotoxicol Environ
Saf. 1981 Dec;5(4):389-400.
.
(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 death 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)(a) 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; & Matthews 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, Matthews 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; & (b)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;
& (c) C. Gooch et al, Eleanor & Lou Gehrig MDA/ALS Center at
Columbia-Presbyterian Medical Center in New York; ALS Newsletter Vol. 6, No. 3
June 2001
(445) Clifford Lab, Dental
Materials Biocompatability Testing, Colorada Springs, Colo.; & Peak Energy
Performance, inc., Dental Materials Biocompatibility Testing, www.peakenergy.com
(449) Long-term
vitamin E supplementation associated with reduced risk of ALS, American
Journal of Epidemiology, March 15, 2011; & Vitamin E intake and
risk of amyotrophic lateral sclerosis. Ascherio A, Weisskopf MG, O'reilly EJ,
Jacobs EJ, McCullough ML, Calle EE, Cudkowicz M, Thun MJ. Ann Neurol. 2005
Jan;57(1):104-10.
(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; & (b) Tabner BJ, Turnbull S, El-Agnaf OM, Allsop D.
Formation of hydrogen peroxide and hydroxyl radicals from A(beta) and
alpha-synuclein as a possible mechanism of cell death in Alzheimer's disease
and Parkinson's disease. Free Radic Biol Med. 2002 Jun 1;32(11):1076-83;
&(c) Ho PI, Collins SC, et al; Homocysteine potentiates beta-amyloid neurotoxicity:
role of oxidative stress. J Neurochem. 2001 Jul;78(2):249-53.
(463) Johnson S. The
possible role of gradual accumulation of copper, cadmium, lead and iron and
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;
& White AR, Cappai R, Neurotoxicity from glutathione depletion is
dependent on extracellular trace copper. J Neurosci Res. 2003 Mar
15;71(6):889-97.
(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
(466) Chen KM, Department of Neurology, Guam Memorial Hospital;
Disappearance of ALS from Guam: implications for exogenous causes, 2000.
(468) M.M. van Benschoten,
““Acupoint Energetics of Mercury Toxicity and Amalgam Removal with Case
Studies,”” American Journal of Acupuncture, Vol. 22, No. 3, 1994, pp. 251-262;
& M.M. Van Benschoten and Associates, Reseda, Calif. Clinic;
http://www.mmvbs.com/
(469)BrainRecovery.com,
the book, by David 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
& Michael Guthrie,
R.Ph. ImmuneSupport.com 07 18 2001 Mycoplasmas – The Missing Link in
Fatiguing Illnesses, www.immunesupport.com/library/showarticle.cfm?ID=3066;
&
D.Cooper,
ImmuneSupport.com, Professor Garth Nicolson’s Studies and Treatments Explained,
www.immed.org/reports/treatment_considerations/ImmuneSuppcom01114a.htm; &
Dr. G. Nicholson, Institute for Molecular Medicine, New Treatments for Chronic
Infections Found in Fibromyalgia Syndrome, Chronic Fatigue Syndrome, Rheumatoid
Arthritis, Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and Gulf War
Illnesses, www.immed.org/reports/autoimmune_illness/rep1.html & Nicolson G,
Nasralla M, Haier J, Pomfret J. High frequency of systemic mycoplasmal
infections in Gulf War veterans and civilians with Amyotrophic Lateral
Sclerosis (ALS). J Clin Neurosci 2002 Sep;9(5):525; & (b) Immunosciences
Lab, www.immuno sci lab.com/index2.html
(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;
& www.lymelink.com/chronic.htm
(477) Lars Landner and
Lennart Lindestrom. Swedish Environmental Research Group(MFG), Copper
in society and the Environment, 2nd revised edition. 1999;
& White AR, Cappai R, Neurotoxicity from glutathione depletion is
dependent on extracellular trace copper. J Neurosci Res. 2003 Mar
15;71(6):889-97.
(485) Hulda Clark, The Cure for all
Diseases, 2000, www.drclark.net (amalgam replacement ,dental infection
revision, detoxification, and treatment for parasites) (U.S. CDC confirms
parasites common in those with chronic immune conditions) http://www.drclark.net/en/testimonials/dental/index.php
http://www.drclark.net/en/testimonials/neuro/index.php
(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, Kristinsson 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.
(490) (a) Analysis of SOD1 mutations in a Chinese population with
amyotrophic lateral sclerosis: a case-control study and literature review. Wei
Q et al; Sci Rep. 2017 Mar 14;7; &(b) Longitudinal assessment of metal
concentrations and copper isotope ratios in the G93A SOD1 mouse model of
amyotrophic lateral sclerosis. Enge TG et al; Metallomics. 2017
Feb 22;9(2):161-174; & (c ) Resveratrol treatment reduces the vulnerability
of SH-SY5Y cells and cortical neurons overexpressing SOD1-G93A
to Thimerosal toxicity through SIRT1/DREAM/PDYN pathway. Laudati G et al; Neurotoxicology. 2018 Nov 29;71:6-15; & (d) Changes in the mitochondrial
antioxidant systems in neurodegenerative diseases and acute brain disorders.
Ruszkiewicz J et al; Neurochem
Int. 2015
Sep;88:66-72.
(491) Shibata N, Nagai R,
Kobayashi M. Morphological evidence for lipid peroxidation and protein
glycoxidation in spinal cords from sporadic amyotrophic lateral sclerosis
patients. Brain Res 2001 Oct 26;917(1):97-104 & 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); & Ferrante RJ, Klein
AM, Dedeoglu A, Beal MF. Therapeutic efficacy of EGb761 (Gingko biloba extract)
in a transgenic mouse model of amyotrophic lateral sclerosis. J Mol Neurosci
2001 Aug;17(1):89-96 & 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); &(e) Li Y, Liu L, et al. Vitamin E suppression of
microglial activation is neuroprotective. J Neurosci Res 2001 Oct
15;66(2):163-70
(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, Sanders 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 Ther 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)
Torres 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: & Pons S, Torres-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;
(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.
(502) Vielhaber S, Kaufmann
J, Kunz WS. Effect of Creatine Supplementation on Metabolite Levels in ALS
Motor Cortices. Exp Neurol 2001 Dec;172(2):377-82; & Andreassen OA, Jenkins
BG, Dedeoglu A, Ferrante KL, Beal MF. Increases in cortical glutamate
concentrations in transgenic amyotrophic lateral sclerosis mice are attenuated
by creatine supplementation. J Neurochem 2001 Apr;77(2):383-90; &
Friedlander, R et al, Combination of Creatine and Minocycline increase survival
rate synergistically, Annals of Neurology, Jan 2003
(503) Protective
effects of methylcobalamin, a vitamin B12 analog, against glutamate- induced
neurotoxicity in retinal cell culture. Kikuchi M,Kashii
S, Honda Y, Tamura Y, Kaneda K, Akaike A. Invest
Ophthalmol Vis Sci. 1997 Apr;38(5):848-54; van Rensburg SJ, Kotze MJ, Hon
D, Haug P, Kuyler J, Hendricks M, Botha J, Potocnik
FC, Matsha T, Erasmus RT. Metab Brain Dis. 2006 Sep;21(2-3):121-37. Epub 2006
May 26; & van Rensburg SJ, Kotze MJ, Hon D, Haug
P, Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha
T, Erasmus RT. Metab Brain Dis. 2006 Sep;21(2-3):121-37. Epub 2006
May 26
(504) Activation of methionine
synthase by insulin-like growth factor-1 and dopamine: a target for
neurodevelopmental toxins and thimerosal, Waly
M,Olteanu H, Deth RC et al, Mol Psychiatry. 2004 Apr;9(4):358-70; & Mercury and multiple sclerosis, Clausen J. Acta Neurol
Scand. 1993 Jun;87(6):461-4
(505) Chemical methylation of inorganic mercury with methylcobalamin, a
vitamin B12 analog. Imura N, Pan SK, Ukita T et al. Science. 1971 Jun 18; 172(989): 1248-9; & Cobalamin-mediated mercury methylation by Desulfovibrio
desulfuricans LS, Choi SC, Bartha R. Appl Environ Microbiol. 1993 Jan;59(1):290-5, & Isolation
of the provisionally named Desulfovibrio fairfieldensis from human
periodontal pockets, Loubinoux J.; Bisson-Boutelliez C.; Miller
N.; Le Faou A.E. Oral Microbiology and Immunology, Volume
17, Number 5, October 2002 , pp.
321-323(3)
(506) Leistevuo J, Pyy L,
Osterblad M, Dental amalgam fillings and the amount of organic mercury in human
saliva. Caries Res 2001 May Jun;35(3):163 6
(507) Appel SH, Beers D,
Siklos L, Engelhardt JI, Mosier DR. Calcium: the Darth Vader of ALS. Amyotroph
Lateral Scler Other Motor Neuron Disord 2001 Mar;2 Suppl 1:S47-54;
(513) Niebroj-Dobosz I,
Jamrozik Z, Janik P, Hausmanowa-Petrusewicz I, Kwiecinski H. Anti-neural
antibodies in serum and cerebrospinal fluid of amyotrophic lateral sclerosis
(ALS) patients. Acta Neurol Scand 1999 Oct;100(4):238-43; & Appel SH,
Stockton-Appel V, Stewart SS, Kerman RH. Amyotrophic lateral sclerosis.
Associated clinical disorders and immunological evaluations. Arch Neurol 1986
Mar;43(3):234-8: Pestronk A, Choksi R. Multifocal motor neuropathy. Serum IgM
anti-GM1 ganglioside antibodies in most patients detected using covalent
linkage of GM1 to ELISA plates. Neurology 1997 Nov;49(5):1289-92; &
Pestronk A, Adams RN, Cornblath D, Kuncl RW, Drachman DB, Clawson L. Patterns
of serum IgM antibodies to GM1 and GD1a gangliosides in amyotrophic lateral
sclerosis. Ann Neurol 1989 Jan;25(1):98-102
(517) (a)Earl C, Chantry A,
Mohammad N. Zinc ions stabilize the association of basic protein with brain
myelin membranes. J Neurochem 1988; 51:718-24; & Riccio P, Giovanneli S,
Bobba A. Specificity of zinc binding to myelin basic protein. Neurochem Res
1995; 20: 1107-13; & (b)Sanders B. The role of general and metal-specific
cellular responses in protection and repair of metal-induced damage: stress
proteins and metallothioneins. In: Chang L(Ed.), Toxicology of Metals. Lewis
Publishers, CRC Press Inc, 1996, p835-52; & (c )
Mendez-Alvarez E, Soto-Otero R, et al, Effects of aluminum and zinc on the
oxidative stress caused by 6-hydroxydopamine autoxidation: relevance for the
pathogenesis of Parkinson's disease. Biochim Biophys Acta. 2002 Mar
16;1586(2):155-68.
(518) (a) Aluminum deposition in the central
nervous system of patients with amyotrophic lateral sclerosis from the Kii
Peninsula of Japan; Yasui M, Yase Y, Ota K, Garruto
RM. Neurotoxicology. 1991 Fall;12(3):615-20
; & Intraneuronal
deposition of calcium and aluminium in amyotropic lateral sclerosis of
Guam; Garruto RM, Swyt C, Fiori CE, Yanagihara R,Gajdusek DC. Lancet. 1985 Dec
14;2(8468):1353, & (b)Low-calcium, high-aluminum diet-induced
motor neuron pathology in cynomolgus monkeys; Garruto RM, Shankar
SK, Yanagihara R, Salazar AM, Amyx HL, Gajdusek
DC. Acta Neuropathol. 1989;78(2):210-9; & Magnesium deficiency
over generations in rats with special references to the pathogenesis of the
Parkinsonism-dementia complex and amyotrophic lateral sclerosis of
Guam; Oyanagi K, Kawakami E, Yasui M. et al; Neuropathology. 2006
Apr;26(2):115-28; & [Similarities in calcium and magnesium metabolism
between amyotrophic lateral sclerosis and calcification of the spinal cord in
the Kii Peninsula ALS focus ] [Article in
Japanese] ; Yasui M, Yoshida M, Tamaki T, Taniguchi
Y, Ota K. No To Shinkei. 1997 Aug;49(8):745-51;
& Comparative study of chronic aluminum-induced neurofilamentous
aggregates with intracytoplasmic inclusions of amyotrophic lateral
sclerosis; Wakayama I, Nerurkar VR,Strong
MJ, Garruto RM. Acta Neuropathol. 1996 Dec;92(6):545-54
(519) Kong J, Xu Z. Mitochondrial degeneration in motor neurons
triggers the onset of ALS in mice expressing a mutant SOD1 gene. J Neurosci
1998; 18:3241-50; & (b)Cassarino DS, Bennett JPJ,Mitochrondrial
mutations and oxidative pathology, protective nuclear responses, and cell death
in neurodegeneration. Brain Res Brain Res Rev 1999; 29:1-25.
(520) Mitchell JD. Heavy metals and trace elements in amyotrophic
lateral sclerosis. Neurol Clin 1987 Feb;5(1):43 60; & Sienko DG, Davis
JP, Taylor JA. ALS: A case-control study following detection of a cluster in a
small Wisconsin community. Arch Neurol 1990, 9:255-62; & Provinciali L,
Giovagnoli A. Antecedent events in ALS: do they influence clinical onset and
progression? Neuroepidemiology 1990, 9:255-62; Roelofs-Iverson RA, Elveback LR.
ALS and heavy metals, Neurology 1984, 34:393-5; & ArmonC, O’Brien PC,
Epidemiologic correlates of sporadic ALS. Neurology 1991, 41:1077-84; &
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; & Yase Y. Environmental contribution to
the ALS process. In: Serratrice Gea(Ed.),
Neuromuscular Diseases, New York, Raven Press, 1984. P335-9.
(521) Guermonprez L, Ducrocq C, Gaudry-Talarmain YM. Inhibition of
acetylcholine synthesis and tyrosine nitration induced by peroxynitrite are
differentially prevented by antioxidants. Mol Pharmacol 2001 Oct;60(4):838-46;
& & (b)Mahboob M, Shireen KF, Atkinson A, Khan AT. Lipid
peroxidation and antioxidant enzyme activity in different organs of mice
exposed to low level of mercury. J Environ Sci Health B. 2001
Sep;36(5):687-97. & Miyamoto K, Nakanishi H, et al, Involvement
of enhanced sensitivity of N-methyl-D-aspartate receptors in vulnerability of
developing cortical neurons to methylmercury neurotoxicity. Brain Res. 2001 May
18;901(1-2):252-8; & (c) Anuradha B, Varalakshmi P. Protective role of
DL-alpha-lipoic acid against mercury-induced neural lipid peroxidation.
Pharmacol Res. 1999 Jan;39(1):67-80.
(522) Kawashima T, Doh-ura K, Iwaki T. Cognitive dysfunction in
patients with amyotrophic lateral sclerosis is associated with spherical or
crescent-shaped ubiquitinated intraneuronal inclusions in the parahippocampal
gyrus and amygdala, but not in the neostriatum. Acta Neuropathol (Berl) 2001
Nov;102(5):467-72
(524) Urushitani M, Shimohama S. The role of nitric oxide in
amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord
2001 Jun;2(2):71-81; & Torreilles F, Salman-Tabcheh S, Guerin M, Torreilles
J. Neurodegenerative disorders: the role of peroxynitrite.Brain
Res Brain Res Rev 1999 Aug;30(2):153-63; & Aoyama K, Matsubara K, Kobayashi
S. Nitration of manganese superoxide dismutase in cerebrospinal fluids is a
marker for peroxynitrite-mediated oxidative stress in neurodegenerative
diseases. Ann Neurol 2000 Apr;47(4):524-7; & Guermonprez L, Ducrocq C,
Gaudry-Talarmain YM. Inhibition of acetylcholine synthesis and tyrosine nitration
induced by peroxynitrite are differentially prevented by antioxidants. Mol
Pharmacol 2001 Oct;60(4):838-46
(525) Edited GluR2
(glutamate receptors), a gatekeeper for motor neurone survival? ; Buckingham SD, Kwak S, Jones AK, Blackshaw
SE, Sattelle DB. Bioessays. 2008 Nov;30(11-12):1185-92
(526) Ahlbom II, Cardis E, Green A, Linet M, Savitz D, Swerdlow A.
Review of the Epidemiologic Literature on EMF and Health. Environ Health
Perspect 2001 Dec;109 Suppl 6:911-933.
(527) N. A. Lanson, A. Maltare, H. King, R. Smith, J. H. Kim, J.
P. Taylor, T. E. Lloyd, U. B. Pandey. A Drosophila model of FUS-related
neurodegeneration reveals genetic interaction between FUS and TDP-43. Human
Molecular Genetics, 2011; DOI: 10.1093/hmg/ddr150
(565) Beuter A, de Geoffroy A, Edwards R. Quantitative
analysis of rapid pointing movements in Cree subjects exposed to mercury and in
subjects with neurological deficits. Environ Res. 1999 Jan;80(1):50-63.
(572) (b) “Decreased phagocytosis of myelin by macrophages with
ALA. Journal of Neuroimmunology 1998, 92:67-75; & (c)
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);
& McCarty MF. Versatile cytoprotective activity of lipoic acid may reflect
its ability to activate signalling intermediates that trigger the heat-shock
and phase II responses. Med Hypotheses 2001 Sep;57(3):313-7 & 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);
& Patrick L. Mercury toxicity and antioxidants: Part 1: role of
glutathione and alpha-lipoic acid in the treatment of mercury toxicity. Altern
Med Rev. 2002 Dec;7(6):456-71. (d) & Z.Gregus
et al, “Effect of lipoic acid on biliary excretion of glutathione and metals”,
Toxicol APPl Pharmacol, 1992, 114(1):88-96;
(575) [Healing of Amyotrophic
Lateral Sclerosis: A Case Report];
Mangelsdorf I, Mutter J;
Complement Med Res. 2017;24(3):175-181.
(577) Joachim Mutter et
al, Alzheimer Disease: Mercury as pathogenetic factor and apolipoprotein E as a
moderator, Neuroendocrinol Lett 2004; 25(5):331–339; & Apolipoprotein E genotyping
as a potential biomarker for mercury neurotoxicity. Godfrey ME et
al; J
Alzheimers Dis. 2003 Jun;5(3):189-95.
(580) Life Enhancement
Foundation (MDs), Disease Prevention and Treatment, Expanded 4th Edition,
2003. www.life-enhancement.com
(582) Aluminum Hydroxide:
Another Poison Pediatricians Inject in Babies; IMVA, http://imva.info/index.php/vaccines/aluminum-hydroxide/ ; & (b) “Vaccines Show Sinister Side” March
23,2006, www.straight.com/content.cfm?id=16717 ; (c) Blaylock, Russell. The Blaylock Wellness Report Vol 1, Issue 1;
& (d) Cave, Stephanie, Mitchell, Deborah
“What Your Doctor May Not Tell You About Children’s Vaccinations”, Warner
Books, 01 September, 2001; & (e) Waly, M. et al Activation of methionine
synthase by insulin-like growth factor-1 and dopamine: a target for
neurodevelopmental toxins and thimerosal. Department of Pharmaceutical
Sciences, Northeastern University. Molecular Psychiatry (2004) 1-13; & (f)
Haley, Boyd. Mercury and Thimerosal Toxicity: A Factor in Autism; & (g) Dr.
Fudenberg’s comments above were from his speech at the NVIC International Vaccine
Conference, Arlington VA September, 1997; & (h) http://www.chinadaily.com.cn/china/2006-03/25/content_552145.htm
(589)
Association between dental amalgam fillings
and Alzheimer's disease: a population-based cross-sectional study in
Taiwan. Sun YH, Alzheimers
Res Ther. 2015 Nov
12;7(1):65; & (d) Associations of blood mercury, inorganic mercury, methyl mercury and
bisphenol A with dental surface restorations in the U.S. population, NHANES
2003–2004 and 2010–2012. Lei Yin et
al; Ecotoxicology and Environmental Safety, 2016;
134: 213: & (c ) Mercury Involvement in Neuronal Damage and in
Neurodegenerative Diseases. Cariccio VL et el; Biol
Trace Elem Res. 2018 May 18.
(590) Proc Natl Acad Sci USA, 08; 105:2052-2057
& Dr. D G Williams, Alternatives, Vol 12, No. 13, July 2008; &
Neuroscience, 03; 117:55-61 & Neuropsychopharmcology 00;23(S2):S39 &
Lancet 00; 356:1241-42; & Combined lithium and
valproate treatment delays disease onset, reduces neurological deficits and
prolongs survival in an amyotrophic lateral sclerosis mouse model; Feng HL, Leng
Y, Ma CH, Zhang J, Ren M, Chuang DM. Neuroscience. 2008 Aug
26;155(3):567-72. Epub 2008 Jun 21.
(592) Should
Depressive Syndromes Be Reclassified as "Metabolic Syndrome Type
II"? Ann Clin Psychiatry. 2007
Oct-Dec;19(4):257-64. McIntyre RS, Soczynska JK, Kennedy SH et al;& Inflammation, depression and dementia: are they
connected? Neurochem Res. 2007 Oct;32(10):1749-56. Epub 2007
Aug 20 Leonard BE.
(593) Vaccines, Depression and Neurodegeneration
After Age 50, By Russell L. Blaylock, www.flcv.com/vaxinfla.html; & &(b)Immunoexcitotoxicity, R L Blaylock, Alt Ther Health Med, 2008,
14:46-53; & (c) Beat Depression and Anxiety with Diet/Nutrition, Blaylock
Report, Dec 2010.
(595) High fructose
consumption combined with low dietary magnesium intake may increase the
incidence of the metabolic syndrome by inducing inflammation. Magnes
Res. 2006 Dec;19(4):237-43. Rayssiguier Y, Gueux E, et al; &
(b) Dietary magnesium and fiber intakes and inflammatory and metabolic
indicators in middle-aged subjects from a population-based cohort. Am
J Clin Nutr. 2006 Nov;84(5):1062-9 Bo S, Durazzo M, Pagano G. et
al; & (c) Hypomagnesemia, oxidative stress, inflammation, and metabolic
syndrome. Diabetes Metab Res Rev. 2006 Nov-Dec;22(6):471-6. Guerrero-Romero
F, Rodríguez-Morán
(596) Effects of
antidiabetic and antihyperlipidemic agents on C-reactive protein. Mayo
Clin Proc. 2008 Mar;83(3):333-42, Dandona P; & Role of advanced
glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell
Biochem Biophys. 2007;49(1):48-63, Vasdev S, Gill
V, Singal P.
(597) Effects of
mercuric chloride on glucose transport in 3T3-L1 adipocytes. Toxicol
In Vitro. 2005 Mar;19(2):207-14. Barnes DM, Kircher EA;
& Effects of inorganic HgCl2 on adipogenesis. Toxicol Sci. 2003
Oct;75(2):368-77. Epub 2003 Jul 25, Barnes DM, Hanlon PR, Kircher
EA; & (b) Heavy metal-induced inhibition of active transport in the rat
small intestine in vitro. Interaction with other ions. Comp Biochem
Physiol C. 1986;84(2):363-8, Iturri SJ, Peña A; & Interaction
of the sugar carrier of intestinal brush-border membranes with HgCl2. Biochim
Biophys Acta. 1980 May 8;598(1):100-14, Klip A, Grinstein S, Biber
J, Semenza G.
(598) Overcoming Depression, Dr. Russell
Blaylock, The Blaylock Wellness Report, Vol 5, No. 3, March 2008, & Food
Additives, What you eat can kill you, Vol 4, No.
10, www.blaylockreport.com/
(599) Documentation of mercury exposure levels from dental amalgam
fillings, B. Windham (ED), www.flcv.com/damspr1.html
(600) B. Windham, Annotated bibliography: Exposure levels and
health effects related to mercury/dental amalgam and results of amalgam
replacement, 2002; (over 3000 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.flcv.com/amalg6.html & www.flcv.com/hgremove.html
(601) B. Windham, Cognitive and Behavioral Effects of Toxic Metal
Exposures, 2002; (over 150 medical study references) www.flcv.com/tmlbn.html
(602) The mechanisms by
which mercury causes chronic immune and inflammatory conditions, B.Windham (Ed.), 2002,www.flcv.com/immunere.html
(603) The environmental
effects of mercury from amalgam affect everyone. B. Windham(Ed.)
(Gov’t studies)
*******