Toxic
Exposures and Parkinsons: the Mercury Connection
Bernard Windham(Ed.)-
Chemical Engineer/Biostatistician
I.
Introduction.
There
has been a huge increase in the incidence of degenerative neurological
conditions in virtually all Western countries over the last 2 decades(574,303). The increase in Parkinson’s and other
motor neuron disease has been over 50%.
The primary cause appears to be increased exposures to toxic pollutants
such as toxic metals, pesticides, etc. resulting in brain inflammation and oxidative damage
of free-radicals(574,580,598).
Dental amalgam fillings are the
largest source of mercury in most people with daily exposures documented to
commonly be above government health guidelines (49,79,183,199,506,600,217).
This is due to
continuous vaporization of mercury from amalgam in the mouth, along with galvanic currents from mixed metals in
the mouth that deposit the mercury in the gums and oral cavity(605,580). 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(601,303,592). All of these are highly neurotoxic and are
documented to cause
neurological damage which can result in chronic neurological
conditions over time, as well as ADHD, mood, and behavioral disorders (580,598,601,602,303). A study found that those with occupational
exposure to lead, arsenic, or copper have more than double the incidence of
Parkinson’s than normal(560).
Mercury is one of the most toxic substances
in existence and is known to bioaccumulate in the body of people and animals
that have chronic exposure(600). Mercury exposure is cumulative and comes
primarily from 4 main sources: silver(mercury) dental
fillings, food(mainly fish), vaccinations, and occupational exposure. Whereas
mercury exposure from fish is primarily methyl mercury and mercury from
vaccinations is thimerosal(ethyl mercury), mercury from occupational exposure and dental
fillings is primarily from elemental mercury vapor. Developmental and
neurological conditions occur at lower levels of exposure from mercury vapor
than from inorganic mercury or methyl mercury(606). Mercury in amalgam fillings, because of its high vapor pressure and
galvanic action with other metals in the mouth, has been found to be
continuously vaporized and released into
the body, and has been found to be the
directly correlated to the number of
amalgam surfaces and the largest source of mercury in the majority of people
(49,183,199,209,79,99,600), typically between 60 and 90% of the total. The level of daily exposure of those with
several amalgam fillings commonly exceeds the U.S. EPA health guideline for
daily mercury exposure of
0.1 ug/kg body weight/day, and the oral mercury level commonly
exceeds the mercury MRL of the U.S.ATSDR
of 0.2 ug/ cubic meter of air(217,600).
When amalgam fillings are replaced, levels of mercury in the blood,
urine, saliva, and feces typically rise temporarily but decline between 60 to 90%
within 6 to 9 months (79,600.).
The
main factors determining whether chronic conditions are induced by metals
appear to be exposure and genetic susceptibility,
which determines individuals immune sensitivity and ability to detoxify metals(405). Very low
levels of exposure have been found to seriously affect relatively large groups
of individuals who are immune sensitive to toxic metals, or have an inability
to detoxify metals due to such as deficient
sulfoxidation or metallothionein function or other inhibited enzymatic
processes related to detoxification or excretion of metals
II.
Mechanisms by which mercury causes neurological conditions found in Parkinson’s
and neurodegenerative diseases.
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 inflamatory cytokine Tumor Necrosis
Factor-alpha(TNFa) (126), reactive oxygen species and oxidative
stress(13,43a,56a,296b,495), reduced glutathione levels(56,126a,111a), liver
enzyme effects and inhibition of protein kinase C and cytochrome
P450(43,84,260), nitric oxide and peroxynitrite toxicity (43a,521,524),
excitotoxicity and lipid peroxidation(490,496), excess free cysteine levels
(56d,111a,33,330),excess glutamate toxicity(13b, 416), excess dopamine toxicity
(56d,13a), beta-amyloid generation(462), increased calcium influx toxicity
(296b,333,416,432,462c,507) and DNA fragmentation(296,42,114,142) and
mitochondrial membrane dysfunction (56de, 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. This has been found to be a factor in conditions like Parkinson’s.
The mechanisms by which mercury causes(often synergistically
along with other toxic exposures) all of these conditions and neuronal
apoptosis will be documented.
TNFa(tumor
necrosis factor-alpha) is a cytokine that controls a wide range of immune cell
response in mammals, including cell death(apoptosis) in neuronal and immune
cells. 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 mechansim for the TNFa
apoptosis mechanism(126a). Gluthathione is an amino acid that is a normal cellular
mechanism for controlling apoptosis.
When glutathione is depleted in the brain, reactive oxidative species
increased, and CNS and cell signaling mechinsisms are disrupted by toxic
exposures such as mercury, neuronal cell apoptosis results and neurological
damage. Mercury has been
shown to induce TNFa and deplete glutathione, causing inflamatory effects and
cellular apoptosis in neuronal and immune cells(126b,126c).
Mercury’s biochemical damage at the
cellular level include DNA damage, inhibition of DNA and RNA synthesis
(42,114,142,197,296,392); alteration of
protein structure (33,111,114,194,252,442);
alteration of the transport of calcium(333,43b,254,263,416,462,507);
inhibitation of glucose transport(338,254), and of enzyme function,protein
transport, and other essential nutrient transport (96,198,254,263,264,33,330,331,338,339,347,
441,442); induction of free radical
formation(13a,43b,54,405,424), depletion of cellular gluthathione(necessary for
detoxification processes) (111,126,424), inhibition of glutathione peroxidase
enzyme(13a,442), inhibits glutamate uptake(119,416), induces peroxynitrite and
lipid peroxidation damage(521b,119b), causes abnormal migration of neurons in
the cerebral cortex(149), immune system
damage (34,111,194, 226,252,272,316,325,355); and inducement of inflammatory
cytokines (126,181).
Oxidative
stress and reactive oxygen species(ROS) have been implicated as major factors
in neurological disorders including stroke, Parkinson’s Disease(PD),
Alzheimer’s, ALS, etc.(13,424,442.303). 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)
(13,441,443). Only a few micrograms of
mercury severely disturb cellular function and inhibit nerve growth
(147,149,226,255, 305,442). Exposure to
mercury results in metalloprotein compounds that have genetic effects, having
both structural and catalytic effects on gene expression (114,241,296,442).
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).
Some of the processes affected by such metalloprotein control of genes
include cellular respiration, metabolism, enzymatic processes, metal-specific
homeostasis, and adrenal stress response systems. Significant physiological changes occur when
metal ion concentrations exceed threshold levels. Such metalloprotein formation also appears to
have a relation to autoimmune reactions in significant numbers of people (114,60,313,342,368,369,405, 442). Increased formation of reactive oxygen species(ROS) has also been found to increase formation of
advanced glycation end products(AGEs) that have been found to cause activation
of glial cells to produce superoxide and nitric oxide, they can be considered
part of a vicious cycle, which finally leads to neuronal cell death in the
substantia nigra in PD(424).
Mercury
exposure causes high levels of oxidative stress/reactive oxygen
species(ROS)(13), 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 congugates are found to be
highest in the brain substantia nigra with similar congugates formed with
L-Dopa and dopamine in Parkinson’s disease(56). 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 Parkinson’s disease(33,56,442).
Exposure to mercury vapor and methyl mercury is well documented to commonly
cause conditions involving tremor and/or ataxia, with populations exposed to
mercury experiencing tremor on average proportional to exposure level (250,565,98). One study
found higher than average levels of mercury in the blood, urine, and hair of
Parkinson’s disease patients(363). Another study(169)
found blood and urine mercury levels to be very strongly related to Parkinson’s
with odds ratios of approx. 20 at high levels of Hg exposure. Other studies (145) that reviewed
occupational exposure data found that occupational exposure to manganese and
copper have high odds rations for relation to PD, as well as multiple exposures
to these and lead, but one study noted that this effect was only seen for
exposure of over 20 years. Occupational exposure to mercury has been found to
cause Parkinson’s(98). One study found the EDTA
chelation was effective in reducing some of the effects(145b).
Glutamate is the most abundant amino acid in the
body and in the CNS acts as excitory neurotransmitter(346,386),
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(119,333).
Mercury and other toxic metals inhibit astrocyte function in the brain
and CNS(119), causing increased glutamate and calcium
related neurotoxicity(119,333,226) which are responsible for much of the
fibromylgia symptoms. This is also a factor in
conditions such as CFS, Parkinson’s, and ALS(346,416).
Parkinson's disease involves the aggregation of
alpha-synuclein to form fibrils, which are the major constituent of
intracellular protein inclusions (Lewy bodies and Lewy neurites) in
dopaminergic neurons of the substantia nigra(564).
Occupational exposure to specific metals, especially manganese, copper, lead,
iron, mercury, aluminum, appears to be a risk factor for Parkinson's disease
based on epidemiological studies(98,145,518,564,580). Elevated levels of
several of these metals have also been reported in the substantia nigra of
Parkinson's disease subjects (564,580,518).
Exposure to aluminum hydroxide in vaccines also appears to sometimes
cause symptoms similar to Parkinson’s or other neurological conditions (592).
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 Parkinson’s cases there was an
elevation in plasma serum digoxin and a reduction in serum magnesium, RBC
membrane Na(+)-K+ ATPase activity (263).
The activity of all serum free-radical scavenging enzymes, concentration
of glutathione, alpha tocopherol, iron binding capacity, and ceruloplasmin
decreased significantly in PD, 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 Parkinson’s (13a,111,288,442,521b,43,56,etc.)
Many
studies of patients with major neurological or degenerative diseases have found
evidence amalgam fillings may play a major role in development of conditions such as such as Alzheimers
(66,67,158,166,204, 207,221,242,244,257,295,300), ALS(92,97,325,442),
MS(102,163,170,184,212,213,285,291,302,324,326), Parkinson’s(98,145,169,248,250,256,258,
363,405,56,84), etc. Mercury exposure
causes high levels of oxidative stress/reactive oxygen species(ROS)(13),
which has been found to be a major factor in neurological disease(56). Mercury and quinones form conjugates with
thiol compounds such as glutathione and cysteine and cause depletion of
glutathione, which is necessary to mitigate reactive damage. Such congugates are found to be highest in
the brain substantia nigra with similar congugates formed with L-Dopa and
dopamine in Parkinson’s disease(56,442). Mercury depletion of GSH and damage to
cellular mitochrondria and the increased lipid perxodation in protein and DNA
oxidation in the brain appear to be a major factor in Parkinson’s disease(33,56,442).
An EKM system for
evaluating nerve and muscle function ability using a set of 5 measures (precision, imprecision, tremor, Fitts'
constant, and irregularity) and tested on a group of Cree Indians with mercury
exposure from fish eating(565). Ninety-six participants, including 30
controls subjects, 36 Cree subjects exposed to mercury, 21 subjects with
Parkinson disease, 6 with presumed cerebellar deficit, and 3 with essential
tremor, participated in the study. An
ANOVA on the three largest groups generated significant results for tremor,
Fitts' constant, and irregularity between the Cree and the control subjects and
on Fitts' constant and irregularity between the subjects with Parkinson's
disease and the control subjects. Three
subgroups of the same mean age composed of six subjects each were selected. One
was composed of Cree subjects with the highest level of mercury exposure,
another with Cree subjects having a low level of mercury exposure, and a third
with control subjects. An ANOVA on
these three groups revealed a significant difference between both groups of
Cree subjects and the control group for Fitts' constant and irregularity. These
preliminary results suggest that the EKM system is able to discriminate the
performance of different groups of subjects and found significant evidence that
mercury exposure is related to nerve and muscle function conditions such as
tremor and Parkinson’s(565).
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, and platelet aggregation through interfering with
the sodium pump.
Studies
have found
mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and
myelin basic protein(MBP) (39b,269ag,405,478,515,516). Mercury and cadmium also have been found to
interfere with zinc binding to MBP(517b) which affects
MS symptoms since zinc stabilizes the association of MBP with brain
myelin(517a). MS has also been found to
commonly be related to inflammatory activity in the CNS such as that caused by
the reactive oxygen species and cytokine generation caused by mercury and other
toxic metals (405,478,515,126,303,516,35c). Antioxidants like lipoic acid which
counteract such free radical activity have been found to alleviate symptoms and
decrease demyelination (494,572). A
group of metal exposed MS patients with amalgam fillings were found to have
lower levels of red blood cells, hemoglobin, hemocrit, thyroxine, T-cells, and
CD8+ suppresser immune cells than a group of MS patients with amalgam replaced,
and more exacerbations of MS than those without(102a). Immune and autoimmune mechanisms are thus
seen to be a major
factor in neurotoxicity of metals. Mercury
penetrates and damages the blood brain barrier allowing penetration of the
barrier by other substances that are neurotoxic (20,38,85,105,301,311/262). Such damage to the blood brain barrier’s
function has been found to be a major factor in chronic neurological diseases
such as MS and studies have found mercury related mental effects to be
indistinguishable from those of MS patients(207,212,222,244,271,286,289,291,302,324,326,183,184). MS patients have been found to have much
higher levels of mercury in cerebrospinal fluid compared to controls (163,35,139). Large German studies
including studies at German universities have found that MS patients usually
have high levels of mercury body burden, with one study finding 300% higher
than controls(271).
Most recovered after mercury detox(369), with
some requiring additional treatment for viruses and intestinal dysbiosis.
Similarly thousands of MS patients
have been documented to have recovered or significantly improved after amalgam replacement (35,212,228,291,302,600,etc.
)
Mercury has been found to
accumulate preferentially in the primary motor function related areas 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). There is considerable indication this may be
a factor in development of ALS and other neurodegenerative conditions(48,325,405,442). Treatment using IV glutathione, vitamin C,
and minerals has been found to be very effective in the stabilizing and
amelioration of some of these chronic neurological conditions by neurologists
such as Perlmutter in Florida(469).
Low levels of toxic metals have been
found to inhibit dihydroteridine reductase, which affects the neural system
function by inhibiting brain transmitters through its effect on phenylalanine,
tyrosine and tryptophan transport into neurons(122,257,258,289,372). This was found to cause severe impaired
amine synthesis and hypokinesis. Tetrahydro-biopterin, which is essential in
production of
nerurotransmitters, is significantly decreased in patients with
Alzheimer’s, Parkinson’s, and MS. Such patients have abnormal inhibition of
neurotransmitter production(432).(supplements which
inhibit breach of the blood brain barrier such as bioflavonoids have been found
to slow such neurological damage).
Clinical tests of patients with
MND,ALS, 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), and in
general being poor sulphur oxidizers.
Mercury has been shown to diminish and block sulphur oxidation and thus
reducing glutathione levels which is the part of this process involved in
detoxifying and excretion of toxics like mercury(33,442).
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). Mercury has also been found to play a part in
neuronal problems through blockage of the P-450 enzymatic process(84). Other toxic metals and toxics such as
pesticides have also been found to cause the types of damage seen in
Parkinson’s and to exposure to have positive correlation to Parkinson’s (400,98,145). Another
exposure that affects some appears to be hexane(505). There are synergistic effects of various
toxics that result in conditions like Parkinson’s(524b,13c). Determination of one’s factors by history
assessment and tests is a first step in improving the condition.
One genetic difference found in animals
and humans is cellular retention differences for metals related to the ability
to excrete mercury(426). For example it has been found that
individuals with genetic blood factor type APOE-4 do not excrete mercury
readily and bioaccumulate mercury, resulting in susceptibility to chronic
autoimmune conditions such as Alzheimer’s, Parkinsons, etc. as early as age 40,
whereas those with type APOE-2 readily excrete mercury and are less
susceptible. Those with type APOE-3 are
intermediate to the other 2 types(437,35).
The Huggins Clinic(35) using total dental
revision(TDR) has successfully treated over a thousand patients with chronic
autoimmune conditions like MS, Parkinson’s,Lupus, ALS, AD, diabetes, etc.,
including himself with the population of over 1000(approx. 85%) who experienced
significant improvement in MS. Jaw bone
cavitations were found to be common significant factors in some of these
conditions such as Parkinson’s(35,580).
Huggins Total Dental
Revision Protocol(35):
(a) history questionnaire and panel of tests.
(b) replace amalgam fillings starting with filling with highest
negative current or highest negative
quadrant, with supportive vitamin/mineral supplements.
© extract
all root canaled teeth using proper finish protocol.
(d) test and treat cavitations and amalgam tattoos where
relevant
(e) supportive supplementation, periodic monitoring tests,
evaluate need for further treatment(not
usually needed).
(f) avoid acute
exposures/challenges to the immune system on a weekly 7/14/21 day pattern.
Tests suggested by Huggins/Levy(35)
for evaluation and treatment of mercury toxicity:
(a) hair element test(386)
(low hair mercury level does not indicate low body level)(more than
3 essential minerals out of normal range indicates likely metals
toxicity)
(b) CBC
blood test with differential and platelet count
© blood serum profile
(d) urinary
mercury (for person with average exposure with amalgam fillings, average
mercury level is 3 to 4 ppm; lower
test level than this likely means person is poor excretor and accumulating
mercury, often mercury toxic(35)
(e) fractionated porphyrin urine test(note test results
sensitive to light, temperature, shaking)
(f) individual tooth electric currents(replace high negative
current teeth first)
(g) patient questionnaire on exposure and symptom history
(h) specific gravity of urine(test for pituitary function,
s.g>1.022 normal; s.g.< 1.008 consistent with depression and suicidal
tendencies(35)}
Note: during initial exposure to mercury
the body marshals immune system and other measures to try to deal with the challenge, so many test indicators will
be high; after prolonged exposure the body and immune system inevitably lose
the battle and measures to combat the challenge decrease- so some test
indicator scores decline. Chronic
conditions are common during this phase.
Also high mercury exposures with low hair mercury or urine mercury level usually indicates body
is retaining mercury and likely toxicity problem(35). In such cases where (calcium> 1100 or < 300 ppm) and low
test mercury,manganese,zinc,potassium; mercury
toxicity likely and hard to treat since
retaining mercury.
Test results indicating mercury/metals toxicity(35):
(a) white blood cell count >7500 or < 4500
(b) hemocrit > 50% or
< 40%
© lymphocyte count
> 2800 or < 1800
(d) blood protein level > 7.5 gm/100 ml
(e) triglycerides > 150 mg %ml
(f) BUN
> 18 or < 12
(g) hair mercury > 1.5 ppm
or < .4 ppm
(h) oxyhemoglobin level < 55% saturated
(I)
carboxyhemoglubin > 2.5% saturated
(j) T
lymphocyte count < 2000
(k) DNA
damage/cancer
(l) TSH > 1 ug
(m) hair aluminum > 10 ppm
(n) hair nickel > 1.5 ppm
(o) hair manganese > 0.3 ppm
(p) immune reactive to mercury, nickel, aluminum, etc.
(q) high hemoglobin and hemocrit and high alkaline
phosphatase(alk phos) and lactic dehydrogenese(LDA) during initial phases of exposure; with low/marginal hemoglobin and hemocrit
plus low oxyhemoglobin during long term
chronic fatigue phase.
note: after treatment of many cases of
chronic autoimmune conditions such as MS, ALS, Parkinson’s, Alzheimer’s, CFS,
Lupus, Rheumatoid Arthritis, etc., it has been observed that often mercury
along with root canal toxicity or cavitation toxicity are major factors in
these conditions, and most with these conditions improve after TDR if protocol
is followed carefully(35).
There are extensive documented cases (many
thousands) where removal of amalgam fillings led to cure of serious health
problems such as MS(94,95,102,170,212,213,222,271,291,302, 34 ,35,229,405),
ALS(229,325,405,535,35), Parkinson’s/ muscle tremor (222,228,248,229,233c,271,212,322,469,557,94,98,35),
Alzheimer’s(204,35), muscular/joint pain/ fibromyalgia (222,293,317,322,369,35,94), anxiety & mental confusion
(94,212,222,229,233,271,317,303,320,322,57,35), Chronic Fatigue Syndrome
(212,293,229,222,232,233,271,313,317,303,320,368,369, 376,595,35), memory
disorders(94,222,303,595,35)
Medical
studies and doctors treating fibromylagia have found that supplements which
cause a decrease in glutamate or protect against its effects have a positive
effect on fibromyalgia. Some that have
been found to be effective in treating metals related autoimmune conditions such
as Parkinson’s include Vit B6, CoenzymeQ10,
methyl cobalamine(B12), L-carnitine, choline, ginseng, Ginkgo biloba,
vitamins C and E, nicotine, octacosanol, phosphatifylserine,and omega 3 fatty
acids(fish and flaxseed oil), tumeric, lipoic acid, proteolytic enzymes ,and
Hydergine(417,444,580). Reduced glutathione(GSH) and N-acetyl cysteine(NAC) have been found
to be protective against cellular apoptosis seen in Parkinson’s and other
neurodegenerative conditions( 56ab,462c, 149b).
High levels of Vitamins C and E along with zinc (517) have also been
found protective against oxidative stress and some effects of mercury toxicity
including for Parkinson’s (41,63,462c,580,56a). CoQ10 at 600 mg per day was
found effective at reducing Parkinson’s effects (580). IGF-1 treatments have
also been found to alleviate some of the symptoms of ALS(424).
There is also evidence that melatonin and curcumin may have beneficial effects
on reducing metal toxicity(591,497,580). Turmeric/curcumin has been found to reduce
some of the toxic and inflammatory effects of toxic metals. Lithium
supplements (lithium carbonate and lithium oratate) have been found to be
effective in protecting neurons and brain function from oxidative and
excitotoxic effects. A recent study demonstrated that combined
treatment with lithium and valproic acid elicits synergistic neuroprotective
effects against glutamate excitotoxicity in cultured brain neurons (590).
Doctors
affiliated with Life Enhancement Foundation have developed a diet and
supplementation protocol to reduce Parkinson’s effects and delay the start time
of daily levodopa therapy (page 1139) (580).
Dietary considerations include avoidance of alcohol, sugar, red meats,
cow’s milk products, gluten, fried foods, aspartame, MSG, pesticides.
Some clinics have found root canals,
cavitations, and amalgam tattoos to also be a factor in such autoimmune
conditions and that treatment of them improves prognosis in recovery from these
conditions(35,437,580).
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Note: etc. when it is used in a list of references means
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for example, but doesn’t
think them necessary here.
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edits (590)