Alzheimer’s Disease
and Other Autoimmune Degenerative Conditions: the Mercury Connection. B. Windham (Editor)
I.
Introduction and Mercury Exposure
There has been a huge increase in
the incidence of degenerative neurological conditions in virtually all Western
countries over the last 2 decades(574,580,594). Alzheimer’s
disease is the leading cause of dementia in the elderly. The increase in
Alzheimer’s and other dementia has been over 300%. The primary cause appears to be brain
inflammation related to increased exposures to toxic pollutants and bad dietary
habits, as well as oxidative stress and depletion of neurotransmitters such as
acetylcholine (445,574,577,580,594,598,158,etc.). These appear to be factors in formation of
advanced glycation end products (AGEs) and senile plaques of beta-amyloid
peptides, hyper-phosphorylation of Tau, and neurofibrillary tangles-as seen in
Alzheimer’s patients.
Mercury
is known to be one of the most toxic substances commonly encountered and to be
along with lead the toxic substances adversely
affecting the largest numbers of people (276).
Mercury in the presence of other metals in the oral environment
undergoes galvanic action, causing movement out of amalgam and into the oral
mucosa and saliva (174,183,192,436,199). Mercury in solid form is not stable
due to its vapor pressure and oral galvanism of mixed metals so that it
evaporates continuously from amalgam fillings
in the mouth, being transferred over a period of time to the host
(49,79,83,85,183,199,335, etc.). The
daily total exposure of mercury from fillings is from 3 to 1000 micrograms per
day, with the average exposure for those with several fillings being above 30
micrograms per day and the average uptake over 7 ug/day
(49,183,199,79,83,85,335,603, etc.), with the majority of the rest
excreted through the feces and often
being over 30 ug/day (79,335,603). The average amount of mercury in the feces
of a group with amalgams was over 10 times that of controls(79,603).
A 2009 study found that inorganic mercury levels in people have been increasing
rapidly in recent years(543b). It used data from the
U.S. Centers for Disease Control and Prevention’s National Health Nutrition
Examination Survey (NHANES) finding that while inorganic mercury was detected
in the blood of 2 percent of women aged 18 to 49 in the 1999-2000 NHANES survey, that level rose to 30 percent of women by 2005-2006.
Surveys in all states using hair tests have found dangerous levels of mercury
in an average of 22 % of the population, with over 30% in some states like
Florida and New York(543c). A large
U.S. Centers for Disease Control epidemiological study, NHANES III, found that those
with more amalgam fillings(more mercury exposure) have significantly higher
levels of chronic health conditions(543a).
Amalgam fillings are the largest source of mercury in most
people with daily exposures documented to commonly be above government health
guidelines (49,79,183,199,506,594,600,607,217). This is due to continuous vaporization of
mercury from amalgam in the mouth, along with galvanic currents from mixed
metals in the mouth that deposit the mercury in the gums and oral
cavity(605). Due to the high daily
mercury exposure and excretion into home and business sewers of those with
amalgam, dental amalgam is also the largest source of the high levels of
mercury found in all sewers and sewer sludge, and thus according to government
studies a significant source of mercury in rivers, lakes, bays, fish, and
crops(603). People also get significant
exposure from vaccinations, fish, and dental office vapor(600).
When amalgam was placed into teeth
of monkeys and rats, within one year mercury was found to have accumulated in
the brain, trigeminal ganglia, spinal ganglia, kidneys, liver, lungs, hormone
glands, and lymph glands(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(600,601). All of these are highly
neurotoxic and are documented to cause neurological damage which can result
in chronic neurological conditions over time, as well as ADHD, mood, and
behavioral disorders(594,600,601,577).
Another
major source of mercury exposure is vaccines such as flu vaccines which have
large amounts of mercury and aluminum, and have been linked to conditions like
depression,Parkinson’s, ALS, and dementia(445,585,598). It has been found that
vaccines contain adjuvants like aluminum plus mercury thimerosal which overstimulate
the immune system and brain, causing high levels of inflammation over long
periods of time. There is evidence of a link between the aluminum hydroxide in
vaccines, and symptoms associated with Alzheimer’s, Parkinson's, and ALS(585). It has been found that those who get at least 5
flu shots have an increased risk of inflammatory conditions like Alzheimer’s of
at least 500%.
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(85,600,577,594).
Mercury exposure is cumulative and comes primarily from 4 main sources: mercury
amalgam 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. However
bacteria, yeasts, and Vitamin B12 methylate inorganic mercury to methyl mercury
in the mouth and intestines (607,505) and mercury inhibits functional
methylation in the body, a necessary process (504). 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 low 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, and feces typically rise temporarily but decline between 60 to 85%
within 6 to 9 months (79,600.).
II.
Cytotoxic, Neurotoxic, and Immunotoxic Effects of Mercury
Mercury vapor from amalgam readily crosses
cell membranes and binds to the -SH (sulphydryl) groups, resulting in
inactivation of sulfur processes and blocking of enzyme functions such as
cysteine dioxygenase(CDO), sulfite oxidase, and gamma‑glutamyltraspeptidase(GGC)
, producing sulfur metabolites with extreme toxicity that the body is unable to
properly detoxify(33,111,114,194,258,330,331,333), along with a deficiency in
sulfates required for many body functions.
Sulfur is essential in enzymes, hormones, nerve tissue, and red blood
cells. These exist in almost every
enzymatic process in the body. Blocked
or inhibited sulfur oxidation at the cellular level has been found in most with
many of the chronic degenerative diseases, including Parkinson’s, Alzheimer’s,
ALS, MS, lupus, rheumatoid arthritis, MCS,
etc (330,331,33,35,56,194,258), and appears to be a major factor in
these conditions. 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 also blocks the metabolic action of
manganese and the entry of calcium ions into cytoplasm(333). Oxidative stress and reactive oxygen
species(ROS) have also been implicated as major factors in neurological
disorders including stroke, PD, Alzheimer’s, ALS, etc. (13,56,84,169,207b,424,442,453,462).
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(490,496,593),
excess free cysteine levels (56d,111a,33,330), excess glutamate toxicity(13b,
416,445,593,598), 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
(56defg, 416,444d). The
mechanisms by which mercury causes all of these conditions and neuronal
apoptosis are documented in this review (often
synergistically along with
other toxic exposures).
Chronic neurological conditions such
as Alzheimer’s 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
(592,593,598,56g). 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(13,585,593,595-598)
Acetylcholine depletion has been found to be a major factor in Alzheimer’s, and
aluminum has been found to inhibit
choline transport and reduce neuronal choline acetyltransferase, which can lead
to acetylcholine deficiency (580).
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 Alzheimer’s can result (593). Mercury and other toxic metals inhibit
astrocyte function in the brain and CNS(119), causing
increased glutamate and calcium related neurotoxicity (119,333,416,496,593).
Mercury and increased glutamate activate free radical forming processes like
xanthine oxidase which produce oxygen radicals and oxidative neurological damage(142,13).
Nitric oxide related toxicty caused by peroxynitrite formed by the
reaction of NO with superoxide anions, which results in nitration of tyrosine
residues in neurofilaments and manganese Superoxide Dimustase(SOD) has been
found to cause inhibition of the mitochondrial respiratory chain, inhibition of
the glutamate transporter, and glutamate-induced neurotoxicity involved in
ALS(524,521,56g).
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. (585,593,598,600,etc.)
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 depletes GSH and damages cellular mitochrondria, which along
with the increased lipid peroxidation in protein and DNA oxidation in the brain
appears to be major factors in conditions such as autism, Parkinson’s disease,
Alzheimer’s, etc. (33,56,416,442,56g). Some prevention
and repair of such damage to mitochondria has been documented using pyroquinoline
quinine(PQQ) (56g).
Reduced
levels of magnesium and zinc are related to metabolic syndrome, insulin
resistance, and brain inflammation and are protective against these conditions(595,43).
Mercury and cadmium inhibiting magnesium and zinc levels as well as
inhibiting glucose transfer are other mechanisms by which mercury and toxic
metals are factors in metabolic syndrome and insulin resistance/diabetes (43,198,338,597).
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 inflamatory 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,598). 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 (96,198,254,263,264,33,330,331,339,347, 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(119,416,445), induces peroxynitrite
and lipid peroxidation damage(521b), 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 inflamatory
cytokines(126,181). Homocysteine has
been found to facilitate and increase mercury toxicity (19c).
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 Alzheimer’s cases there was a
reduction in serum magnesium and RBC membrane Na(+)-K+
ATPase activity and an elevation in plasma serum digoxin (263). The activity of all serum free-radical
scavenging enzymes, concentration of glutathione, alpha tocopherol, iron
binding capacity, and ceruloplasmin decreased significantly in Alzheimer’s, 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 Alzheimer’s (13a,111,288,442,521b,43,56,263etc.)
Autoimmunity has also been found to be
a factor in chronic degenerative autoimmune conditions such as ALS, with
genetic susceptibility a major
factor in who is affected. One
genetic factor in Hg induced autoimmunity is major histocompatibility complex(MHC) linked.
Both immune cell type Th1 and Th2 cytokine responses are involved in autoimmunity(425c).
One genetic difference found in animals and humans is cellular retention
differences for metals related to the ability to excrete mercury(426). For example it has been found that
individuals with genetic blood factor type APOE-4 do not excrete mercury
readily and bioaccumulate mercury, resulting in susceptibility to chronic
autoimmune conditions such as Alzheimer’s, Parkinson’s, etc. as early as age
40(437b), whereas those with type APOE-2 readily excrete mercury and are less
susceptible (437,35). Those with type APOE-3 are intermediate to
the other 2 types. The incidence of
autoimmune conditions have increased to the extent this is now one of the
leading causes of death among women(450). Also when a condition has been initiated and
exposure levels decline, autoimmune antibodies also decline in animals or humans(233,234c,60,369,405)
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 (85,577). Dozens of studies have documented that
exposure to inorganic mercury causes memory loss and memory problems(435,600). Mercury has been found to cause memory loss
by inactivating enzymes necessary for brain cell energy production and proper
assembly of the protein tubulin into microtubules(258).
In a recent study, mercury at extremely low levels found commonly in those with
amalgam fillings was found to disrupt membrane structure and linear growth
rates of neurites in most nerve growth cones exposed, causing
tubulin/micortubile structure to disintegrate.
The study also found that mercury also interferes with formation of
tubulin producing neurofibrillary tangles in the brain similar to those
observed in Alzheimers patients(207,462,594), as well as causing neuronal
somata to fail to sprout. The process
was found to result in low levels of zinc in the brain(158,43). There is evidence that certain redox active
metal ions including copper and mercury are important in exacerbating and
perhaps facilitating Abeta‑mediated oxidative damage and amyloid deposits
in Alzheimer's disease(462,488,590,594). Mercury has also been shown to induce cell
cytotoxicity and oxidative stress and increases beta‑amyloid secretion
and tau phosphorylation in neuroblastoma
cells resulting in amyloid plaques which is found in Alzheimer’s patients, and
to also cause the formation of the neurofibrilla tangles found in the
Alzheimer’s patient brain(462,258).
Mercury and the induced neurofibrillary tangles also appear to produce a
functional zinc deficiency in the of AD sufferers(242), as well as
causing reduced lithium levels which is another factor in such diseases. Lithium protects brain cells against excess
glutamate induced excitability and calcium influx (280,416,445,56).
These studies clearly implicate mercury as having the ability to cause
neurodegeneration in the brain and CNS, at levels of 20 ppb, which is lower
than that of many with several amalgam fillings or dental occupational exposure(462).
Researchers at Geriatric and Psychiatric Univ. Clinics in Basel,
Switzerland concluded that inorganic mercury appears to be a causative factor
in Alzheimer’s and the Swizz Dental Assoc. recommended avoidance of amalgam use
in those with neurological disorders(462). Clinical experience has also found that DMSO
has some ability to repair tubulin damage(594).
Clinical tests of patients with MND,ALS, Parkinson’s, Alzheimer’s,
Lupus(SLE), rheumatoid arthritis and
autism have found that the patients generally have elevated plasma cysteine to
sulphate ratios, with the average being 500% higher than
controls(330,331,56,33d), and in general being poor sulphur oxidizers. This means that these patients have
insufficient sulfates available to carry out necessary bodily processes and
that cysteine levels build up in the brain and CNS to neurotoxic levels. Mercury has been shown to diminish and block
sulphur oxidation and thus reducing glutathione levels which is the part of
this process involved in detoxifying and excretion of toxics like mercury(33). Glutathione is produced through the sulphur
oxidation side of this process. Low levels of available glutathione have been
shown to increase mercury retention and increase toxic effects(111), while high
levels of free cysteine have been demonstrated to make toxicity due to
inorganic mercury more severe(333,194,56,33d).
Mercury has also been found to play a part in inducing intolerance and
neuronal problems through blockage of the P-450 enzymatic process(84,33d).
Mercury also blocks the immune
function of magnesium and zinc (198,427,43,38), whose
deficiencies are known to cause significant neurological effects(461,463,443).
The low Zn levels result in deficient CuZnSuperoxide dismustase (CuZnSOD),
which in turn leads to increased levels of superoxide due to toxic metal exposure(443). Mercury is known to damage or inhibit SOD activity(33,111). Mercury induced lipid peroxidation
has been found to be a major factor in mercury’s neurotoxicity, along with
leading to decreased levels of glutathione peroxidation and superoxide dismustase(SOD)(13,254,489,494-496).
Mercury inhibits sulfur ligands in
MT and in the case of intestinal cell membranes inactivates MT that normally
bind cuprous ions(477), thus allowing buildup of
copper to toxic levels in many and malfunction of the Zn/Cu SOD function. Modern amalgams commonly used in the U.S.
have higher levels of copper than the traditional silver amalgams and result in
much higher exposure levels to mercury and copper(258).
This is a factor in higher incidence of neurodegnerative condidtions like
Alzheimer’s. Exposure to mercury
results in changes in
metalloprotein compounds that have genetic effects, having both
structural and catalytic effects on gene
expression(114,241,296,442,464,477,495).
Some of the processes affected by such MT control of genes include
cellular respiration, metabolism, enzymatic processes, metal-specific
homeostasis, and adrenal stress response systems. Significant physiological
changes occur when metal ion concentrations exceed threshold levels.
Copper is an essential trace metal
which plays a fundamental role in the biochemistry of the nervous system(489,495,464).
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 and
similar effects on Cu/Zn SOD to be a factor in other conditions such as autism,
Alzheimer’s, Parkinson’s, and non-familial ALS(489,495,464,111). This condition can result in zinc deficient
SOD and oxidative damage involving
nitric oxide, peroxynitrite, and lipid peroxidation(495,496,489), which
have been found to affect glutamate mediated excitability and apoptosis of
nerve cells and effects on mitochondria (416,445,495, 496,119) These effects
can be reduced by zinc supplementation(464,495,517), as well as supplementation
with antioxidants and nitric oxide-suppressing agents and peroxynitrite
scavengers such as Vit C, Vit E, lipoic acid, Coenzyme Q10, carnosine, gingko
biloba, N-acetylcysteine, turmeric, etc.(444,464,494,495,469,497). Some of the
antioxidants were also found to have protective effects through increasing
catalase and SOD action, while reducing lipid peroxidations(494a). Curcumin as an antioxidant, anti-inflammatory
and lipophilic action improves the cognitive functions in patients with AD(497). A growing body of evidence indicates that oxidative
stress, free radicals, beta amyloid, cerebral deregulation caused by bio-metal
toxicity and abnormal inflammatory reactions contribute to the key event in
Alzheimer's disease pathology. Due to various effects of curcumin, such as
decreased Beta-amyloid plaques, delayed degradation of neurons,
metal-chelation, anti-inflammatory, antioxidant and decreased microglia
formation, the overall memory in patients with AD has improved. Ceruloplasmin
in plasma can be
similarly affected by copper metabolism disfunction, like SOD function, and is often
a factor in neurodegeneration(489).
Studies
showed that metals can induce A-beta aggregation and toxicity and are
concentrated in Alzheimer's brain. There
is accumulating evidence that interactions between beta-amyloid and copper,
iron, and zinc are associated with the pathophysiology of Alzheimer's disease
(AD) (590). A significant dyshomeostasis
of copper, iron, and zinc has been detected, and the mismanagement of these
metals induces beta-amyloid precipitation and neurotoxicity. Chelating agents
offer a potential therapeutic solution to the neurotoxicity induced by copper
and iron dyshomeostasis. Currently, the copper and zinc chelating agents clioquinol and desferroxamine represent a potential
therapeutic route that may not only inhibit beta-amyloid neurotoxicity, but may
also reverse the accumulation of neocortical beta-amyloid. There is also evidence that melatonin and
curcumin may have beneficial effects on reducing metal toxicity(591,497).
Turmeric/curcumin has been found to
reduce some of the toxic and inflammatory effects of toxic metals(497,498).
Low levels of mercury and toxic
metals have been found to inhibit dihydroteridine reductase, which affects the
neural system function by inhibiting transmitters through its effect on
phenylalanine, tyrosine and tryptophan transport into neurons
(122,257,289,342,372). This was found
to cause severe impaired amine synthesis and hypokinesis. Tetrahydrobiopterin, which is essential in
production of
neurotransmitters, is significantly decreased in patients with
Alzheimer’s’s, Parkinson’s, MS, and
autism. Such patients have abnormal inhibition of neurotransmitter production.
Some studies have also found persons with
chronic exposure to electromagnetic fields(EMF) to
have higher levels of mercury exposure and excretion(38).
Magnetic fields are known to induce current in metals and would increase the
effects of galvanism. Occupational
exposure to higher levels of EMF have also been found in many studies to result
in much higher risk of chronic degenerative neurological conditions such as ALS(39) and Alzheimer’s Disease(40) Since EMF causes increased mercury exposure
in those with amalgam, and mercury is also known to cause these conditions,
again it is not clear the relative importance of the factors since the studies
were not controlled for mercury levels or number of amalgam fillings.
Studies have also found a correlation between high levels of aluminum
exposure and dementia such as Alzheimer’s(470,580),
and concluded based on extensive
literature that the neurotoxic effects of aluminium are beyond any doubt, and
aluminium as a factor in some AD cannot be discarded (470b). It is well
documented that neurological effects of toxics are synergistic. Flu shots have mercury and aluminum which
both are known to accumulate in the brain over time. A study of people who
received flu shots regularly found that if an individual had five consecutive flu shots between 1970
and 1980 (the years studied) his/her chances of getting Alzheimer's Disease is
ten times higher than if they had one or no shots(475).
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 Alzheimer’s (66,67,158,166,204, 207,
221,238,242,244,257,300,303,369,444d,462,35,38d) and significantly improve
after dental amalgam replacement and dental infection cleanup. 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(122,257,289,372). This was found to cause severe impaired
amine synthesis and hypokinesis. Tetrahydro-biopterin, which is essential in
production of
neurotransmitters, is significantly decreased in patients with
Alzheimer’s’s, Parkinson’s, and MS. Such patients have abnormal inhibition of
neurotransmitter production.(supplements which inhibit
breach of the blood brain barrier such as bioflavonoids have been found to slow
such neurological damage).
Also mercury binds with cell membranes interfering
with sodium and potassium enzyme functions, causing excess membrane
permeability, especially in terms of the blood-brain barrier
(155,207,311). Less than 1ppm mercury
in the blood stream can impair the blood- brain barrier. Mercury was also found to accumulate in the
mitochondria and interfere with their vital functions, and to inhibit
cytochrome C enzymes which affect energy supply to the brain(43,84,232,35). Persons with the APO-E4 gene form of apolipoprotein E which transports
cholesterol in the blood, are especially
susceptible to this damage(207,221,346,437,580), while those with APO-E2 which
has extra cysteine and is a better mercury scavenger have less damage. The majority have an intermediate form
APO-E3. This appears to be a factor in susceptibility to Alzheimer’s
disease, Parkinson’s disease and multiple sclerosis(291). Ones susceptibility can be estimated by
testing for
this condition. Repeated exposure to pesticides has
also been found to increase Alzheimer's Disease risk(586).
A major systematic review of all medical studies found on the connection of mercury exposure and Alzheimer’s Disease was recently carried out by MDs and PhDs. (435) Studies were screened according to a pre-defined protocol. The author’s noted that mercury is one of the most toxic substances known to humans and in addition to being widespread in the environment has also been used extensively in vaccinations and dental amalgam. Studies were screened according to a pre-defined protocol. Most of the studies testing memory in individuals exposed to inorganic mercury(IM), found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. “ In vitro models showed that IM reproduces all pathological changes seen in AD, and in animal models IM produced changes that are similar to those seen in AD. Its high affinity for selenium and selenoproteins suggests that IM may promote neurodegenerative disorders via disruption of redox regulation.” IM appears to play a role as a co-factor in the development of AD. It appears to also increase the pathological influence of other metals through adverse effects on the blood brain barrier. “ Our mechanistic model describes potential causal pathways. It concludes: “As the single most effective public health primary preventive measure, industrial, and medical usage of mercury should be eliminated as quickly as possible.”
“Earlier research on the biochemical abnormalities of the Alzheimer’s Diseased (AD) brain showed that mercury, and only mercury, at very low levels induced the same biochemical abnormalities when added to normal human brain homogenates or in the brains of rats exposed to mercury vapor.” (438) "Since the brain is more vulnerable to oxidative stress than any other organ, it is not surprising that mercury, which promotes oxidative stress, is an important risk factor for brain disorders."
III.
Insulin resistance as a factor in Alzheimer’s
Higher insulin and glucose levels in
the blood and deficiency of glucose in brain cells that need it has been found
to lead to neurological problems such as Alzheimer’s (580,581). Those with
either type I or type II diabetes have been found to be more likely to have
other chronic conditions including heart disease, strokes, kidney disease,
Alzheimer’s, eye conditions and blindness (580,581). Diabetes also impacts memory by increasing the
risk blood vessels will become obstructed, restricting blood flow to the brain.
High blood glucose levels also impact cognition through formation of
sugar-related toxins called advanced glycation end products (AGEs). AGEs have been found to be a factor in aging,
diabetes, and Alzheimer’s. Glycotoxins
are formed when sugars interact with proteins and lipids, damaging the
structure of proteins and membranes, rendering them less able to carry out
their many vital processes. (581). Studies have shown that AGEs are a key
factor in cross-linking of harmful beta-amyloid plaques in the brain that are
implicated in Alzheimer’s. As
previously documented mercury and aluminum exposure increase insulin resistance
and amalgam replacement and detoxification reduce insulin resistance.
Inflammation induced by vaccine
adjuvants like aluminum and mercury or by excitotoxins like MSG has been found
to play a significant role in insulin resistance (type-2 diabetes) and in high
levels of LDL cholesterol (597,598,585,593). Reduced levels of
magnesium and zinc are related to metabolic syndrome, insulin resistance, and
brain inflammation, and these are protective against these conditions (599,43). Mercury and
cadmium by inhibiting magnesium and zinc levels as well as inhibiting glucose
transfer are other mechanisms by which mercury and toxic metals are factors in
metabolic syndrome and insulin resistance/diabetes (43,198,338,597). Mercury inhibits
production of insulin and is a factor in diabetes and hypoglycemia, with significant
reductions in insulin need after replacement of amalgam filings and normalizing
of blood sugar(35,502). Iron overload has also been found to be a cause of insulin
resistance/type 2 diabetes(582).
IV. Treatment of Alzheimer’s
In some cases replacement of amalgam
fillings or toxic metals chelation has been found to result in cure or
significant improvement in Alzheimer’s patients (204,35,38c).
Alzheimer’s patients commonly are
found to be deficient in omega 3 fatty acids, vit C, B12, SAMe, vit K, etc. and
clinical experience has found supplementing these to be beneficial in some
cases (580). 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 . Supplements with clinical experience
indicating benefit in many Alzheimer’s/dementia cases include pantothenic
acid(B5), vit B12, vit B1, vit B6, Vit E, Ginkgo Biloba, Vit C,
Acetyl-L-Carnatine, CoQ10, EFAs(DHA/EPA), N-Acetyl-Cysteine(NAC), SAMe, folate,
inositol, melatonin, carnosine (580).
Two treatments shown to be significantly beneficial in the majority of
Alzheimer’s patients using the supplement are Huperzine A and Kami-Umtan-To
(KUT) (580). 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 (280).
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Exposure levels and health effects related to mercury/dental amalgam and
results of amalgam replacement, 2002;B Windham(Ed.),(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
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everyone. B. Windham(Ed.) (Gov’t studies) www.flcv.com/damspr2f.html
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Disrupting Chemicals" (including mercury),
Annotated Bibliography ,2004, B.Windham,
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Note: etc. when it is used in a list of references means
that Author knows of several more references supporting the statement, in #600
for example, but doesn’t
think them necessary here.
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