Chronic fatigue syndrome, Fibromyalgia, Scleroderma, Lupus, Rheumatoid
Arthritis, MCS: the mercury
connection. B. Windham (Ed.) 2009.
I.
Introduction.
Chronic
fatigue syndrome(CFS) is characterized by fatigue,
neurologic symptoms including headaches, brain fog, mood disorders, and motor
dysfunction. Millions of people in the U.S. suffer from CFS. An estimated three to six million patients in
the US are affected by fibromyalgia (FMS) (581). Spect scans of those with CFS have found that
the majority have over 5 times more areas of regional brain damage and reduced
blood flow in the cerebral cortex area of the brain(471)
than controls. The majority studied were also found to
have increased Th2 inflammatory cytokine activity and a blunted DHEA response
curve to I.V. ATCH
indicative of hypothalamic/adrenal deficiency such as relative glucocorticoid
deficiency (472).
CFS
and Fibromyalgia patients have also been found to commonly have abnormal
enzymatic processes that affect the sodium‑potassium ATPase energy channels(473), which appears to be a major factor in the
condition and for which mercury is a
known cause(43,288,498). This also has
been found to result in inflammatory processes that cause muscle tissue damage
and result in higher levels of urinary excretion of creatine
, choline, and glycine in CFS, and higher levels of excretion of
choline, taurine, citrate, and trimethyl amine oxide in FM(474,593,594). Supplementation of creatine has been found to
result in improved muscle mitochondrial function in such patients(502). FM is further characterized by muscle and
fibrous tissue pain, and its prevalence has been estimated at greater
than 7% in women aged 60-79 years and 3.4% for all women(528). A Swedish study found that in one county,
11.6% of women over 35 surveyed had symptoms of Fibromyalgia, while 5.5% of men
reported such symptoms(368). A study found that for a group of patients
that had both CFS and FM, all had high homocysteine levels, a marker of
inflammation (580,Regland et al, 1997). Other factors in CFS and Fibromyalgia include
oxidative stress, metal sensitivity,adrenal fatigue,
autoimmunity, leaky gut,
organic acid imbalances, food allergies, IBS,
digestive malabsorption of essential nutrients, along with overgrowth of
intestinal yeasts, bacteria, or parasites (386a,580.581,586). Research suggests
that as many as 75% of individuals with fibromyalgia have bacterial overgrowth
in the small bowel. Clinical experience has found that the pathogen overgrowths
cannot be fully eliminated without detoxification of mercury and toxic metals
which facilitate the pathogen overgrowths(581).
Tests also
found mercury accumulation in the limbic system and muscle tissues of a sample
of fibromyalgia patients tests, and significant improvement after dental
revision to replace amalgam fillings and deal with toxic root-canal teeth and cavitations(586).
II. Mercury
sources and exposure levels.
Amalgam
fillings are the largest source of mercury in most people with daily exposures
documented to commonly be above government health guidelines(49,79,506,600).
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
(600). 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 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 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). Antioxidants have been found to protect
against such mercury neurotoxicity(494,572).
Mercury (especially mercury vapor) rapidly
crosses the blood brain barrier and is
stored preferentially in the pituitary
gland, hypothalamus, thyroid gland, adrenal gland, and occipital cortex in
direct proportion to the number and extent of amalgam surfaces (20, many
studies referenced in (600)) Thus
mercury has a greater effect on the functions of these areas. The range in one study was 2.4 to 28.7
parts per billion(ppb), and one study found on average
that 77% of the mercury in the occipital cortex was inorganic(600).
III. Effects of Mercury (and toxic metal) Exposure
Some of the factors documented
to be involved in inflammatory conditions like CFS, FMS, Lupus, Rheumatoid
Arthritis, etc and in programmed cell death, apoptosis, of neurons and immune
cells in degenerative neurological conditions like ALS, Alzheimer’s, MS,
Parkinson’s, etc. include inducement of
the inflammatory cytokine Tumor Necrosis Factor-alpha(TNFa) (126), reactive
oxygen species and oxidative stress (13,43a,56a,296b,386a), reduced glutathione
levels(56,126a,111a), liver enzyme effects and inhibition of protein kinase C
and cytochrome P450(43,84,260), nitric oxide and peroxynitrite toxicity (43a,521,524),
excitotoxicity and lipid peroxidation(490,496), excess free cysteine levels
(56d,111a,33,330),excess glutamate toxicity(13b, 416), excess dopamine toxicity
(56d,13a), beta-amyloid generation(462,56a), increased calcium influx toxicity
(296b,333,416,432,462c,507) and DNA fragmentation (296,42,114,142) and
mitochondrial membrane dysfunction (56de, 416), and autoimmunity
(313,342,382,405,513). As will be
documented, mercury and toxic metals exposure causes all of these factors.
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
conditions like CFS, FM, RA, Lupus, etc. and in 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 inflammatory and apoptosis mechanism(126a). glutathione is an amino acid that is a normal cellular mechanism for controlling
inflamation and apoptosis. When
glutathione is depleted in the brain, reactive oxidative species increase, 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 (42,114,142,197,296,392);
alteration of protein structure (33,111,114,194,252,263,442); alteration of the transport and signaling
mechanisms of calcium(333,43b,254,263,416d,462,507); inhibitation of glucose
transport(338,254), and of enzyme function and transport/absorption of other
essential nutrients (96,198,254,263,264,33,330,331,338,339,347,441,442); induction of free radical formation(13a,43b,54,405,424),
depletion of cellular glutathione(necessary for detoxification processes)
(56,111,126,424), inhibition of glutathione peroxidase enzyme(13a,442),
inhibits glutamate uptake(119,416), induces peroxynitrite and lipid
peroxidation damage(521b,56b), causes abnormal migration of neurons in the
cerebral cortex(149), immune system
damage (111,126,181,194,226,252, 272,316,355); affects dopamine uptake by
neuronal synaptosomes(288), inducement
of inflammatory cytokines(126,152,181), and induces autoimmunity
(181,313,342,382,405,etc.). Mercury’s
activation of inflammatory cytokines and Th2 helper immune cells suppresses the
cytotoxic response of T-cells and natural killer immune cells that are the
body’s main defense against viruses and such biological pathogens(181,472,580).
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: Lupus (SLE) (331a,330a,33,113,126,181,234,260d,288a,405,270,226,
314,316,263c,456) & Scleroderma (330a,33,126,181,234,468,405,263c) &
Rheumatoid
Arthritis(287,288a,416f,331b, 330a,33,126,181,405,263d,260d), as well as CFS and FMS that are also related
to inflammatory cytokine processes and autoimmunity
(181,118,313,314,342,382,405,126, 330, 33,263,582,etc.). One study found that
insertion of amalgam fillings or nickel dental materials causes a suppression
of the number of T‑lympocytes(270), and impairs
the T‑4/T‑8 ratio. Low T4/T8 ratio has been found to be a factor in
lupus, anemia, MS, eczema, inflammatory bowel disease, and glomerulonephritis.
Mercury
induced autoimmunity in animals and humans has been found to be associated with
mercury's expression of major histocompatibility complex(MHC)
class II genes(314,181,226,425c). Both
mercuric and methyl mercury chlorides caused dose dependent reduction in immune
B‑cell production(316). B‑cell expression of IgE receptors were
significantly reduced(316,165), with a rapid and
sustained elevation in intracellular levels of calcium induced(316,333).
Mercury
and other toxic metals also form inorganic compounds with OH, NH2, CL, in
addition to the SH radical and thus inhibits many cellular enzyme processes,
coenzymes, hormones, and blood cells(405,600). Mercury has been found to impair conversion
of thyroid T4 hormone to the active T3 form as well as causing autoimmune
thyroiditis common to such patients(342,382). In general, immune activation from toxic
metals such as mercury resulting in cytokine release and abnormalities of the
hypothalamus‑pituitary‑adrenal (HPA)
axis can cause changes in the brain, hypocortisolism, fatigue, and severe psychological symptoms
(348,342,375,379‑382,385,386a,405,118) such as profound fatigue,
muscoskeletal pain, sleep disturbances, gastrointestinal and neurological
problems as are seen in CFS, Fibromyalgia, and autoimmune thyroiditis. Such hypersensitivity has been found most
common in those with genetic predisposition to heavy metal sensitivity (60,313,342,405),
such as found more frequently in patients with human lymphocyte antigens (HLA‑DRA)
(381-383). A
significant portions of the population appear to fall in this category.
Mercury exposure through dental fillings
appears to be a major factor in chronic fatigue syndrome(CFS) and Fibromyalgia through
its effects on ATP and immune system(lymphocyte reactivity, neutraphil
activity, effects on T‑cells and B‑cells) as well as its promotion of
growth of Candida albicans in the body and the methylation of inorganic mercury
by candida and intestional bacteria to the extremely toxic methyl mercury form,
which like mercury vapor crosses the blood‑brain barrier, and also
damages and weakens the immune system (222,225,226,234,235,265,293,60,313,314,342,404,581,
590). Mercury vapor or Inorganic
mercury have been shown in animal studies to induce autoimmune reactions and
disease through effects on immune system T cells(226,268,269,270,314). Chronic immune activation is common in CFS,
with increase in activated CD8+ cytotoxic T-cells and decreased NK cells(518).
Numbers of suppressor-inducer T cells and NK cells have been found to be
inversely correlated with urine mercury levels(270ad). CFS and FMS patients usually improve and
immune reactivity is reduced when amalgam fillings are replaced (342,383,405,581,590,293).
Heavy
metal toxicity has been found to be a common co-factor in FMS
, as well as root canaled teeth and jawbone cavitations (582). Nickel
has been often found to be a factor in chronic autoimmune conditions like CFS
and Lupus (342,456, etc.)
Chronic
neurological conditions 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, 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(13,595-598,386a,etc.) Exposures to heavy metal toxins can impair
energy production and burden the detoxification system(386a). Oxidative stress caused by unstable free
radical molecules can damage the energy-producing mechanisms inside the body’s
cells. Fatigue and/or muscle pain can
develop from toxic stress when the body is unable to detoxify harmful waste
products or toxins from the environment (386a).
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 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).
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 (598). Inflammation also
disrupts brain neurotransmitters resulting in reduced levels of serotonin,
dopamine, and norepinephrine which can lead to depression.
(593) Some of the main causes of such
disturbances that have been documented include vaccines, mercury, aluminum,
other toxic metals, MSG, aspartame, etc. (593,598,600,etc.)
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 (43,196,338,597).
Fatigue is a hallmark symptom of thyroid
or adrenal hormone imbalances (386a,581). Mercury
lymphocyte reactivity, effects on glutamate in the CNS, and mercury induced hypothyroidism induce
CFS type symptoms including profound tiredness, musculoskeletal pain, sleep
disturbances, gastrointestinal and neurological problems along with other CFS
symptoms and Fibromyalgia (342,346,405,293). Mercury has been found to be a
common cause of Fibromyalgia (293,346,342,523,527,581). 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 and facilitating
neurotransmission, 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 Fibromyalgia symptoms. This is also a
factor in conditions such as CFS, Parkinson's, and ALS(346,416).
Animal studies have confirmed that increased levels of glutamate(or
aspartate, another amino acid excitory neurotransmitter) cause increased
sensitivity to pain , as well as higher body temperature‑ both found in
CFS/Fibromyalgia. Mercury and increased glutamate activate free radical forming
processes like xanthine oxidase which produce oxygen radicals and oxidative
neurological damage(142,346,13). Medical studies and
doctors treating Fibromyalgia have found that supplements which cause a
decrease in glutamate or protect against its effects have a positive effect on
Fibromyalgia. Some that have been found to be effective include Vit B6, methyl
cobalamine(B12), L‑carnitine, choline, ginseng, Ginkgo biloba, vitamins C
and E, nicotine, and omega 3 fatty acids(fish and flaxseed
oil-GLA,EPA,DHA)(417,229). Other supplements
that also have been found to help are magnesium and malic acid(488,489). Avoidance of exictotoxins like MSG and
aspartame have been found to eliminate symptoms in some with Fibromyalgia(490).
Clinical tests of patients with
chronic neurological conditions, 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 (330,331,600,33e), and in general being poor sulphur oxidizers. This
means that these patients have insufficient sulfates available to carry out
necessary bodily processes. Mercury has been shown to diminish and block
sulphur oxidation and thus reducing glutathione levels which is the part of
this process involved in detoxifying and excretion of toxics like mercury(33). Glutathione is produced through the sulphur
oxidation side of this process. Low levels of available glutathione have been
shown to increase mercury retention and increase toxic effects(111),
while high levels of free cysteine have been demonstrated to make toxicity due
to inorganic mercury more severe(333,194,33e). Mercury has also been found to
play a part in inducing intolerance and neuronal problems through blockage of
the P‑450 liver enzymatic process(84,33e).
Mercury from amalgam interferes with
production of cytokines that activate macrophage and neutrophils, disabling
early control of viruses and leading to enhanced infection(131,251).
Mercury’s activation of inflammatory cytokines and Th2 helper immune cells
suppresses the cytotoxic response of T-cells and natural killer immune cells
that are the body’s main defense against viruses and such biological pathogens(181,472,580). Animal studies have confirmed that
mercury increases effects of the herpes simplex virus type 2 for example(131). Mercury damages the immune system and in those
with chronic conditions has been found to commonly facilitate infestation by
pathogens such as viruses, harmful bacteria, candida, mycoplasma, and parasites(131,251,386a,404,460,470, 473,485). The majority
of those tested who have CFS or FMS have been found to have infections of
mycoplasma, Human Herpes Virus-6,XMRV, Cytomeglivirus,
or bacterial infections such as intracellular chlamydia(470,575,580). Clinics treating these conditions commonly
find such pathogens to be a factor in the condition (470,473,485,487,488, 580). Mercury detoxification and treatment of these
pathogens results in significant improvement in the majority of those treated
(470,485,488,489, 230,581,600). Studies
have also found bilberry extract, curcumin, carotenoids, and chlorophyll
supplements to be effective in suppressing effects of viruses such as
Epstein-Barr (580) or XMRV(575). Supplementation with chlorella has been found
to result in beneficial effects when used in patients chronic conditions such
as ulcerative colitis, hypertention, or Fibromyalgia(304).
Doctors such as D. Klinghardt (581) have suggested that the mechanism by which
chlorella improves treatment of such conditions is metals detoxification, which
is the main mechanism of action of chlorella and has been found to greatly
improve intestinal function.
Mercury exposure causes high levels of oxidative
stress/reactive oxygen species(ROS)(13,386a), 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 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)
IV.
Multiple Chemical Sensitivity
Many
cases of Multiple Chemical Sensitivity (MCS) develop following exposures to
heavy metal toxins such as mercury(386a). Mercury
exposure results in oxidative stress, reduced glutathione, increased
peroxynitrite, found in virtually all with MCS or CFS or FM, which have
overlapping symptoms and factors. Oxidative stress from reactive free radicals
or deficient glutathione and the resulting increased peroxynitrite can
inactivate important mitochondrial enzymes and interfere with energy production
in MCS or CFS (386a,580). Inherited impairments in detoxification
function can also interact with environmental factors to promote MCS. Defects
in the body’s ability to neutralize environmental chemicals lead directly to
the accumulation of toxins. The body’s
ability to neutralize and excrete environmental toxins depends on the
availability of key nutrients. Some cases of MCS may be secondary to ‘leaky
gut’ and the passage of toxins or food particles into the system. Maldigestion of critical nutrients, as
well as intestinal infection (bacteria, yeast, or parasites) may aggravate
MCS. Intestinal overgrowth of yeast and
the passage of Candida toxins into the system or parasites may further chemical
sensitivities in MCS or CFS(386a,580).
V.
Treatment of CFS, Fibromyalgia, Multiple Chemical Sensitivity, etc.
It has been well documented by hundreds
of medical studies including thousands of tested subjects and by scientific
panels that "amalgam fillings" are the largest source
of mercury in people and that those with several amalgam
fillings often have daily exposures exceeding the Government Health Standards
for mercury(600). Thus among those most susceptible, significant neurological
and immune effects related to amalgam fillings are common. Symptoms of those
with CFS, Fibromyalgia, or thyroid related conditions usually improve
significantly after proper amalgam replacement.
In thousands of cases undergoing amalgam replacement, the majority
recovered or had significant improvement in symptoms for muscular/joint pain/ Fibromyalgia
(222,293,317,322,342,440,469,470,523,527, 94), Chronic Fatigue Syndrome(CFS)
(8,27,60,212,230,293,229,222,232,233,271,293,313, 317,320,342,375,376,382,440,469,470,485,590,35),
lupus (342,113,222, 229,233,323,35), autoimmune thyroiditis (342,382), multiple
chemical sensitivities (26,27,35,60,62,95,222,229,232,233,115,313,321, 342,537,583),
as well as many other
conditions(600). Of one group of 86 patients with CFS symptoms, 78% reported significant health improvements after replacement of amalgam
fillings within a relatively short period, and the MELISA
immune reactivity test found significant reduction in lymphocyte reactivity
compared to pre removal tests(342,375). The
improvement in symptoms and lymphocyte reactivity imply that most of the Hg‑induced
lymphocyte reactivity is allergenic in nature. Although patch tests for mercury
allergy are often given for unresolved oral symptoms, this is not generally
recommended as a high percentage of such problems are resolved irrespective of
the outcome of a patch test (60,87,90,etc.) Exposure to organochlorine
compounds such as DDT/DDE and hexachlorobenzene have also been found to be
highly correlated with chronic fatigue.
Other Treatments for CFS and FM
Nutrition and nutritional support have
been found to play significant roles in CFS/FM alleviation(580,386a,etc.). An adequate supply of
vitamins and essential minerals as well as antioxidants have been found
to benefit such conditions to counteract free radicals and oxidative stress
caused by the conditions. Glyconutrients such as Mannatech Ambrotose and
Immunostart have also been found to be effective in reducing the effects of CFS
and FM(528). Immunostart has been documented to be
effective in detoxing toxic metals.
Some of the conditions found in people
with CFS or FM or MCS include immune effects, energy metabolism problems,
inflammation, adrenal fatigue, homocystein metabolism, fatigue, stress, brain
neurotransmitter imbalances, leaky gut. (580,386a,etc.) In addition to metals detox, supplementation has been
found clinically effective to deal with these conditions. Immune(ginseng,
echineacea, EFAs, curcumin); energy metabolism(CoQ10, NADH, L-carnatine,
magnesium) ; Adrenal fatigue(DHEA,
licorice, sodium); Stress(glutamine, Adapton); neurotransmitters(tyrosine);
homocysteine(B6,B12,folic acid, SAMe); inflammation(antioxidants:
N-acetyl-cysteine, alpha lipoic acid), fatigue(ginseng, Mate), digestive
support(digestive enzymes, probiotics) (580)
Tests are
readily available to check for hormone levels often out of imbalance in these
conditions such as DHEA, cortisol, thyroid, and testosterone in older men (386a,580,etc.).
B.E.Vickery’s testing showed all
Fibromyalgia patients to have five common conditions, regardless of their
symptoms: 1)protein deficiency 2)degenerating spinal
disks 3)sulfur deficiency 4) heavy metal toxicity , and 5) viral infection.
(585) It is claimed that if
they follow the Vickory Protocol their bodies are able to heal.
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.
(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
(26)
A.F.Zamm, “Removal of dental mercury: often an effective treatment for very
sensitive patients”, J Orthomolecular
Med, 1990, 5(53):138-142. (22 patients)
(33) (a) Markovich et al, "Heavy metals
(Hg,Cd) inhibit the activity of the liver and kidney sulfate transporter Sat‑1",
Toxicol Appl Pharmacol, 1999,154(2):181‑7; &
(b)2S.A.McFadden, “Xenobiotic metabolism and adverse environmental response:
sulfur- dependent detox
pathways”,Toxicology, 1996, 111(1-3):43-65; &(c) S.C. Langley-Evans et al, “SO2: a potent
glutathion depleting agent”, Comp Biochem Physiol Pharmocol Toxicol Endocrinol,
114(2):89-98; & (d)Alberti A, Pirrone P, Elia M, Waring RH,
Romano C. Sulphation
deficit in “low-functioning” autistic children. Biol Psychiatry 1999,
46(3):420-4.
(34) 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; &
CFS, www.hugginsappliedhealing.com/fatigue.php
(42) Rodgers JS,
Hocker JR, et al,
Mercuric ion inhibition of eukaryotic transcription factor
binding to DNA. Biochem Pharmacol. 2001 Jun
15;61(12):1543-50; & K.Hansen et al A survey of metal induced
mutagenicity in vitro and in vivo, J
Amer Coll Toxicol , 1984:3;381‑430;
(43) (a)Knapp LT; Klann
E. Superoxide‑induced stimulation
of protein kinase C via
thiol modification and modulation of zinc content. J Biol Chem
2000 May 22; & P.Jenner,“Oxidative mechanisms in PD”, Mov Disord, 1998;
13(Supp1):24-34;&(b) Rajanna B et al, “Modulation of protein kinase
C by heavy metals”, Toxicol Lett, 1995, 81(2-3):197-203: & Badou A et al,
“HgCl2-induced IL-4 gene expression in T cells involves a protein kinase
C-dependent calcium influx through L-type calcium channels”J Biol Chem. 1997
Dec 19;272(51):32411-8., & D.B.Veprintsev, 1996, Institute for Biological
Instrumentation, Russian Academy of Sciences,
Pb2+ and Hg2+ binding to alpha‑lactalbumin”.Biochem Mol Biol Int
1996 ;39(6): 1255‑65; & M. J. McCabe, University of Rochester
School of Medicine & Dentistry, 2002, Mechanisms of Immunomodulation by
Metals, www.envmed.rochester.edu/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
(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, 77(3):461-71
(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.
(60)V.D.M.Stejskal, Dept. Of Clinical Chemistry, Karolinska
Institute, Stockholm, Sweden LYMPHOCYTE IMMUNO‑STIMULATION ASSAY ‑MELISA"
& VDM Stejskal et al, "MELISA: tool for the study of metal
allergy", Toxicology in Vitro, 8(5):991‑1000, 1994. http://www.melisa.org
(62)
Dr. J.E. Hardy, Mercury Free: the wisdom behind the growing consumer moverment
to ban silver dental fillings, 1998.
(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).
(87)A. Skoglund, Scand
J Dent Res 102(4): 216‑222, 1994; and 99(4):320‑9,1991(40 cases);
& P.O.Ostman et al, "Clinical & histologic changes after removal
of amalgma", Oral Surgery, Oral Medicine, and Endodontics, 1996, 81(4):459‑465;
& S.H.Ibbotson et al, "The relevance of amalgam replacement on oral
lichenoid reactions", British Journal of Dermatology, 134(3):420‑3,
1996; & J.Bratel et al, "Effect of Replacement of Dental Amalgam on
OLR", Journal of Dentistry, 1996, 24(1‑2):41‑45(. (431 cases)
(90)P.Koch et al,
"Oral lesions and symptoms related to metals", Dermatol,1999,41(3):422‑430; & "Oral lichenoid
lesions,mercury hypersensitity, ...", Contact Dermatitis, 1995, 33(5): 323‑328;
& S.Freeman et al, "Orallichenoid lesions caused by allergy to mercury
in amalgam", Contact Dermatitis, 33(6):423‑7, Dec 1995 (Denmark)
(94) F.Berglund, Case reports spanning 150 years
on the adverse effects of dental amalgam,
Bio-Probe, Inc.,Orlando,Fl,1995;ISBN 0-9410011-14-3(245 cured); &
Tuthill JY, "Mercurial neurosis resulting from amalgam
fillings", The Brooklyn Medical Journal, December 1898, v.12, n.12,
p725-742
(95)H.J.Lichtenberg,
"Elimination of symptoms by removal of dental amalgam from mercury
poisoned patients", J Orthomol Med 8:145-148, 1993(120 patients);
& “Symptoms before and after proper
amalgamremoval in relation to serum globulin reaction to metals”,J of Orthomol
Med., 1996, 11(4):195-9. (118 cases) http://www.lichtenberg.dk/symptoms_before_and_after_proper.htm
(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.
(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;
(113)T.A.Glavinskiaia
et al, "Complexons in the treatment of lupus erghematousus", Dermatol
Venerol, 1980,12: 24‑28; & A.F.Hall, Arch
Dermatol 47, 1943, 610‑611.
(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) Tibbling L,
Stejskal VDM, et al, Immunolocial and brain MRI changes in patients with
suspected metal intoxication", Int J Occup Med Toxicol 4(2):285‑294,1995.
(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; & 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.
(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.
(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
(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.
(181)P.W.
Mathieson, "Mercury: god of TH2 cells",1995, Clinical Exp
Immunol.,102(2):229‑30;& &
Heo Y, Parsons PJ, Lawrence DA, Lead differentially modifies cytokine
production in vitro and in vivo. Toxicol
Appl Pharmacol, 196; 138:149-57; & Murdoch RD, Pepys J; Enhancement of
antibody and IgE production by mercury and platinum salts. Int Arch Allergy
Appl Immunol 1986 80: 405-11.
(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;
(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;
(212)Ziff, M.F.,
"Documented Clinical Side Effects to Dental Amalgams", ADV. Dent.
Res.,1992; 1(6):131‑134; & S.Ziff,Dentistry without Mercury, 8th
Edition, 1996, Bio‑Probe, Inc., ISBN 0‑941011‑04‑6;
& Dental Mercury Detox, Bio‑Probe, Inc. http://www.bioprobe.com.
(cases:FDA Patient Adverse Reaction Reports‑762, Dr.M.Hanson‑Swedish
patients‑519, Dr. H. Lichtenberg‑100 Danish patients,Dr. P.Larose‑
80 Canadian patients, Dr. R.Siblerud, 86 Colorado patients,Dr. A.V.Zamm, 22
patients)
(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;
(225)S. Yannai et
al, "Transformationss of inorganic mercury by candida albicans and
saccharomyces cerevisiae", Applied Envir Microbiology,1991, 7:245‑247;
& N.E.Zorn et al, " A relationship between Vit B‑12, mercury
uptake, and
methylation", Life Sci, 1990, 47(2):167‑73; & W.P.Ridley et al,
Environ Health Perspectives, 1977, Aug 19, 43‑6; & R.E.DeSimone et
al, Biochem Biophys Acta, 1973,May 28; & Yamada, Tonomura"Formation of
methyl Mercury Compounds from inorganic Mercury by Chlostridium
cochlearium" J Ferment Technol1972 50:159‑1660
(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); & Andrew Hall Cutler, PhD, PE; Amalgam Illness:Diagnosis and Treatment; 1996 , www.noamalgam.com/
(230) Rogers S(MD),
The E.I. Syndrome: An Rx for Environmental Illness, Keats Publishing, Amazon Books
(233)F.Berglund,Bjerner/Helm,Klock,Ripa,Lindforss,Mornstad,Ostlin),
“Improved Health after Removal of
dental amalgam fillings”, Swedish Assoc.
Of Dental Mercury Patients, 1998. http://iaomt.org/articles/files/files214/Hansen-%20effects%20of%20amal%20removal.pdf
(234) P.E. Bigazzi,
"Autoimmunity and Heavy Metals", Lupus, 1994; 3: 449‑453; &
Pollard KM, Pearson Dl, Hultman P. Lupus‑prone mice as model to study
xenobiotic‑induced autoimmunity. Environ Health Perspect 1999;
107(Suppl 5): 729‑735;
& &
Nielsen JB; Hultman P. Experimental
studies on genetically determined susceptibility
to mercury‑induced autoimmune response.
Ren Fail 1999 May‑Jul;21(3‑4):343‑8; & Feighery L, Collins C, Anti-transglutaminase antibodies and the
serological diagnosis of coeliac disease.
Br
J Biomed Sci. 2003;60(1):14-8; & & Mayes
MD. Epidemiologic studies of
environmental agents and systemic autoimmune diseases. Environ Health Perspect.
1999 Oct;107 Suppl 5:743-8; &. Bigazzi PE.
Metals and kidney autoimmunity.
Environ Health Perspect. 1999 Oct;107 Suppl 5:753-65
(235) H.J.Hamre,
Mercury from Dental Amalga and Chronic Fatigue Syndrom", The CFIDS
Chronicle, Fall 1994, p44‑47.
(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.
(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; & Kurup RK, Kurup
PA. Hypothalamic digoxin, cerebral
chemical dominance and myalgic encephalomyelitis. Int J Neurosci. 2003 May;113(5):683-701,
& (c) Kurup RK, Kurup PA. Hypothalamic
digoxin, hemispheric dominance, and neuroimmune integration. Int J Neurosci. 2002
Apr;112(4):441-62; & (d) Kurup RK, Kurup PA, Hypothalamic digoxin and
hemispheric chemical dominance--relation to the pathogenesis of senile
osteoporosis, degenerative osteoarthritis, and spondylosis. Int J Neurosci.
2003 Mar;113(3):341-59.
(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
(265)K.Lohmann et
al, "Multiple Chemical Sensitivity Disorder in patients with neuroltoxic
illnesses", Gesundheitswesen, 1996, 58(6):322‑31.
(268)J.J.Weening et
al, "mercury induced immune complex glomerulopathy", Chap 4, p36‑66,
VanDendergen, 1980, & P.Duuet et al, "Glomerulonephritis induced by
heavy metals", Arch Toxicol. 50:187‑194,1982 & Transplantation
Proceedings,Vol
XIV(3),1982,482‑
(269)(a)C.J.G.Robinson
et al, "Mercuric chloride induced anitnuclear antibodies In mice",
Toxic Appl Pharmacology, 1986, 86:159‑169. &(b) P.Andres, IgA‑IgG
disease in the intestines of rats ingesting HgCl", Clin Immun Immunopath,
30:488‑494, 1984; &(c) F.Hirsch et al, J Immun.,136(9), 3272‑3276,
1986 & (d)J.Immun.,136(9):3277‑3281; & (e)J Immun.,
137(8),1986,2548‑ & (f)Cossi et al, "Benefiecial effect of human
therapeutic IV‑Ig in mercury indueced autoimune disease" Clin Exp
Immunol, Apr, 1991; & (g)El‑Fawai HA, Waterman SJ, De Feo A, Shamy
MY. Neuroimmunotoxicology: Humoral Assesment of Neurotoxicity and Autoimmune
Mechinisms. Contact Dermatitis 1999; 41(1): 60‑1.
(270)D.W.Eggleston,
"Effect of dental amalgam and nickel alloys on T‑lympocytes",J
Prosthet Dent. 51(5):617‑623, 1984; & (d)
Park SH et al, Effects of occupational metallic mercury vapor exposure on
suppressor-inducer(CD4+CD45RA+) T lymphocytes and CD57+CD16+ natural killer
cells, Int Arch Occup Environ Health, 2000, 73(8): 537-42.
(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;
(287) (Kurup RK, Kurup PA.
Hypothalamic digoxin, cerebral chemical dominance, and pathogenesis
of pulmonary diseases Int J Neurosci. 2003 Feb;113(2):235-58;
& 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; &
Walczak-Drzewiecka A, Wyczolkowska J, Dastych J. Environmentally Relevant Metal and Transition
Metal Ions Enhance Fc Epsilon RI-Mediated Mast Cell Activation. Environ Health Perspect. 2003
May;111(5):708-13. ); & Hunter I,
Cobban HJ, Vandenabeele P, MacEwan
DJ, Nixon GF. Tumor necrosis
factor-alpha-induced activation of RhoA in airway smooth muscle cells: role in the Ca2+ sensitization
of myosin light chain20 phosphorylation.
Mol Pharmacol. 2003
Mar;63(3):714-21 )
(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 & TE Levy,
"cerebrospinal fluid protein changes in MS after Dental amalgam removal", Alternative Med
Rev, Aug 1998, 3(4):295‑300; & H.A. Huggins, Solving the MS Mystery, 2002, & http://www.hugginsappliedhealing.com/ms.php
(293)H.Huggins,Burton
Goldberg, & Editors of Alternative Medicine Digest,Chronic Fatigue
Fibromyalgia & Environmental Illness, Future Medicine Publishing, Inc,
1998, p197; & CFS, http://www.hugginsappliedhealing.com/fatigue.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, 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.
(304) Dietary Supplementation with Chlorella
pyrenoidosa Produces Positive Results in Patients with Cancer or Suffering from
Certain Common Chronic Illnesses, R.E. Merchant and C.A. Andre, Townsend Letter
for Doctors & Patients, Feb/Mar 2001
(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
(313)
V.D.M.Stejskal et al, "Mercury‑specific Lymphocytes: an indication
of mercury allergy in man", J. Of Clinical Immunology, 1996, Vol 16(1);31‑40.
(314) M.Goldman et
al,1991,"Chemically induced autoimmunity ...",Immunology Today,12:223‑;
& K. Warfyinge et al, "Systemic autoimmunity due to mercury vapor
exposure in genetically susceptible mice", Toxicol Appl Pharmacol,
1995, 132(2):299‑309;&
L.M. 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.
(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)
(317) S.Zinecker, “Amalgam:
Quecksilberdamfe bis ins Gehirn”, der Kassenarzt, 1992, 32(4):23; “Praxiproblem Amalgam”, Der
Allgermeinarzt, 1995,17(11):1215-1221. (1800 patients)
(321) R.L.Siblerud, “Relationship between dental amalgam and health”,
Toxic Substances Journal, 1990b. 10:425-444; & “Effects on
health following removal of dental amalgams”, J Orthomolecular Med,5(2):
95-106, & “Relationship between
amalgam fillings and oral cavity health” Ann Dent, 1990, 49(2): 6-10, (86 cured)
(323) Dr. Kohdera,
Faculty of Dentistry, Osaka Univ, Internationsl Congress of Allergology and
Clinical Immunology, EAACI, Stockholm, June 1994; & Heavy Metal Bulletin,
Vol 1, Issue 2, Oct 1994. (160 cases cured‑eczema,etc.); Tsunetoshi
Kohdera, MD, dermatology, allergology, 31 Higashitakada‑cho Mibu Nakagyo‑ku
Schimazu Clinics Kyoto 604 Japan e‑mail:smc‑inet@mbox.kyoto‑inet.or.jp
& G. Ionescu, Biol Med, 1996, (2): 65‑68; (these clinics use MELISA
test for diagnosis of immune reactivity) Neukirchen (clinic)(Germany, near
Czech border). Director; Gruia Ionescu, owns 2 Clinics, cases paid by insurance
companies in Germany. Email: Spezialklinik‑Neukirchen@toolpool.de fax:
0049 9947 10 51 11
(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.
(331) C.Gordon et al, “Abnormal sulphur
oxidation in systemic lupus erythrmatosus(SLE)”, Lancet,
1992,339:8784,25-6; &(b) 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; &
(c)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; & H.Iioka et al, “The effect of inorganic mercury on
placental amino acid transport”, Nippon sanka Fujinka Gakkai Zasshi, 1987,
39(2): 202-6.
(342)
Stejskal VDM, Danersund A, Lindvall A, Hudecek R, Nordman V, Yaqob A et al.
Metal‑ specific memory lymphoctes: biomarkers of sensitivity
in man. Neuroendocrinology Letters, 1999; 20: 289-298; & Sterzl I, Prochazkova J, Stejaskal VDM et al,
Mercury and nickel allergy: risk facotrs in fatigue and autoimmunity. Neuroendocrinology Letters 1999;
20:221‑228.; & The beneficial
effect of amalgam replacement on health in patients with autoimmunity.
Prochazkova J, Sterzl I, Kucerova H, Bartova J, Stejskal VD;
Neuro Endocrinol Lett. 2004 Jun;25(3):211-8. http://www.nel.edu/pdf_/25_3/NEL250304A07_Prochazkova_.pdf
(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, p3‑6.
(348) A Kistner, “Quecksilbervergiftung durch Amalgam: Diagnose und
Therapie” ZWR, 1995,104(5):412-417; &(b) Villegas J, Martinez R, Andres A,
Crespo D. Accumulation of mercury in
neurosecretory neurons of mice after long-term exposure to oral
mercuric chloride. Neurosci Lett 1999;
271: 93-96; &(c) Kozik MB, Gramza G.
Histochemical changes in the neurosecretory hypothalic nuclei as a
result of an intoxication with mercury compounds. Acta Histochem Suppl 1980; 22:367-80.
(368) Olin R, Paulander J, Axelsson P; FMS,CFS, and TMS- Prevalences in
a Swedish County, An oral examination
based study, Preventive Dental Health Care Center, Karlstad, Sweden,
1998.
(379) MacDonald EM, Mann AH, Thomas HC.
Interferons as mediatorors of psychiatric morbidity. The Lancet 1978; Nov 21, 1175‑78; & Hickie I,
Lloyd A. Are cytokines associated with neuropsychiatric syndrome in humans? Int
J Immunopharm 1995; 4:285‑294.
(380) Komaroff AL,
Buchwald DS. Chronic fatigue syndrom: an update. Ann Rev Med 1998; 49: 1‑13;
& Buchwald DS, Wener MH, Kith
P. Markers of inflamation and immune activation in CFS. J Rheumatol 1997;
24:372‑76.
(381) Demitrack
MA,Dale JK. Evidence for impaired activation of the hypothalamic‑pituitary‑
adrenal axis in patients with
chronic fatigue sydrome. J Clin endocrinol Metabol 1991; 73:1224‑ 1234;
& Turnbull AV, Rivier C. Regulation
of the HPA axis by cytokines. Brain Behav Immun 1995; 20:253‑75.
(382) Sterzl I,
Fucikova T, Zamrazil V. The fatigue syndrome in autoimmune thyroiditis with
Polyglanular activation of
autoimmunity. Vnitrni Lekarstvi 1998; 44: 456‑60; & Sterzl I, Hrda
P, Prochazkova J, Bartova J, Reactions
to metals in patients with
chronic fatigue and autoimmune endocrinopathy. Vnitr Lek 1999 Sep;45(9):527‑31
(383) Saito K.
Analysis of a genetic factor of metal allergy‑polymorphism of HLA‑DR‑DO
gene. Kokubyo Gakkai Zasschi 1996; 63: 53‑69; &
Prochazkova J, Ivaskova E, Bartova J, Stejskal VDM. Immunogentic findings in
patients with altered tolerance to
heavy metals. Eur J Human Genet 1998; 6: 175.
(385) Kohdera T,
Koh N, Koh R. Antigen‑specific lympocyte stimulation test on patients
with psoriasis vulgaris. XVI
International Congress of Allergology and Clinical Immunology, Oct 1997,
Cancoon, Mexico; & Ionescu
G. Schwermetallbelastung bei atopischer
Dermatitis und Psoriasis. Biol Med 1996; 2:65‑68.
(386)
Genova Diagnostics,[click: Tests, Search by Disease, see Disease in question
& Heavy Metal Toxicity], www.genovadiagnostics.com/ ; &
Doctors Data Lab
,http://www.doctorsdata.com , inquiries @doctors data.com, & MetaMatrix
Lab, http://www.metamatrix.com &
Biospectron Lab .......
(404) M. E.
Godfrey, Candida, Dysbiosis and Amalgam. J. Adv. Med. vol 9 no 2 (1996).
(405) Jenny Stejskal,
Vera Stejskal. The role of metals in autoimmune diseases and the link to
neuroendocrinology
Neuroendocrinology Letters, 20:345‑358, 1999; www.melisa.org
& ………..Factors in susceptibility to mercury toxicity, www.flcv.ccom/suscept.html
(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
(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) 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;
(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 .
(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;
(440) Kidd RF.
Results of dental amalgam removal and mercury detoxification. Altern Ther Health Med 2000 Jul;6(4):49‑55.
(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.
(456) Panasiuk J , Peripheral blood lymphocyte transformation
test in various skin diseases of allergic origin. (nickel & lupus) Przegl
Dermatol 1980;67(6):823‑9 [Article in Polish] ; & Barnett JH, Discoid lupus erythematosus exacerbated by contact dermatitis. Cutis 1990
Nov;46(5):430‑2 (nickel &
lupus) & Nickel Allergy Is Found in a Majority of Women with
Chronic Fatigue Syndrome and Muscle Pain– And May Be Triggered by Cigarette
Smoke and Dietary Nickel Intake; Journal of Chronic Fatigue Syndrome, Vol. 8(1)
2001
(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.
(468) Overzet K,
Gensler TJ, Kim SJ, Geiger ME, van Venrooij WJ, Pollard KM, Anderson P, Utz PJ.
Small nucleolar RNP scleroderma autoantigens associate with phosphorylated
serine/arginine splicing factors during apoptosis. Arthritis Rheum 2000
Jun;43(6):1327‑36
(469)BrainRecovery.com, the book, by David Perlmutter MD; Perlmutter Health Center, Naples, Florida, www.perlhealth.com/about.htm; & 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, , Reseda, Calif. Clinic; www.mmvbs.com
(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; & New Treatments
for Chronic Infections Found in Fibromyalgia Syndrome, Chronic Fatigue
Syndrome, Rheumatoid Arthritis, and Gulf
War Illnesses,
http://www.immed.org/reports/autoimmune_illness/rep1.html ; & Prof. Garth L. Nicolson,
Chronic Fatigue Syndrome, Fibromyalgia Syndrome and Other Fatigue
Conditions, http://www.immed.org/illness/fatigue_illness_research.html
(471) Schwartz RB, Garada BM, Komaroff AL, Gleit M, Holman BL.
Detection of intracranial abnormalities in patients with chronic fatigue
syndrome: comparison of MRI and SPECT. Am J Roentgenol, 1994, 162(4):935‑41;
& Spect Imaging: comparison of findings in patients with CFS, AIDA dementia
complex, and major unipolar depression,
Am J Roentgenol 1994, 162(4): 943‑51; & Ichiso M, Salit IE,
Abbey SE. Assessment of regional
cerebral perfusion by SPECT in CFS. Nucl Med Commun 1992; 13:767-72.
(472) Patarca‑Monero R, Klimas NG, Fletcher MA. Immunotherapy of
chronic fatigue syndrome. Journal of Chronic Fatigue Syndrome. 2001, 8(1): 3‑37;
& DeBecker P, De Meirleir K, Joos E, Velkeniers B. DHEA response to I.V.
ACTH in patients with CFS. Horm Metab Res 1999, 31(1): 18‑21.
(473) De Meirleir K, Bisbal C, Campine I, De Becker, et al. A 37 kDa 1‑5A
binding proein as a potential biochemical marker for CFS. Am J Med 2000,
108(2): 99‑105; & Suhadolnik RJ, Peterson DL, Obrien K, et al, Biochemical
evidence for a novel low molecular weight 2‑5A‑dependent Rnase L in
CFS. J Interferon Cytokine Res, 1997, 17(7): 377‑85; & Chaudhuri A, Watson WS, Pearn J, Behan
PO. The symptoms of chronic fatigue
syndrome are related to abnormal ion
channel function. Med Hypotheses 2000
Jan;54(1):59‑63
(474) Richards SCM, Bell J, Cheung, YL, Cleare A, Scott DL. Muscle
metabolites detected in urine in FM and CFS suggest ongoing muscle damage. Conference Proceedings of the British
Scociety of Rheumatologists, April
2001, Scotland, Abstract 382;
http://freespace,virgin.net/david.axford/me_nb_o4.htm.
(485) Hulda Clark, The
Cure for all Diseases, 2000, www.drclark.net.
(487) Straus SE et
al, CFS and allergy, J Allergy Clin Immunol, 1988, 81(5): 791-95; Straus SE et
al, Evidence of Epstein-Barr virus
infection in CFS, Annals of Internal Med, 1985, 102(1): 7-16; & Jones JF et
al, Annals of Internal Med, Evidence
for active Epstein-Barr Virus in patients with chronic unexplained illness,
1985, Annals of Internal Med,
102(1): 1-6; & Tyler AN, Influenza A virus: factor in fibromyalgia?, 1997,
2(2): 82- 86.
(488) Teitelbaum J,
Bird B; Effective treatment of CFS, report on 64 patients, J Musculoskeletal
Pain, 1995, 3(4): 91-100.
(489) Behan PO et
al; Effect of high doses of essential fatty acids on postviral fatigue
syndrome, Acta Neurol Scand, 1990,
82: 209-216; & Abraham GE, Flechas JD; Rationale for the use of magnesium
and malic acid in fibromyalgis
treatment, Journal of Nutritional Medicine, 1992, 3:40-52.
(490) Smith JD, Terpening CM, Schmidt SO, Gums JG. Relief of fibromyalgia symptoms following discontinuation of dietary
excitotoxins. Ann Pharmacother 2001
Jun;35(6):702‑6.
(490) 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; & (Bridi R, Crossetti FP,
Steffen VM, Henriques AT. The antioxidant activity of standardized
extract of Ginkgo biloba (EGb 761) in rats. Phytother Res 2001 Aug;15(5):449-51 ;&(c)Li Y,
Liu L, Barger SW, Mrak RE, Griffin WS. Vitamin E suppression of microglial
activation is neuroprotective. J Neurosci Res 2001 Oct 15;66(2):163-70.
(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
(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.
(518) Landay AL,
Jessop C, Lenette ET, chronic fatigue syndrome: clinical condition associated
with immune activation. Lancet 1991;
338:707-12; & (b)Caliguri M, Murray C, Buchwald D. Phenotypic and functional deficiency of
natural killer cells in patients with CFS.
J Immunol 1987; 139:3306-13; & Barker E, Fujirmura SF, Fadern
MB. Immunologic abnormalities associated
with CFS. Clin Infect Dis 1994; 18:
136-41.
(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.
(523) CBS Television Network,” 60 Minutes”, television program narrated by Morley
Safer, December 12, 1990
(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
(527) Cline Medical Center, Vancouver Island, http://www.oceansidemedicine.com/Default.htm
(528) Goldenberg DL;. Fibromyalgia, chronic
fatigue syndrome, and myofascial pain. Curr
Opin Rheumatol. 1996; 8: 113-123.
(529) GLYCONUTRITIONAL
IMPLICATIONS IN FIBROMYALGIA AND CHRONIC FATIGUE SYNDROME http://www.glycoscience.org/glycoscience/start_frames.wm?FILENAME=G005&MAIN=glyconutritionals&SUB=disease
(537)
Amalgam replacement with detox using NDF, case histories, www.healthydetox.org/cases.html
(572) 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.
(575)
XMRV-
CFS/ME http://www.youtube.com/watch?v=_WEUC7hRXzM
& www.wpinstitute.org/xmrv/xmrv_qa.html
(580) Life Extension
Foundation (MDs), Disease Prevention and Treatment, Expanded 4th
Edition, 2003 , http://www.life-enhancement.com/
(582) R.F. Kidd, Results of Dental Amalgam Removal and
Mercury Detoxification, Alternative Therapies, July 2000, vol 6, no. 4, p49-55.
(583)
Dr. Ronald King, DDS, Patient Experience
After Amalgam Replacement, http://www.kingtooth.com/My-Histories-11-20-04.htm
(585) Fibromyalgia causes and treatment, B. E. Vickory, http://www.abctohealth.com/8.html?sm=11953
(586) (304) Fibromyalgia Syndrome and Heavy
Metal Toxicity, Dietrich Klinghardt, MD, Ph.D. www.neuraltherapy.com/FibromyalgiaHeavyMetal.doc
(590)
Mercury toxicity presenting as
chronic fatigue, memory impairment and depression: Diagnosis, treatment,
susceptibility, and outcomes in a New Zealand general practice setting
(1994–2006), D.
P. Wojcik, M. E. Godfrey, D. Christie3 & B. E.
Haley, Neuroendocrinology Letters Volume 27 No. 4 September 2006
(594)
(a) Hidden Causes of GI Dysfunction,
C.D. Meletis, Vitamin Research
News, vol 22, no.4,
April 2008; & (b) Are You the Victim of Hidden Allergies?, The Blaylock Wellness
Report, Vol 4, No. 11, Nov 2007; & (c)
Food Additives: What You Eat Can Kill You, The Blaylock Wellness Report, Vo. 4,
No. 10, Oct 2007 www.blaylockreport.com &
(d) www.flcv.com/autismgc.html;
(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/
(600) B. Windham, Annotated bibliography: Exposure levels and health
effects related to mercury/dental amalgam and
results of amalgam replacement, 2002; (over 1500 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/damspr1.html (exposure
levels) &
www.flcv.com/amalg6.html
(effects,recovery)
(601) B. Windham, Cognitive and Behavioral Effects of Toxic Metal
Exposures, 2002; (over 150 medical study references)
www.flcv.com/tmlbn.html & www.flcv.com/kidshg.html
(602) The mechanisms by which mercury causes chronic immune and
inflamatory condtions, B.Windham(Ed.), 2002,
www.flcv.com/immunere.html & www.flcv.com/inflamhg.html
(603) B. Windham(Ed.), The environmental effects of dental amalgam
affect everyone, 2002,