Immune Reactive
Conditions: The mercury connection to eczema, psoriasis, lupus, asthma,
scleroderma, rheumatoid arthritis, and allergies (snipped from larger
study)
Bernard
Windham(Ed.)
I. Introduction.
This paper documents
that a significant percentage of people are allergic or immune reactive to
mercury to varying degrees, and that millions are adversely affected by such
conditions, including many disabled by related autoimmune conditions. The incidence of allergic and immune
reactive conditions such as allergies, asthma, eczema, lupus, psoriasis, MS, etc.
have been increasing rapidly in recent years (1-3,21,23).
Autism incidence rate had a 10 fold increase in the
last decade and ADHD had major increases likewise(16,116). At least 50 million
have allergies(19%)(1d) and according to the U.S.
CDC(1c) approximately 20 million have asthma(7.7%). The largest increase has
been in infants (1,2,6,7,21,23,16), and
approximately 10 % of infants- approximately 15 million in the U.S. with
systemic eczema(1ab,9,16). Studies
researching the reason for these rapid increases in infant reactive conditions
seem to implicate earlier and higher usage of vaccines containing mercury
(thimerasol) as a likely connection (2,6,21,23,16),
plus fetal and neonatal exposure from mother’s blood and milk (115). It has been estimated that by age 3 the
typical child has received over 235 micrograms of mercury thimerasol from
vaccinations which is considerably more than Federal mercury safety guidelines,
in addition to significant levels of mercury exposure from other sources for
many(2,21,23,16). Infants during this period have undeveloped immune systems
and blood brain barriers, and much of the mercury goes to the brain, resulting
in significant adverse neurological effects in those that are most
susceptible. Many thousands of parents
have reported that their child got such conditions after vaccination, and tests
have confirmed high levels of mercury in many of those tested, along with other
toxic exposures. Many of those diagnosed with high mercury levels have also
been found to have significant improvement after mercury detoxification (16,23,11,12,etc.). Thimerasol
had been previously removed from similar preservative uses in eye drops and eye
medications after evidence of a connection to chronic degenerative eye
conditions. After over 15,000 law suits
were filed in France over adverse effects of the Hepatitis B vaccine, the
French Minister of Health ended the mandatory hepatitis B vaccination program
for all school children. Adverse effects included neurological disorders and
autoimmune disorders such as multiple sclerosis and lupus.
People with
chronic and immune reactive problems are increasingly finding dental materials
are a factor in their problems and getting biocompatibility tests run to test
their immune reactivity to the various dental materials used. A high percentage of such
patients test immune reactive to mercury and some of the other toxic metals. Of the many thousands who have had the
Clifford immune reactivity test and the similar Peak Lab test, over 90% tested
immune reactive to mercury and often to other metals as well(46). The extreme immunotoxicity of mercury and
resulting damage to immune system cells and the immune system by mercury
exposure is likely a factor in this.
MELISA is an immune reactivity test developed to measure “significant”
immune reactivity to substances to the degree that often results in autoimmune
reactions and autoimmune conditions like CFS, Fibromyalgia, oral lichen planus,
MS, rheumatoid arthritis, lupus, etc. Of a
population of over 3000 with chronic health problems tested by the immune
lymphocyte reactivity test(MELISA,12a), 20% tested positive for inorganic
mercury, 13% for phenyl mercury, 8% for methyl mercury, and 7% for mercury thimerasol. For people with autoimmune conditions such as
CFS, Fibromyalgia, or Multiple Chemical Sensitivity, the percentage testing
immune reactive to mercury was much higher-
28% percent were immune reactive to palladium, 26% to gold, 23% to
inorganic mercury, 23% to phenyl mercury, and 12% to methyl mercury, as
compared to less than 5% for controls.
Of 98 patients who had amalgam fillings replaced, 76% had long term
health improvement and significant improvement in MELISA scores.
II. Allergic
health effects related to mercury exposure.
Many studies including hundreds of thousands of clinical cases
as well as Scientific Panels have found that the number one source of mercury
in adults is mercury amalgam fillings and exposures to those with amalgam
commonly exceed government health guidelines for mercury (199,134). Amalgam has
also been found to be the largest source of methyl mercury in most who have amalgam fillings
(134,199). Amalgam fillings of mothers is also a significant source of exposure
to infants as mercury in the mother crosses the placenta in levels higher than
in the mother and significant exposure also occurs through breast milk(115).
Studies have found
mercury to be a major factor in allergic/immune reactive conditions including
lupus(27-32,46d,47,88), contact dermatitis (3-10,91),eczema (3-9,18-20, 34,31),
psoriasis(33-38,54,31, 11) , oral lichen planus (11,39-42), systemic eczematous contact-type dermatitis (baboon
syndrome)(7),
stomatitis(10b,54), scleroderma(47,87), allergies(11-15,31,43-49), asthma
(47-51,65,16), and rheumatoid arthritis(47,49,88). Mercury
has been shown to be a factor that can cause rheumatoid arthritis by activating
localized CD4+ T-cells
which trigger production of immune macrophages and immunoglobulin(Ig) producing
cells in joints(12,513,514).
Allergic contact eczema is the most frequent
occupational disease(1,91), occurring in over 10% of
children in some areas; and the most common cause of contact eczema is exposure
to toxic metals(1, 5-9). The metals most
commonly causing allergic immune reactivity are nickel, mercury, chromium,
cobalt, and palladium(5-15,60,91,200). Nickel
in stainless steel braces and crowns is a source of reactivity and autoimmunity
along with gold and palladium in crowns(32bc,11,12) The highest level of sensitization is to
Infants, who are most reactive to thimerosal, a form of mercury that has been
used as a preservative in vaccines and eye drops(6,5b,16). There is strong suggestive and clinical
evidence for a connection between toxic metals and autism (16,21,2,23-25,81,86). Although nickel has historically been the
number one source of metal allergy and contact allergy, with many dozens of
medical studies documenting the connection to conditions such as contact
eczema, in recent years the largest increase in infant reactivity appears to be
related to mercury exposure(6,7, 32,86,16). Also mercury has been found to be
the most significant factor in large numbers of reactive autoimmune allergic
and neurological conditions(11-15,201) Thus in assessing mechanisms by which these
conditions are related to metals, this paper will focus more on mercury. Some of this would be similar for other
metals however.
Mercury causes release of inflammatory cytokines
such as Tumor Necrosis Factor-alpha(TNFa) and Interleukin-4 which are
documented to be factors in the chronic inflammatory conditions discussed here,
including asthma, lupus, rheumatoid arthritis, scleroderma, celiac and chron’s
disease, etc. (47,49,65,87-92) and also is involved in chronic heart problems.
TNFa(tumor necrosis factor-alpha) is a cytokine
that controls a wide range of immune cell response in mammals, including cell
death(apoptosis). This process is
involved in inflammatory and degenerative neurological conditions like ALS, MS,
Parkinson’s, rheumatoid arthritis, etc.
Cell signaling mechanisms like sphingolipids are part of the control
mechanism for the TNFa apoptosis mechanism(101a). 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 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(101b,101c).
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(94). Studies have found that in asthma, lupus, rheumatoid
arthritis, scleroderma, celiac/chron’s/IBS, and eczema cases there was a
reduction in serum magnesium and RBC membrane Na(+)-K+ ATPase activity and an
elevation in plasma serum digoxin
(87-90,65). The activity of some
free-radical scavenging enzymes, concentration of glutathione decreased
significantly, 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 that
mercury is a cause of most of these conditions (30,29,65,87-90,95,96,etc.)
Dental staff have been found to have significantly
higher prevalence of eye problems, conjunctivitis, atopic dermatitis, and contact
urticaria(91c). Finnish dental staff have the highest
occupational risk of contact dermatitis with 71% affected over time(91b) with plastics, rubber, and mercury the most common
causes of sensitization. Korean dental
technicians have a high incidence of contact dermatitis, with dental metals the
most common sensitizers. Over 25% had contact dermatitis with over 10%
sensitive to 5 metals, chromium, mercury, nickel, cobalt, and palladium(91a). 16.3%
were immune reactive to mercury.
One mechanism of mercury’s
affect on contact sensitivities is the inhibition of glutathione S- transferase(92), which is a modulator of inflammation.
Mercury also causes intestinal damage and leaky gut, causing metabolic damage
and increasing food sensitivities(93).
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
these allergic/immune reactive conditions(13,15,16,23-31,56-58). For example mercury has been found to
strongly inhibit the activity of dipeptyl peptidase (DPP IV) which is required
in the digestion of the milk protein casein(25,26,16).
Studies involving a large sample of autistic and schizophrenic patients found
that over 90 % of those tested had high levels of the milk protein
beta-casamorphin-7 in their blood and urine and defective enzymatic processes
for digesting milk protein(24). Casamorphin is a morphine like compound that results in neural
disfunction. Elimination of milk
products from the diet has been found to improve the condition. As noted previously, such populations have
also been found to have high levels of mercury and to recover after mercury detox(23,11,12,16).
As mercury levels are reduced the protein binding is reduced and
improvement in the enzymatic process occurs(16,200).
Additional cellular level enzymatic effects of mercury’s binding with proteins
include blockage of sulfur oxidation processes, enzymatic processes involving
vitamins B6 and B12, effects on the cytochrome-C energy processes, along with
mercury’s adverse effects on cellular mineral levels of calcium, magnesium,
zinc, and lithium(16,200). And along
with these blockages of cellular enzymatic processes, mercury has been found to
cause additional neurological and immune system effects in many through
immune/autoimmune reactions(11-15,201). But the effect on the immune system of
exposure to various toxic substances such as toxic metals and environmental
pollutants has also been found to have additive or synergistic effects and to
be a factor in increasing eczema, allergies, asthma, and sensitivity to
other lesser allergens. Many of the
immune reactive children tested for toxic exposures have found high or reactive
levels of other toxic metals, and organochlorine compounds(11,12,4). Other than the organochlorines or toxic
metals which are discussed later, four common pollutants that have been
documented to have effects on such conditions are traffic and industrial
pollutants nitrogen oxide, sulfur dioxide, power plant residual oil fly ash,
and organochlorine pollutants(4).
Mercury
vapor exposure at very low levels adversely affects the
immune system (11-15, 44-46,
56-62). From animal studies it has
been
determined that mercury damages T-cells
by generating reactive oxygen
species(ROS), depleting the
thiol reserves of cells, damaging and
decreasing the dimension of
mitochondria, causing destruction of
cytoplasmic organelles with loss
of cell membrane integrity, inhibiting
ability to secrete interleukin
IL-1 and IL-2R, causing activation of glial cells
to produce superoxide and
nitric oxide, and inactivating or inhibiting
enzyme systems involving the
sulphydryl protein groups(13-6,45,57,200).
Mercury caused adverse
effects on both neutrophil and macrophage
function and after depletion of
thiol reserves, T-cells were susceptible to
Hg induced cellular
death (apoptosis)(15,63,64). Interferon syntheses
was reduced in a
concentration dependent manner with either mercury or
methyl mercury as well as
other immune functions(13-15,200), and low
doses also induce
aggregation of cell surface proteins and dramatic
tyrosine phosporlation of
cellular proteins related to asthma(49-51) and
allergic diseases such as
eczema and lupus(27-38,201), and
autoimmunity(11-15,56-58). One study found that insertion of amalgam
fillings or nickel dental
materials causes a suppression of the number of T-
lymphocytes(60), 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
(56,14,15,57c).
Both mercuric and methyl mercury chlorides caused dose
dependent reduction in immune
B-cell production (59). B-cell
expression
of IgE receptors were
significantly reduced(59), with a rapid and sustained
elevation in intracellular
levels of calcium induced(59,65).
Antigen specific
LST-test was performed
on a large number of patients with atopic
eczema(33), using T-cells of
peripheral blood. 87% showed LST positive
reactions to Hg, 87% to Ni, 38%
to Au and 40% to Pd They removed LST
positive dental metals from the
oral cavities of patients. Improvement of
symptoms was obtained in 82%
(160/196) of the patients within 1-10
months. Similar results have been obtained at other clinics(11,34-38).
Mercury and toxic
substances effects on suppressing the immune system also are documented to
cause increased susceptibility to other pathogens such as viruses, mycoplasma,
bacterial infections, and parasites. The majority of those with autoimmune
conditions like ALS, CFS, FMS, MS have been found to also be infected with
mycoplasma and other pathogens(98-100).
Many studies have found
that the body’s basic building blocks, amino acids with SH hydroxyl radicals
form strong bonds with the toxic metals such as mercury, resulting in compounds
which the immune system recognizes as “foreign” or non-functional in the basic
digestive enzymatic processes that use them as fuel and building blocks in cell
structure. This results in activation of
the immune system, and when there is a chronic exposure can lead to an autoimmune
process that results in significant symptoms and various autoimmune diseases
and conditions such as these systemic allergic conditions as well as others
such as chronic fatigue(CFS), multiple chemical
sensitivities(MCS), and fibromyalgia(11-15,201).
As previously noted,
many occupational and children’s studies have found mercury and other toxic
metals to be a common cause of immune reactivity and contact and systemic skin
conditions including eczema(4-12,31-38). One of the confusions about mercury is that
there are several forms of mercury, with different mechanisms of exposure for
the different forms, as well as different mechanisms in which the forms of
mercury affect the body and immune system.
However all have been documented to be extremely
neurotoxic and immunotoxic, and to cause autoimmunity in susceptible
individuals. Many studies
including patch tests and immune reactivity tests have been carried out to
assess the level of mercury sensitivity in different populations. They have found that there is a
significant portion of the population that are reactive and sensitive to
mercury and such have significant effects.
In a group of medical students tested by patch test, 12.8 % were
sensitive to mercury(17). The mercury sensitized students were found to
have more than average number of amalgam fillings, higher urine mercury than
non-sensitized students, and more allergic reactions to other things such as
cosmetics, soaps, shampoos, etc. Many
other studies have found similar levels of sensitization in recent years, with
those populations with higher exposures such as those with many fillings or
dental staff tending to have higher levels of sensitization(11,12,200)
and more adverse health effects. In a
group of 8 with contact eczema patch tested for mercury in Spain, all were
positive for mercurochrome, six to inorganic mercury, and some to thimerosal(18). This
study like several others noted the danger in patch tests for mercury as 2 of
the patients suffered anaphylactic shock after the patch test due to the
extreme immune reactivity of some to mercury.
Inorganic mercury was found to be a cause of systemic eczema and
digestive problems by a
Japanese study(19). There
is consensus among researchers and dental authorities that amalgam fillings is
the main cause of oral lichen planus and the condition is usually cured by
amalgam removal(39-42,54).
Mercury blocks the immune function of magnesium and zinc (125-128), whose
deficiencies are known to cause significant neurological effects(129-131). The
low Zn levels result in deficient CuZnSuperoxide dismustase (CuZnSOD),
which in turn leads to increased levels of superoxide due to toxic metal
exposure.
III. Autoimmunity caused by Mercury: Connection to Immune and
Neurological Conditions
Mercury has been documented to cause
autoimmune disease (139,140,118,60,82,141,11,12) and
many researchers have concluded that autoimmunity is a factor in the
major chronic neurological diseases such as MS, ALS, PD, SLE, RA, etc. Mercury
and other toxic metals also form inorganic compounds with OH, NH2, CL, in
addition to the SH radical and thus inhibits many cellular enzyme processes,
coenzymes, hormones, and blood cells(12b,200). 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(142,12). In general, immune activation from toxic
metals such as mercury resulting in cytokine release and abnormalities of the
hypothalamus‑pituitary‑adrenal(HPA) axis can cause changes in the
brain, fatigue, and severe psychological symptoms (12,143,144-147,12b,118) such
as profound fatigue, muscosketal pain, sleep disturbances, gastrointestinal and
neurological problems as are seen in CFS, fibromyalgia, and autoimmune
thyroidititis. Such hypersensitivity has been found most common in those with
genetic predisposition to heavy metal sensitivity(11,12,142),
such as found more frequently in patients with human lymphocyte antigens (HLA‑DRA)
(142,146,147,12). A
significant portions of the population appear to fall in this category.
The enzymatic
processes blocked by such toxic substances as
mercury also result in chronic formation of metal‑protein
compounds (HLA
antigens or antigen-presenting
macrophages) that the body’s immune
system(T-lymphocytes) does not recognize, resulting in autoimmune
reactions (103,12a,12b). The metals bind to SH-groups on proteins
which
can then be recognized as
“foreign” and attacked by immune lymphocytes
Such has been extensively
documented by studies such as the
documentation of the autoimmune
function test MELISA, a sophisticated
immune/autoimmune test which was
developed to test for such
reactions(11,12b).
Very low doses and short term
exposures of inorganic Hg (20-200 mug/kg) exacerbates lupus and
accelerates mortality in mice. Low dose
Hg exposure increases the severity and prevalence of experimental autoimmune
myocarditis induced by other factors. In
a study of small-scale gold mining using mercury, there was a positive interaction between Hg
autoimmunity and malaria. These results suggest a new model for Hg
immunotoxicity, as a co-factor in autoimmune disease, increasing the risks and
severity of clinical disease in the presence of other triggering events, either
genetic or acquired(28e).
Autoimmune reactions to inorganic and
methyl mercury have been found to be relatively independent, occurring in over
10% of controls. Among a population of
patients being tested for autoimmune problems, 94% of such patients had
significant immune reactions to inorganic mercury(MELISA test,11,12a,12b) and
72% had immune reactions to low concentrations of HgCl2(<0.5 ug/ml). Of a
population of 86 patients with CFS symptoms who had amalgam fillings replaced,
78% reported significant health improvement in a relatively short time period
after replacement, and MELISA test scores had a significant reduction in
lymphocyte reactivity compared to pre- replacement(12). The MELISA test has proved successful in diagnosing and
treating environmentally caused autoimmune diseases such as MS, SLE, oral
lichen planus, CFS,etc. (11,12,148).
A high percentage of patients subjectively diagnosed with CNS and
systemic symptoms suggestive of mercury intoxication have been found to have
immune reactivity to inorganic mercury(MELISA test,148),
and likewise for MRI positive patients for brain damage. Controls without CNS problems did not have
such positive correlations. Nickel,
palladium, and gold have also been found to induce autoimmunity in genetically
predisposed or highly exposed individuals (11,12,13,149). Tests have found a significant portion of people(over 10%) to be in this category and thus more
affected by exposure to amalgam than others.
Once compromised by a toxic substance that depletes the immune
protectors and causes autoimmunity, the immune system is more susceptible to
being sensitized to other toxic chemicals, a factor in multiple chemical sensitivity(MCS).
Mercury also causes a reduction in thyroid production(150)
and an accumulation in the thyroid of radiation. Among those with chronic immune system
problems with related immune antibodies, the types showing the highest level of
antibody reductions after amalgam removal include glomerular basal membrane,
thyroglobulin, and microsomal thyroid antigens(140,142,12).
Toxic metals appear to be only one of the factors
involved in chronic autoimmune conditions and appear to often be cofactors with
other triggering effects(28e). Very low doses and short term exposures of inorganic Hg (20-200 mug/kg) exacerbates
lupus and accelerates mortality in mice.
Low dose Hg exposure increases the severity and prevalence of
experimental autoimmune myocarditis induced by other factors. In a study of small-scale gold mining using
mercury, there was a
positive interaction between Hg autoimmunity and malaria. These
results suggest a new model for Hg immunotoxicity, as a co-factor in autoimmune
disease, increasing the risks and severity of clinical disease in the presence
of other triggering events, either genetic or acquired(28e). Pathogens such as viruses, mycoplasma,
bacteria and parasites have been found to usually be present and a factor to
deal with in treating those with chronic degenerative conditions and weakened
immune systems such as MS(97e,98 ,99,100) and other
autoimmune conditions.
Mercury’s biochemical damage at the cellular level
include DNA damage, inhibition of DNA and RNA synthesis (102-105); induction of free radical formation (12,95),
depletion of cellular glutathione (necessary for detoxification processes) (30de,106,101),
inhibition of glutathione peroxidase enzyme(95), inhibition of glutamate
uptake(108), induces peroxynitrite and lipid peroxidation damage(109), inducement of inflammatory cytokines(101,111,14),
causes abnormal immune system damage (15,63,69,107,110); and autoimmunity (12-15,63,112,etc.)
Metals
like mercury bind to SH-groups(sulphydryl) in sulfur
compounds like amino acids and proteins, changing the structure of the compound
that it is attached to. This often
results in the immune systems T-cells not recognizing them as appropriate
nutrients and attacking them(13-15,112). Such binding and autoimmune damage has been
documented in the fat-rich proteins of the myelin sheaths and of collagen(12b), which are
affected in MS. Metals by binding to SH
radicals in proteins and other such groups can cause autoimmunity by modifying
proteins which via T-cells activate B-cells that target the altered proteins
inducing autoimmunity as well as causing aberrant MHC II expression on altered
target cells(115de,117). Studies have
also found mercury and lead cause autoantibodies to neuronal proteins,
neurofilaments, and myelin basic protein(MBP) (118ag,12,119,120,121). Mercury and cadmium also have been found to
interfere with zinc binding to MBP(122b) which affects
MS symptoms since zinc stabilizes the association of MBP with brain myelin(122a). MS has also been found to commonly be related
to inflammatory activity in the CNS such as that caused by the reactive oxygen
species and cytokine generation caused by mercury and other toxic metals (12,119,120,121).
Antioxidants like lipoic acid which counteract such free radical activity have
been found to alleviate symptoms and decrease demyelization(123,124). A group of metal exposed MS patients with
amalgam fillings were found to have lower levels of red blood cells,
hemoglobin, hemocrit, thyroxine, T-cells, and CD8+ suppressor immune cells than
a group of MS patients with amalgam replaced, and more exacerbations of MS than
those without(80).
Immune and autoimmune mechanisms are thus seen to be a major factor in neurotoxicity of
metals.
Autoimmunity
has also been found to be a factor in chronic degenerative autoimmune
conditions such as MS,ALS, etc., with genetic
susceptibility a major factor in who is affected. One genetic factor in Hg induced
autoimmunity is major histocompatibility complex(MHC)
linked. Both immune cell type Th1 and
Th2 cytokine responses are involved in autoimmunity(57c). One genetic difference found in animals and
humans is cellular retention differences for metals related to the ability to
excrete mercury(58).
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(132), whereas those with type APOE-2
readily excrete mercury and are less susceptible (132).
Those with type APOE-3 are intermediate to the other 2 types. The incidence of autoimmune conditions has
increased to the extent this is now one of the leading causes of death among women(135). Also
when a condition has been initiated and exposure levels decline, autoimmune antibodies
also decline in animals or humans (136,28c,11,118,137,12)
Exposure
to mercury results in metalloprotein compounds that have
genetic effects,
having both structural and catalytic effects on gene
expression(114). Some
of the processes affected by such metalloprotein
control of genes include cellular respiration, metabolism,
enzymatic
processes, metal-specific homeostasis, and adrenal stress
response
systems.
Significant physiological changes occur when metal
ion concentrations
exceed threshold levels.
Such metalloprotein formation also appears to
cause a change in antigenicity and autoimmune reactions
in significant
numbers of people(103,11,12a,12b). Much mercury in saliva
and the brain is also organic, the most neurotoxic
form(138,63), since
mouth bacteria and other organisms in the body methylate
inorganic
mercury to organic mercury(134,133). Dental amalgam has
been found to
be the largest source of methyl mercury in most with
mercury amalgam
fillings(134,199,etc.).
IV.
Recovery from Chronic Immune and Neurological Related Diseases After Amalgam Removal and
Mercury Detoxification
Much
of the direct chronic exposure to toxic metals for persons with the autoimmune
diseases discussed here appears to be from use of metals in dental work. The most common dental metals that have been
documented to be causing widespread adverse health effects are mercury, nickel,
palladium, gold, and copper. Although
chronic exposure clearly is affecting a much larger population, nickel has been
found to be a major factor in many cases of MS and lupus, with palladium having
very similar effects to nickel.
Many clinics and studies involving thousands of patients have found
that patients with allergic reactive conditions such as oral lichen planus,
eczema, chronic allergies etc. usually recover or have significant improvements
after amalgam replacement. Of a group of
86 patients with CFS symptoms, 78% reported significant health improvements
after replacement of amalgam fillings within a relatively short period, and
MELISA test found significant reduction in lymphocyte reactivity compared to
pre removal tests(11,12). The improvement in symptoms
and lymphocyte reactivity imply that most of the Hg-induced lymphocyte
reactivity is allergenic in nature. Patients
with other systemic neurological or immune symptoms such as arthritis, myalgia,
CFS, MCS, MS, etc. also often recover after amalgam replacement(11,12,200).
A
large epidemiological study of 35,000 Americans by the National Institute of
Health, the nation's principal health statistics agency, found that there was a
significant correlation between having a greater than average number of dental
amalgam surfaces and having the a chronic condition such as epilepsy, MS, or
migraine headaches. Fewer of those with this condition have zero fillings than
those of the general population while significantly more of those with the
condition have 17 or more surfaces than in the general population (155)
There are extensive documented cases (many
thousands) where removal of amalgam fillings led to cure of serious health
problems such as
eczema
(22,33,34,38,52-54,67-69,11,12),
psoriasis(33-38,12), asthma(49-52,68,72,98), lupus(12,27,32,33,68,70,71,31),
allergies(31,32,43,48,51,49,52,53,66-74), oral lichen planus(39-42), chronic
multiple chemical sensitivities (32,68,70,71,73,75-77,154, 11,12,31), ALS(51,99,154,31),
arthritis(31,52,67,68,72,73,78,79,98,11), MS(52,67-70,73,80-83,31c,99,100,151-154), CFS (11,12,31,33,52-54,66-68,70,71,75,84,85,98,99,153,154)
muscular/joint
pain/fibromyalgia (11,12,31,53,68,69,72,84,85,98,99,151) and over 20 other
chronic health conditions(200). Any
references not found in this paper can be found in the bigger paper(200), from which much of this paper is excerpted and
which contains clinical documentation of over 60,000 cases of recoveries after
amalgam replacement. In several of the studies, over 75% of those with MS and
having amalgams replaced recovered or had significant improvement ( 212(a),(b),(e),302,222,*31). Some of the studies reported similar success
rates for SLE but with lower number of cases treated.
Clinical studies have found that patch
testing is not a good predictor of success of amalgam removal, as a high
percentage of those testing negative also recovered from chronic conditions
after replacement of fillings (86,87,90). Follow up tests for autoimmune reaction to
inorganic mercury after amalgam replacement have found that in most patients
tested, the immune reaction as well as most symptoms disappear over time
(11,313,12b,etc.)
References
(1)
American Academy of Dermatology, Press Release, February, 2000; &(b) National Institute of
Arthritis and Musculoskeletal and Skin Diseases, (U.S.) National Institute of
Health, 2003; & (c) CDC. Behavioral
Risk Factor Surveillance System Survey. Atlanta, Georgia: U.S. Department of
Health and Human Services, CDC, 2001; &(d) American Academy of Allergy,
Asthma and Immunology (AAAAI). The Allergy Report: Science
Based Findings on the Diagnosis & Treatment of Allergic Disorders,
1996-2001; & (e) S. Redd, U.S. Centers for Disease Control, National Center
for Environmental Health, 1998.
(2)Gary Null, Second Opinion:
Vaccinations, Gary Null and Associates,Inc., 2000. www.garynull.com.
(3) Silhan P, Arenberger P. Standard epicutaneous tests in ambulatory
care of patients.
Cas Lek Cesk 1999, 138(15):469-73; & Lindemayr H, Drobil M. Eczema of the lower leg and
contact allergy. [German]
Hautarzt, 1985, 36(4): 227-3.
(4) Reichrtova E et al, “Cord Serum Immunoglobulin E Related to
Environmental Contamination of Human Placentas with Oganochlorine Compounds”, Envir Health Perspec, 1999,
107(11):895-99; & Gavett SH et
al. Residual Oil Fly Ash Amplifies
Allergic Cytokines, Airway Responsiveness, and Inflamtion in Mice. Am J Respir Crit Care Med, 1999,
160(6):1897-1904; & Kramer U et al,
Traffic-related air pollution is associated with atopy in children living in urban
areas. Epidemiology 2000, 11(1): 64-70;
& S.C. Langley-Evans et al, “SO2: a potent glutathione depleting
agent”,
Comp Biochem Physiol Pharmocol Toxicol Endocrinol, 114(2):89-98
(5) Romaguera C, Vilaplana J. Contact dermatitis in children: 6 years
experience. Contact Dermatitis 1998; 39(6): 277-80; & Manzini BM, Ferdani
G, Simonetti V, Donini M, Sedernari S.
Contact sensitization in children.
Pediatr Dermatol 1998; 15(1): 12-17.
(6)
Brasch J, Geier J, Schnuch A.
Differentiated contact allergy lists serve in quality improvement. Hautarzt 1998; 49(3): 184-91; & Audicana MT, Munoz D, del Pozo MD,
Fernandez E, Gastaminza G, Fernandez de Corres L. Allergic contact dermatitis from mercury
antiseptics and derivatives: study protocol of tolerance to intramuscular
injections of thimerosal. Am J
Contact Dermat. 2002 Mar;13(1):3-9.;
& Patrizi
A, Rizzoli L, Vincenzi C, Trevisi P, Tosti A.
Sensitization to thimerosal in atopic children. Contact Dermatitis, 1999, 40(2): 94-7.
(7)
Nakada T, Higo N, Iijima M, Nakayama H, Maibach HI. Contact Dermatitis.
1997 May;36(5):237-9.;
(8) Sun CC. Allergic contact dermatitis of the face from
contact with nickel and ammoniated mercury.
Contact Dermatitis 1987, 17(5):306-9;. & Schafer T, Bohler E, et al, Epidemiology of contact allergy in adults.
Allergy. 2001 Dec;56(12):1192-6.
(9) Xue C, He Z, Zhang H, Li S. Study on the contact allergen in patients
with dermatitis and eczema. Wei Sheng
Yen Chiu 1997, 26(5): 296-8; &
Meding B, Jarvholm B. Hand eczema in
Swedish adults and children - J Invest
Dermatol 2002 Apr;118(4):719-23; & Lindemayr H, Drobil M, .[Eczema of the lower
leg and contact allergy] [German] Hautarzt. 1985 36(4): 227-31.
(10) Aberer W, Holub H, Strohal R,
Slavicek R. Palladium in dental alloys-
the dermatologists responsibility to warn? Contact Dermatitis 1993. 28(3): 163-5; & Veien NK. Stomatitis and systemic dermatitis from
mercury in amalgam dental restorations.Dermatol Clin. 1990 Jan;8(1):157-60.
(11)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;
& 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. www.melisa.org
& (b) Alanko K, Kanerva L, Jolanki R,
Kannas L, Estlander T. Oral mucosal
diseases investigated by patch testing with a dental screening series. Contact
Dermatitis. 1996 Apr;34(4):263-7.
(12) Stejskal VDM, Danersund A, Lindvall A,
Hudecek R, Nordman V, Yaqob A et al. Metal- specific memory lymphocytes: biomarkers of sensitivity in
man. Neuroendocrinology Letters, 1999;
& (b)Jenny Stejskal, Vera Stejskal.
The role of metals in autoimmune diseases and the link to
neuroendocrinology Neuroendocrinology
Letters, 20:345‑358, 1999. &(c) Sterzl I, Prochazkova J, Stejaskal
VDM et al, Mercury and nickel allergy: risk factors in fatigue and
autoimmunity. Neuroendocrinology Letters
1999; 20:221-228; &(d) 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; www.melisa.org; & (e)Valentine-Thon E, Schiwara
HW, Validity of MELISA for metal sensitivity testing; Neuroendocrinol Lett,
2003, Feb-Apr, 24(1-2): 57-64.
(13) S.Ellermann-Eriksen et al,
"Effect of mercuric chloride on macrophage-mediated resistance mechinisms
against infection", Toxicology, 93:269-297,1994; & M.Kubicka-Muranyi et al, “Systemic autoimmune disease induced by
mercuric chloride”,
Int Arch Allergy Immunol;1996, 109(1):11-20
& M.M.Christensen et al, Institute o Medical Microbiology, “Comparision of interaction of meHgCl2
and HgCl2 with murine macrophages”, Arch Toxicol, 1993, 67(3):205-11;
& 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;
(14)P.W. Mathieson, “Mercury: god of TH2 cells”,1995, Cliical Exp
Immunol.,102(2):229-30; & Parronchi
P, Brugnolo F, Sampognaro S, Maggi E.
Genetic and Environmental Factors Contributing to the Onset of Allergic Disorders. Int Arch Allergy Immunol
2000 Jan;121(1):2-9.
(15)
L.M. Bagentose 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; 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”
and “Immune suppression of human T-cell activation”, Immunopharmacologicol Immunotoxical, 1992, 14(3):555-77; &“Mercury-induced autoimmunity”, Clin
Exp Immunol, 1998, 114(1):9-12.
(16) Windham, B. Annotated
Bibliography: The mercury connection to childhood neurolgical and developmental
conditions, http://www.flcv.com/kidshg.html
(17) Sato K, Kusaka Y, Miyakoshi S. An
epideomological study of factors relating to mercury sensitization.
Arerugi 1995; 44(2):86-92; & Chen L, Nordlind K, Liden S,
Sticherling M., Increased expression of keratinocyte interleukin-8 in human
contact eczematous reactions to heavy metals.
APMIS. 1996 Jul-Aug;104(7-8):509-14.
(18) Galindo PA, Feo F, Fernadez
F. Mercurochrome allergy: immediate and
delayed hypersensity. Allergy 1997; 52(11):
1138-41;
(19) Koizumi A et al, Mercury
poisoning as cause of smelter disease. Lancet 1994; 343(8910): 1411-2.
(20) Ulukapi I. Mercury
hypersensitivity from amalgam: report of case. ASDC J Dent Child
1995;62(5):363-4.
(21)
Halsey, NA. Limiting Infant Exposure
to Thimerosal in vaccines. J. of the
Amer. Medical Assoc., 282: 1763-66.
(22) Redhe O, Pleva J. Recovery from asthma and allergies after
removal of dental amalgam fillings. Int
J of Risk & Safety in Medicine 1994; 4:229-236.
(23) Autism: a unique form of mercury
poisoning. http://www.autismwebsite.com/ari/vaccine/mercurylong.htm ; &
(b) Elferink JG.
Thimerosal: a versatile sulfhydryl reagent, calcium mobilizer, and cell
function‑modulating agent. Gen
Pharmacol 1999 Jul;33(1):1‑6; & Forstrom L, Hannuksela M, Kousa M,
Lehmuskallio E. Merthiolate
hypersensitivity and vaccination. Contact Dermatitis. 1980 Jun;6(4):241-5;
& Schafer T, Bohler E, et al,
Epidemiology of contact allergy in adults. Allergy. 2001 Dec;56(12):1192-6.
(24) J.R. Cade et al, Autism and schizophrenia linked to
malfunctioning enzyme for milk protein digestion. Autism, Mar
1999. http://www.hsc.ufl.edu/post/post0399/post03_19/1.html
(25) Puschel G, Mentlein R, Heymann E,
'Isolation and characterization of dipeptidyl peptidase IV from human placenta', Eur J Biochem 1982
Aug;126(2):359-65; & 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
(26) Stefanovic V. et al, Kidney
ectopeptidases in mercuric chloride-induced renal failure. Cell Physiol Biochem 1998; 8(5): 278-84.
(27) 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.
(28) P.E. Bigazzi, “Autoimmunity and Heavy Metals”, Lupus, 1994; 3: 449-453; &
(b)Pollard KM, Pearson Dl,
Hultman
P. Lupus-prone mice as model to study
xenobiotic-induced autoimmunity.
Envriron 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;
& Hultman P, Enestrom S, Mercury induced antinuclear antibodies in
mice,
Clinical
and Exper Immunology, 1988, 71(2): 269-274;
& (d) Via CS, Nguyen P, Silbergeld EK, et
al,
Low-dose exposure to inorganic mercury accelerates disease and mortality in
acquired murine
lupus,
Environ Health Perspect. 2003, 111(10): 1273-7; &(e) Silbergeld EK, Silva IA,
Nyland JF. Mercury
and autoimmunity: implications for occupational and environmental health. Toxicol
Appl Pharmacol. 2005 Sep 1;207(2 Suppl):282-92.
(29)
C.Gordon et al, “Abnormal
sulphur oxidation in systemic lupus erythrmatosus(SLE)”, Lancet, 1992,339:8784,25-6; &
P.Emory et al, “Poor
sulphoxidation in patients with rheumatoid arthitis”, Ann Rheum Dis, 1992, 51:3,318-20; & P.Emory et al, Br J
Rheumotol, 1992, 31:7,449-51; &
C.M. Tanner et al,“Abnormal
Liver Enzyme Metablolism in Parkinson’s”,Neurology, 1991, 41(5): Suppl 2, 89-92; &
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;
& Hisatome I, 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.
(30)S.A. McFadden, “Xenobiotic metabolism and adverse
environmental response: sulfur-dependent detox pathways”,Toxicology, 1996,
111(1-3):43-65; ;& (b) 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;&(c)Alberti
A, Pirrone P, Elia M, Waring RH, Romano C.
Sulphation deficit in “low-functioning” autistic children. Biol Psychiatry 1999, 46(3):420-4;
&(d) Quig D, Doctors Data
Lab,"Cysteine metabolism and metal
toxicity", Altern Med Rev, 1998;3:4,
p262‑270, &(e) 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‑;
(31 Huggins HA, Levy,TE, Uniformed Consent: the hidden
dangers in dental care, 1999, Hampton Roads Publishing Company Inc; &
(b)Hal Huggins, Its All in Your Head, 1993; & (c) Huggins HA,
Levy,TE, Solving the MS Mystery:
Help, hope and recovery, 2002
& Center for Progressive Medicine, 1999, http://www.hugnet.com
(32) 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)
& (b) Schultz JC, Connelly E, Glesne L,
Warshaw EM. Cutaneous and oral eruption from oral exposure to
nickel in dental braces. Dermatitis. 2004 Sep;15(3):154-7;
& Genelhu MC, Marigo M et al;
Characterization of nickel-induced allergic contact stomatitis associated with
fixed orthodontic appliances, Am J Orthod Dentofacial Orthop. 2005
Sep;128(3):378-81; & (c) &(c) Marcusson
JA, Contact allergies to nickel sulfate,
gold sodium thiosulfate and palladium chloride in patients claiming
side-effects from dental alloy components,
Contact Dermatitis, 1996 May, 34:5, 320-3
(33) 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); 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 & P.Dallmann,”kon
nen durch Quecksilber entstehen? PeDa_Eigenverisg, 1995;& SS
Tsyganok, “Unithiol
in treatment of dermatoses”,
Vestn.Dermatol.Venerol., 1978, (9): 67-69.
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
(these clinics use
MELISA test for diagnosis of immune reactivity)
(34) 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