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1 21st June 10:30
jdrew63929
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Default Dental Amalgam Removal Improves Health


http://www.toxicteeth.net/natCamp_IntScene_SwedenArticle.cfm


Dental amalgam removal improves health


2002; 23:459-482**pii: NEL235602A12**PMID: 12500173


NEUROENDOCRINOLOGY LETTERSincluding Psychoneuroimmunology,
Neuropsychopharmacology,
Reproductive Medicine, Chronobiology and Human Ethology, ISSN 0172-780X

Key words: amalgam, metal exposure, mercury, chronic fatigue,
removal, antioxidants, plasma, questionnaire, quality of life

Removal of dental amalgam and other metal alloys supported by antioxidant
therapy alleviates symptoms and improves quality of life in patients with
amalgam-associated ill health


by Ulf Lindh, Romuald Hudecek, Antero Danersund, Sture Eriksson & Anders
Lindvall

Submitted: July 29, 2002 Accepted: August 1, 2002


SETTING AND DESIGN: We included 796 patients in a retrospective study using a
questionnaire about symptom changes, changes in quality of life as a
consequence of treatment and assessment of care taking.

METHODS: Treatment of the patients by removal of offending dental metals and
concomitant antioxidant therapy was implemented according to the Uppsala model
based on a close co-operation between physicians and dentists.

RESULTS: More than 70% of the responders, remaining after exclusion of those
who had not begun or completed removal, reported substantial recovery and
increased quality of life. Comparison with similar studies showed accordance of
the main results. Plasma concentrations of mercury before and after treatment
supported the metal exposure to be causative for the ill health.

MAIN FINDINGS: Treatment according to the Uppsala model proved to be adequate
for more than 70% of the patients. Patients with a high probability to respond
successfully to current therapy might be detected by symptom profiles before
treatment.

CONCLUSIONS: The hypothesis that metal exposure from dental amalgam can cause
ill health in a susceptible part of the exposed population was supported.
Further research is warranted to develop laboratory tests to support
identification of the group of patients responding to current therapy as well
as to find out causes of problems in the group with no or negative results

* * *


ABBREVIATIONS

ANOVA -- ****ysis of variance
bcl-2 -- Anti-death gene
DTT -- Dithiothreitol
GABA -- gamma-aminobutyric acid
GSH -- Glutathione, reduced
Hg -- Mercury
hSkM1 -- Gene product of SCN4a (sodium channel a-subunit) being the human
homologue of rSkM1, the tetrodotoxin-sensi tive sodium channel characteristic
of adult rat skeletal muscle
ICP-MS --- Inductively Coupled Plasma Mass Spectrometry
IL -- Interleukin
IRE -- Iron responsive element
IRP-1 -- Iron regulatory protein 1
MAP -- Mitogen activated protein
MELISA® -- Memory Lymphocyte Immuno Stimulation Assay
Ras -- One of a family of guanosine nucleotide-binding proteins
RIC -- Restoration with Individually Compatible Dental Materials
RID -- Removal of Incompatible Dental Materials
ROS -- Reactive Oxygen Species
TNF -- Tumor Necrosis Factor


Introduction

Dental amalgam was used very early in China. "Silver paste" is mentioned in the
materia medica of Su Kung in 659 A.D. The name used is probably the historical
reason why this material in some countries is called "silver amalgam" although
its main ingredient always has been mercury. French chemists and dentists
experimenting with various mixtures of metals in the end of the 18th century
initiated the use of amalgam in the western world. Introduction of dental
amalgam is usually ascribed to the French brothers Crawcour in 1831. They used
a mixture of mercury and filings of French silver coins. Two years later the
Crawcour brothers introduced the filling material in New York and they falsely
pretended to be dentists.

Discussions about the rationale in using mercury as the main component in
dental amalgams have been going on more than 160 years. In fact, the debate
started immediately after the introduction of the material in the U.S.A.
American medical-dentists at that time started a merciless crusade against
their foreign rivals. They declared that not only was silver amalgam a lousy
filling material but it also caused mercury poisoning. This had among other
things the consequence that professional dentists started a dental association
(The American Society of Dental Surgeons) in New York in 1840 to "increase the
standing of the profession and to counteract charlatanry". The first amalgam
war had begun.

Almost ignored were the results of studies in which warnings were issued for
negative health effects associated with exposure to mercury from dental
amalgams [1, 2]. Later during the 1920s, the German chemist Alfred Stock warned
about the danger with mercury vapor [3, 4]. As late as in 1939 he issued
enhanced warnings [5]. The latest phase in these amalgam wars started in the
late 1970s and has been especially intense in Scandinavia but also in the
U.S.A. and Germany. Various attempts to estimate risks from dental amalgams
have been published advancing conclusions of increased risk of disease [6] as
well as no correlation between amalgams and health problems [7]. The latter
study, however, demonstrated negligence of combinations of gold and amalgam
causing increased corrosion and mercury vapor emission. Richardson [8-10]
concludes that a significant portion of all age groups exceeds the proposed
reference dose for mercury exposure (0.98 mg Hg/day - tolerable daily intake)
more than fives times due to dental amalgam. He also concludes that data
suggest that approximately 19 to 20% of the general population may experience
sub-clinical central nervous system and/or kidney function impairment as a
result of the presence of amalgam fillings. Berlin [11] arrives at the
conclusion that the prevalence of side effects from mercury in amalgam on the
nervous system, immune system and kidneys should fall in the interval 0.1-10%
with the highest probability of 1%. This makes the probable side effects from
amalgams a significant health problem.

Do***ented effects of amalgam removal appeared already in 1842 [1]. However,
probably the first comprehensive study was published in 1928 as a consequence
of Stock's warnings [15]. Seven patients with a completed treatment reported
substantially improved health or complete health. Fleischmann [15] interpreted
the symptoms as an expression of "hypersensitivity" and recommended dentistry
to abandon copper amalgam of that time immediately and silver amalgam when
equivalent materials were available. Several contemporary studies have been
published dealing with implications, both in general health, oral pathology and
laboratory medicine, of removal of dental amalgam [16-35]. A drawback of most
of these studies is, however, that there are few indications of the treatment
quality.

The rationale for highlighting clinical effects of chronic low-dose mercury
exposure is the advancement of modern research in the behavior of mercury in
tissues. This metal has a lot of potentially toxic effects on various levels in
a living organism. Mercury exposure decreases the DNA content and increases
collagenase-resistant protein formation in synovial tissues. This leads to an
increased risk for reduced joint function and decreased ability to repair joint
damage [36] partly explaining the joint problems in the patient group.

Decreased amounts of available selenium are also a consequence of exposure to
heavy metals, in particular mercury, which compounds the oxidative burden on
the body [37]. Mercury also decreases levels of glutathione (GSH) in the body
[38]. Mercury binds irreversibly to GSH causing the loss of up to two GSH
molecules per mercury ion. The GSH-Hg-GSH complex is excreted via the bile into
the feces. Part of the irreversible loss of GSH is due to the inhibition of GSH
reductase by mercury, which is used to recycle oxidized glutathione and return
GSH to the pool of available antioxidants [39]. At the same time, mercury also
inhibits GSH synthetase, so a lesser amount of new GSH is created. Since
mercury promotes formation of hydrogen peroxide, lipid peroxides and hydroxyl
radicals, it is evident that mercury sets up a scenario for a serious imbalance
in the oxidant/antioxidant ratio of the body [40].

Central nervous affection by exposure to mercury may in part be explained by
that Hg0 and Hg2+ are ac***ulated in motor neurons and Purkinje cells in the
brain [41]. Important intracellular effects of mercury are intimately connected
to enzymes. All enzymes with sulfur amino acids as well as selenocysteine are
open for attack by Hg2+ with a probable outcome of impairment of function.
Cells presented with Hg0 will not be able to stop penetration through membranes
due to the lipophilicity of uncharged mercury atoms. This opens for a multitude
of possible symptoms from various organs in the body. First order thiol binding
constant of Hg2+ is 1030-40, which demonstrates the extreme affinity of mercury
for thiol groups [42]. Additionally, the ligand exchange rate constant of Hg2+
among thiol groups is among the highest known (109 s-1), again showing the
extreme properties of the mercuric ion [43].

Exposure of workers to 0.0058 mg m-3 mercury vapor (0.007-0.021 mg m-3)
affected the chemotaxis of polymorphonuclear leukocytes significantly [44].
This exposure is in good agreement to what could be expected from a "normal"
set of amalgam fillings [45]. A sensitive subgroup of the population,
therefore, has to be expected to suffer from impairment of circulating blood
cells. Furthermore, neutrophil activity has been shown to be inhibited by
mercury [46]. Even damages to DNA has been attributed to mercury exposure [47].
Mercury interacts with the GABAA receptor by way of alkylation of thiol groups
of cysteinyl residues found in GABAA receptor subunit sequences [48]. This has
the consequence that the binding site of benzodiazepine is modulated.

Structural alteration of the mitochondrial inner membrane with consequent
dissipation of membrane potential and disruption of oxidative phosphorylation
is another cellular effect of mercuric ions [49-51]. The intracellular calcium
homeostasis is altered by mercury inducing mitochondrial release of calcium
[51, 52]. Cellular influx of calcium also seems to be a consequence of human
exposure to mercury and other metals from dental amalgam [13]. Mercury-induced
stress may transform innocuous astrocytes into potentially lethal sources of
cytotoxic oxygen free radicals [53].

Low levels of mercuric ions alter the normal pattern of protein tyrosine
phosphorylation in B-lymphocytes during antigen receptor-stimulated signal
transduction, suggesting that low levels of mercuric ions interfere with signal
transduction pathways that are mediated by receptor-associated tyrosine kinases
[54]. Additionally, Mattingly et al. [55] showed that low concentrations of
mercuric ions interfere with the normal activation of Ras and MAP kinase during
antigen receptor-mediated signal transduction in T lymphocytes. The regulation
of cell growth is interfered by low and non-toxic levels of ionic mercury [56].
Mercury-induced apoptosis seems to be species dependent in human lymphoid cells
in a comparison between the effects of methylmercuric chloride and mercuric
chloride [57]. Each of the mercurial species trigger the apoptotic cascade,
however, there are profound differences in the mechanism of action at the
mitochondrial level. This disparity of mode of action may be linked to
differential effects on the anti-death gene, bcl-2. Low-dose exposure to
silver, copper, mercury and nickel ions alters the metabolism of human
monocytes [58]. These authors conclude that the levels of metals released from
dental alloys may be significant to monocytic function.

Mercury as well as cadmium binds iron regulatory protein 1 (IRP-1) with high
affinity, compared with iron. These metals may cause the disruption of iron
metabolism by inhibiting posttranscriptional regulation of iron-related
proteins, such as ferritin and transferrin receptor. The effects of these toxic
metals on inactivation of IRP-1/IRE binding and activation of aconitase may
explain part of the cell toxicity [59]. Even ion channels may be adversely
affected by mercury exposure. Divalent mercury blocked human skeletal Na+
channels (hSkM1) in a stable dose-dependent manner in the absence of reducing
agent. Dithiothreitol (DTT) significantly prevented Hg2+ block of hSkM1 and
Hg2+ block was also readily reversed by DTT [60].

Mercury is additionally well known to have adverse effects on the immune system
with increased IgE in blood and deposits of immune complexes in the renal
mesangium [61, 62]. Immunomodulation is but one of the facets of mercury
exposure. Experimental animal studies and observations in humans indicate that
immunomodulatory properties of metals such as mercury are heterogeneous and are
not restricted to contact allergy [63]. Mercury causes induction of oligoclonal
T cell responses skewed toward type-2 reactions [64]. There are numerous
studies showing the induction of autoimmunity by mercury exposure [65-69]. Even
neurological diseases have been hypothesized to be, at least partly, due to
induction by exposure to heavy metals such as mercury [70-72].

During the last twenty years an increasing number of patients have sought
dental and/or medical care for problems possibly associated with dental
amalgam. These patients have observed a relationship in time between
odontological treatment and occurrence or increase of their symptoms. The metal
syndrome was conceived by our group as a collective term describing such
patients with a series of symptoms for which no other etiologic diagnosis could
be found in spite of thorough examination and laboratory tests [12]. Most other
possible causes, except for metal exposure from amalgams, for the disease of
these patients have been excluded by meticulous investigations performed by
several specialist physicians. A differential diagnostic procedure had thus
been thoroughly implemented. These patients suffered from several general,
neurological, psychiatric and oral symptoms.

Soon additional laboratory tests were included in these studies. Nuclear
microscopy of single isolated blood cells revealed that patients, in contrast
to healthy controls, displayed distorted profiles of trace elements in blood
cells [13]. In addition, changes of trace elements in blood plasma assessed by
X-ray fluorescence were observed.

Hypersensitivity or allergy to metals comprising dental alloys was suspected
rather early. To avoid potential side effects of traditional patch testing, an
in vitro test was applied. This test being called MELISA® (MEmory Lymphocyte
Immuno Stimulation Assay) is a development of the common lymphocyte
transformation test. MELISA® applied to 3000 patients with suspected side
effects from metals in dental restorative materials in three ****ytical centers
demonstrated a reasonable degree of conformity [14].

The aim of the present study was to evaluate the treatment of patients at the
former Department of Clinical Metal Biology at the University Hospital in
Uppsala, Sweden. A questionnaire comprising questions about symptoms, quality
of life as well as care-taking assessment was constructed and sent to patients.
The study design was, therefore, a before-after design in which patients
constituted their own controls and was undertaken in retrospect and
longitudinally. This design has the attractive advantage of setting aside
genetic differences between cases and controls. Even if the study had been
prospective, it would not have been possible to adopt a double-blind
placebo-controlled design for obvious reasons.
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2 21st June 10:30
noyb
External User
 
Posts: 1
Default Dental Amalgam Removal Improves Health


No double-blind placebo control group? And the "medical" evaluation to see
if patients' health improved was a "questionnaire"?!?!? Bwahahahahahaha!
You *have* to be joking!

I especially liked this "scientific" portion of the study:

"The study design was, therefore, a before-after design in which patients
constituted their own controls."

Can you say "placebo effect"?


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3 21st June 10:30
jdrew63929
External User
 
Posts: 1
Default Dental Amalgam Removal Improves Health


If you wish to remain in denial, you can use any ole excuse.

WHEN CORRECT PROTOCOL IS FOLLOWED!

http://www.home.earthlink.net/~berniew1/index.html

I. DENTAL AMALGAM FILLINGS PAGE- do***ents high common mercury exposure levels
from dental amalgam fillings; and common adverse health effects on people and
dental staff; plus results of 60,000 clinical cases of significant improvements
to chronic conditions after amalgam replacement and treatment- as followed and
do***ented by doctors; plus environmental effects of amalgam that affect
everyone.
(over 1500 peer-reviewed medical study or Gov't Agency references do***enting
mechanisms by which mercury from amalgam causes over 30
chronic health conditions)


http://www.lichtenberg.dk/experience_after_amalgam_removal.htm

http://www.lichtenberg.dk/symptoms_before_and_after_proper.htm

http://www.rmdentalcentre.com/article.cfm?artid=4&catid=1

http://www.positivehealth.com/permit/Articles/Dentistry/burrow45.htm

http://www.notdoctors.com/mercfill.html

http://www.geocities.com/toothk/bernieref1.html

http://216.239.53.100/search?q=cache:2MRH9H-lc08J:www.melisa.org/articles/
engel-e.pdf+people+finding+improvements+from+removal+of+ amalgams&hl=en&ie=UTF-8

http://www.web-light.nl/AMALGAM/EN/frame_r.html#V

http://www.positivehealth.com/permit/Articles/Dentist/crawford76.htm

http://www.cqs.com/amalgam.htm

Jan
The world is a dangerous place to live; not because of the people who are evil,
but because of the people who don't do anything about it."
Albert Einstein
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4 21st June 10:30
joel m. eichen d.d.s.
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Posts: 1
Default Dental Amalgam Removal Improves Health


This was a psychiatric study right?

Would it also apply to sane patients?


Joel

--
Joel M. Eichen, .
Philadelphia PA
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5 21st June 10:31
joel m. eichen d.d.s.
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Posts: 1
Default Dental Amalgam Removal Improves Health


Ye Olde Boye and girle Clubbe in deNILE, and lowering their own
incomes **** plenty of hard cash to be made with composite
compatibility testing, NICO, and other unproven nonsense from Janster.

--
Joel M. Eichen, .
Philadelphia PA
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