Amalgam in
Alzheimer's Disease*
* Studies have shown that the brains of the deceased Alzheimer patient
have 4-times as much mercury and 2-times as much aluminum as is found in
patients without Alzheimer. Also,
tumors contain more mercury than is
found in their environment.
Source
<http://babelfish.altavista.com/babelfish/trurl_pagecontent?lp=de_en&url=http%3a%2f%2fwww.power-for-life.com%2fSchwermetall%2fschwermetall.html>
*
------------------------------------------------------------------------
Kip Sullivan is an attorney from Minneapolis that has recovered from an
"incurable" illness after having his amalgam fillings removed.
Since
then he has been an advocate for making this treatment more readily
accepted and available to others suffering from neurological diseases,
and has done extensive research which is documented in a memo that he is
presenting to several well known Alzheimer's medical researchers in the
Minneapolis area. The following are excerpts from the memo, presented
here with Kip's permission, without the extensive footnotes, references
and tables contained within the memo. Anyone wishing additional
information with regard to the content presented here should contact Kip
at (612)823-1459.
------------------------------------------------------------------------
Robert Terry et al. are the authors of a book which reviews current
knowledge about Alzheimer's Disease (AD). The book was recently
described as "the best single book on the topic" by the New
England
Journal of Medicine and as "a most useful reference for
practitioners of
medicine" by the Journal of the American Medical Association. At
page
363 of this book, Terry et al. state: "Taken together, these
studies
suggest that chronic low level Hg toxicity in AD should be considered as
a potential pathogenetic factor in AD." Because amalgam is the
dominant
source of human exposure to mercury <hg.htm>, one may paraphrase
this
conclusion as follows: "Chronic low level exposure to mercury from
amalgam should be considered as a factor in AD."
The scientific evidence supports the following statements:
1. People with amalgams have
much more mercury in their bodies,
including their brains, than
people without amalgams; the extra
mercury carried by people
with amalgams constitutes half to
three-fourths of all mercury
found in their bodies;
2. People who die of AD have
elevated levels of mercury in their
brains; in rat brains and
human brain homogenate, mercury blocks a
biochemical process that is
also blocked in the brains of AD
victims; mercury causes
emotional and mental symptoms frequently
found in AD patients;
3. Twin studies suggest an
environmental cause of AD; epidemiological
evidence (the temporal and
racial distribution of AD) suggests
mercury from amalgams plays
a role in AD;
4. The hypothesis that mercury
causes AD is consistent with other
hypotheses about the
etiology of AD, namely, that apolipop
status is a strong predictor
of AD, that education and estrogen
p
5. Mercury may be a cause of
other diseases of the central nervous
system, including
amyotrophic lateral sclerosis, multiple
sclerosis, and Parkinson's
Disease.
------------------------------------------------------------------------
*
Overview of mercury body
burden studies
*
The typical amalgam filling is 50% mercury, 30% silver, and 20% other
metals. The appendix presents the research which documents the
conclusion that mercury escapes amalgam and accumulates in tissue
throughout the body, including the brain. The great majority of these
studies were performed on people, not animals. I summarize them briefly
here.
Mercury escapes from the amalgam in three ways: (a) corrosion, caused by
electrical currents passing through the filling; (b) what one expert
calls "direct dry evaporation;" and (c) removal of small
pieces of the
fillings caused by chewing. The liberated mercury is taken into the body
via (a) inhalation, (b) swallowing and (c) absorption into nearby mouth
and nasal tissue. People with amalgams have at least twice as much
mercury vapor in their mouths, twice as much mercury in their blood,
three to six times as much in their urine, at least six times as much in
their kidneys, and double the amount of mercury in their brains and
other body parts as people without amalgams. Several of these mercury
burden studies found a correlation between the number of amalgam
surfaces and mercury levels in the brain. One of the latest and most
disturbing of these studies found that women with ten or more filled
teeth give birth to babies with twice as much mercury in their bodies as
mothers with two or fewer filled teeth.
------------------------------------------------------------------------
*
*
That amalgams can double the body's mercury level and triple the urine's
mercury level suggests that mercury from amalgams is the source of at
least half to two-thirds of all the mercury humans are exposed to. Over
the last four or five years, a substantial body of evidence has emerged
which indicates that most of the mercury absorbed by people in
industrial nations comes from their amalgam fillings.
In 1991 the World Health Organization...... concluded the daily dose of
mercury from the environment is 2.6 ug......... If the correct figure
for absorption of mercury from amalgam turns out to be 8 ug, then the
total mercury absorbed per day from all sources -- the environment plus
amalgam -- is 10.6 ug, according to the WHO data. This means amalgam
mercury constitutes three-fourths of all mercury absorbed by the body (8
ug is 75% of 10.6 ug). If 10 ug turns out to be the correct figure for
mercury taken up from amalgams, then the total absorbed is 12.6, which
means about four-fifths of all mercury absorbed comes from amalgams (10
ug is 79% of 12.6 ug).
In a 1995 report prepared for Health Canada (Canada's national health
department), Richardson estimated that amalgam mercury constitutes half
of the mercury absorbed daily by adult Canadians.
Whether amalgam mercury is the source of 50% of all mercury absorbed, as
Richardson's data indicates, or three-fourths, as the WHO data suggests,
mercury from amalgams contributes a substantial portion of the mercury
absorbed each day, not a "very small" portion as the ADA would
have the
public believe.
------------------------------------------------------------------------
All the studies that directly link mercury to Alzheimer's Disease have
been done at the University of Kentucky. Three of these found higher
mercury levels in AD brains than in age-matched, neurologically normal
brains. The first of these, published by Ehmann et al. in 1986, examined
levels of 16 trace elements in the cerebral cortex of 14 AD and 28
control brains. The authors reported significant differences in eight of
the 16 elements; the largest differences were in mercury and bromine
(elevated in AD brains) and rubidium (reduced in AD brains). Two years
later Thompson et al. examined levels of 14 trace elements in three
areas of the brain that undergo marked change in AD victims -- the
hippocampus, amygdala, and nucleus basalis of Meynert (nbM) (11 AD and
11 control brains). They found the same imbalances in these regions of
the brain that they had found in the cerebral cortex in their earlier
study (with the exception of rubidium). The mercury imbalance in nbM was
the largest of these differences. In 1990, Wenstrup et al. measured 13
trace elements at the "subcellular level" in material taken
from the
temporal lobe of ten AD patients and 12 normal controls. They reported
significant differences for five elements: elevated mercury and bromine,
and diminished selenium, zinc, and rubidium. The authors noted that
selenium "is known to play a p
against mercury toxicity" and that zinc may also play a p
"by forming a zinc-thioneine complex with which the mercury will
replace
zinc forming a less toxic mercury-thioneine complex."
In this last study, the authors discussed three mechanisms by which
mercury could cause AD symptoms: reducing the brain's ability to utilize
tubulin, a p
membranes; and other forms of cell dysfunction caused by the loss of
zinc and selenium, a loss "possibly" due to the role zinc and
selenium
plan in detoxifying mercury. The University of Kentucky researchers have
conducted several studies examining the first hypothesis.
Tubulin is a p
element of mic
tracks, transporting molecules between the cell body and nerve
terminals." The hypothesis that AD brains cannot use tubulin to
make
mic
University of Kentucky researchers has been to show that mercury may be
the cause of this defect. Three studies by these scholars support this
hypothesis. The first demonstrated that the
tubulin-guanosine-5'-triphosphate (GTP) interaction is greatly reduced
in AD brains; the second that EDTA "complexed" with mercury
reduces
GTP-tubulin interaction in normal human brain homogenates; the third,
that the brains of rats exposed to mercury vapor demonstrate the same
marked reduction in tubulin-GTP interaction demonstrated in humans in
the first study. In the third study (which was done with scholars at the
University of Calgary medical school), rats were exposed to mercury
vapor at 300 micrograms per cubic meter for four hours a day for periods
ranging up to 28 days. The authors noted that 300 micrograms is "a
level
detectable in mouths of some human subjects with large numbers of
amalgam fillings." The authors found that by the fourteenth day the
rate
of tubulin-GTP binding had been reduced by 75 percent. "The
identical
neurochemical lesion of similar magnitude is evident in Alzheimer brain
homogenates. . .," stated the authors.
------------------------------------------------------------------------
A large body of research on the effect of accidental mercury poisoning
indicates that mercury causes emotional and mental disturbances very
similar to those that appear in many AD victims. Here is a summary of
the emotional and mental symptoms commonly associated with AD:
Patients with Alzheimer's exhibit changes in personality and social
skills. They . . . may become socially uninhibited or lose all
initiative and interest in activities. These patients often have
delusions, hallucinations, and sleep disorders. They sometimes show
grossly inappropriate judgement and sometimes are misdiagnosed as being
depressed or psychotic.
Every one of these symptoms are common symptoms of mercury poisoning.
The American Dental Association and its state affiliates cite a 1995
study of 129 elderly nuns as conclusive evidence that amalgams cannot
cause AD. But this study lacked a control group, and is therefore
useless. The authors divided 129 nuns into five groups depending on how
many teeth and how much occlusal amalgam surface they had. The authors
referred to these groups as "risk categories," which is to say
the
authors assumed that an old woman's risk of contracting Alzheimer's-like
symptoms is higher if, at the time of the study, she had teeth with
amalgams than if she had no teeth. The reader is led to think, in other
words, that the edentulous (toothless) nuns were the least likely to get
AD because their amalgam load at the time of the study was lower than
that of nuns in the other four categories. This is an absurd assumption.
No one other than the authors of this study postulates that mercury from
amalgams causes AD overnight. If amalgam mercury causes AD in elderly
women, it does so over decades, beginning possibly when the women got
their first fillings, which for most people occurs when they are
children. Having made this untenable assumption, the authors proceeded
to measure the mental abilities of the nuns with the Mini-Mental State
Examination, a commonly used test of mental function, and other tests,
and found no difference in test scores among the five "risk
categories."
"In fact," note the authors in an attempt to get the reader to
think the
edentulous group was the control group, "the group with the highest
amalgam surface area had the same mean Mini-Mental State Examination
score as the edentulous group." Nowhere in this article does the
phrase
"control group" appear.
What the authors of this study should have done was to measure the
lifetime exposure of the nuns to amalgam mercury as well as mercury
levels in their brains during autopsy, and see if there is a correlation
between lifetime exposure and brain mercury levels, or between either of
these variables and performance on cognitive skills tests. In such a
study, nuns edentulous by the time of the study may turn out to be the
"risk category" with the highest exposure to amalgam mercury. After
all,
a toothless person has almost certainly suffered from greater tooth
decay than someone with teeth, and, therefore, has probably been exposed
to more amalgam mercury for a substantial period of time than someone
who remains dentate. Because mercury stays in the brain for decades, one
could be edentulous for a very long time and still have more brain
mercury than someone who is dentate and has a lot of amalgams.
------------------------------------------------------------------------
Like Parkinson's and other adult-onset diseases of the central nervous
system that now afflict humanity, AD was rare or nonexistent prior to
the onset of the Industrial Revolution. The Industrial Revolution, which
greatly increased human exposure to mercury in the work place and in the
environment, got underway in the mid-1700s. Amalgam was invented in
Europe around 1820 and was widely used throughout Europe and North
America by 1850. Parkinson's, MS, and ALS were first mentioned in
medical journals in the 1800s. It was not until 1906 that German
psychiatrist Alois Alzheimer announced that he had found a "strange
disease of the cerebral cortex" in the course of performing an
autopsy
on a demented 56-year-old woman. The woman's brain contained an unusual
number of the plaques and tangles now considered to be the defining
symptoms of AD.
Scholars affiliated with the University of Minnesota and the Minnesota
Pollution Control Agency have demonstrated that atmospheric mercury
levels rose dramatically during the 1800's. In a 1992 article published
in Science, they reported that the rate at which mercury accumulated in
seven lakes "increased by a factor of 3 to 4 during the past 140
years."
Because the seven lakes are a
mercury and are spread out over a large area encompassing northern
Wisconsin and northern and central Minnesota, and because "the
deposition rates are relatively uniform" across the seven lakes,
the
authors concluded that the mercury sources were "regional if not
global." Data for six of the seven lakes indicated a substantial
increase in deposition rates around 1850 and another increase around
1920. Subsequent research indicates mercury deposition rates may have
peaked in the 1970s.
Amalgam is the dentist's stock in trade. Today a typical adult carries
ten amalgams weighing a total of about ten grams, of which five grams is
mercury. What little research there is on the rate at which mercury
escapes amalgam suggests about half a gram of mercury will escape from
these ten fillings over the ten-year life of these fillings, and most of
this mercury will be absorbed by the bearer of the amalgams. To put a
half-gram in context, consider these facts: Half a gram of mercury
dropped into a ten-acre lake warrants the promulgation of a fish
advisory for the lake in Minnesota; the tennis shoes with mercury in
them that were banned by the Minnesota legislature in 1994 contained
half a gram of mercury per shoe. (0.5 gram in a 180 lb. body, produces a
concentration of 6.168 PPM. Compare this level, to the elements in the
"Water of Life" <hydros0l.htm>. TRC)
Mammals have been evolving on this earth for 70 million years. A
permanent tripling or quadrupling of environmental mercury levels over a
mere century may well have had some impact on human health even if
amalgams had never been invented. If in fact amalgam accounts for at
least half of all mercury absorbed today, then we may say with some
accuracy that the introduction of amalgam coupled with the increase in
atmospheric mercury exposed humanity to at least a six-fold increase in
mercury over approximately 100 years. A century is a very short period
of time for any organism to develop new defense mechanisms against
unprecedented levels of something as toxic as mercury.
------------------------------------------------------------------------
Blacks have far fewer amalgams in their heads than whites; they also die
far less frequently from AD and MS. According to a 1996 report from the
Centers for Disease Control, white people are nearly two times more
likely to die from AD than blacks. According to a 1978 study of MS,
"The
. . . US Army suggests that the risk of MS for white males is 2.5 times
the risk for black males." Blacks in the US and England have long
had
much lower rates of caries than whites. According to the latest health
survey by the National Center for Health Statistics (which was conducted
over the 1988-91 period), adult blacks had only one-third the number of
"filled surfaces" as whites (8.5 versus 22.8). A small part of
this
difference was due to more untreated decay among blacks, but most of it
was accounted for by less decay in blacks. The small difference in
longevity in blacks and whites is too small to account for a two-fold
difference in AD mortality rates.
------------------------------------------------------------------------
*
AD as an inflammatory
response
*
The hypothesis that AD is caused by mercury from amalgam and the
environment is consistent with the theory that AD is an inflammatory
disease caused by the body's reaction to an infection or environmental
insult. The evidence that AD "fits the paradigm of the idiopathic
rheumatic disorders" was recently presented by Aisen and Davis.
"According to this model," w
circumstances results in an initial insult triggering an inflammatory
reaction in the brain. The inflammation becomes self-propagating, or it
continues because the obscure inciting factors persist." They argue
that
the acute phase response may augment production of beta-amyloid, the
p
"cytokines, acute phase p
all mechanisms which can be triggered by the acute phase response of the
immune system, are "involved" with AD, either as causes or
consequences,
and that anti-inflammatory drugs may "alter" the progression
of AD.
Mercury may well be one of the "obscure inciting factors" that
triggers
the inflammatory response.
Some direct evidence that anti-inflammatory drugs may delay the onset of
AD already exists. McGeer et al. reported data suggesting that "the
prevalence of Alzheimer disease in patients with rheumatoid arthritis is
unexpectedly low and that [the use of] anti-inflammatory therapy might
be the explanation." Aisen and Davis cite two other studies that
reach
the same conclusion.
------------------------------------------------------------------------
*
ApoE status
*
Researchers at Duke University have recently shown an association
between AD and the presence of a blood p
type-four (apoE4). People with two apoE4 genes have eight times the risk
of developing late-onset AD as those with two apoE3 genes, and those
with two apoE2 genes have an even lower risk. The Duke researchers
subsequently found that mic
people with apoE4 than E3 genes. They surmise that this breakdown is
caused by the inability of a p
construction of mic
al. indicating the breakdown may be caused by the AD brain's reduced
ability to utilize another p
mic
Haley hypothesizes that the apoE4-AD correlation is due to the inability
of apoE4 p
statement by David Kennedy, a dentist and researcher on amalgam
toxicity, summarizes Haley's theory:
The function of [the apoE] p
of the brain... The difference
between apoE2, E3 and E4 is that E2
has two cysteines, in E3 one
cysteine is replaced by an arginine,
[and] in E4 both cysteines are
replaced by arginine. [Haley]
explained that unlike cysteine
the arginine does not pick up mercury
since it contains no sulfur. Sulfur
is called a mercaptan (Latin for
mercury capture). Mercury
loves sulfur more than other molecules. It
will drop whatever it is
attached to and bind with sulfur.... E2
people, who are less likely to
get AD, have a p
mercury as well as cholesterol
out of the brain by binding mercury
with sulfur seats.
Haley's explanation of the relationship between apoE status and AD is
consistent with a 1988 study of trace element levels in hair and nails
of AD patients done at the University of Kentucky by Vance et al. The
study found no difference in hair mercury levels of patients with and
without AD; it found that AD patients had lower mercury levels in their
nails than did the non-AD controls. In his review of the literature on
amalgam toxicity, Richardson cited the study by Vance et al. as evidence
against the conclusion that amalgams cause AD. If Haley's description of
apoE is correct, or if research demonstrates some day that for other
reasons some humans are have diminished capacity to scavenge and excrete
mercury, we should expect to find that AD victims have the same or lower
mercury levels in hair and nails despite having above-average levels in
their brains.
If Haley's thesis is correct, the following hypothesis seems quite
plausible: because of a reduced capacity to excrete mercury, mercury
(from amalgam and nonamalgam sources) builds up more rapidly in the
brains of people with the epoE4 gene; rising mercury levels in the brain
eventually cause the destruction of mic
neuron death; rising mercury levels trigger an inflammatory response
that accompanies, and may contribute to, neuron death.
AD afflicts many who do not carry the apoE4 gene. What that signifies is
that an intolerable level of mercury can build up in people regardless
of their apoE status. This intolerable level may be reached (1) because
of exposure to high levels of mercury, (2) because of exposure to other
toxins and stressors that reduce the ability to cope with mercury, (3)
because of genes other than those controlling apoE status, or (4) some
combination of these three conditions.
------------------------------------------------------------------------
*
Other theories: estrogen,
education, head trauma,
electromagnetic fields, and
smoking
*
The hypothesis that mercury causes AD is consistent as well with other
theories of AD etiology.
Evidence supports the claim that estrogen supplements reduce the risk of
AD in women. Animal experiments indicate that estrogen stimulates nerve
growth, perhaps indirectly by its effect on nerve growth factor. Higher
education levels may also p
(or perhaps the habits of mind that higher education encourages) may
help the brain maintain or construct neurons. These findings are
consistent with the mercury hypothesis.
p
destruction caused by mercury.
Trauma to the head is occasionally mentioned in the literature as a
factor associated with a higher incidence of AD. At least one expert
believes head trauma is a risk only for people with the apoE4 gene. A
blow to the head may aggravate the toxic effect of mercury in at least
two ways: it might stress the body and thereby weaken the body's ability
to withstand the presence of mercury; the trauma may fracture fillings
and increase the victim's exposure to mercury.
I base the latter explanation on my familiarity with the health history
of June Varner, a Little Falls woman who overcame nearly paralyzing
confusion by getting her amalgams removed. Her inability to concentrate
and make decisions set in after a 1978 car accident. The problem was
severe. June stated in a letter to me, "I can remember looking down
at
my shoelaces months after the accident; I could not remember how to tie
them. I knew that I knew how to do it but I could not remember." Other
symptoms that appeared after the accident included headaches, vertigo,
nausea, extreme fatigue, and memory loss. These symptoms persisted until
1992 when her dentist discovered that several teeth in the upper right
side of her mouth with amalgams in them were cracked. The replacement of
these amalgams with crowns eliminated the mental confusion and the other
symptoms that came with the confusion. June speculates that the blow to
her head suffered during her auto accident allowed mercury from her
fillings to gain access to her brain.
Golden mentions a study done by Eugene Sobel at the University of
Southern California which found "that the onset of Alzheimer's is
unusually high in dressmakers and tailors," possibly because sewing
machines create large electromagnetic fields (EMFs). EMFs could augment
the damage that mercury does to the brain in two ways. They may render
the blood-brain barrier more permeable to toxic material, including
mercury; they may accelerate the release of mercury from amalgams (see
discussion of the role of electricity in releasing amalgam mercury in
attachment).
Finally, smoking seems to play a p
for this may be that nicotine has the opposite effect on
neu
of, or otherwise reduces the effect of, dopamine, norepinephrine,
se
neu
smoke more than people without amalgams.
------------------------------------------------------------------------
*
ANECDOTAL EVIDENCE
*
Mary and Monica are, like me, patients of a Bloomington dentist under
attack by the Minnesota Board of Dentistry for his stance on amalgam (he
won't use them, and he takes them out). Mary, Monica and I have come to
know each other well in the course of working together to defend him and
other mercury-free dentists. Monica and Mary both recovered from
Alzheimer's-like symptoms after the dentist took their amalgams out.
Monica's symptoms were mild; she would say one word when she meant
another, and her memory deteriorated. She overcame these symptoms with a
combination of amalgam removal and supplements. Because Monica's mother
had AD for many years, Monica has little doubt she has the genes that
make her susceptible to AD. Upon her mother's death, Monica and her
sister asked the Mayo Clinic to determine the levels of aluminum, nickel
and mercury in their mother's brain. The results: aluminum, normal;
nickel and mercury, extremely high.
Mary's symptoms were severe, especially for a woman in her thirties
which is when Mary's health deteriorated. She suffered from memory loss
so severe she could not remember people she had known for years or how
to drive to places she had driven to for years. She suffered fits of
rage so intense she had to lock herself in the bathroom to avoid hurting
her children. She recovered quickly after having her amalgams removed.
We can only speculate whether Mary and Monica had the plaques and
tangles of fully developed AD.
I am told dozens, perhaps hundreds, of other Americans could tell
similar stories. I have the phone numbers of several of them.
------------------------------------------------------------------------
*
Overview of the evidence
linking amalgam mercury to ALS
The evidence supporting the hypothesis that amalgam mercury is a cause
of ALS is as strong as the evidence implicating amalgam in the onset of
AD. Like AD, ALS was not described until well after the Industrial
Revolution had begun. According to Felmus et al., "[T]he original
description of amyotrophic lateral sclerosis" appeared in 1869. Like
the
evidence linking amalgam with AD, the evidence linking amalgam to ALS
includes research showing elevated mercury in ALS patients and anecdotal
evidence of recovery from ALS after amalgam removal. Unlike the AD
literature, the literature on ALS includes at least five articles
describing the appearance of ALS symptoms in people exposed to organic
mercury and mercury vapor, and, for some victims, the disappearance of
these symptoms after exposure to mercury ceased. Like the literature on
AD, the literature on ALS contains speculation that ALS may be an
inflammatory disease caused by a toxin. I find it intriguing that
familial ALS and AD "have [both] been mapped to chromosome
21."
The scientific literature on mercury, amalgam and ALS
The first of several reports on ALS-like symptoms triggered by exposure
to mercury appeared in 1954. The article described an ALS-like syndrome
in a 39-year-old farmer who absorbed organic mercury from a fungicide he
used on oats. At least three similar articles have been published since.
One described ALS symptoms in 11 Iranians who ingested bread made with
wheat treated with a fungicide containing ethyl mercury; another
reported ALS symptoms in two men exposed to mercuric oxide and mercury
vapor in a factory that manufactured mercuric oxide; the third described
a 54-year-old man who developed ALS symptoms three-and-a-half months
after he spent two days gathering liquid mercury from old thermometers.
A number of people who have had amalgams removed have recovered from
ALS. In a 1994 article, Redhe and Pleva described such a recovery by a
29-year-old Swedish woman. She had been diagnosed with ALS by the
neurology department at the University Hospital in Umea, Sweden. This
same department pronounced her free of ALS in August 1984, five months
after her amalgams were removed. Nine years later the woman was still
free of ALS symptoms.
Mercury has also been implicated by studies examining health histories
of groups of people diagnosed with ALS. Felmus et al. found that 25 ALS
patients were more likely to be exposed to mercury and lead than a
control group of sick people with non-ALS diagnoses (although the two
groups did not differ in number of amalgams). Sienko et al. sought to
explain the sudden appearance of ALS in six residents of Two Rivers,
Wisconsin over the 1975-1983 period. They found that the ALS victims
suffered more instances of physical trauma, reported more cancer in
their families, and had eaten more fish from Lake Michigan than had 12
controls.
Some of the University of Kentucky scholars who examined mercury levels
in AD victims were among the authors of a similar study of ALS patients.
They found that seven deceased ALS victims had more mercury in their
brains than did nine deceased controls who did not have ALS, and that
blood cells of 40 living ALS patients contained more mercury than the
blood cells taken from 31 living controls. Interestingly, ALS victims
had lower levels of selenium in blood serum. Selenium has been shown to
"p
as mercury . . . ."
------------------------------------------------------------------------
Unpublished anecdotal evidence of recovery from ALS after amalgam
removal
The Redhe-Pleva article on the Swedish woman who recovered from ALS
after amaglam removal is the only such report in the peer-reviewed
literature I know of. However, similar but unpublished stories are
numerous. I recount one here. Cynthia Hughes is a Nevada woman who
recovered from ALS after her amalgams were removed by Dr. Hal Huggins, a
Colorado dentist who practiced mercury-free for 23 years until the
Colorado Board of Dental Examiners took his license because of his
public criticism of amalgam. Cynthia and the neurologist who diagnosed
her appeared on a four-part television report entitled "Toxic
Teeth"
which aired on a Las Vegas TV station in the early 1990s. The reporter
stated: "Cynthia could not walk or talk until she had her mercury
fillings removed. Even her doctor was amazed by her sudden
improvement."
At this point the camera showed a doctor sitting at his desk with his
name and specialty shown on the screen -- "Dr. Hal Griffith,
neurologist." Dr. Griffith stated, Cynthia "had a dramatic . .
.
complete recovery."
------------------------------------------------------------------------
*
Evidence linking amalgam
mercury
with multiple sclerosis and
Parkinson's
*
Like AD and ALS, MS and Parkinson's are adult-onset diseases that either
did not exist or were rare prior to 1800. Like the AD and ALS
literature, the MS and Parkinson's literature offers some evidence that
toxins in general and mercury in particular plays a critical role in the
etiology of these diseases. Finally, there is substantial anecdotal
evidence that amalgam removal reduces MS symptoms dramatically in many
MS patients. I know only two Parkinson's patients who have had their
amalgams removed, and one of them improved.
------------------------------------------------------------------------
Evidence that mercury is
swallowed and absorbed
into mouth tissue: the
corrosion studies
Although experts think most amalgam mercury enters the body is mercury
that escaped via evaporation and inhaled, I start with a review of the
evidence that mercury is released via corrosion because that evidence is
the oldest. Electrical currents, created by the amalgams themselves,
liberate mercury from the filling and allow it to travel into the saliva
and mouth tissue, including gums and pulp. The liberation of mercury and
other metals from the amalgam by electrical currents is called corrosion
and, sometimes, "oral galvanism."
It has been known since at least 1878 that amalgams create these
electrical currents. It has been known since at least 1881 that amalgams
discolor and soften the dentin (the soft material between the enamel and
the pulp), and since at least 1953 that one phenomenon causes the other,
that is, that the electrical currents in the mouth cause fillings to
corrode and release metals that then travel into the dentin causing
discoloration. The 1953 study examined 300 freshly extracted teeth
containing amalgams and found a "greenish to grayish black
discoloration" in the dentin of 85% of the teeth. In this
discolored
dentin the authors found "relatively large amounts of mercury . . .
with
smaller amounts of silver, zinc, tin and copper. . . ." The authors
recreated this same greenish-black color in the dentin by running
electric currents through the amalgam, leading the authors to conclude
that the migration of mercury and other materials from the amalgam was
precipitated by "intermitten
amalgam filling itself." Other studies have confirmed this finding.
By
the 1970s it was established that mercury was migrating into the gums,
pulp, and, by the 1980s, the jawbone.
------------------------------------------------------------------------
*
Evidence that mercury is
inhaled: the vapor studies
*
A report in 1979 that fillings give off mercury vapor led to the revival
of the amalgam debate in this country. Prior to 1979 the position of the
ADA and most dentists was that a newly inserted filling would give off
mercury vapor for a few hours but after that mercury vaporization
ceased. The 1979 study was important because it established that chewing
released mercury vapor even from old fillings. The study was done by
three researchers at the University of Iowa. They announced preliminary
results in a letter to Lancet, a widely read British medical journal.
They reported that chewing gum for 15 minutes caused mercury vapor
levels in expired air to rise by as much as 17 times in five individuals
with amalgams whereas gum chewing by two subjects without amalgams had
no effect on the amount of mercury in their breath. Although other
research was also published that year linking amalgams to mercury levels
in the blood, the Lancet announcement is the one cited throughout the
scientific literature as the first study in recent times demonstrating
that mercury escapes from fillings. The final report on the Iowa
research published two years later concluded that chewing increased the
amount of mercury vapor in the breath of subjects with amalgams by an
average of 15.6-fold and that, even before chewing, subjects with
amalgams had three times as much mercury in their breath as the
non-amalgam subjects.
Patterson and two other New Zealand researchers reported in 1985 that
brushing one's teeth with a soft tooth brush for one minute also
stimulates mercury vapor release. Mercury vapor levels rose from an
average of 3.1 ng/L of expired air before brushing to 8.2 ng/L after
brushing. Even eating musli, a soft cereal, raised mercury vapor levels.
In 1988, Langworth et al. published a study of "intratracheal
mercury
levels" (that is, mercury levels in the air in the windpipe) of ten
subjects (all, apparently, with amalgams). Prior to brushing their
teeth, tracheal mercury vapor levels were below the instrumental
detection limit of 1 ug/m^3 for five subjects and ranged from 1-6 ug/m^3
for the other five. After brushing, the average level for all ten
subjects rose to 56.4 ug/m^3 .
The last study of oral mercury vapor levels was published in 1994 by
Siblerud et al. They reported that people with amalgams had twice as
much mercury vapor in their mouth air as people without amalgams prior
to chewing and four times as much after chewing.
The reader should note that the breath levels just reported are averages
among the people volunteering for the various studies and therefore do
not reveal the high levels of mercury vapor reached in some people's
mouths. Dr. Wayne King, a Georgia dentist, in testimony before the FDA
Dental Panel in 1991, made this remark indicating that oral mercury
vapor levels can reach very high levels in some of his patients: "I
have
been absolutely horrified to see some of the numbers that I have
measured coming out of some of the mouths of my patients; for instance,
200 micrograms per cubic meter in a suicidally depressed patient."
That mercury vapor is released by amalgams is no longer debatable. As
one expert who defends amalgams put it at the 1991 National Institute of
Dental Research conference, "The question is not if, but how much
mercury vapor is released."
------------------------------------------------------------------------
Those interested in more information may contact Kip Sullivan at
(612)823-1459.
------------------------------------------------------------------------
Chelation Therapy <../riddick/rwaters.htm>
Heavy Metal Toxicology <heavmet.htm>
Hydroponic Reference Center <makhydro.htm>
Site Link List <../link.htm> - Mercury <hg.htm> - Silver <Ag.htm>
Mercury Free and Healthy <http://www.amalgam.org>
The Dental Amalgam Issue
Advanced Therapy for Heavy Metal Detoxification
<../ext/hastobe.htm>
Symptoms of Toxic Elements - From the Merck Index. <../toxic.htm>
The Tortoise Shell "Science
of Health" Newsletter
<../news.htm> *
? Putting an End to Disease on Our Planet ? *
*Tortoise Shell Life Science Puzzle Box ? Front Page
<../index.html> *
*View this page Full Frame <amalgam.htm> *
*Excerpts from memo by **Kip Sullivan*
<http://www.lightparty.com/Health/SilverFillings.html>