Re: Mercury Amalgams

[Guest guest]

Just a few minor points for the nephew who claims to be a dentist.

Jan

http://www.algonet.se/~leif/AmFAQk03.html#TOXLEV

Reports stating that groups of people, suspecting that they have a

(non-allergic-) amalgam-related illness, have reduced their symptoms, by up

to 80%, after removing their amalgam-fillings have been presented

(Lichtenberg 1993, Lindqvist 1996, Siblerud 1990). Also presented are

case-reports of people regaining their health after amalgam-removal

(Barregard 1995, Godfrey 1990, Langworth 1996, Redhe 1994).

Berglund (1995) has reviewed the case-reports of adverse effects to amalgam,

available in the literature, and found that:

" Removal of amalgam was the common measure that led to improvement or cure "

Subject: Re: amalgams

>| From: Kip King <A HREF= " mailto:wodi007@... " >wodi007@...</A>

>| Date: 11/5/00 10:54 PM Eastern Standard Time

>| Message-id: <3A062B62.404EB0A3@...>

>|

>| I tested out with extreme mercury poisoning (100 ug/g creatinine,

>| reference rage 0-3 ug/g creatinine) on Feb. 9, 1999 by Doctor's Data,

>| Inc. (urine test). I had no other possible sources of mercury except

>| amalgams. I've had many chelation treatments since then that have

>| reduced my mercury to 18 ug/g creatinine on May 3, 2000. Amalgams can

>| indeed cause extreme mercury poisoning.

http:www.amalgam.org/

This web page presents information pertaining to the dental amalgam issue.

Subjects presented in the contents list are linked to subsequent portions of

the web page.

Contents List

I) Introduction

I a) Fundamental Health Flaws

I The Truth and the Hippocratic Oath

I c) Historical Overview of Mercury Use in Dentistry

Id) Has the US Food and Drug Administration Approved the Mixed Dental Amalgam?

II) Paramount Scientific Documents

II a) Review

II Dental Mercury Impairs Kidney Function

II c) Dental Mercury Provokes an Increase in Oral and Intestinal Floras

II d) Dental Amalgam Mercury in the Human Population

II d1) Dental Mercury is Source of Two-Thirds of Mercury in Population

II d2) Neurological Behavioral Effects from Exposure to Dental Amalgam

Mercury (focuses on dental personnel)

II d3) Mobilization of Mercury and Arsenic in Humans by DMPS (including

dental personnel)

II e) Mercury Exposure via Breast Milk

II f) Infertility

IIg) Mercury Associated with Cardiac Dysfunction

III) Fetal Malformations

III a) Sheep Study

III Rat Studies

III c) Human Study

IV) Alzheimer's Disease Studies

IV a) Trace Elements in Alzheimer's Disease Brains

IV Mercury Vapor Inhalation Inhibits Tubulin in Rat Brain

IV c) HgEDTA Complex Inhibits Tubulin

IV d) Increased Blood Mercury Levels in Patients with Alzheimer's Disease

IVe) Mercury Induces Cell Cytotoxicity and Oxidative Stress and Increases

ß-Amyloid Secretion and Tau Phosphorylation in SHSY5Y Neuroblastoma Cells

V) Amalgam Removal

V a) Patient Preparation for Amalgam Removal

V Dental Procedures for Patient Protection During amalgam Removal

V c) Amalgam Removal without Patient Protection

V d) Amalgam Removal with Patient Protection

V e) Pregnancy Precaution

V f) Patient Reports

VI) Dental Mercury A Source of Air and Water Pollution

VIa) Mercury in Dental Clinic Wastewater Discharge

VII) American Dental Association's (ADA) Position

VII a) Journal of the American Dental Association

VII Superior Court Demurrer

VII c) ADA Code of Ethics

VII d) ADA Internet Site

http://www.ada.org/public/faq/fillings.html#safe

Are dental amalgams safe?

Yes. Dental amalgam has been used in tooth restorations worldwide for more

than 100 years. Studies have failed to find any link between amalgam

restorations and any medical disorder. Amalgam continues to be a safe

restorative material for dental patients.

Woops. Do you see any mention of studies that proved them to be safe??

Studies in animals and human have been done and have shown problems, so this

line stating they have failed is NOT true, as well as the next line saying

they are still safe. Still? They haven't been proven to be safe at all let

alone *still*.

Studies have failed to show any link between amalgam restorations and medical

disorder. See below taken from http://www.amalgam.org

III a) Sheep Study

Vimy, M.J., Y. Takahashi, and F.L. Lorscheider " Maternal-fetal distribution

of mercury (203Hg) released from dental amalgam fillings. " Am. J. Physiol.

258 (Regulatory Integrative Comp. Physiol. 27): R939-R945 (1990).

ABSTRACT: In humans, the continuous release of Hg vapor from dental amalgam

tooth restorations is markedly increased for prolonged periods after chewing.

The present study establishes a time-course distribution for amalgam, Hg in

body tissues of adult and fetal sheep. Under general anesthesia, five

pregnant ewes had twelve occlusal amalgam fillings containing radioactive

203Hg placed in teeth at 112 days gestation. Blood, amniotic fluid, feces,

and urine specimens were collected at 1- to 3-day intervals for 16 days. From

days 16-140 after amalgam placement (16-41 days for fetal lambs), tissue

specimens were analyzed for radioactivity, and total Hg concentrations were

calculated. Results demonstrate that Hg from dental amalgam will appear in

maternal and fetal blood and amniotic fluid within 2 days after placement of

amalgam tooth restorations. Excretion of some of this Hg will also commence

within 2 days. All tissues examined displayed Hg accumulation. Highest

concentrations of Hg from amalgam in the adult occurred in kidney and liver,

whereas in the fetus the highest amalgam Hg concentrations appeared in the

liver and pituitary glands. The placenta progressively concentrated Hg as

gestation advanced to term, and milk concentration of amalgam Hg postpartum

provides a potential source of Hg exposure to the newborn. It is concluded

that accumulation of amalgam Hg progresses in maternal and fetal tissues to a

steady state with advancing gestation and is maintained.

III Rat Studies

Fredriksson, A., Dencker, L., Archer, T., sson, B.R. " Prenatal

Coexposure to Metallic Mercury Vapor and Methyl Mercury Produce Interactive

Behavioral Changes in Adult Rats. " Neurotoxicol Teratol., 18(2): 129-34,

(1996).

ABSTRACT: Pregnant rats were either 1) administered methyl mercury (MeHg) by

gavage, 2 mg/kg/day during days 6-9 of gestation, 2) exposed by inhalation to

metallic mercury (Hg) vapor (1.8 mg/m3 air for 1.5 hours per day) during

gestation days 14-19, 3) exposed to both MeHg by gavage and Hg vapor by

inhalation (MeHg + Hg), or 4) were given combined vehicle administration for

each of the two treatments (control). The inhalation regimen corresponded to

an approximate dose of 0.1 mg Hg/kg/day.

Clinical observations and developmental markers up to weaning showed no

differences between any of the groups. Testing of behavioral functions was

performed between 4 and 5 months of age and included spontaneous motor

activity, spatial learning in a circular bath, and instrumental maze learning

for food reward.

Offspring of dams exposed to hg vapor showed hyperactivity in the motor

activity test chambers over all three parameters: locomotion, rearing and

total activity; this effect was potentiated in the animals of the MeHg + Hg

group. In the swim maze test, the MeHg + Hg and Hg groups evidenced longer

latencies to reach a submerged platform, which they had learned to mount the

day before, compared to either the control or MeHg group. In the modified,

enclosed radial arm maze, both the MeHg + Hg and Hg groups showed more

ambulations and rearings in the activity test prior to the learning test.

During the learning trial, the same groups (i.e., MeHg + Hg and Hg) showed

longer latencies and made more errors in acquiring all eight pellets.

Generally, the results indicate that prenatal exposure to Hg causes

alterations to both spontaneous and learned behaviors, suggesting some

deficit in adaptive functions. Coexposure to MeHg, which by itself did not

alter their functions at the dose given in this study, served to

significantly aggravate the change.

S. Soderstrom, A Fredriksson, L. Dencker, T. Ebendal, " The effect of mercury

vapour on cholinergic neurons in the fetal brain: studies on the expression

of nerve growth factor and its low- and high-affinity receptors, "

Developmental Brain Research 85, 96-108 (1995)

ABSTRACT: The effects of mercury vapour on the production of nerve growth

factor during development have been examined. Pregnant rats were exposed to

two different concentrations of mercury vapour during either embryonic days

E6-E11 (early) or E13-E18 (late) in pregnancy, increasing the postnatal

concentration of mercury in the brain from 1 ng/g tissue to 4 ng/g tissue

(low-dose group) or 11 ng/g (high-dose group). The effect of this exposure in

offspring was determined by looking at the NGF concentration at postnatal

days 21 and 60 and comparing these levels to age-matched controls from

sham-treated mothers. Changes in the expression of mRNA encoding NGF, the

low- and high-affinity receptors for NGF (p75 and p140 trk. respectively) and

choline acetyltransferase (ChAT) were also determined. When rats were exposed

to high levels of mercury vapour during early embryonic development there was

a significant (62%) increase in hippocampal NGF levels at P21 accompanied by

a 50% decrease of NGF in the basal forebrain. The expression of NGF mRA was

found to be unaltered in the dentate gyrus. The expression of p75 mRNA was

significantly decreased to 39% of control levels in the diagonal band of

Broca (DB) and to approximately 50% in the medial septal nucleus (MS) whereas

no alterations in the level of trk mRNA expression were detectabe in the

basal forebrain. ChAT mRNA was slightly decreased in the DB and MS,

significantly in the striatum. These findings suggest that low levels of

prenatal mercury vapour exposure can alter the levels of the NGF and its

receptors, indicating neuronal damage and disturbed trophic regulations

during development.

Aschner M, Lorscheider FL, Cowan KS, Conklin DR, Vimy MJ, Lash LH

" Metallothionein induction in fetal rat brain and neonatal primary astrocyte

cultures by in utero exposure to elemental mercury vapor (Hg0). " Brain Res

1997 Dec 5;778(1):222-32

ABSTRACT: Brain metallothionein (MT) protein and mRNA levels were determined

in the fetal rat following in utero (gestational days 7-21) exposure to

elemental mercury vapor (Hg0; 300 microg Hg/m3; 4 h/day). Total RNA was

probed on Northern blots with [alpha-32P]dCTP-labeled synthetic cDNA probes

specific for rat MT isoform mRNAs. The probes for MT-I and MT-II mRNA

hybridized to a single band of approximately 550 and 450 nucleotides,

respectively. Expression of whole brain MT-I mRNA in full-term fetal rats

(day 21) was significantly increased (P < 0.03) by in utero exposure to Hg0

compared to nonexposed controls. This corresponded to a 14-fold increase (P <

0.001) in fetal brain Hg concentration after in utero Hg0 exposure. In

addition, astrocytes from both control and in utero Hg0-exposed fetuses were

isolated, and neonatal primary astrocyte cultures were established and

maintained in vitro for up to 3 weeks without additional experimental

intervention. Astrocyte monolayers derived from in utero Hg0-exposed fetuses

consistently expressed increased abundance of MT-I mRNA transcripts after 1,

2, and 3 weeks in culture (P < 0.03, P < 0.01, and P < 0.03, respectively)

compared with controls. The abundance of astrocyte MT-II mRNA was unchanged

at 1 and 2 weeks in culture, but was significantly increased at 3 weeks in

cultures derived from brains of Hg0-exposed fetuses (P < 0.04). Consistent

with the increase in MT mRNA, an increase in astrocytic levels of MT proteins

was noted by Western blot analysis and MT-immunoreactivity. These studies

suggest that in utero exposure to Hg0 induces brain MT gene expression, and

that MT mRNAs and their respective proteins are useful quantitative

biochemical markers of intrauterine exposure to Hg0, a potentially cytotoxic

challenge to astrocytes in the developing brain. It is concluded that

induction of MT by fetal/neonatal astrocytes represents an attempt by these

glial cells to protect against Hg cytotoxicity in maintaining cerebral

homeostasis.

III c) Human Study

Drasch et. al. " Mercury Burden of Human Fetal and Infant Tissues " European

Journal of Pediatrics (August 1994).

ABSTRACT: The total mercury concentrations in the liver (Hg-L), the kidney

cortex (Hg-K) and the cerebral cortex (Hg-C) of 108 children aged 1 day- 5

years, and the Hg-K and Hg-L of 46 fetuses were determined. As far as

possible, the mothers were interviewed and their dental status was recorded.

The results were compared to mercury concentrations in the tissues of adults

for the same geographical area. The Hg-K (n=38) and Hg-L (n=40) of fetuses

and Hg-K (n=35) and Hg-C (n=35) of older infants (11-50 weeks of life)

correlated significantly with the number of dental amalgam fillings of the

mother. The toxicological relevance of the unexpected high Hg-K of older

infants from mother with higher numbers of dental amalgam fillings is

discussed. Conclusion: Future discussion on the pros and cons of dental

amalgam should not be limited to adults or children with their own amalgam

fillings, but also include fetal exposure. The unrestricted application of

amalgam for dental restorations in women before and during the child-bearing

age should be reconsidered. Abbreviations: Hg-C total mercury concentration

in the cerebral cortex (ng/g wet weight). Hg-K total mercury concentration in

the renal cortex (ng/g wet weight). Hg-L total mercury concentration in the

liver (ng/g wet weight).

Kenny S. Crump, Tord Kjellstrom, Annette M. Shipp, Abraham Silvers, Alistair

" Influence of Prenatal Mercury Exposure Upon Scholastic and

Psycholgical Test Performance: Benchmeark Analysis of a New Zealand Cohort "

Risk Analysis, Vol.18, No. 6, 1998.

This paper presents benchmark (BMD) calculations and additional regression

analyses of data from a study in which scores from 26 scholastic and

psychological tests administered to 237 6- and 7- year old New Zealand

children were correlated with the mercury concentration in their mothers'

hair during pregnancy. The original analyses of five test scores found an

association between high prenatal mercury exposure and decreased test

performance, using category variables for mercury exposure. Our regression

analyses, which utilized the actural hair mercury level did not find

significant associations between mercury and children's test scores. However,

this finding was highly influenced by a single child whose mother's mercury

hair level (86 mg/kg) was more thatn four times that of any other mother.

When that child was ommited, results were more indicative of a mercury effect

and scores on six tests were significantly associated with the mothers' hair

mercury level. BMDs calculated from five ttests ranged from 32 to 73 mg/kg

hair mercury, and corresponding BMDs (95% lower limits on BMDs) ranged form

17 to 24 mg/kg. When the child with the highest mercury level was omitted,

BMDs ranged from 13 to 21 mg/kg, and corresponding BMDLs ranged from 7.4 to

10 mg/kg.

IV) Alzheimer's Disease Studies

Many on-going studies have linked many aspects of amalgam mercury to brain

tissue damage found in patients with Alzheimer's Disease. Abstracts from

these on-going studies are presented below.

IV a) Trace Elements in Alzheimer's Disease Brains

Wenstrup, D., Ehmann, W.D., and Markesbery W.R., " Trace Element Imbalances in

Isolated Subcellular Fractions of Alzheimer's Disease Brains " Brain Research,

533 125-131 Elsevier Science Publishers (1990).

ABSTRACT: Concentrations of 13 trace elements (Ag, Br, Co, Cr, Cs, Fe, Hg, K,

Na, Rb, Sc, Se, Zn) in isolated subcellular fractions (whole brain, nuclei,

mitochondria, microsomes) of temporal lobe from autopsied Alzheimer's disease

(AD) patients and normal controls were determined utilizing instrumental

neutron activation analysis. Comparison of AD and controls revealed elevated

Br (whole brain) and Hg (microsomes) and diminished Rb (whole brain, nuclear

and microsomes), Se (microsomes) and Zn (nuclear) in AD. The elevated Br and

Hg and diminished Rb are consistent with our previous studies in AD bulk

brain specimens. Comparison of element ratios revealed increased Hg/Se, Hg/Zn

and Zn/Se mass ratios in AD. Se and Zn play a protective role against Hg

toxicity and our data suggest that they are utilized to detoxify Hg in the AD

brain. Overall our studies suggest that Hg could be and important toxic

element in AD. Whether Hg deposition in AD is a primary or secondary event

remains to be determined.

Basun H, Forssell LG, Wetterberg L, Winblad B. " Metals and trace elements in

plasma and cerebrospinal fluid in normal aging and Alzheimer's disease. " J

Neural Transm Park Dis Dement Sect 1991;3(4):231-58

ABSTRACT: Cerebro-spinal fluid (CSF) and blood levels of aluminum, cadmium,

calcium, copper, lead, magnesium, and mercury were studied in 24 subjects

with dementia of the Alzheimer type (DAT) and in 28 healthy volunteers.

Furthermore, arsenic, bromine, chrome, iron, manganese, nickel, rubidium,

selenium, strontium, and zinc were measured only in blood. There were

significant changes in the DAT group when compared to the controls. The

plasma levels of aluminum, cadmium, mercury and selenium were increased and

the contents of iron and manganese were lower in the DAT group as compared to

control subjects. In CSF there were low levels of cadmium and calcium and

increased content of copper in DAT cases. Iron and zinc levels in blood and

calcium in both blood and CSF of DAT patients correlated with memory and

cognitive functions. Iron, manganese and strontium levels of DAT sufferers in

blood and aluminum in CSF were related with changes in behavior.

C.R. Cornett, W.R. Markesbery, and W.D. Ehmann, " Imbalances of Trace Elements

Related to Oxidative Damage in Alzheimer's Disease Brain " NeuroToxicology

19(3): 339-346 (1998).

ABSTRACT: Four elements that have been implicated in free radical induced

oxidative stress in Alzheimer's Disease (AD) were measured by instrumental

neutron activation analysis (INAA) in seven brain regions from 58 AD patients

and 21 control subjects. A statistically significant elevation of iron and

zinc was observed in multiple regions of AD brain, compared with controls.

Mercury was elevated in AD in most regions studied, but the high variability

of mercury levels in both AD and control subjects prevented the AD-control

difference from reaching significance. Selenium, a protective agent against

mercury toxicity, was significantly elevated only in AD amygdala. The

elevation of iron and zinc in AD brain has the potential of augmenting neuron

degeneration through free radical processes.

IV Mercury Vapor Inhalation Inhibits Tubulin in Rat Brain

C. Pendergrass, Boyd E. Haley, Murray J. Vimy, A. Winfield and

Fritz L. Lorscheider, " Mercury Vapor Inhalation Inhibits Binding of GTP to

Tubulin in Rat Brain: Similarity to a Molecular Lesion in Human Alzheimer

Brain. " NeuroToxicology 18(2): 315-324, 1997.

ABSTRACT: Mercury (Hg) interacts with brain tubulin and disassembles

microtubules that maintain neurite structure. Since it is well known that Hg

vapor is continuously released from " silver " amalgam tooth fillings and is

absorbed into brain, rats were exposed to Hg 4 hr/day for 0, 2, 7, 14, and 28

days at 250 or 300 mcg Hg/m3 air, concentrations present in mouth air of some

humans with many amalgam fillings. Average rat brain Hg concentrations

increased significantly (11-47 fold) with duration of Hg exposure. By 14 days

of Hg exposure, photoaffinity labeling of the B-subunit of the tubulin dimer

with (a32P)8N3GTP in brain hamogenates was decreased 41-74% , upon analysis

of SDS-PAGE autoradiograms. The identical neurochemical lesion of similar or

greater magnitude is evident in Alzheimer brain homogenates from

approximately 80% of patients, when compared to human age-matched controls.

Since the rate of tubulin polymerization is dependent upon binding of GTP to

tubulin dimers, we conclude that chronic inhalation of low-level Hg can

inhibit polymerization of tubulin essential for formation of microtubules.