Thimerosal Containing Vaccines and Neurodevelopment Outcomes - Boyd Haley

[Guest guest]

" The synergistic effects of different compounds with thimerosal are not all

known but some do exist. For example, the commonly used antibiotic,

tetracycline, is known to enhance thimerosal toxicity. " [what is the

synergeistic effect of other antibiotics - we don't know as no one has

looked.........Sheri]

" One fact that has become extremely obvious to me during this past 11 years

is that it is impossible to determine the exact toxic level of mercury or

mercury containing compounds that is safe for all humans. There are several

reasons why mercury should not be considered safe for humans at the

measurable levels currently reported as ' safe " by current government

monitoring agencies. One of these is the obvious effects of other metals on

increasing the toxicity of identical levels of mercury. An example is that

of zinc ion, an essential metal for normal cell function. Yet, in the

presence of mercuric ion, the addition of zinc enhances the toxicity level

significantly (see Figure 4). Cadmium and lead are even more potent at

enhancing the toxicity of mercuric ion. This concept of synergistic

toxicity of mercury with other metals is supported by prior research that

demonstrated that a mixture of mercury and lead at LD I levels of each

metal produced a mixture with an LD 100 effect, at least 50 times the

additive effect minimally expected (Schubert, J., Riley, E.J. and Tyler,

S.A., Combined Effects in Toxicology-A Rapid Systematic Testing Procedure:

Cadmium, Mercury and Lead. J. of Toxicology and Environmental Health, 4:

763 776, 19 8). "

http://www.vran.org/vaccines/mercury/mer-haley.htm

GENERAL VACCINE ISSUES:

MERCURY - THIMERSOL & NEURODEVELOPMENT OUTCOMES

Affidavit Of Boyd E. Haley. Professor And Chair. Department Of Chemistry.

University Of Kentucky

Thimerosal Containing Vaccines and Neurodevelopment Outcomes

FORWARD:

Thimerosal or merthiolate is a derivative of thiolsalicylate where ethyl

mercury is attached though the sulfur. It is defined as a preservative or

anti microbial in medical use. This anti microbial action is dependent on

thimerosal breaking down releasing ethyl mercury that can penetrate cell

membranes and bind to intracellular enzymes, inhibiting them, and causing

cell death. Further, in certain biological environments the ethyl mercury

can further break down releasing mercury cation (Hg2+). Hg2+ is also very

reactive with enzymes and proteins inhibiting their biological functions

and causing cell injury or death. Both ethyl mercury and Hg2+ are very

neuro toxic compounds. However, ethyl mercury is more rapidly partitioned

into the hydrophobic (fatty) tissues of the central nervous system and is a

more potent neuro toxin than Hg2+ based on this " partitioning factor " . It

is this partitioning factor that makes organic mercurials such as dimethyl

mercury so neuro toxically lethal (this is the compound that caused the

death of a Dartmouth University chemistry professor after she was exposed

to a drop or two on her gloved hand). The concern with organic mercurials,

such as thimerosal, is that such compounds can be perceived as " pro

toxicants " just as certain pharmaceuticals can be classified as " pro

drugs " . This means that the original compound, e.g. thimerosal, is less

reactive giving the compound time to partition into certain areas of the

body before it breaks down releasing the ethyl mercury and then further

releasing Hg2+. However, while attaching ethyl mercury to thiolsalicylate

makes the ethyl mercury less reactive it most likely allows increased

partitioning into the central nervous system before the ethyl mercury is

released and thereby, increases the neuro toxicity per unit ethyl mercury

involved. Considerable caution must be taken when stating what is the

" toxic level " of mercury and any mercury containing compound. Humans are

not rats in a pristine cage where their environment can be controlled to

ensure that other toxicities and infections are not occurring. The level of

mercury that would cause toxicity in a healthy individual is much higher

than what would be needed to cause a toxic effect in an individual that is

ill or under oxidative stress. This is because additional stresses lower

the amount of protective compounds that bind mercury and render it less

harmful. If an individual is low on these protective compounds, then less

mercury or thimerosal would be needed to cause a clinical effect. Below I

will present my interpretation of our research and that from other

laboratories that focus on the potential toxicity of injected thimerosal in

the vaccine mixture.

BIOCHEMICAL TOXICITY STUDIES:

In my laboratory we have recently done an evaluation of the potential in

vitro toxicity of vaccines containing thimerosal as a " preservative " versus

those vaccines not containing thimerosal. In these preliminary studies,

vaccines with thimerosal added consistently demonstrated in vitro toxicity

that was markedly greater than the non thimerosal or low thimerosal

containing vaccines. We also compared the toxicity of the vaccine solutions

with solutions of pure thimerosal and with solutions of mercury chloride.

Mercury is a known neurotoxin and its mechanism of neurotoxicity has been

studied in our laboratory for the past 10 years. To determine the relative

toxicity we used two different biological testing systems: (i) brain

homogenates and (ii) a mixture of four purified mammalian enzymes. In human

brain homogenates we had earlier observed that mercuric ion rapidly

inhibited tubulin viability at low micromolar levels. mimicking the

situation in Alzheimer's diseased brain, but was less toxic to actin (see

Figures 1 & 2). Both tubulin and actin are polymerizing proteins that are

actively involved in neurite growth cone activity. In contrast to mercuric

ion, vaccines containing thimerosal inhibited both tubulin and actin

viability (see Figure 3). This would indicate that thimerosal has the

potential to be much more damaging to neurite development than equivalent

levels of mercuric ion. It is my hypothesis that thimerosal releases ethyl

mercury which most certainly interferes with neurite growth and neuronal

development in infants through rapid inhibition of several thiol sensitive

enzymes/proteins including actin, tubulin and creatine kinase. This

supports the concept that thimerosal in biological solutions injected into

the human body could cause a number of systemic problems identified as

disease states.

CELL CULTURE WORK ON THIMEROSAL

The toxicity results obtained in our biochemical toxicity studies were not

at all unexpected since thimerosal and other compounds containing a similar

thiol organic mercury group are widely known to be especially potent

neurotoxic agents. Our biochemical toxicity results are very consistent

with the reported toxicity of thimerosal containing vaccines versus

nonthimerosal containing vaccines as observed in cell culture studies

(Kravchenko et al., Evaluation of the Toxic Action of Prophylatic and

Therapeutic Preparations on Cell (cultures 111. The Detection of Toxic

Properties in Medical Biological Preparations by the [Degree of Cell Damage

in the L132 Continuous Cell Line. Zh. Microbiological Epidemiol.

Immunobiol. (3):87 92, 1983). The results of this research demonstrated the

toxicity of thimerosal (merthiolate) by showing cell damage of the 1

:10,000 concentration found in vaccines after dilution of this mixture to I

part per 128. The conclusion was that thimerosal use for medical and

biological preparation (i.e. vaccines) manufacturing is inadmissible,

especially in pediatrics. Other studies on cytotoxicity of thimerosal

compared it to another mercury containing preservative (phenylmercuric

acetate) and thimerosal was 5 times more toxic with only a two minute

exposure to the cells. The LD50 for thimerosal was 2.2 micrograms/ml for a

24 hour exposure to human conjunctival cells and the comment was made that

" the longer the contact time of these preservatives, the severer the damage

to the ocular tissue " .

In collaboration with another professor in our department we have now

included toxicity studies using human brain neurons in culture. Our initial

studies have shown that thimerosal is quite toxic to these neurons in

culture. Further, studies using vaccines with and without thimerosal

present demonstrated that the presence of thimerosal greatly enhanced the

toxicity. The neuron toxicity studies mirror the results we observed in the

enzyme toxicity studies mentioned above with the thimerosal being more

toxic than inorganic mercury. Further studies are underway at the present

time.

(top)

CASE HISTORIES ON THE TOXICITY OF THIMEROSAL AND OTHER ETHYL MERCURY

RELEASING COMPOUNDS:

A recent review covers much of the case history literature on the little

that is known about ethyl mercury toxicity (L. Magos Review on the Toxicity

of Ethyl mercury Including it.s Presence as a Preservative in Biological

and Pharmaceutical Products, J. Applied Toxicology 21. 1 5, 2001). The

conclusions reached by the author of this review is that " ethyl mercury may

present a risk when blood mercury concentrations approaches or exceeds 1.0

microgram per ml and severe intoxication occurs when blood mercury

concentration approaches or exceeds 2 micrograms per ml. " In the context of

the literature reviewed the conclusions by Dr. Magos seems reasonable.

However, this conclusion was based primarily on ethyl mercury and

methylmercury exposures from occupational exposures, dietary intake,

externally applied tinctures along with vaccination data on adults. It

should be noted that in considering deceased patients the one infant had a

blood mercury (from an externally applied tincture) that was measured at

1.34 micrograms per ml, a young boy had a blood mercury of 5 micrograms per

ml (from eating pork from a pig feed ethyl mercury) and adults had 15

micrograms per ml (from eating bread made with seed treated with a compound

that generated ethyl mercury). Without the needed extensive data to make a

conclusion, it appears as if the younger the patient the more deadly or

toxic the ethyl mercury is at a lower concentration. This is further

supported by the other (Kostial, K., et al. Influence of Age on Metal

Metabolism and Toxicity, Environmental Health Perspectives, v25, 81 86,

1978) who state " results obtained in sucklings show a very high intestinal

absorption of all metals which is partly attributed to milk diet; a higher

whole body retention, higher blood levels and a much higher accumulation in

the brain " . Certainly, no conclusion of sate levels of exposure to ethyl

mercury on infants could be made from the data reviewed by Dr. Magos.

The exposures reviewed were from different delivery modalities and there is

a considerable difference in the toxicity of many materials when oral

intake is compared to injections via the vaccine route. Total mercury in

the blood stream does not distinguish between bound mercury (e.g. that

coupled with glutathione and being removed from the body) and unreacted

mercury (that available to cause further damage). Ratios of bound and free

ethyl mercury are likely to be different if ethyl mercury is eaten or

inhaled versus injected, bypassing the protective systems available in the

intestines. It was also pointed out in the review that the blood/urine

ratios varied from 3.4 to 18 indicating that urine mercury levels are

inferior for monitoring ethyl mercury exposures. However, since ethyl

mercury should partition between blood and urine at a consistent ratio this

data could also be interpreted to indicate that the mercury in some of

these patients is coming from more than just ethyl mercury (e.g. dental

amalgams that are the major source of human mercury body burden). In a

report on mercury levels in squirrel monkeys treated intranasally with

thimerosal (Blair, A., , B., e, A and Wood, P., Tissue

Concentrations of f Mercury After Chronic Dosing of Squirrel Monkeys with

Thimerosal Toxicology, v3, 171176, 1975) it was shown that exposure to

0.002% thimerosal daily for 6 months, with a total of 2,280 ,ug given, lead

to a 174/29 or about 6.0 ratio of mercury in the brain/blood ratio

indicating that thimerosal leads to a more rapid build up of brain versus

blood mercury. However, it was pointed out that the highest brain total

(250ng/g) was still below the 3 9 ug/g where neurological symptoms appear,

but this later value would depend on the oxidative stress of the patient

and could be much lower.

The review states that " ethyl mercury in medicinal preparations declines

with time " and gave examples of 38%, 64% and 85% decreases in ethyl mercury

in plasma and immunoglobin G samples. This mercury did not disappear and

the loss of ethyl mercury has to be due to ethyl mercury reacting

covalently with the protein thiols in the medicinal preparations. In aged

medicinal preparations, increased ethyl mercury reaction with protein

thiols in the preparations would likely change the neurotoxity effects of

the resulting mercury complexes compared to pure ethyl mercury How this pre

reacted ethyl mercury would contribute to blood levels of mercury appears

unknown, but it is likely to be quite different from pure ethyl mercury

However, what is known is that ethyl mercury retains its severe toxicity

after prolonged exposure in living animals. This is supported by a case

mentioned in the Magos review where ethyl mercury obtained by " consumption

of meat from a pig fed with ethyl mercury " caused severe damage to adults

and killed two young boys. It seems as if ethyl mercury can retain its

severe toxicity after a period of incubation time in a living pig,

butchering and storage of meat, followed by cooking. Then the concept that

the faster decomposition of ethyl mercury, relative to methylmercury,

decreases its toxicity compared to methylmercury seems to be such a small

difference as to be insignificant. What is solidly observed is that ethyl

mercury (and other organic mercurials) can withstand considerable exposure

to a living system, storage in a biological environment, exposure to high

heat in the presence of muscle tissue, and still produce a lethal toxicity

when taken orally.

In a 1972 a (National Geographic Quicksilver and Slow Death, vl 42, #4,

507527, 1972) a similar report was presented where the pig was fed seed

coated with Panogen, a methylmercury pesticide. The family ate the pig as

above and the four children suffered severe neurological damage. But, in

contrast to the ethyl mercury poisoning above, they all lived. One of the

children was in utero during the consumption of the pork, suffered the most

and was born blind and mentally retarded. Again, this supports the concept

that the younger the human the more detrimental the toxic effect the

organic mercury compounds will have.

It appears certain that much of the blood level mercury in these patients

presented in the Magos review could be from sources other than pure ethyl

mercury In my opinion, I do not believe that a safe level of ethyl mercury

can be arrived at by only comparing blood levels of mercury if we do not

know the chemical nature of all of the contributing mercury sources, the

initial source of the mercury or if the presence of other compounds were

involved (e.g. antibiotics that bind heavy metals such as tetracycline and

enhance thimerosal toxicity:see below in Synergistic Toxicity).

It is of major concern that ethyl mercury from thimerosal in vaccines is a

special situation. It is injected with millimolar levels of aluminum and it

is probable that thimerosal, a negatively charged molecule, has formed a

salt compound with the positively charged aluminum cation that would change

its partitioning, breakdown rate, and may have a synergistic effect on the

toxicity of any mercuric ion produced from the ethyl mercury Aluminum is a

known neurotoxin and to be causally involved in macrophagic myofasciitis.

The enhanced toxicity of ethyl mercury in the presence of other toxic

agents is to be expected. Few of the clinical cases included in the Magos

review were from vaccine but the one that was discussed problems which

occurred in a 44 year old adult with a blood mercury of 0.104 ,ug per ml,

so low that Dr. Magos called the diagnosis " unconvincing " . Perhaps co

administration of thimerosal with aluminum in the Hepatitis B vaccine

represents the " other aetiological factors than ethyl mercury " that might

have been responsible for his mercury like induced symptoms at such low

concentrations. The authors of the report on this patient state " this

patient had evidence of previous environmental exposure to mercury " and

this data can imply that thimerosal is more toxic in patients previously

exposed to materials that sensitize them.

(Top)

DR. MAGOS REPORT TO THE IOM, SUMMER 2001:

Dr. Magos makes several statements that reasonable individuals with

scientific experience could disagree about. First, " The consequence of

faster decomposition is that, compared with methylmercury. The neurotoxic

potential of ethyl mercury declines faster.?' This requires the assumption

that ethyl mercury breaks down to Hg2+ as a toxic factor. What if the

breakdown product was a conjugate of cysteine known to enhance the toxicity

of mercuric ion? What if the breakdown was caused by reactive oxygen

species generated in response to an infection? It is known that ethyl

mercury breaks down 10 times faster in the presence of reactive oxygen

species (Suda, 1, and Takahashi, [l., Degradation of methyl and ethyl

mercury into inorganic mercury by other reactive oxygen species besides

hydroxyl radical. Arch. Toxicol. 66, 34 39, 1992) making the production of

toxic Hg2+ occur more rapidly at sites of high level of reactive oxygen,

and in the body this would be at sites of infection or inflammation or

within mitochondria, the important energy producing organelle. In my

opinion, the enhanced chemical ability to breakdown ethyl mercury versus

methyl mercury at sites of reactive oxygen production (usually sites of

oxidative stress) makes ethyl mercury a much more dangerous compound than

methylmercury as it attacks chemically at a site of infectious damage.

In section 2.b.a Dr. Magos quotes his research as showing that

methylmercury treated rats had 1.55 (males) and 2.4 (females) the mercury

in their brains as did ethyl mercury treated rats. In addition, the ethyl

mercury treated rats had 3.4 fold more inorganic mercury in their brains.

He states that this " excludes the possibility that the cleavage itself or

the formed inorganic mercury is responsible for the brain damage. If this

were the case, the brain ethyl mercury treated rats would be more affected

than the brain of methylmercury treated rats (which didn't occur by his

analysis). " The problem with this conclusion is that Dr. Magos expects the

damage caused by methylmercury to be the same as that caused by a

combination of ethyl mercury and 3.4 fold extra Hg2+. This is not likely as

methyl and ethyl mercury would partition into the hydrophobic areas of the

brain whereas Hg2+ would most likely react in the hydrophilic aspect of the

brain. The inhibition of specific brain enzymes by thimerosal (ethyl

mercury) compared to Hg2+ are markedly different.

SYNERGISTIC TOXICITY WITH THIMEROSAL:

Since about 1989 my laboratory has been actively involved in research

regarding the toxic effects of elemental mercury and the relationship of

this toxicity to neurological diseases, primarily Alzheimer's disease. One

fact that has become extremely obvious to me during this past 11 years is

that it is impossible to determine the exact toxic level of mercury or

mercury containing compounds that is safe for all humans. There are several

reasons why mercury should not be considered safe for humans at the

measurable levels currently reported as ' safe " by current government

monitoring agencies. One of these is the obvious effects of other metals on

increasing the toxicity of identical levels of mercury. An example is that

of zinc ion, an essential metal for normal cell function. Yet, in the

presence of mercuric ion, the addition of zinc enhances the toxicity level

significantly (see Figure 4). Cadmium and lead are even more potent at

enhancing the toxicity of mercuric ion. This concept of synergistic

toxicity of mercury with other metals is supported by prior research that

demonstrated that a mixture of mercury and lead at LD I levels of each

metal produced a mixture with an LD 100 effect, at least 50 times the

additive effect minimally expected (Schubert, J., Riley, E.J. and Tyler,

S.A., Combined Effects in Toxicology-A Rapid Systematic Testing Procedure:

Cadmium, Mercury and Lead. J. of Toxicology and Environmental Health, 4:

763 776, 19 8).

The synergistic effects of different compounds with thimerosal are not all

known but some do exist. For example, the commonly used antibiotic,

tetracycline, is known to enhance thimerosal toxicity. Crook and Freeman,

Reactions Ind'~ced by the Concurrent Use of Thimerosal and Tetracycline,

American J. of Optometry & Physiological Optics v60,#9, pp759761 1983,

reported that the use of tetracycline in humans induced and increased the

irritation and inflammation of the ocular tissues caused by thimerosal.

These results were confirmed in studies using rabbits. Therefore, it is

obvious that concurrent treatment of infants with other drugs and/or

antibiotics has the possibility to enhance the toxic effects of thimerosal

exposures. Further, it was postulated that the synergistic effects of

tetracycline was due to the metal binding properties of this antibiotic

that may have delivered the toxic metal more effectively to the site(s)

inducing enhanced toxicity. This data clearly demonstrates that there is no

know level of safety for the use of thimerosal, especially in infants being

treated with other medicinals that would enhance the toxicity of the ethyl

mercury released such as occurred with tetracycline (a commonly used

antibiotic).

Since each human would likely have a level of toxicity from other mercury

and non mercury containing sources it would be impossible to determine the

exact level of mercury that would induce observable toxicity in each human.

Many environmental toxicants could work synergistically with ethyl mercury

rendering the ethyl mercury much more toxic than it would be in the absence

of these other toxicants (e.g., elemental mercury from dental amalgams,

cadmium from smoking, lead from paint and drinking water, aluminum, etc.).

Humans are not rats in a pristine cage, eating rat chow carefully prepared

to eliminate any toxicants. Humans smoke, drink alcohol, have numerous

mercury emitting amalgam fillings, eat questionable food, and drink water

known to contain other toxicants. Finally, it is impossible to state the

toxic effect of any injection of thimerosal unless one knows the toxic

exposure of the individual to other heavy metals or other environmental

toxicants.

(Top)

THE EFFECTS OF AGE AND HEALTH ON THIMEROSAL TOXICITY:

The detrimental effect of any specific level of mercury or mercury

containing compound would have on any one individual's metabolic system

would be directly proportional to both the level of' protective big

compounds " (e.g., glutathione, metallothioine) that exist within that

person on the time of exposure and, the ability to physiologically clear

such toxicants from the body. The level of the protective compounds would

certainly be directly dependent on two factors, age and health. Infants,

with their immature physiology and metabolism would not be expected to

handle mercury as efficiently as mature adults. The elderly have been shown

to have decreased " protective " glutathione levels compared to middle aged

and young adults. Melatonin, a hormone, is known to be decreased in the

aged and melatonin is known to increase the neuron and cellular

concentration of glutathione. Glutathione is the natural compound that

binds mercuric ion and aids in its removal from the body. This explains

partly why the aged are also more susceptible to oxidative toxicants such

as mercury.

The elderly also have weakened immune systems and are more susceptible to

microbial infections are known to lower their chemical energy levels and,

further, to reduce their ability to synthesize the proteins that protect

them from heavy metals. Infants have their own weaknesses regarding toxic

exposures. Infants do not make much bile in their early months of life and

are less able to remove mercury through bilary transport the major route

for mercury removal. They also do not have a fully developed renal system

that would remove other heavy metals (e.g. aluminum! as effectively as

adults. The age factor must always be considered for response to heavy

metal exposure as well as spurious microbial infections.

THE EFFECTS OF GENETIC SUSCEPTIBILITY ON MERCURY TOXICITY:

Genetically susceptibility is of critical importance. For example, other

researchers have shown that genetic carriers of the brain protein APO E2

are protected against Alzheimer's disease (AD) whereas genetic carriers of

the APO E4 genotype are at enhanced risk factor for developing AD. APO E

proteins are synthesized in the brain with the assigned physiological task

of carrying waste material from the brain to the cerebrospinal fluid,

across the blood brain barrier into the plasma where the material is

cleared by the liver. The biochemical difference between APO E2 and APO E4

is that APO E2 has two additional thiol groups, capable of binding and

removing mercury (and ethyl mercury) that APO E4 does not have. The second

highest concentration of APO E proteins is in the cerebrospinal fluid.

Therefore, it is my opinion that the protective effects of APO E2 is due to

its ability to protect the brain from exposure to oxidants like mercury and

ethyl mercury by binding these toxicants in the cerebrospinal fluid and

keeping them from entering the brain. I strongly object to labeling those

" genetically susceptible " as " having a genetic disease " because they are

the first injured on exposure to modern toxicants. Humans did not evolve

breathing mercury vapor or having organic mercury compounds injected in

them as infants.

SIMILARITY TO ACRODYNIA:

The argument that the thimerosal containing vaccines could not deliver the

amount of mercury to cause a systemic illness is somewhat refuted by the

history of the disease classified as acrodynia. Perhaps autism will end up

like acrodynia, where the removal of the causative material (i.e. the

mercury containing teething powders) lead to cessation of the disease and

the identification of the cause. Due to the perceived low levels of mercury

in the teething powders and the wide spread use of mercury in medicine at

that time it was 10 years after the removal of the mercury containing

teething powders before medicine acknowledged that mercury exposure was the

causal factor. It is significant to notice that many of the symptoms of

acrodynia are similar to the clinical symptoms of children identified today

as autistic, with attention deficit disorder, etc. that have no family

history of such diseases or illness classifications.

SUMMARY:

It is the inability to see the effects of chronic, low level toxicities on

human health that has been, and remains, our greatest failing as

intelligent beings. For example, within the past year two publications in

refereed scientific journals have emerged from major foreign research

universities demonstrating that mercury can induce the formation of three

major pathological diagnostic hallmarks of Alzheimer's disease. The

production of these diagnostic hallmarks occurred at non lethal

concentrations near or below the levels of mercury reportedly found in most

human brains. First, mercury has been shown to induce an increase in

amyloid protein secretion (the component of amyloid plaques) and to

increase the phosphorylation of a protein called Tau {see Oliveri et al.,

J. of Neurochemistry, V 74, p231, 2000}, and to produce neurofibillary

tangles {Leon " et al., NeuroReports V12(4), 733, 2001 }. All of this was

done with neurons in culture and represent observations found and

considered diagnostic of Alzheimer's disease. Further, in a very recent

article by Dr. Bush in the journal Neuron it is implied that

Alzheimer's disease may be caused by heavy metal buildup. This article

focused on removal of zinc and copper by chelation decreasing amyloid

plaque formation in rats mercury was not studied. However, these metals,

along with silver, are the components of dental amalgams. This work is in

agreement with data published earlier from my laboratory in refereed

articles and summarized in one single article {Pendergrass and Haley, Metal

Ions in Biological Systems V34, Chspter 16, Mercury and Its Effects on

Environment and Biology, Siegel and Sigel EDS., Marcel Dekker, Inc. I 996}.

This data basically demonstrated that addition of very low amounts of

mercury to normal human brain homogenates inhibited critical thiol

sensitive enzymes (creatine kinase, glutamine synthetase and tubulin) that

are also dramatically inhibited in Alzheimer's diseased brain. Research in

our laboratory clearly demonstrates that thimerosal rapidly inhibits these

enzymes as well as several other metabolically important enzymes.

Further, data presented in Aschner et al. in Methylmercury Alters Glutamate

Transport in Astrocvtes Neurochemistry International, v37, #2 3, pp 199

206, 2000 indicate that organic mercury compounds dysregulate excitatory

amino acid homeostasis and may cause glutamate mediated excitotoxic

mechanisms to be involved on exposures that cause neuron death or injury.

Glutamate toxicity is one hypothesis proposed to explain the slow

deterioration of AD as it was reported that the enzyme, glutamine

synthetase, that removes toxic glutamate was elevated in AD cerebral spinal

fluid (D. Gunnersen and B. Haley, PNAS, USA, v89, 11949, 1992) and

inhibited in AD brain (Butterfield et al., J. Neurochemistry, v68, 2451,

1997). Glutamine synthetase is rapidly inhibited by the divalent mercuric

ion as it has two divalent metal ion (manganese) binding sites required for

activity. It is obvious that ethyl mercury from thimerosal would have the

same effect on glutamine synthetase as mercury and methyl mercury and

impair nervous system glutamate metabolism. Consistent with this concept is

the reported ability of astrocytes (the brain cells that contain glutamine

synthetase that converts toxic glutamate to non toxic glutamine) to

preferentially concentrate brain organic mercury (Ashner, Astrocytes as

Modulators of Mercury lnduced Neurotoxicity Neurotoxicology vl 7, #3 4,

pp663 669 1996). The straight forward conclusion is that any exposure to

mercury or mercury containing compounds (e.g. thimerosal) would exacerbate

any medical condition affected by the inability to metabolize glutamate.

The chemical rationale for the neurotoxicity of thimerosal is that this

compound would release ethyl mercury as one of its breakdown products.

Ethyl mercury is a well known neurotoxin. Further, combining thimerosal

with the millimolar levels of aluminum cation plus significant levels of

formaldehyde, also found in these vaccines, would make the vaccine mixture

of even greater risk as a neurotoxic solution. The synergistic effects of

mercury toxicity with other heavy metal toxicities (Pb, Cd, Zn) has been

established in the literature for many years. Further, using this vaccine

mixture on infants who are ill and do not have fully developed bilary

(liver) and renal (kidney) systems could greatly increase the toxic effects

compared to that observed in healthy adults.

The toxic effects of exposure to thimerosal to adults and infants and

always been reported to have dire consequences, including death. Similar

exposures, even at lower level, in infants should have more severe

consequences compared to those observed in adults made toxic by exposure to

similar ethyl mercury containing compounds. Mercury is primarily removed

through the bilary system and aluminum is removed by the renal system.

Inability to rid the body of these toxicants would greatly increase the

damage they are capable of doing.

While one can understand the necessity of using an anti microbial

" preservative " in vaccines to prevent contamination it represents poor

judgment to use a " preservative " that breaks down into a well known

neurotoxin when safer " preservatives " were available. Further, it has come

to my attention through several parents that a significant number of

physicians encourage mothers to have their infants receive multiple

vaccinations during one visit. In one report a 13 pound baby was given 4

vaccinations. This would result in the equivalent of a 130 pound adult

receiving 40 vaccinations in one day. This is quite unreasonable in my

opinion, but appears to happen with a great deal of regularity in practice.

Physicians do this as they are not warned of the possible consequences and

are regularly informed by vaccine providers that the vaccines are totally

safe. No steps were taken to recommend against this procedure.

It is very difficult to prove that mercury or organic mercury compounds

cause any specific disease that is identified by its related symptoms. This

is due to the fact that mercury toxicity from various types of mercury

containing materials may be considerably different and the genetic

susceptibility and age of the victim would alter the response. This

difficulty is further compounded due to the high numbers of confounding

factors presented in the current human environment. However, since infants

get autism and related disorders, and many of our aged are afflicted with

AD, we know that they have crossed the thin red line into the

neurologically diseased state. There can be no doubt that the purposeful

use of mercury in medicine and dentistry, especially if it was prolonged

and excessive, would significantly contribute to the onset of their

disease. In my opinion, this is especially true in the case of the

injection of thimerosal via vaccines in day old infants and toddlers.

FIGURE 1: COMPARISON OF THE VIABILITY OF BRAIN TUBULIN IN CONTROL (NON

DEMENTED) VERSUS AI ZI IEIMER'S DISEASED BRAIN.

FIGURE 2: A COMPARISON OF THE EFFECTS OF MERCURIC ION ADDITION ON CONTROL

(NON DEMENTED) AND ALZHEIMER'S DISEASED BRAIN.

FIGURE 3: A COMPARISON OF THE EFFECTS OF THIMEROSAL ADDITION ON CONTROL

(NON DEMENTED) AND Al ZHEIMER'S DISEASED BRAIN.

Please refer to Dr. Haley's website for more mercury/thimerosal/vaccine

information http://www.altcorp.com/DentalInformation/thimerosal.htm

http://iquebec.ifrance.com/autismemtl/2002/program_en.html

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Sheri Nakken, former R.N., MA, Hahnemannian Homeopath

Vaccination Information & Choice Network, Nevada City CA & Wales UK

Vaccines - http://www.wellwithin1.com/vaccine.htm Email classes start in

January