ALZHEIMERS, AUTISM, AND MERCURY TOXICITY
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We also received a letter from a Florida M.D., Dr. David Minkoff, expressing "wariness" of the Alzheimers vaccine mentioned in our last issue. "All the data points to mercury as the key culprit in Alzheimers disease," reads the letter. "In the lab it causes amyloid plaques and tau protein. See http://www.altcorp.com on this... 'Alzheimers' is not a disease. It's a toxic condition. Vaccines don't cure toxic conditions but rather cause one to look elsewhere (in error) for the reason that will never be found."

The letter prompted further search into the question of mercury and other heavy metal toxicity. Ironically, certain vaccines appear to be part of the problem -- not directly, but through a mercury-containing preservative called thimerosal. Its usage is too recent to have a known impact on Alzheimers, but the link to autism is widely acknowledged. Other studies have established a connection between Alzheimers and the mercury contained in silver amalgam fillings.

A study was conducted in 1990 by three psychiatrists [Wenstrup et al, "Trace element imbalances in isolated subcellular fractions of Alzheimer's disease brains", Brain Research¸ Vol 553, p125-131, 1990] to look for trace element imbalances in the brains of Alzheimers patients. The brains from ten autopsied Alzheimers patients and 12 control patients of the same age were evaluated. The most significant imbalance of metals found in the Alzheimers patients was an elevated mercury level and an elevated level of bromine. Leading Edge Research tells us, "levels of mercury were especially significant in the cerebral cortex, especially in an area called the nucleus basalis of Meynert, a primary center of memory retention. Short term memory loss is initially the most common complaint. Researchers have also found significant levels of mercury in the hippocampus and amygdala, which are also structures that relate to memory."

In an article titled "Claims for Autism Caused By Childhood Vaccinations Containing Thimerosal or Mercury," the website of law firm Ashcraft & Gerel tells us:

"A full generation of children in America was exposed to dangerous doses of highly toxic ethyl mercury from 1990 through 2000. Children were injected with the toxic mercury that was a major ingredient in a chemical product called thimerosal, an additive and biological preservative packaged into multi-dose vials of many childhood vaccines. With each dose of vaccine that contained thimerosal, a child would also get an injection of toxic mercury. Each one of those mercury injections exposed the child to levels of toxic mercury in excess of the federal government's own safety guidelines.

"Mercury is widely known to cause neurological damage, often permanent. Current clinical and epidemiological research suggests that the mercury-laden thimerosal so widely given to children by the drug companies in the 1990's might cause a range of neurological and neurodevelopmental injuries, including autism. Compounding this public health disaster is that the toxic exposure was entirely avoidable. The thimerosal was added merely as product packaging for the multi-dose vials, and is not needed as a preservative when the vaccines are packaged in single-dose vials or single-use syringes."

Vaccine protocols in the U.S. in 1990 included 33 Doses of 10 Different Viral and Bacterial Vaccines by the Age of 5.

My Mom was recently diagnosed with Alzheimer's. She has had at least 12 flu shots the past years. Although I had read articles about the link between Flu shots and Alzheimer's I didn't know that it kills as well as neurologically impairs. The most surprising find though, is the similarities between autism behaviors and those of Alzheimer's patients. For those who have autistic children you should see this
yourself in the information below:

Moderate or Middle Stage AD

By this stage, Alzheimer's disease damage has spread further to the areas of the cerebral cortex that control language, reasoning, sensory processing, and conscious thought. Affected regions continue to atrophy and signs and symptoms of the disease become more pronounced  and widespread. Behavior problems, such as wandering and agitation, can occur. More intensive supervision and care become necessary, and this can be difficult for many spouses and families.

Behavior is the result of complex brain processes, all of which take place in a fraction of a second in the healthy brain. In AD, many of these processes are disturbed, and this is the basis for many distressing or inappropriate behaviors. For example, a person may angrily refuse to take a bath or get dressed because he does not understand what his caregiver has asked him to do.  If he does understand, he may not remember how to do it. The anger is a mask for his confusion and anxiety. Or, a person with AD may constantly follow her husband or caregiver and fret when the person is out of sight. To a person who cannot remember the past or anticipate the future, the world around her can be strange and frightening. Sticking close to a trusted and familiar caregiver may be the only thing that makes sense and provides security. Taking off clothes may seem reasonable to a person with AD who feels hot and doesn't understand or remember that undressing in public is not acceptable.


Symptoms: Increasing memory loss and confusion.
Shorter attention span.
Problems recognizing close friends and/or family.
Repetitive statements and/or movements.
Restless, especially in late afternoon and at night.
Occasional muscle twitches or jerking.
Perceptual motor problems.
Difficulty organizing thoughts, thinking logically.
Can't find right words -- makes up stories to fill in blanks.
Problems with reading, writing and numbers.
May be suspicious, irritable, fidgety, teary or silly.
Loss of impulse control -- sloppy -- won't bathe or afraid to bathe -- trouble dressing.
Gains and then loses weight.
May see or hear things that are not there.
Needs full-time supervision.

Examples:

Can't remember visits immediately after you leave. Repetitive movements or statements. Sleeps often, awakens frequently at night and may get up and wander. Perceptual motor problems -- difficulty getting into a chair, setting the table for a meal. Can't find the right words.  Problems with reading, numbers -- Can't follow written signs, write name, add or subtract. Suspicious -- May accuse spouse of hiding things, infidelity, may act childish. Loss of impulse control -- sloppier table manners; may undress at inappropriate times or in the wrong place. Huge appetite for junk food and other people's food; forgets when last meal was eaten, then gradually loses interest in food.

Severe Stage AD

In the last stage of AD, plaques and tangles are widespread throughout the brain, and areas of the brain have atrophied further. Patients cannot recognize family and loved ones or communicate in any way. They are completely dependent on others for care. All sense of self seems to vanish.

At the end, patients may be in bed much or all of the time. Most people with AD die from other illnesses, frequently aspiration pneumonia. This type of pneumonia happens when a person is not able to swallow properly and breathes food or liquids into the lungs.

Symptoms:

Can't recognize family or image of self in mirror. Loses weight even with good diet. Little capacity for self care. Can't communicate with words. May put everything in mouth or touch everything. Can't control bowels, bladder. May have seizures, experience difficulty with swallowing, skin infections.

Examples:

Looks in mirror and talks to own image. Needs help with bathing, dressing, eating and toileting. May groan, scream or make grunting sounds. Sleeps more.

Sources:

1. Care of Alzheimer's Patients: A Manual for Nursing Home Staff by Lisa P. Gwyther ACSW, Member, Committee on Patient and Family Services, Alzheimer's Association.

2. National Institute on Aging, National Institutes of Health, Alzheimer's Disease, Unraveling the Mystery. (Text and pictures.)

 

Is Hidden True Cause Of Alzheimer's Your Toothpaste?
From Paul Kuhlman
5-3-3

Hello Jeff...

I am a truck driver, and have hauled just about everything over the past 13 years. I read your site's article postulating that naturally occurring aluminum found in water might be the key to Alzheimer's disease. I'll go one better than that.

I once picked up a 44,000 pound load of aluminum dioxide powder in the aptly-named town of Bauxite, Arkansas. Noting that the destination for the load was not a processing plant or a mill,
I enquired as to why this load was destined for the Colgate-Palmolive Company. The shipping agent said that the quality of bauxite (Aluminum dioxide) found in Arkansas was too low grade for manufacturing purposes, but was fine for toothpaste.

"Toothpaste?" I enquired. He then went on to explain that common white toothpaste is made largely from Aluminum Dioxide, which is a mildly abrasive, brilliantly white powder. They'll simply add a sudsing agent to make the bubbles, a flavoring agent to make it palatable, perhaps a food coloring agent, some water, and presto - toothpaste.

Go read the ingredients on your tube of toothpaste. It'll list one or two 'active ingredients'...notice the combined total amounts of 'active ingredients' is usually less than 1%. What about the other
99%?

* Were you aware that every day of your life, you are filling your mouth with a gob of nearly pure aluminum dioxide?

* Can you imagine the possible health effects?

* Do you see how this is the number one entry point for aluminum to enter the body?

* Can you guess why the inactive ingredients aren't listed?

* Imagine the outcry from all the millions of health conscious Americans who suddenly discovered that they are being poisoned!

*Yes, that's why they aren't listed.

So, if you and your vast readership are concerned about getting too much aluminum in their diets, you can all relax about naturally occurring aluminum in the water, or cooking with pots and pans. These are trivial sources of aluminum compared with the several pounds of aluminum directly swallowed or absorbed through the tissues while brushing our teeth.

On the bright side, we can all still have a beautiful smile in our old age, if only we can remember how to smile.

From KT Feller
5-4-3
 

Hi all.
Just to let you know that Procydin (gape seed extract) is a very powerful antioxidant and I have noticed the improvement since using it for mercury poisoning. Used in conjunction with DMSA seems good.The ailments it is used for amongst the general public are all mercury toxicity symptoms. This leads me to think they have ,perhaps by mistake, found an excellent natural source of chelation for mercury. It seems very good at cleaning up free radicals from remote areas in the body.(Eg: athritis, high bood pressure, cholestrol) Recent studies by Dr Hal Huggins and his scientists, have found amalgam fitment increase/decrease blood pressure, increase cholestrol (drastically). When removed from these volunteers, their levels retuned to normal ! To protect the lining of the arteries from the corrosive effects of Hg in the blood, the body increases the amount of cholestrol (a soft buttery substance) to negate these effects. As we all know, heart disease starts when the lining of the arteries is damaged by free radicals like Hg, and this results in buildup of cholesterol and calcium on this "rough", damaged area, eventually blocking the arteries, resulting in the all too common heart attack.

According to some figures checked up on: About half Alzheimers patients have had their gallbladder removed. The liver chelates mercury from the body and puts it out in the bile. Bile is stored in the gallbladder until ejected onto the passing stools. As this Hg contaminated bile is held in the gallbladder it gradually damages it. Once the damaged gallbladder is removed surgically, the bile is pumped straight into the colon and mercury (which is originally from amalgams) is reabsorbed into the body through the colon wall ,as the body absorbs it the same way as fats. This causes more poisoning and contributes to worsened Hg poisoning/Alzheimers.
The highest level of Hg found in the brain of an Alzheimers patient (post mortem) was about 53 times the amount found in non-amalgam brains.
 

 
Alzheimer's surge predicted
An "epidemic of Alzheimer's" over the next few decades could be far worse than previously thought, experts suggest. The number of people with Alzheimer's could treble by 2050, say US researchers, as the population surges and existing patients live longer. In the UK, predictions from the Alzheimer's Society are for a 150% increase in prevalence over the next 50 years.

The US team, from Rush Institute on Healthy Aging, claimed that the huge rise could effectively bankrupt the country's medicare system, and called for more funding for research into treatments. Their study, based on US Census data, suggested that by the middle of the 21st century, up to 16 million Americans will have Alzheimer's.

We have learned more about the brain in the last fifty years than in the previous 5,000 Harry Caton, The Alzheimer's Society Previous estimates had placed the figure at up to 14.3 million. The primary cause of the rise is the fact that many more people are expected to live into their 80s and 90s in the future.

Beyond 80, as many as one in five people has some form of dementia.

Many require highly expensive health and social care, and it is possible that the disease will not greatly alter their lifespan. Sheldon Goldberg, president and CEO of the US Alzheimer's Association, said: "This study represents a significant step forward in confirming what we're up against. "If we don't find answers soon, it will be devastating on multiple fronts."

Research hope

However, a more upbeat message was delivered by the Alzheimer's Society, despite similar predictions of increasing numbers living with the disease. Its chief executive, Harry Caton, said: "In the UK we estimate about 150% increase by the year 2050. "But the important message is that in fifty years there will be huge advances in research. "We have learned more about the brain in the last fifty years than in the previous 5,000. "So the likelihood is there will be effective treatments, prevention or even a cure in fifty years' time."

However, he added: "But for this to happen we need a real increase in funding for research, which lags well behind other major health problems such as cancer and heart disease. The study was published in the journal Archives of Neurology.


Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/1/hi/health/3161523.stm

Published: 2003/08/19 04:27:10 GMT

© BBC MMIII

 

INTERNATIONAL IMMUNIZATION NEWS

"A Dose of Hope vs. Alzheimer's"
USA Today (www.usatoday.com) (07/28/03) P. 1D; Fackelmann, Kathleen

A 2002 study of Elan's experimental Alzheimer's disease vaccine AN-1792 was stopped early because the medicine caused brain swelling in some patients, but the treatment's benefit--of breaking up the amyloid plaques that are thought to be associated with Alzheimer's disease--suggests that a safe and effective vaccine against the disease may be closer than originally thought.  Researchers at Elan and other companies are trying to create a vaccine similar enough to AN-1792 that it provides the same plaque-busting powers but different enough that its side effects no longer include the life-threatening brain swelling, a development that could have a vaccine on the market within five years.  There is a question, however, that the plaques really are associated with the forgetfulness and personality changes associated with Alzheimer's disease or whether they are simply another sign of the illness; as such, a vaccine that breaks up the plaques may not change the other problem of memory loss.  Either way, early results from the suspended AN-1792 trial suggested that the vaccine could slow the disease's progression, and in some patients it appeared to actually reverse problems associated with Alzheimer's.
 

http://www.palmbeachpost.com/accent/content/auto/epaper/editions
/tuesday/accent_f31fa83285daa1340008.html

Removing brain metals may aid Alzheimer's

By Jane E. Allen, Los Angeles Times
Tuesday, December 30, 2003


Thinking and memory among Alzheimer's patients may decline more slowly if metals are removed from the toxic plaques that accumulate in their brains. For years, scientists have experimented with ways to inhibit the production and accumulation of the protein beta-amyloid in the plaques associated with Alzheimer's disease. Excessive amounts of copper and zinc have been observed in the plaques, so researchers from the University of Melbourne in Australia tried a novel approach called chelation therapy. (Unlike chelation therapy used to draw toxic metals, such as mercury, out of the blood, this type can penetrate into the brain.)

In a preliminary experiment, they gave patients the antibiotic clioquinol, which they hypothesized could remove zinc and copper from the beta-amyloid and help dissolve the protein. In a 36-week study of 36 patients with moderate to severe Alzheimer's, half received twice-daily doses of clioquinol and half received a placebo. All underwent periodic tests of thinking and memory, and blood measurements of beta-amyloid. Beta-amyloid levels dropped among those who got the drug, but increased among placebo recipients. The treated group scored higher on cognitive tests than the placebo group, but disease progression was slowed only in the most severely affected Alzheimer's patients.

The study appears in the December issue of the Archives of Neurology.

A U.S. trial is being planned, but researchers must prove they can protect patients from several nerve-damaging illnesses that led to the withdrawal of oral clioquinol from the U.S. market in the 1970s, when it was predominantly used for intestinal infections. It's still used topically.

 

Boyd Haley shared another citation wherein research showed the mercury is related to two markers of Alzheimers. Boyd wrote, "Oliveri et al. in the J. Neurochemistry v74, 231, 2000, showed that mercury at nanomolar levels doubled the production of beta-amyloid protein and increased the hyperphosphorylation of tau protein, both factors in AD brain.  However, all of the work on heavy metals and neurological diseases have, in my opinion, been trashed at NIH."  (See  WSJ article in cite 3).

To obtain a free pdf of cite 1, go to
http://www.blackwell-synergy.com/rd.asp?code=JNC&goto=journal Then enter 74 in volume field and 231 in page field.

The second cite describes an estrogen effect.

1: J Neurochem. 2000 Jan;74(1):231-6.
Mercury induces cell cytotoxicity and oxidative stress and increases beta-amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells.
Olivieri G, Brack C, Muller-Spahn F, Stahelin HB, Herrmann M, Renard P, Brockhaus M, Hock C.
Neurobiology Laboratory, Psychiatric University Hospital, Basel, Switzerland.
Olivieri@ubaclu.unibas.ch

Concentrations of heavy metals, including mercury, have been shown to be altered in the brain and body fluids of Alzheimer's disease (AD) patients. To explore potential pathophysiological mechanisms we used an in vitro model system (SHSY5Y neuroblastoma cells) and investigated the effects of inorganic mercury (HgCl2) on oxidative stress, cell cytotoxicity, beta-amyloid production, and tau phosphorylation. We demonstrated that exposure of cells to 50 microg/L  (180 nM) HgCl2 for 30 min induces a 30% reduction in cellular glutathione (GSH) levels (n = 13, p<0.001). Preincubation of cells for 30 min with 1 microM melatonin or premixing melatonin and HgCl2 appeared to protect cells from the mercury-induced GSH loss. Similarly, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) cytotoxicity assays revealed that 50 microg/L HgCl2 for 24 h
produced a 50% inhibition of MTT reduction (n = 9, p<0.001). Again, melatonin preincubation protected cells from the deleterious effects of mercury, resulting in MTT reduction equaling control levels. The release of beta-amyloid peptide (Abeta) 1-40 and 1-42 into cell culture supernatants after exposure to HgCl2 was shown to be different: Abeta 1-40 showed maximal (15.3 ng/ml) release after 4 h, whereas Abeta 1-42 showed maximal (9.3 ng/ml) release after 6 h of exposure to
mercury compared with untreated controls (n = 9, p<0.001). Preincubation of cells with melatonin resulted in an attenuation of Abeta 1-40 and Abeta 1-42 release. Tau phosphorylation was significantly increased in the presence of mercury (n = 9, p<0.001), whereas melatonin preincubation reduced the phosphorylation to control values. These results indicate that mercury  may play a role in pathophysiological mechanisms of AD.


2: Neuroscience. 2002;113(4):849-55.
The effects of beta-estradiol on SHSY5Y neuroblastoma cells during heavy metal induced oxidative stress, neurotoxicity and beta-amyloid secretion. Olivieri G, Novakovic M, Savaskan E, Meier F, Baysang G, Brockhaus M, Muller-Spahn F. Neurobiology Laboratory, Psychiatric University Hospital, CH-4025 Basel, Switzerland. gianfranco.olivieri@pharma.novartis.com

The role of estrogen as a neurotrophic/neuroprotective agent in neurodegenerative diseases such as Alzheimer's and Parkinson's diseases is increasingly being shown. In this study we examine the neuroprotective  effects of beta-estradiol on SHSY5Y neuroblastoma cells which have been exposed to the heavy metals cobalt and mercury. The results show that cobalt and mercury are able to induce oxidative stress and cell cytotoxicity and increase the secretion of beta-amyloid 1-40 and 1-42. These deleterious effects are reversed by the pretreatment of cells with beta-estradiol. It is further shown that beta-estradiol exerts its neuroprotective action through mechanisms which reduce oxidative stress and reduce beta-amyloid secretion. Pre-treatment of the  cells with alpha-estradiol did not alleviate the toxic effects of the heavy metals. Our results are significant as they contribute to a better understanding of the mode of action of estrogen with relevance to its use in the treatment of neurodegenerative disorders. Copyright 2002 IBRO PMID: 12182891

3. Is Alzheimer's field blocking R&D into other causes?
By SHARON BEGLEY
The Associated Press - 4/9/04 9:42 AM
<http://www.mlive.com/newsflash/business/index.ssf?/newsflash/get_story.ssf?
/>http://www.mlive.com/newsflash/business/index.ssf?/newsflash/get_story.ssf
?/ cgi-free/getstory_ssf.cgi?f0029_BC_WSJ--ScienceJournal&&news&newsflash-finan
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4:  Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer diseased brain. Neurotoxicology. 1997;18(2):315-24.
Pendergrass JC, Haley BE, Vimy MJ, Winfield SA, Lorscheider FL.
College of Pharmacy, University of Kentucky, Lexington 40536, USA.

Hg2+ interacts with brain tubulin and disassembles microtubules that maintain neurite structure. Since it is well known that Hg vapor (Hg0) is continuously released from "silver" amalgam tooth fillings and is absorbed into brain, rats were exposed to Hg0 4h/day for 0, 2, 7, 14 and 28 d at 250 or 300 micrograms 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 Hg0 exposure. By 14 d Hg0 exposure, photoaffinity labelling on the beta-subunit of the tubulin dimer with [alpha 32P] 8N3 GTP in brain homogenates 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 neurological controls. Total tubulin protein levels remained relatively unchanged  between Hg0 exposed rat brains and controls, and between Alzheimer brains and controls. Since the rate of tubulin polymerization is dependent upon binding of GTP to tubulin dimers, we conclude that  chronic inhalation of low-level Hg0 can inhibit polymerization of brain tubulin essential for formation of microtubules. PMID: 9291481 [PubMed - indexed for MEDLINE]
 

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

PRESENTATION CONTENTS OF BOYD E. HALEY, PROFESSOR AND CHAIR, DEPARTMENT OF
CHEMISTRY, UNIVERSITY OF KENTUCKY

In Vitro studies of pure thimerosal and vaccines with and without thimerosal added as a preservative: Comparison to Hg(II) toxicity.

SUMMARY: Data will be presented comparing Hg2+ and thimerosal toxicity as well as that of vaccines with and without thimerosal added. Aspects of the biochemical mechanisms of these toxicants will be addressed. An extensive evaluation of the potential in vitro toxicity of thimerosal and vaccines containing thimerosal as a "preservative" versus those vaccines not containing thimerosal has been the objective of recent research done in my laboratory. In these preliminary studies pure thimerosal has been shown to be more toxic to enzymes of the central nervous system than Hg2+. Further, vaccines with thimerosal added as a preservative consistently demonstrated in vitro enzyme toxicity that was markedly greater than the non-thimerosal or low thimerosal containing vaccines. We also compared the toxicity of thimerosal to solutions of mercury chloride. The data indicate that thimerosal is usually a more potent toxicant to mammalian enzymes and brain tubulin polymerization than is Hg2+. Additionally, the toxicity of thimerosal to pure enzymes is rapid and does not require break down of the released ethylmercury into Hg2+. Also, the inhibitory profile of thimerosal with enzymes of human brain homogenates is very different from the inhibitory profile of Hg2+. This is further proof that the ethylmercury released from thimerosal has its own inhibitory properties independent of any further break down to Hg2+. It seems chemically sensible that ethylmercury ( CH3CH2-Hg+) could exert its toxic effects by disrupting the internal, hydrophobic located, dithiol linkages (-S-S-) of cystine that are necessary for normal enzyme structural conformations as well as binding to the reduced thiol groups of cysteines (-SH). Such data indicate that Hg2+ and ethylmercury could act synergistically to enhance toxicity.

Additional studies on the killing of human neurons in culture show that thimerosal displays toxicities in the nanomolar range. This supports our enzyme/tubulin observations. Also, recent studies on neurons in culture have demonstrated that only Hg2+ at 10-7 to 10-10 molar concentration, of several heavy metals tested, was capable of disrupting neurite structures by causing the abnormal polymerization of tubulin baring the neurofibrils and leaving a body similar to neurofibillary tangles, a diagnostic hallmark of Alzheimer’s disease. This is also in agreement with previous research from our laboratory demonstrating that Hg2+, and only Hg2+, under chelation conditions found in brain tissue could cause the abnormal tubulin behavior observed in Alzheimer’s disease. The growth of neurite processes is well known to require the presence of two structural proteins, tubulin and actin. Hg2+ appears to be much more toxic to tubulin biochemical properties than to actin. Thimerosal, in contrast, appears to be about equally toxic to both tubulin and actin. This biochemical difference, along with partitioning vectors, may help explain the toxicity differences observed between Hg2+ versus organic mercuricals such as methyl and ethylmercury. Using vaccines with and without thimerosal added to determine their toxicity to human neurons in culture also follows the biochemical
observations. Vaccines with out added thimerosal are much less toxic than vaccines containing thimerosal.

With all toxicants one has to consider synergistic toxicities. In the case of thimerosal there was a reported sensitization to this mercurical by the presence of an antibiotic, tetracycline. We have done preliminary studies with tetracycline and ampicillin one the neuron killing capability of thimerosal. Both antibiotics appeared to enhance the toxicity of thimerosal. This may be due to the interactions of these antibiotics with the heavy metal portion of ethylmercury that may enhance delivery of the toxicant to specific sites in the neurons. This area should be of concern as many infants are placed on antibiotics. It would be important to evaluate this aspect of thimerosal toxicity with additional research.

INTRODUCTION: 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 but was less toxic to actin. Both tubulin and actin are polymerizing proteins that are actively involved in neurite growth cone activity. In contrast, vaccines containing thimerosal inhibited both tubulin and actin viability. This would indicate that thimerosal has the potential to be much more damaging to neurite development than equivalent levels of mercuric ion. It is therefore my hypothesis that thimerosal rapidly releases ethyl-mercury which most certainly could interfere directly with neurite growth and neuronal development in infants through inhibition of several dithiol and thiol-sensitive enzymes/proteins. Below I will present my interpretation of this research and that from other laboratories that focus on the potential toxicity of injected thimerosal in the vaccine mixture.

PRESENTATION CONTENTS: Thimerosal, and other compounds containing a similar thiol-organic mercury group, are widely known to be especially potent neurotoxic agents. The toxicity results we obtained were not at all unexpected since our results are very consistent with the previously reported toxicity of thimerosal containing vaccines versus non-thimerosal containing vaccines as observed in cell culture studies reported in 1986. The chemical rationale for the neurotoxicity of thimerosal is that this compound would release ethylmercury as one of its breakdown products. Ethylmercury 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 in the presence of other heavy metalS (Pb, Cd, Zn) is well established in the literature (see below).

Exposing infants who are ill and do not have fully developed bilary (liver) and renal (kidney) systems to a vaccine mixture could greatly increase the toxic effects compared to that observed in healthy adults. The toxic effects of exposure to thimerosal in infants cannot be reasonably compared to those observed in adults made toxic by exposure to similar ethylmercury or methylmercury containing compounds. Mercury is primarily removed through the bilary system and aluminum is removed by the renal system. Inability of the infant to rid the body of these toxicants would greatly increase  the damage they are capable of doing.

The necessity of using an anti-microbial "preservative" in vaccines to prevent contamination is obvious and acceptable. However, using a "preservative" that breaks down into a well-known neurotoxin does not appear well thought out. Especially when infants are given multiple thimerosal containing vaccinations during one office visit. Toxicity is determined by units of toxicant per unit body weight. So, if a 10 pound baby was given 4 vaccinations this would result in the equivalent of a 150 pound adult receiving 60 vaccinations in one day. This appears to happen with a great deal of regularity in practice and steps should be taken to recommend against this procedure.

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. First, ethylmercury has its own toxic properties and does not have to break down to Hg2+ to be toxic. Therefore, to evaluate the toxicity of thimerosal delivered mercury levels by comparison to the toxicity levels of elemental mercury is scientifically invalid. Further, each human would likely have a level of toxicity from other mercury and non-mercury containing sources. These environmental toxicants could work synergistically with ethylmercury rendering the ethylmercury 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. Our laboratory has tested the toxicity in vitro of the combination of elemental mercury with some of the other toxicants. The data, not unexpectedly, shows a great increase in toxicity of equally added amounts of mercury. Our results are supported by prior research that demonstrated that a mixture of mercury and lead at LD-1 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&endash;A Rapid Systematic Testing Procedure: Cadmium, Mercury and Lead. J. of Toxicology and Environmental Health, 4:763-776, 1978). Therefore, it is impossible to state the toxic effect of an injection of thimerosal unless one knows the toxic exposure of the individual to other heavy metals or other environmental toxicants, or
perhaps the properties of the antibiotic given simultaneously.

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 bio-compounds" (e.g., glutathione, APO-E, 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 and melatonin levels compared to middle aged and young adults. The aged are also more susceptible to oxidative toxicants such as mercury. The elderly also have weakened immune systems and are more susceptible to infections that are known to lower the chemical energy levels needed to remove toxicants. This also reduces 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 unable 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 as effectively as adults. Therefore, the age factor must always be considered for response to heavy metal exposure as well as spurious microbial infections.

Genetic 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 ethylmercury by binding these toxicants in the cerebrospinal fluid and keeping them from entering the brain. There are physicians looking at APO-E proteins as a risk factor for autism and early reports indicate that a relationship may exist.

One argument I have heard against thimerosal causing autism is the low number of children getting the disease versus the number receiving vaccinations. I think the same argument could have been made regarding acrodynia (Pinks Disease) being caused by teething powder. 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.

In my opinion, it is the inability to see the effects of chronic, low level toxicities on human health that is most likely 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, and only mercury, can induce the formation of the two major pathological diagnostic hallmarks of Alzheimer’s disease. Mercury does this at nanomolar concentrations. This near or below the levels of mercury found in most reports where human brains have been tested for mercury levels. First, mercury at 10-9M levels has been shown to induce an increase in amyloid protein secretion (the component of amyloid or senile 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 {Leong 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. Ashley 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 mercury and silver, are the components of dental amalgams. Most of 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, Cahpter 16, Mercury and Its Effects on Environment and Biology, Siegel and Sigel EDS., Marcel Dekker, Inc. 1996}. This data basically demonstrated that addition of very low amounts of mercury to normal human brain homogenates inhibited critical enzymes (creatine kinase, glutamine synthetase and tubulin) that were also dramatically inhibited in Alzheimer’s diseased brain. The straight-forward conclusion is that any exposure to mercury or mercury containing compounds would exacerbate the medical condition classified as Alzheimer’s disease and one would even have to consider low level chronic exposure to mercury as a possible etiology for this disease.

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 mostly 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.

Academic medicine has searched long and hard without success to identify vectors that cause many of the neurological diseases such as AD, ALS, MS, Parkinson’s, etc. The NIH has spent huge amounts of funds on the study of amyloid protein, tau protein and neuro-fibillary tangles in the search for the cause of AD---now it has been demonstrated that mercury at low concentrations can cause neurons in culture to form these protein abnormalities. Exposure of brain tissue to mercury also specifically inhibits other enzymes/proteins known to be inhibited in AD brain. Yet, there has been a paucity of NIH funds spent to study the potential neuro-toxicity of mercury routinely placed in human contact by medicine and dentistry. Further, our regulatory agencies, such as the FDA, routinely dismiss basic research showing the unique toxicity of mercury at very low concentrations and continue to allow the use of this material without testing. Certain organizations routinely use toxic mercury containing materials without experimental proof of their safety. They then argue that damage by mercury has not been "validly" proven as their defense and the FDA buys into this. Common sense implies that safety should be proven before use of toxicants in medicine and dentistry, not after. Common sense implies that the mere presence of mercury demonstrates toxicity at some level. Nowhere was this lack of common sense more evident than in the exposure of infants to thimerosal without prior testing in the recent past vaccine program.

Boyd E. Haley, Ph.D.

Boyd E. Haley is Professor and Chair at Department of Chemistry, University of Kentuccky, KY. He graduated from Franklin College in 1963 with a BA in Chemistry-Phyrsics, completed an MS in Organic Chemistry at the University of Idaho, and his Ph.D. in Chemistry-Biochemistry at Yale University Medical Center in 1971. In 1985, he was appointed a permanent member of the National Institutes of Health Biomedical Sciences Section. Dr. Haley is the author of over 114 investigational papers. Since 1997, he is Chairman and full Professor in the Department of Chemistry at the University of Kentucky.

 

Atlanta Emergency Milk Recall

From the Associated Press 10/25/05 (9:15 AM)

"Flagship Atlanta Dairy has issued a voluntary produce recall of whole milk.

...a limited amount of whole milk was formulated on October 22nd with excess Vitamin D and does NOT meet the dairy's product specifications." The product recall affects whole milk in the following brands: Parmalat, Farm Fresh, Wayfield, Piggly Wiggly,  Kirkland and Kinnett."

The milk was distributed to consumers on October 22nd. Milk purchasers have had four days to drink this tainted product. Could excess Vitamin D be dangerous to their health? Consider that Vitamin D is a steroid hormone when reading the following:

"Vitamin D increases aluminum absorption, and high aluminum levels in the body may cause an Alzheimer's- like disease."

Canadian Medical Association Journal,m1992 147(9)

"Consuming as little as 45 micrograms of Vitamin D-3 in young children has resulted in signs of overdose." (one quart of milk should contain 10 micrograms)."

Pediatrics, 1963; 31

"Testing of 42 milk samples found only 12% within the expected range of Vitamin D content...Vitamin D is toxic in overdose."

New England Journal of Medicine, 1992, 326

If you've been exposed to Flagship Atlanta Dairy's toxic milk, you can reach the general manager, Ted Young, at: 404-688-2671 x-421. Should you call, ask for the number of his attorney and insurance company. Thousands of people may have been affected. This
might be cause for an enormous lack of class-action lawsuit.