Amalgam Perpetuates Social Injustice

While middle class consumers opt for mercury-free filling materials, people in developing nations, low-income families, minorities, military personnel, prisoners, and people with disabilities are still subjected to amalgam. Racial minorities are more likely to receive amalgam; for example, dentists place almost 25% more mercury fillings in American Indian patients than in white patients. In his testimony before Congress, former Virginia state NAACP president Emmitt Carlton described this injustice as "choice for the rich, mercury for the poor."

Excerpt of http://www.toxicteeth.org/

Nick Cannon Mercury Poisoned!

@NickCannon has lupus, and Lupus is Mercury Poisoning of the Kidneys.  Heavy Metal Chelation will make Nick healthy. 

http://www.livingnetwork.co.za/chelationnetwork/chelation-the-andy-cutler-protocol/
 

Mercury Poisoning From Interior Latex Paint

Editorial Note: Phenylmercuric acetate is routinely added by some paint manufacturers to interior latex (water-based) paint as a fungicide and bactericide to prolong the paint's shelf-life. EPA permits interior latex paint to contain less than or equal to 300 ppm elemental mercury and exterior latex paint to contain less than or equal to 2000 ppm. However, neither the presence nor the concentration of mercury in the paint is required to be labeled on the paint can. Mercury may not lawfully be used in oil-based paint (1,2). 

Cut and pasted from the below article.

http://www.cdc.gov/mmwr/preview/mmwrhtml/00001566.htm?mobile=nocontent

Lisa Marie Presley Mercury Poisoned

Excerpt from her Rolling Stone interview.

"My body started to deteriorate. I started to have panic attacks. I went through two years of baffling every doctor from East to West Coast. One week it was asthma . . . hypoglycemia . . . candida . . . reflux . . . I had everything. My gall bladder just. . . stopped working, and I had to get it taken out. This was when the tabloids said I tried to kill myself or something like that. We settled out of court. But anyway, I wound up in the hospital. I had everything happening; my body completely fell apart. And nobody knew what the hell was wrong with me." She was allergic to everything. "I had to eat chicken and broccoli for a year," she remembers. "I was absolutely falling apart, physically and emotionally, for a two-year period." At times she thought of death. "It was the constant physical breakdowns that were going on that I didn't understand."

"I really thought it. It was just non-stop. "Then she went to a homeopathic doctor, told him all her symptoms, and he asked her to open her mouth. He told her to get her fillings removed. "But once I started to get it out, it all stopped." (She now thinks her problems were caused by a mixture of mercury fillings and extreme stress.) "Mercury can make you go...crazy. That term 'mad as a hatter' comes from mercury: people working in felt factories and going crazy. They try to say mercury is safe, but it's the second-deadliest poison known to man, underneath plutonium, and it's in people's...teeth."

Mercury Poisoning and Endometriosis

Amalgam fillings, nickel and gold crowns are major factors in reducing pituitary function. Replacement of metals in the mouth can normalize pituitary function and stabilize menstrual cycle problems, endometriosis, and increase fertility.

http://www.evolvedental.com.au/amalgam-fillings-and-mercury

Incredible Research of ALS vs Mercury Poisoning

Here is an excerpt from the research paper.

Due to the high daily mercury exposure and excretion into home and business sewers of those with amalgam, dental amalgam is also the largest source of the high levels of mercury found in all sewers and sewer sludge, and thus according to government studies a significant source of mercury in rivers, lakes, bays, fish, and crops(603). People also get significant exposure from vaccinations, fish, and dental office vapor(600).

The full paper may be read here:
http://www.flcv.com/als.html

FDA Approves Fake Silver Dental Amalgams with 50% Mercury

Ask yourself this question, does the FDA state what level of Mercury Poisoning is safe in this article?

Here is a quote from their introduction.

FDA Issues Final Regulation on Dental Amalgam

The U.S. Food and Drug Administration today issued a final regulation classifying dental amalgam and its component parts – elemental mercury and a powder alloy—used in dental fillings. While elemental mercury has been associated with adverse health effects at high exposures, the levels released by dental amalgam fillings are not high enough to cause harm in patients.


http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm173992.htm

Julia Roberts Mercury Poisoned

Her current symptoms sound like Mercury Poisoning 

'My GP hasn't confirmed it's post-polio syndrome yet, but I think I'm heading that way,' says Julia. 'I'm much more tired than I used to be and my left leg is thinner. If it gets any worse, I'll seek professional advice.'


http://www.dailymail.co.uk/health/article-2358540/Julia-thought-shed-beaten-polio-50-years-ago-Now-returned-haunt--timebomb-affect-thousands-more.html

Mercury poisoning from amalgam fillings causes acne, dermatitis, psoriasis, and rosacea.

Any swelling or infection of the face may be caused by toxic mercury from leaking dental fillings.  Silver amalgam fillings contain 50% toxic mercury.  Treatment for the condition without removing the underlying cause will only be treating the symptom.

 Acne rosacea is a common disorder affecting facial skin. Its most persistent feature is a bright red flush. People affected are usually in the 35-50 range of age, most are females, but severity is generally greater in males. Fair skinned people are more often affected.

Recurrent flushing and blushing is present and late in the disease the nose may be enlarged with thick red skin, a condition known as "rhinophyma." Enlargement of the nose is more common in males. Also, along with thicker skin, the oil glands of the face enlarge and are more active giving an oily appearance. Swelling of the face may be present along with stinging of the cheeks, forehead and ears.

A likely cause of acne rosacea, acne vulgaris, sebhorrheic dermatitis, perioral dermatitis is an overload of mercury, usually from dental amalgams, and Thimerasol in vaccines and/or cosmetics.
Unless the cause is identified and treated, this tends to be a chronic progressive disease which comes and goes and generally slowly increases.

For perioral dermatitis a course of doxycycline and topical erythromycin may help.

To chelate the underlying cause, the heavy-metal-bioaccumulative mercury out of our bodies, use the Andy Cutler protocol.
http://mercuryconspiracy.blogspot.com/p/chelation-andy-cutler-protocol-oral.html

Kate Winslet Mercury Poisoned

Mercury poisoning may be the root cause of Kate Winslet's adult acne.

http://mercuryconspiracy.blogspot.com/2015/04/mercury-poisoning-from-amalgam-fillings.html

http://www.femalefirst.co.uk/lifestyle-fashion/stylenews/kate-winslet-adult-acne-543147.html

Jameela Jamil - Mercury Poisoned!

The UK Daily Mail won't directly admit that Jameela Jamil was poisoned by MERCURY, they instead run the headline:

Can mercury fillings really poison you or is it just a scare story? Jameela Jamil is convinced they triggered her health issues

A quote from the article:
" ... a review by the EU Commission's Scientific Committee in 2008 concluded there was no risk from amalgam, says Professor Damien Walmsley, the British Dental Association's scientific adviser."

So they are implying mercury in people's mouths is inert.  That's a pretty broad statement.  What if the mercury amalgam comes loose, what then?  What if they eat really acidic foods, or constantly drink hot beverages that heats the mercury creating mercury vapors.  Why don't they just chew on aluminum foil with mercury amalgam in their mouths if there is "no risk". 

Watch the mercury eat away this aluminum I-beam.
 

The original article is here:

http://www.dailymail.co.uk/health/article-3047765/Can-mercury-fillings-really-poison-just-scare-story.html

Tinnitus and Mercury Poisoning

I had tinnitus my entire life.  I believe I was mercury poisoned prenatally.  Not until I chelated for mercury did the tinnitus go away!

http://mercuryconspiracy.blogspot.com/p/chelation-andy-cutler-protocol-oral.html



Excerpt from a great article by Barry Keate

Hearing Loss and Tinnitus
Of particular interest to people with hearing loss and tinnitus, researchers have linked mercury to hearing loss and multiple sclerosis. We know that hearing loss has a direct impact on tinnitus. This study involved seven women who had been diagnosed with MS. They underwent a standard hearing test then all their amalgam fillings were removed. Six to eight months later they retook the hearing test. Six of the seven had significant hearing improvement in the right ear and five of the seven had improvement in the left ear. Hearing improved an average of 8 dB. The researchers concluded that amalgam fillings may be a significant factor in hearing loss experienced by MS patients and could be a factor in hearing loss for others as well.


Here are excerpts from other blogs and comments.

I can confirm from personal experience that heavy metal poisioning can create the conditions necessary for some to contract Tinnitus.
I have medical and Dental records that confirm the day I got my first Mercury fillings as a teenager was the day I got my Tinnitus. Teenagers seem to be much more sensitive to Mercury then adults it seems.

Who is Eli Lilly?

From the early 1900’s through the 1950’s,

Eli Lilly marketed baby teething powders with Calomel.

However, many of these infants suffered horribly.  Doctors named the condition Acrodynia, or Pink Disease because it turns the hands and feet pink.

Many infants died from Pink Disease, and many were left with lifelong debilitating conditions.

In fact, so many children died that the American and British governments had to pass laws outlawing Calomel.

The chief ingredient in Calomel is mercuric chloride.

Eli Lilly has made Thimerosal since 1927.  Thimerosal is used in vaccines and antiseptic ointments, creams, jellies, sprays, nasal sprays, eye drops, and contact lens solutions.

Thimerosal contains mercury.  Mercury rarely remains un-bonded to other elements, readily bonding with sulfur in the human body.  Mercury is an extremely dangerous neurotoxin in any form.  Some of the major symptoms of mercury poisoning are anxiety and depression.  For anxiety and depression, doctors often prescribe antidepressants like Prozac.  Who do you think invented Prozac?  Eli Lilly?  YES! 

What is the 2nd most profitable classification of drugs for Eli Lilly?
Diabetes drugs of course.

Links Between Root Canals and Other Diseases

The Links between Root Canals and Other Diseases

One of the most common questions we get is “why don’t you believe in root canals?” For years we have talked about the links between root canals and all kinds of systemic health problems (including certain cancers). To drive the point home further, we have developed the following list of some of the most common bacteria found in root canals and the links between that bacteria and other diseases.
Up to 400 percent more bacteria are found in the surrounding tissues of the root canal tooth than in the tooth itself, indicating that the dead tooth works as an incubator for bacteria that feed on the periodontal ligament where they mutate, grow in number and eventually invade the bone surrounding the root canal.This is just a PARTIAL list and by no means is meant to be considered all-inclusive.

Growing Evidence of Bacteria Commonly Found in Root Canal Cavitations

Bacteria can be identified using DNA analysis, whether they’re dead or alive, by looking at their DNA signatures. The Toxic Element Research Foundation (TERF) used DNA analysis to examine root canal teeth, and they found bacterial contamination in 100% of the samples tested. They were able to identify more than 40 different species of anaerobic bacteria in each sample. In cavitations, 67 different bacteria were identified among the 85 samples tested, with 19 to 53 types of bacteria each individual sample.
Examples of the many diseases that have been associated with the bacterium discovered hidden within dental procedures are MS, ALS, AD, leukemia and diabetes. With proper dental treatment and recognition of these sources of toxins and their eradication, many patients can be improved, and clearly most could have been avoided entirely.
The bacteria found by clinical tests conducted by both TERF and independent laboratories reveal the following most types present in root canals and cavitations:

• Acinetobacter baumanii – linked to Pneumonia and Periodontal disease
• Gemella morbillorum – linked to invasive endocarditis, Meningitis & Arthritis
• Klebsiella – linked to pneumonia Lung infections, infections of the Urinary Tract, biliary tract & Osteomyelitis & Meningitis
• Porphyromonas gingivalis – Protein metabolism, Biofilms, leads to Bone destruction and Premature labor
• Pseudomonas aeruginosa – linked to Central Nervous System disorders, Endocarditis, Brain abscesses & increase in liver enzymes, Prosthetic heart valve invasion
• Streptococcus mitis – found in Strep Throat, Scarlet fever and linked to heart failure –
• Rhpumatir fpvpr– known to affect the heart, nerves, kidneys, brain, and sinus cavities.
• Capnocytophagaochraceavi – known to affect the heart, nerves, kidneys, brain, and sinus cavities.
• Fusobacteriumnucleatumvii – known to affect the heart, nerves, kidneys, brain, and sinus cavities.
• Leptotrichiabuccalis – known to affect the heart, nerves, kidneys, brain, and sinus cavities.
• Porphyromonas gingivalis ix – known to affect the heart, nerves, kidneys, brain, and sinus cavities.
• Veillonella parvula – pathology associated with heart disease and destruction of the Central Nervous System.
• Candida albicans – as it changes from yeast to the fungal state, it becomes invasive, causing small holes to occur in the intestinal tract resulting in „leaky gut syndrome?.  Also increases porphyrin excretion in urine leading to reduced ATP and heme formation, thus reducing overall energy to cells of the nervous system.
• Capnocytophaga ochracea – can cause frontal lobe brain abscesses – associated with dental infections and diseases of the Central Nervous System
• Porphyromas gingivalis – alters the integrity of endothelium of blood vessels.  Enhances atherosclerosis.
• Actinomyces naeslundii –associated with draining sinuses (generally clear up within a week of root canals and cavitation treatment)
• Candida albicans –associated with ALS
• Capnocytophaga ochracea –frontal lobe brain abscesses of dental origin – microbe thought to originate in dental decay.
• Gemella morbillorum –associated with meningitis.
• Neisseria meningitides –associated with seizures.
• Escherichia coli –and Staph aureus –are both capable of increasing porphyrins, which will cause less ATP to be available to neural tissues.
• Streptococcus intermedius –Cervical spinal cord abscesses –associated with high mortality and neurologic morbidity.

http://naturaldentistry.us/3047/the-links-between-root-canals-and-other-diseases/

Hair Analysis

New York State has made it illegal to do a hair test analysis.  Even doctors can not order the test.  Why would this be?

Here is their reasoning:

seeks to ensure the accuracy and reliability of results of laboratory tests on specimens obtained within the state through on-site inspections, proficiency testing and evaluation of the qualifications of personnel of state permit-holding clinical laboratories and blood banks. The proper performance of diagnostic laboratory tests is a matter of vital concern, affecting the public health, safety and welfare of all NYS residents. Clinical laboratories and blood banks provide essential public health services in aiding the medical practitioner by furnishing information invaluable in the diagnosis and treatment of disease. Substandard performance of such tests may and has contributed to erroneous diagnoses and/or the selection of inappropriate treatment protocols.²

This is excerpted from this article:
http://legalgenealogist.com/blog/2012/12/23/ny-and-md-limits-on-23andme/


We understand that Complete Nutrition and Wellness in NJ can order the test.  Here is their web site.

http://www.completenutritionandwellness.com/testing-services/hair-analysis/

Eric's Journal of Mercury Chelation

For those of us who have chelated without keeping a great journal, Eric's notes of his experiences are encouraging.  My experiences chelating are almost identical.

Eric's timeline of chelation:
http://howirecovered.com/my-dose-timeline/

Lessons learned:
http://howirecovered.com/lessons-learned/


http://howirecovered.com/my-story/

Celiac Disease and Amalgam Fillings

An Italian research team has found a strong correlation between Celiac Disease and mercury poisoning!

Thank goodness for independent research!

http://www.hindawi.com/journals/grp/2015/953042/

Center for the Prevention and Diagnosis of Celiac Disease, Gastroenterology and Endoscopy Unit, Fondazione

Dan Burton Speech to Congress

Congressman Burton's Statement- Congressional Hearings on Mercury Updated January 31, 2009 On May 8, 2003 I attended the hearings in Washington D.C. conducted by Congressman Dan Burton R-Indiana) and Congresswoman Diane Watson (D-California). These hearings were part of the Committee on Government Reform, Subcommittee on Human Rights and Wellness, a Subcommittee Hearing entitled "Consumer Choice and Implementing Full disclosure in Dentistry." This was the second hearing on dental mercury. The first hearing of the Government Reform Committee, "Mercury in Dental amalgams: An Examination of the Science" was held November 14, 2002. You can access transcripts of the 2002 hearings at the Government Printing office website. The link to http://www.gpo.gov/fdsys/pkg/CHRG-107hhrg10784699/pdf/CHRG-107hhrg10784699.pdf is below. Mercury in Dental Amalgams: An Examination of the Science Burton said his commitee started doing this investigation into mercury in 1999 when he started examining the use of mercury [thimerosal] in baby vaccines. He said this was a "no win situation for the child and family," because the state mandates shots for the child before going to school. Burton said his grandson Christian became profoundly autistic overnight. He developed autism at the age of 18 months after taking the MMR vaccine and other shots. (The MMR does not contain mercury.) Burton said that his grandson received nine vaccines that day and six of them contained mercury. (In a former SafeMinds.org article, his granddaughter Burton said, also had a close encounter with death due to the Hepatitis B vaccine.) Burton said the incidence of autism used to be 1 in 10,000 twenty years ago, but now was 1 in 250. Congressman Burton vowed, "We are not going away. We are going to keep on collecting evidence and holding hearings. Then we are going to publish the evidence. What I want to know is why can't the the NIH and the ADA find a connection between mercury and health effects? Sweden found 700 credible papers about the harmful effects of mercury, but the NIH and the ADA can't find one." This following is the statement released by Congressman Burton previous to the hearings. He read from this statement on May 8th. ONE HUNDRED EIGHTH CONGRESS Congress of the United States House of Representatives Committee on Government Reform 2157 Rayburn House Office Building Washington, DC 20515-6143 TOM DAVIS, VIRGINIA (CHAIRMAN) HENRY A. WAXMAN, CALIFORNIA (RANKING MINORITY MEMBER) Majority (202)225-5074 Minority (202) 225-5051 To: Members, Subcommittee on Human Rights and Wellness From: Dan Burton, Chairman Date: May 5, 2003 Subject: Subcommittee Hearing entitled, "Consumer Choice and Implementing Full Disclosure in Dentistry." Thursday, May 8, 2003, 2 PM 2154 Rayburn House Office Building The Subcommittee on Human Rights and Wellness will hold an oversight hearing on Thursday, May 8, 2003 in 2154 Rayburn House Office Building at 2 PM, entitled, "Consumer Choice and Implementing Full Disclosure in Dentistry." BACKGROUND The Subcommittee is continuing an investigation into medical and dental exposures to mercury that was initiated by the full Government Reform committee during the 107th congress. Previously, the Committee reviewed concerns about thimerosal in vaccines and its links to developmental, speech, and language delays. It also examined mercury in dental amalgams and their health implications. This hearing will focus primarily upon new information relating to possible health implications of mercury in the human body, and upon disclosing adequate information to patients to enable them to make informed choices about the type of dental restorative material that is used in their treatment. Mercury is one of the most toxic minerals found in nature, second only to radioactive materials. Dental amalgam consists of a mixture of powdered metals (alloy) and liquid mercury, with mercury constituting 50 percent or slightly more of the amalgam by weight. After the ingredients are mixed and inserted into a cavity, the mixture quickly hardens. For many years it was thought that after amalgamation, the mercury was permanently bound to the other ingredients and was rendered inert. However, during the last 30 plus years, scientists have come to realize that small amounts of mercury continuously leach from amalgams, and that the leaching may go on for many years. It should be noted that mercury is an element. It cannot be broken down or changed into a different substance. Whether in its vapor, liquid, or solid form, mercury is still mercury. The human body does not have an effective filter or elimination system for mercury, since it is a substance that humans were not designed to ingest. Moreover, mercury in the human body accumulates over time. The most common sources of human mercury toxicity are through vaccinations, dental amalgams, and fish consumption. Unfortunately, most of the Federal government's attention seems to have been focused on the hazards of fish consumption, rather than on the hazards of vaccinations and amalgams. The Food and Drug Administration (FDA), Environmental Protection Agency (EPA), and many state government agencies have issued frequent warnings that vulnerable populations, such as pregnant and lactating women and young children, should limit their consumption of fish from mercury-polluted waters. Those warnings are entirely appropriate. But United States government agencies seem to have been far less vigilant in their efforts to examine the health implications of mercury-containing vaccinations and amalgams, in spite of growing evidence that those sources of mercury may contribute to a substantial array of tragic problems, and very likely add more mercury burden to the average American body than any other source. Mercury toxicity has been linked to tremors, attention deficit disorder (ADD), attention deficit hyperactivity disorder (ADHD), autism, Alzheimer's disease (AD), cardiovascular problems, fertility problems, impairment of kidney function, impairment of the immune system, impairment of fetal development, modest declines in intelligence quotient (IQ), and death. Mercury is especially neurotoxic to the development brains of fetuses and young children. Mercury from mothers is passed through the placenta to the unborn baby, and some of that mercury may accumulate in the brain. After birth, breast-feeding can continue the bioaccumulation process. Neurological development continues through all of the first decade of life and well into the second decade. That is why various health warnings reference children age 14 and under. Regardless of the source, neurological and renal problems can result from mercury in human cells. When speaking of the health consequences of mercury in the environment on May 1, 2003 in the Dirksen Senate Office Building, noted pediatrician Dr. Katherine Shea, M.D., M.P.H., F.A.A.P. said: "All forms of mercury are toxic. It is a poison in all of its forms. There is no good mercury." 1 In response to a question she went on to explain that mercury damage lasts a lifetime. She stated: "You can't take a pill and fix it."2 A January of 2003 report by the Centers for Disease Control and Prevention (CDC) found that 1 in 12 women of childbearing age has mercury levels above the EPA-safe threshold of 5.8 parts per million in their blood. That could put as many as 320,000 newborns at risk of neurological effects from being exposed in utero.3 A study by the National Research Council Committee on the Toxicological Effects of Methylmercury reviewed the epidemiological and toxicology literature up to the year 2000. The report came up with the much lower estimate that 60,000 U. S. newborns annually are at risk for neurodevelopmental effects due to in utero mercury exposure. Whether the number is 60,000 or 320,000 or some number in between, that is a tragic number of babies to put at risk, especially since most of that risk can be avoided. Some recent developments are noteworthy. The FDA has decided to adopt the EPA reference dose for mercury body burden-the theoretical amount that the typical person con tolerate without any discernable harm. That represents a four-fold decrease in the FDA estimate. The Swedish Dental Material Commission released a report last week authored by Dr. Maths Berlin, Ph. D., who was the former Chair of the World Health Organization (WHO) International project on Chemical Safety. The report entitled "Mercury in Dental-Filling Materials-An Updated Risk Analysis in Environmental Medical Terms" involved a review of 936 scientific papers, of which just over 700 were deemed to be credible. All of the papers were recent, having been published between 1997 through 2002. Among other things, the report indicated that previous estimates of a safety margin of mercury in the human body were wrong-harm may occur in vulnerable individuals at much lower levels than previously thought. A conclusion of the report stated: "With reference to the fact that mercury is a multipotent toxin with effects on several levels of the biochemical dynamics of the cell, amalgam must be considered to be an unsuitable material for dental restoration. This is especially true since fully adequate and less toxic alternatives are available." 4 The report also states: "With reference to the risk of inhibiting influence on the growing brain, it is not compatible with science and tested experience to use amalgam fillings in children and fertile women." 5 The Centers for Disease Control and Prevention (CDC) announced in April, 2003, that lead may impair children's intelligence at far lower levels of exposure than those in current Federal health guidelines, meaning that potentially millions of additional U. S. children than was previously thought may have lower IQs from ingesting contaminated dust. A study conducted by Dr. Mark Geier, which was published in the peer-reviewed Journal of American Physicians and Surgeons, concludes that there has been a documented increase in neurodevelopmental disorders following the use of vaccines containing thimerosal. According to Dr. Geier: "The amount of mercury in thimerosal in childhood vaccines far exceeds Federal safety guidelines...A causal relationship between childhood vaccines containing thimerosal and neurodevelopmental disorders and heart disease appears to be confirmed." Independent research conducted by Dr. Boyd Haley and Dr. James Adams indicated that autistic children represent a subpopulation that cannot effectively excrete mercury from their bodies, and are therefore very susceptible to the toxic methyl-mercury exposure presented during routine childhood vaccinations. More has been learned about the synergistic effects that can result when multiple heavy metals, such as both lead and mercury, are ingested by the same person. That subject will be covered more in-depth in the Subcommittee hearing. A recent court order in California requires implementation of a Proposition 65 warning, to be prominently posted in dental clinics with more than 9 employees. It states: "Amalgam, used in many dental fillings, causes exposure to mercury, a chemical known to the state of California to cause birth defects or other reproductive harm. Root canal treatments and restorations, including fillings, crowns and bridges, use chemicals known to the state of California to cause cancer. The U.S. Food and Drug Administration has studies the situation and approved for use all dental restorative materials. Consult your dentist to determine which materials are appropriate for your treatment." Proposition 65 was adopted by the voters of California in 1986, but it took 17 years to implement in dental offices, and that happened only as a result of a successful lawsuit. California's "Watson Law" (1992) still has not been implemented. It requires the California Dental Board to prepare and distribute a fact sheet about the risks and efficacies of dental fillings. When the board still had not complied in 2001, nine years after enactment of the law, the public outcry led the legislature to shut down the board and create a new one. The new board held hearings on the safety of mercury-containing fillings in 2002, but once again has bogged down as the California Dental Association argues against effective disclosure of risks. There have been major disagreements as to whether state dental boards impose a so called "Gag Rule" on dentist that prohibits them from initiating conversations with patients about the potential removal of amalgams. Although the ADA denies that there is such a rule, many dentist say that is very real and is strictly enforced by state dental boards. Mercury-free dentists contend that they cannot compete openly, as they are not allowed to advertise that they offer "mercury-free" fillings. The "Gag Rule" that inhibits dentists from discussing the potential health risks of amalgam was first inserted into the ADA Code of Ethics while an ADA subsidiary held the patent on amalgam. This raises strong First Amendment issues, and the Attorneys General of Iowa, Oregon, and Minnesota have ruled that the ADA gag rule may not be enforced in their states. Amalgams typically are referred to as "Silver" fillings. While they are silver in color, and there is some silver in the alloy portion of the amalgam, the name obscures the fact that "silver" fillings are 50% or more mercury. The first state that successfully passed a full disclosure law and properly implemented it is Maine. Former State Senate president, present-day Congressman Michael Michaud (ME-02), wrote a disclosure statute in 2001, then oversaw its implementation by the Maine Department of health in 2002. A booklet designed for dental patients advises consumers that the main ingredient of amalgam fillings is mercury, and that it has potential health risks and significant environmental consequences. Proposition 65, the so-called "Gag Rule," and informed consent will be discussed at the Subcommittee hearing. Finally, there is considerable concern about economically-disadvantaged persons for whom no dental choice exists. For most families on Medicaid, the choice is "mercury fillings or no fillings at all" in their teeth. Many moderate-income consumers face almost as bad a situation. Insurance often covers only mercury fillings, forcing those who cannot afford to pay out-of-pocket to accept mercury in their mouths. In view of recent advances in science, it is time to fully inform the American public about the risks, as well as the benefits, of various dental restorative materials. It also may be time to move on to safer alternatives. Legislation During the 107th Congress, Ms. Watson of California (for herself and Mr. Burton of Indiana) introduced H.R. 4163, the Mercury in Dental Filling Disclosure and Prohibition Act, also referred to as the Watson-Burton Bill. This bill was designed to amend the Federal Food, Drug, and Cosmetic Act to ban mercury-containing amalgams intended for use in dental fillings effective January 1, 2007. A transitional provision also would have required a label that disclosed: "Dental amalgam contains approximately 50 percent mercury, a highly toxic element. Such product should not be administered to children less than 18 years of age, pregnant women, or lactating women. Such product should not be administered go any consumer without a warning that he product contains mercury, which is a highly toxic element, and therefore poses health risks." (Editor's note: A revised version of the bill, HR 1680, was reintroduced in the 108th Congress. In the 109th Congress HR 4011 was reintroduced with many added sponsorers. HR 4011 also includes environmental issues that are related to the use of dental amalgam. HR 4011 can be read at http://thomas.loc.gov The name of the bill remains the same-"Mercury in Dental Filling Disclosure and Prohibition Act." Type in HR 4011 to see the bill. (January 2009 editor's note) HR 4011 is no longer the number of the bill as it changes with each new session of Congress. One of the best ways to keep up with the newest number is to go to the Library of Congress website (http://thomas.loc.gov) that I linked to above, and type in the search box "mercury." If you do an advanced search and put Congresswoman Diane Watson from California as one of the sponsors, you will most likely find the latest legislation or resolutions concerning dental mercury. 1 Response to a question at The Environment & Health Forumm presentation in the Dirksen Senate Office Building on May 1, 2003 entitled, "Public Health Implications of Mercury: Protecting the Health of Children and Other Vulnerable Populations." 2 Ibid. 3 Centers for Disease Control, January 2003, Second National Report on Human Exposure to Environmental Chemicals. 4 Mercury in Dental_Filling materials_An Updated Risk Analysis in Environmental Medical Terms, by Maths Berlin, The Dental Material Commission of Sweden. 5 Ibid. Witnesses Panel One Dr. Fritz Lorscheider, Ph.D., Professor Emeritus, Medial Physiology & Biophysics University of Calgary, Calgary, Alberta, Canada. Dr. Boyd Haley, Ph. D., Professor and Chair, Department of Chemistry University of Kentucky, Lexington, KY Dr. Maths Berlin, Professor Emeritus, Environmental Medicine University of Lund, Sweden and Past Chair, Internation Project of Chemical Safety, World Health Organization Dr. Frederick C. Eichmiller, D.D.S., Director, American Dental Association Health Foundation

Paffenbarger Research Center, National Bureau of Standards and Technology Gaithersburg, MD Panel Two Sandra Duffy, Esq., Founding member, Consumers of Dental Choice Northwest Lake Oswego, OR Congressman Mike Michaud (ME-02) Member of Congress, Second district of Maine Dr. Chester Yokoyama, D.D.S., Member, Dental Board of California Los Angeles Mr. Emmitt Carlton, Immediate Past President, Alexandria Virginia Chapter, National Association for the Advancement of Colored People Alexandria, VA

Eye Problems and Mercury

  

Eye problems  related to mercury.  B Windham(ed)

Studies document that mercury and similar toxic metals accumulate in endothelial cells such as those in the eye retina, cornea, and macula depleting glutathione and lipoate by binding to thiols; these are needed to counteract free radicals caused by such as toxic metals that damage the endothelial layers of the the retina, cornea and macula, as major factors in such conditions(see Pub Med abstracts of studies).  Such free radicals generated have been found to cause cataracts and such conditions that can be prevented, slowed, and even reversed to some degree by detox and antioxidant eye drops (according to studies).  Mercurialentis (brown discoloration of anterior capsule of eye lens- caused by mercury, is documented in medical texts as the first sign of mercury toxicity:  It is an indicator and early sign of further eye damage.  Cataracts, retinitis pigmentosa, iritis, color vision problems, and other eye conditions are documented to commonly be caused by mercury/metals toxicity. 

Medical Dictionary, www.medilexicon.com/medicaldictionary.php

It is commonly caused by systemic poisoning from absorption of mercury vapor through the respiratory tract or through the gastrointestinal tract:  www.llnl.gov/es_and_h/hsm/supplement_21.11/inorg.html

 *****

From my experience I know of 5 eye problems related to mercury. There are probablymore.  One eye problem mercury causes is chronic iritis‑ I don't know much about that  but it’s documented in the medical literature and someone else I know had it.  Another is color vision; that’s also documented in the medical literature and several I know have had color vision improve after amalgam removal, including me.

        I have Fuch's disease(clouding of cornea caused by deterioration/ glumping of endothelial cells in the cornea. Aggressive form of cataracts.  Animal studies and in vitro studies have shown mercury causes similar damage to endothelial cells in various parts of the body due to deterioration and free radical effects.  Since having my amalgams removed over the last 2 years, my opthamologist says that the deterioration of the endothelial layer of my corneas has slowed considerably compared to 2 years ago.  My vision has also improved so much that I cannot see at all through my glasses that I got 4 years ago.  My optomitrist who did the glasses and reexamined me was really surprised, said my vision had improved almost 50%.  I no longer wear glasses.

     Another eye problem related to mercury is dry eyes.  Several clinics have had success with improvements after amalgam replacement.       The other eye problem known to sometimes be related to mercury is macula degeneration.  The buildup of mercury in the eye is similar to in Fuch’s, etc. and causes clouding and degeneration.  Someone I know says a relative got better after amalgam replacement.   The following are a few abstracts or references I’m aware of.     (B Windham)

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Strabismus is where one eye moves freely of the other, either  inwardly or outwardly to focus independently. This condition, which  was present at an early age in my now 5 year old, was quickly  corrected by supplementing the RDA of vit A in cis form and cutting  out all other vit A sources (Megson protocol). Pupil dilation was  always a factor in him too. Interestingly, his pupils reacted  normally within the first two doses of DMSA he ever received, but the  dilation returned post-round. After 5 months of chelation, I see  VERY normal eye function, with normal pupil reactivity for the most  part. I believe the dilation is a symptom of mercury toxicity.                                *************

Dilation, poor accomodative function (focussing) and convergence insufficiency - which if severe is strabismus - are characteristic of mercury poisoning. They are all due to a mild, symmetrical impairment of the third cranial nerve. Since this nerve connects to the brain right next to the hypothalamus, where mercury is known to concentrate,

Dr. A. Cutler,   (see his web site)  

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macular degenerationDegeneration of the macula lutea of the eye. Often caused by free radical or oxidation damage.    www.nutritionfocus.com/nutrition_supplementation/glossary/GlossaryM.html

The first symptom I had of mercury toxicity was double vision, then drooping eyelids. I also had floaters for years and bright lights blinded me. When I was 42 my keen eyesight started to go and I had to wear glasses to sew or read. By the time 1998 rolled around I was wearing 250 magnifying glasses. Within a short period of time after amalgam removal I no longer needed reading glasses, and today I do not wear glasses and am able to read any size print.  

  However, I still have very slight double vision to the extreme right and left, I don't have floaters any longer but still have some sensitivity to bright lights.    

  Freya Koss, Frekoss@aol.com

Mercury has been found to be a factor in retinitis pigmentosa and retina degeneration.

        Olynyk F, Sharpe DH; Mercury poisoning in paper pica, New Eng J Med, 1982, Apr 29: 306(17):1056-57;   &  Uchino M, Tanaka Y, Ando M, et al; Neurologic features of chronic minamata disease(organic mercury poisoning) J Environ Sci Health B 1995, Sep; 30(5): 699-715.

Distributions of elements in the human retnal pigment epitheliaum; Arch Ophthalmol, 1990, Jan; 108(1):113-117; Ulshafer RJ, Allen CB, Rubin ML.

Transport of thiol-conjugates of inorganic mercury in human retinal pigment epithelial cells, Bridges CC, Battle JR, Zalups RK.  Toxicol Appl Pharmacol. 2007 Jun 1;221(2):251-60. Epub 2007 Mar 23

Division of Basic Medical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA. bridges_cc@mercer.edu

Inorganic mercury (Hg(2+)) is a prevalent environmental contaminant to which exposure to can damage rod photoreceptor cells and compromise scotopic vision. The retinal pigment epithelium (RPE) likely plays a role in the ocular toxicity associated with Hg(2+) exposure in that it mediates transport of substances to the photoreceptor cells. In order for Hg(2+) to access photoreceptor cells, it must first be taken up by the RPE, possibly by mechanisms involving transporters of essential nutrients. In other epithelia, Hg(2+), when conjugated to cysteine (Cys) or homocysteine (Hcy), gains access to the intracellular compartment of the target cells via amino acid and organic anion transporters. Accordingly, the purpose of the current study was to test the hypothesis that Cys and Hcy S-conjugates of Hg(2+) utilize amino acid transporters to gain access into RPE cells. Time- and temperature-dependence, saturation kinetics, and substrate-specificity of the transport of Hg(2+), was assessed in ARPE-19 cells exposed to the following S-conjugates of Hg(2+): Cys (Cys-S-Hg-S-Cys), Hcy (Hcy-S-Hg-S-Hcy), N-acetylcysteine (NAC-S-Hg-S-NAC) or glutathione (GSH-S-Hg-S-GSH). We discovered that only Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy were taken up by these cells. This transport was Na(+)-dependent and was inhibited by neutral and cationic amino acids. RT-PCR analyses identified systems B(0,+) and ASC in ARPE-19 cells. Overall, our data suggest that Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy are taken up into ARPE-19 cells by Na-dependent amino acid transporters, possibly systems B(0,+) and ASC. These amino acid transporters may play a role in the retinal toxicity observed following exposure to mercury.

Transport of thiol-conjugates of inorganic mercury in human retinal pigment epithelial cells, Bridges CC, Battle JR, Zalups RK.  Toxicol Appl Pharmacol. 2007 Jun 1;221(2):251-60. Epub 2007 Mar 23

Division of Basic Medical Sciences, Mercer University School of Medicine, Macon, GA 31207, USA. bridges_cc@mercer.edu

Inorganic mercury (Hg(2+)) is a prevalent environmental contaminant to which exposure to can damage rod photoreceptor cells and compromise scotopic vision. The retinal pigment epithelium (RPE) likely plays a role in the ocular toxicity associated with Hg(2+) exposure in that it mediates transport of substances to the photoreceptor cells. In order for Hg(2+) to access photoreceptor cells, it must first be taken up by the RPE, possibly by mechanisms involving transporters of essential nutrients. In other epithelia, Hg(2+), when conjugated to cysteine (Cys) or homocysteine (Hcy), gains access to the intracellular compartment of the target cells via amino acid and organic anion transporters. Accordingly, the purpose of the current study was to test the hypothesis that Cys and Hcy S-conjugates of Hg(2+) utilize amino acid transporters to gain access into RPE cells. Time- and temperature-dependence, saturation kinetics, and substrate-specificity of the transport of Hg(2+), was assessed in ARPE-19 cells exposed to the following S-conjugates of Hg(2+): Cys (Cys-S-Hg-S-Cys), Hcy (Hcy-S-Hg-S-Hcy), N-acetylcysteine (NAC-S-Hg-S-NAC) or glutathione (GSH-S-Hg-S-GSH). We discovered that only Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy were taken up by these cells. This transport was Na(+)-dependent and was inhibited by neutral and cationic amino acids. RT-PCR analyses identified systems B(0,+) and ASC in ARPE-19 cells. Overall, our data suggest that Cys-S-Hg-S-Cys and Hcy-S-Hg-S-Hcy are taken up into ARPE-19 cells by Na-dependent amino acid transporters, possibly systems B(0,+) and ASC. These amino acid transporters may play a role in the retinal toxicity observed following exposure to mercury.

Homocysteine, system b0,+ and the renal epithelial transport and toxicity of inorganic mercury, Bridges CC, Zalups RK.  Am J Pathol. 2004 Oct;165(4):1385-94

Mercer University School of Medicine, Division of Basic Medical Sciences, 1550 College St., Macon, GA 31207, USA.

Proximal tubular epithelial cells are major sites of homocysteine (Hcy) metabolism and are the primary sites for the accumulation and intoxication of inorganic mercury (Hg(2+)). Previous in vivo data from our laboratory have demonstrated that mercuric conjugates of Hcy are transported into these cells by unknown mechanisms. Recently, we established that the mercuric conjugate of cysteine [2-amino-3-(2-amino-2-carboxy-ethylsulfanylmercuricsulfanyl)propionic acid; Cys-S-Hg-S-Cys], is transported by the luminal, amino acid transporter, system b(0,+). As Cys-S-Hg-S-Cys and the mercuric conjugate of Hcy (2-amino-4-(3-amino-3-carboxy-propylsulfanylmercuricsulfanyl)butyric acid; Hcy-S-Hg-S-Hcy) are similar structurally, we hypothesized that Hcy-S-Hg-S-Hcy is a substrate for system b(0,+). To test this hypothesis, we analyzed the saturation kinetics, time dependence, temperature dependence, and substrate specificity of Hcy-S-Hg-S-Hcy transport in Madin-Darby canine kidney (MDCK) cells stably transfected with system b(0,+). MDCK cells are good models in which to study this transport because they do not express system b(0,+). Uptake of Hg(2+) was twofold greater in the transfectants than in wild-type cells. Moreover, the transfectants were more susceptible to the toxic effects of Hcy-S-Hg-S-Hcy than wild-type cells. Accordingly, our data indicate that Hcy-S-Hg-S-Hcy is transported by system b(0,+) and that this transporter likely plays a role in the nephropathy induced after exposure to Hg(2+). These data are the first to implicate a specific, luminal membrane transporter in the uptake and toxicity of mercuric conjugates of Hcy in any epithelial cell.

(mercury accumulates in cornea endothelial cells and causes oxidative damage resulting in cataracts, etc.)

********************

SEAFOOD/CATARACTS   Methylmercury in seafood may cause lens clouding, contributing to cataract development. Optometrist Ben Lane noted that his cataract patients liked seafood, while those who didn't like fish were clear-eyed. A study of 17 patients revealed that the cataract patients had eaten salt water fish or shellfish at least once a week on the average, but those cataract-free reported using these foods an average of once every five weeks. The cataract patients showed far higher concentrations of mercury in their hair. Dr. Lane's study showed that the presence of 2.3 ppm or more of mercury in hair samples was related to a 23-fold increase in the risk of cataracts. Dr. Lane encourages his patients to eat such foods as garlic and pectin-rich foods such as apples to help remove the mercury, and to receive adequate, while avoiding excessive, amounts of vitamins A, C, and E.

Dr, Ben Lane, O.D., Methylmercury in seafood contributes to cataract development, Medical World News, December 20, 1982

**********************

I would look into the possibility of mercury poisoning which is capable of causing both cataracts and light sensitivity. (So are other things.) I have seen many babies born with mercury poisoning (further exacerbated by the mercury in vaccinations.) from their mother's dental amalgams. I would get a Hair Mineral Analysis right away. Good luck.Steve Rochlitzrochlitz@wellatlast.com               ******************************************************

Cataract reversal through mercury detox      www.digitalnaturopath.com/treat/T33633.html

Mobilization AND excretion are required for mercury detoxification. Consuming foods high in sulfur such as garlic, onions, beans, and eggs or supplemental sulfur in the form of MSM can help move mercury around but it is only bound loosely and caution is advised. There have been reported cases of reversible cataract development from individuals mobilizing mercury without excreting it. Consult a qualified doctor for a detoxification protocol appropriate for you.           Alan Thal, MD

Antioxidant eye drops (n-acetylcarnosine) have been documented to prevent and sometimes reverse cataracts (such as Can C drops).

******************************************************************

Rudolph CJ, Samuels RT, McDanagh EW. Cheraskin E. Visual Field Evidence of Macular Degeneration Reversal Using a Combination of EDTA Chelation and Multiple Vitamin and Trace Mineral Therapy.In: Cranton EM, ed. A Textbook on EDTA Chelation Therapy, Second Edition. Charlottesville, Virginia: Hampton Roads Publishing Company; 2001

*********************************************

Dr. G. E. Poesnecker, Its Only Natural, 2001, http://www.oneflesh.org/only‑22.html

Disorders that Chelation Can Help

Following is a list of conditions successfully treated by chelation that has been assembled by physicians who did much of the early research work. Many of these problems are common and are generally considered incurable: scleroderma; digitalis intoxication; heavy-metal poisoning (especially acute plumbism); calcinosis (pipestem calcinosis of the vessels, prostatic calcinosis); vascular atheromatous disorders including atherosclerosis, atheromatous deposits, arteriosclerosis obliterans, peripheral vascular insufficiency with intermittent claudication, and acute brain syndrome secondary to cerebral ischemia secondary to calcific atherosclerosis; myocardial or coronary insufficiency; collagenosis; arteriosclerosis including cerebrovascular arteriosclerosis; arthritis including hypertrophic and rheumatoid; calcific tendinosis; calculi; diabetic retinopathy; multiple sclerosis; macular degeneration of the retina; cataracts; Parkinsonism; emphysema; poisonous snake and insect bites; calcified necrotic ulcers; heart valve calcification; hemochromatosis; calcific bursitis; calcified granulomas; and hypertension.

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Mercury accumulates in the uvea and retina of the eye. 

Khayat A, Dencker L.  Whole body and liver distribution of inhaled mercury vapor in the mouse: influence of ethanol and aminotriazole pretreatment. J Appl Toxicol. 1983 Apr;3(2):66-74

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Inorganic mercury has been found to be associated with cataract formation.Hachet E.  Cataracts,  Bull Soc Ophtalmol Fr. 1985 Nov;Spec No:87-107. &&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&Dr. Victoria Buntine, Mercury Effects,  Healthinasia Incorporated, 2001www.healthinasia.com/mercury.html

        The problem with mercury is that  it affects our nervous system.  Mercury accumulates in what we call end organs, like kidneys, brain, thyroid and eyes, and this is why it is detected on hair analysis  It may contribute to cataracts, headaches, numbness and tingling, irritability, joint pain and autism in kids, as well as chronic fatigue syndrome and general allergies.                  *******************************************************

Dr. D.A. Carroll, O.D.& Dr. B.C. Lane,  Preventing mercury related cataracts,

www.medicalvisioncenter.com/prevention.html

Vitamin C also helps to pull out the toxic mercury that results from the consumption of large fish, such as tuna, swordfish and shark. Dr. Lane said that his 1982 study found that mercury, which would accumulate in the crystalline lens, resulted in the depression of enzymes such as superoxide dismutase and glutathione peroxidase. The latter is the primary enzyme that helps prevent mercury cataracts from forming. 'Organic mercury is the worst offender because it's able to penetrate membranes and get into organic tissues,' he said.

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Cavalleri A, Belotti L, Gobba FM, Luzzana G, Rosa P & Seghizzi P.       Colour vision loss in workers exposed to elemental mercury  vapour.      Toxicology Letters 77(1‑3):351‑356 (1995)

ABSTRACT: "We evaluated colour vision in 33 workers exposed to elemental mercury (Hg) vapour and in 33 referents matched for sex age, alcohol consumption and cigarette smoking. The results were expressed as colour confusion index (CCI). In the workers urinary excretion of Hg (HgU) ranged

from 28 to 287 ug/g creatinine. Subclinical colour vision loss, mainly in the blue‑yellow range, was observed in the workers. This effect was related to exposure, as indicated by the correlation between HgU and CCI (r=0.488, P<0.001).

& Urban P, Gobba F, Nerudova J, Lukas E, Cabelkova Z, Cikrt M,.Color Discrimination Impairment in Workers Exposed to Mercury Vapor.  Neurotoxicology. 2003 Aug;24(4-5):711-716;

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If you want to know something about

retinitis pigmentosa (or retinopathia pigmentosa) and mercury poisoning,

you should read the following two articles:

1.   Olynyk F, Sharpe DH: Mercury poisoning in paper pica. (retinitis pigmentosa)

     N Engl J Med 1982 Apr 29;306(17):1056‑1057

2.   Uchino M, Tanaka Y, Ando Y, Yonehara T, Hara A, Mishima I,  Okajima T, Ando M:      Neurologic features of chronic minamata disease (organic  mercury poisoning) and incidence of complications with aging.    J Environ Sci Health B 1995 Sep;30(5):699‑715

Also:     Arch Ophthalmol 1990 Jan;108(1):113‑117

Distributions of elements in the human retinal pigment epithelium.

Ulshafer RJ, Allen CB, Rubin ML

Department of Ophthalmology, College of Medicine, Univ. of Florida, Gainesville 32610.

Distributions of elements above the atomic number of sodium were mapped in the retinal pigment epithelia of eight human eyes. X‑ray energy spectra and maps were collected from cryofixed, freeze‑dried, and epoxy‑embedded tissues using energy‑dispersive x‑ray microanalysis. All eyes had high concentrations of phosphorus in the nuclei of retinal pigment epithelial cells. Melanosomes were rich in sulfur, zinc, calcium, and iron. Lipofuscin and cytoplasm contained only phosphorus and sulfur in detectable amounts. Drusen, when present, contained phosphorus and calcium. Six eyes had a prominent aluminum peak recorded from melanosomes, nuclei, and Bruch's membrane. In one pair of 90‑year‑old eyes, small, electron‑dense deposits

surrounded many melanosomes and contained mercury and selenium. Retinal pigment epithelial melanosomes may bind and accumulate metals and

other potentially toxic ions over time, preventing them from reaching the neural retina.

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Journal of Environmental Science and Health Part B Pesticides Food Contaminants and Agricultural Wastes 30(5): 699-715. 1995

Abstract:      Tessier‑Lavigne M, Mobbs P, Attwell D,  Invest Ophthalmol Vis Sci 1985 Aug;26(8):1117‑1123 “Lead and mercury toxicity and the rod light response”.

Lead and mercury have been reported to alter selectively the rod component of the electroretinogram, and to inhibit the phosphodiesterase in rod outer segments which may be responsible for generating the rods' light response. The authors have investigated the effect of lead and mercury on the voltage response to light of rods, and compared these effects with those of the phosphodiesterase inhibitor papaverine. Lead and mercury, like papaverine, slow the light response. In addition, papaverine increases the light response amplitude while lead decreases it. Mercury initially increases and then decreases the amplitude. The late decrease in amplitude  “produced by mercury is  associated with rod degeneration”:  an effect which may mimic degenerative diseases in which the rod phosphodiesterase is insufficiently active. These results demonstrate that the changes of electroretinogram induced by lead and mercury can be accounted for by the changes in receptor potential these heavy metals produce. The changes in receptor potential seen are consistent with mercury inhibiting the rod phosphodiesterase, and with lead having an action in addition to phosphodiesterase inhibition.

PMID: 2991162, UI: 85260515

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God Zb Med Fak Skopje 1978;24:289‑291

[Changes in the crystalline lens of the eye in workers occupationally exposed to mercury vapors].     [Article in Serbo‑Croatian (Cyrillic)]

Delivanova S, Popovski P, Orusev T    PMID: 757176, UI: 80092857

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Abstract

“Effect of the ophthalmic preservative thimerosal on human and rabbit  corneal endothelium”.

Van Horn DL, Edelhauser HF, Prodanovich G, Eiferman R, Pederson HF

Widespread use of the mercurial‑containing preservative thimerosal as an antibacterial agent in ophthalmic drugs and solutions warranted an investigation into its possible cytotoxic effects on the functional and ultrastructural integrity of the corneal endothelium. No changes in corneal thickness were observed during 5 hours' perfusion of the endothelium of  rabbit and human corneas with 0.0001 and 0.0005 percent thimerosal in  glutathione bicarbonate Ringer's solution (GBR). Scanning electron

microscopy (SEM) and transmission electron microscopy (TEM) of the endothelium of the 0.0001 percent group revealed normal ultrastructure. SEM and TEM of the endothelium of corneas perfused with 0.0005 percent thimerosal for 5 hours revealed condensed mitochondria, cytoplasmic vacuoles, and cytoplasmic flaps at the apical end of the cellular  junctions. Perfusion of higher concentrations (0.001 and 0.005 perecnt) of  thimerosal in GBR resulted in increases in corneal thickness after 2 hours

 and irreversible ultrastructural damage to the endothelial cells by 5 hours. Corneas perfused with 0.01 and 0.1 percent thimerosal in GBR showed a rapid and immediate increase in corneal thickness and endothelial cell death and  necrosis within 1 hour. It is postulated that the mercury in thimerosal

 becomes bound to the cell membrane protein sulfhydryl groups, causing an

increase in cellular permeability; These results suggest that the prolonged exposure of the corneal endothelium to thimerosal in the accepted antimicrobial dosage of 0.005 to 0.001 percent may result in functional and “structural damage to the endothelium”. *

PMID: 844986, UI: 77140310

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       Garron LK, Wood IS, Spencer WH, Hayes TL.  A clinical pathologic study of mercurlalentis medicamentosus.  Trans Am Ophthalmol Soc 1977;74:295‑320

Thirty‑one patients who used eye drops containing the preservative, phenylmercuric nitrate for from 3 to 15 years, developed a brownish pigmentation of the

anterior capsule of the pupillary area. Light and electron microscopic

studies on two lenses demonstrated deposits of dense particulate material

resembling melanin pigment on and in the anterior capsule of the lens in

the area of the pupil. Special studies, including electron microprobe

analysis and neutron activation analysis established the presence of mercury in a lens with mercurialentis. No mercury was found in two lenses used as controls.

PMID: 867632, UI: 77196922

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          Klein, CL; Kohler, H; Kirkpatrick, CJ.

  Increased Adhesion and Activation of Polymorphonuclear Neutrophil Granulocytes to Endothelial Cells under Heavy Metal Exposure in Vitro.              Pathobiology. 62(2):90‑98, 1994.

 ABSTRACT: Heavy metals have been implicated in the mechanisms of endothelial damage. Influences of heavy metal ions on diverse cell types have been studied using a variety of in vitro and in vivo methods. Polymorphonuclear neutrophil granulocytes (PMNs) have physiological and pathological functions, including the modulation of adhesion to  and destruction of endothelial cells (ECs).

PMNs were studied during interaction with human umbilical vein ECs under exposure to zinc, nickel and cobalt using an in vitro model. We studied adhesion processes with the help of a computer‑controlled image‑analyzing system and examined the activation of PMNs by quantification of leukotriene

B4 (LTB4) release. The biphasic effects of the valuated heavy metals on PMN‑EC adhesion, with stimulation at very high and very low molar concentrations, were  observed.  The release of LTB4 by PMNs increased during exposure to very low metal concentrations. The initiation of these important pathogenetic mechanisms of inflammation at very low metal ion concentrations, which give no

morphologic changes, must be regarded as potentially significant with respect to the toxic effects of heavy metals.  BIO‑PROBE COMMENT: Damage to the inner lining of blood vessels (endothelium)

is widely regarded to be the initial step in the disease process that leads to cardiovascular disease. Although mercury was not included in this study, it is a heavy metal that has previously been shown to cause endothelial damage. The three metals examined in this study nickel, cobalt and zinc)

are all used in dental restorative materials. Research, published in peer‑reviewed dental journals, has demonstrated the release and bioavailability of nickel (and mercury). Cardiovascular disease has become widespread only since the 1920's, about the time of increased use of heavy metals in dental

therapy and long after humans consumed eggs, meat, milk, butter and cheese.(other studies documenting mercury damage to is available on the web: use EXCITE search engine or MEDLINE   http:///www.nlm.nih.gov/)

Abstract

Exp Eye Res 1993 Nov;57(5):549‑555

Low levels of inorganic mercury damage the corneal endothelium.

Sillman AJ, Weidner WJ

Section of Animal Physiology, University of California, Davis 95616.

The effect of inorganic mercury on the integrity of the endothelium of  isolated bullfrog (Rana catesbeiana) corneas was examined by spectrophotometric analysis of corneal uptake of the vital stain Janus green, and by both  transmission (TEM) and scanning (SEM) electron microscopy. The uptake of

Janus green by the endothelium is dose related between 1.0 and 30.0 microM  HgCl2. The effect of mercury is not altered by changes in external calcium concentration, nor is it influenced by the calcium ionophore A23187, indicating that inorganic mercury damages the corneal endothelium through a mechanism which does not involve competition with external calcium or  interaction with calcium channels. TEM and SEM demonstrate significant ultrastructural damage to the endothelium exposed to inorganic mercury,  including cellular swelling, increased vacuolization, focal denuding of

Descemet's membrane, and diminished integrity at the intercellular junctions.

PMID: 8282041, UI: 94109509

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       Toimela TA, Tahti H.   Effects of mercuric chloride exposure on the glutamate uptake by  cultured retinal pigment epithelial cells.  Toxicol In Vitro 2001 Feb;15(1):7‑12

                

                  Tampere University Medical School, FIN‑33014 University of Tampere, Finland.

                  The cytotoxicity of mercuric chloride and the effects of mercuric chloride on glutamate and   calcium uptake and the factors regulating glutamate uptake were studied in retinal pigment   epithelium (RPE) cell cultures. RPE cells isolated from pig eyes and human RPE cell line   (D407) cells were cultured to confluency and further subcultured according to the test protocol  in question. The cytotoxicity caused by 15 min of exposure to mercuric chloride (0.01‑‑1000 microM) was evaluated by WST‑1 assay based on the activity of mitochondrial  dehydrogenases. [(3)H]Glutamate uptake was measured after the cells were exposed to  0.1‑‑100 microM mercuric chloride and the selected regulators of protein kinase C (PKC)    pathway: PKC activator SC10, PKC inhibitor chelerythrine chloride, phospholipase A(2)/C    inhibitor manoalide, tyrosine kinase inhibitor lavendustin A, competitive NMDA receptor   antagonist AP7 and IP(3) receptor antagonist heparin. Intracellular calcium was monitored with  Fluo‑3 probe starting immediately after the exposure to 1‑‑1000 microM mercuric chloride.   Mercuric chloride showed concentration‑dependent effects on cell viability, on glutamate   uptake and on intracellular calcium concentration. The results give some support to the concept  that glutamate uptake is affected by PKC. The PKC inhibitor chelerythrine chloride decreased    glutamate uptake by 25%, but the PKC activator SC10 could partly prevent the inhibitory  effect of mercuric chloride. Lavendustin A, manoalide and heparin had smaller, but statistically   significant, effects. All these substances act on mediators which can regulate the activity of  PKC. However, PKC is not likely to be the only regulator of glutamate uptake. The rise                  observed in [Ca(2+)](i) may initiate various cellular events during mercury intoxication.

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Hum Toxicol 1987 May;6(3):253‑256

                                                    

                  Prenatal and early postnatal intoxication by inorganic mercury

                  resulting from the maternal use of mercury containing soap.

                  Lauwerys R, Bonnier C, Evrard P, Gennart JP, Bernard A.

                  A case of slight renal tubular dysfunction associated with cataract and anaemia was diagnosed  in a 3‑month‑old black boy in whom high levels of mercury were found in blood and urine.     Several arguments suggest that the renal, ocular and haematological defects may have resulted  from exposure to mercury during foetal life and the 1‑month lactation period due to the  extensive use of inorganic mercury containing cosmetics by the mother.

**********************************************************

1: Bull Soc Belge Ophtalmol 1978;181:21‑37

    [Cataract of toxic origin(mercury)]                  [Article in French]

                  Michiels J.

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Bull Soc Ophtalmol Fr 1985 Nov;Cataracts:87‑107                                                    

                  [Cataracts(mercury)].

                  [Article in French]

                  Hachet E.

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Oftalmol Zh 1974;29(7):501‑503

                         

                  [Eye manifestations of chronic mercury poisoning].

                  [Article in Russian]

                  Fomicheva IV.

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Bull Environ Contam Toxicol 1991 Feb;46(2):230‑236

Inhibition of corneal epithelial cell migration by cadmium and mercury.

Ubels JL, Osgood TB

Mount Desert Island Biological Laboratory, Salsbury Cove, Maine 04672.

PMID: 2018869, UI: 91208463

**********************************************************

          Klein, CL; Kohler, H; Kirkpatrick, CJ.

  Increased Adhesion and Activation of Polymorphonuclear Neutrophil  Granulocytes to Endothelial Cells under Heavy Metal Exposure in Vitro.    

              Pathobiology. 62(2):90‑98, 1994.

 ABSTRACT: Heavy metals have been implicated in the mechanisms of endothelial damage. Influences of heavy metal ions on diverse cell types have been studied using a variety of in vitro and in vivo methods. Polymorphonuclear neutrophil granulocytes (PMNs) have physiological and pathological functions, including the modulation of adhesion to and destruction of endothelial cells (ECs).

PMNs were studied during interaction with human umbilical vein ECs under exposure to zinc, nickel and cobalt using an in vitro model. We studied adhesion processes with the help of a computer‑controlled image‑analyzing system and examined the activation of PMNs by quantification of leukotriene

B4 (LTB4) release. The biphasic effects of the valuated heavy metals on PMN‑EC adhesion, with stimulation at very high and very low molar concentrations, were  observed.  The release of LTB4 by PMNs increased during exposure to very low metal concentrations. The initiation of these important pathogenetic mechanisms of inflammation at very low metal ion concentrations, which give no

morphologic changes, must be regarded as potentially significant with respect to the toxic effects of heavy metals. 

BIO‑PROBE COMMENT: Damage to the inner lining of blood vessels (endothelium) is widely regarded to be the initial step in the disease process that leads to cardiovascular disease. Although mercury was not included in this study, it is a heavy metal that has previously been shown to cause endothelial

damage. The three metals examined in this study nickel, cobalt and zinc) are all used in dental restorative materials. Research, published in peer‑reviewed dental journals, has demonstrated the release and bioavailability of nickel (and mercury). Cardiovascular disease has become widespread only

since the 1920's, about the time of increased use of heavy metals in dental therapy and long after humans consumed eggs, meat, milk, butter and cheese.

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Toxicology 1996 Mar 18;107(3):189‑200

Mercury accumulation in the squirrel monkey eye after mercury vapour exposure.

Warfvinge K, Bruun A

Department of Ophthalmology, University Hospital of Lund, Sweden.

Squirrel monkeys were exposed to mercury vapour at different concentrations and for different numbers of days. The calculated total mercury absorption ranged between 1.4‑2.9 mg (range of daily absorption 0.02‑0.04 mg). The monkeys were killed at different intervals after the end of exposure (range 1 month ‑ 3 years) and the eyes were enucleated. Eyes from four un‑exposed monkeys were used as control material. Mapping of the mercury distribution in the eye revealed that the non‑myelin‑containing portion of the optic disc was densely loaded with mercury deposits, which are mostly confined to the capillary walls and the glial columns. The white matter of the brain does not accumulate mercury at these exposure levels, which might suggest that the myelinization process inhibits the accumulation of mercury. The pigmented epithelium of the pars plicata of the ciliary body and of the retina contained a considerable amount of mercury. This finding indicates that mercury is trapped within the melanocytes, which keeps potentially dangerous material from reaching the neural retina. In addition, the retinal capillary walls were densely loaded with mercury deposits, even 3 years after exposure. It was also found that the inner layers of the retina accumulated mercury during a 3‑year period. It is known that the biological half‑time of mercury in the brain may exceed years. This seems also to be the case for the ocular tissue.

PMID: 8604479, UI: 96180636

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Toxicology 1988 Sep;51(1):67‑76

Enhanced electroretinogram in cats induced by exposure to mercury acetate.

Gitter S, Pardo A, Kariv N, Yinon U

Institute for Occupational Health, Maurice and Gabriela Goldschleger Eye Research Institute, Chaim Sheba Medical Center, Tel‑Hashomer, Israel.

The present study was undertaken in order to verify whether, and how, retinal functions are affected by subacute poisoning with organic mercury.   Mercury acetate in various concentrations (0.025‑0.25 mg/kg per day) was injected subcutaneously every second day to adult cats (N = 20) throughout a 2.5‑4.0‑week period. The electroretinogram (ERG) was recorded and the Hg2+ concentrations in the blood were determined. In nearly 90% of the intoxicated cats an enhanced electroretinogram (scotopic b‑wave amplitude) was found as compared to its level in the normal control cats (N = 10). The latency of the ERG was found to be appropriately shorter, up to a maximal difference of nearly 20% in comparison to the controls.    Hg2+ was present in the blood of the exposed cats during a 2.5‑month period following the exposure. It is concluded that exposure to mercury acetate   induces a permanent increase in the excitability level of the cat's retina.

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Toxicology 1983 Jan;26(1):1‑9

A cell aggregation model for the protective effect of selenium and vitamin E on

methylmercury toxicity.

Kleinschuster SJ, Yoneyama M, Sharma RP

Histotypic aggregation of embryonic neural retinal cells was chosen as a test model to evaluate mercury toxicity. After 24 h rotational culture with methylmercury (CH3HgCl) at 4 microM, aggregation was completely inhibited. A dose‑response relationship between concentrations of methylmercury and final sizes of aggregates was found. Selenium (Na2SeO3) at concentrations of 1, 3 and 5 microM provided a protective effect for methylmercury (1 microM) toxicity. Vitamin E (DL‑alpha‑Tocopherol acetate) at concentrations 5, 7 and 10 microM also provided protection against the same concentration of methylmercury; however, it was less effective than selenium. Histotypic embryonal retinal cell aggregation may be a useful assay system for in vitro neurotoxic studies in morphogenesis.

PMID: 6829026, UI: 83147085

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Science 1979 Oct 5;206(4414):78‑80

Heavy metals affect rod, but not cone, photoreceptors.

Fox DA, Sillman AJ

Low concentrations of lead, mercury, or cadmium depress the amplitude of the rod receptor potential in the perfused bullfrog retina. Responses from the cones were not affected. The data implicate the rods as a lesion site in animals exhibiting scotopic vision deficits as a result of heavy metal poisoning.

PMID: 314667, UI: 80014468

K.Warfvinge et al, "mercury accumulation in the monkey eye after mercury vapour exposure.  Toxicology, 1996, 107: 189‑200.

 mercury from vapor exposure accumulates over time in the various parts of the eye.

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Kishimoto T, Ohno M, Yamabe S, Tada M

              Methylmercury Injury of Cultured Human Vascular  Endothelial Cells

              Journal of Trace Elements in Experimental Medicine. 6(4):155‑162, 1993

        Abstract The effect of methylmercury chloride (MeHg) on cultured human vascular endothelial (HVE) cells was investigated. Umbilical         vein‑derived HVE cells were collected by enzymatic digestion with collagenase. At concentrations of 0‑50 mu M, MeHg had only barely    detectable effects on cell viability. However, the viability of HVE cells decreased dose‑dependently at concentrations >100 mu M.

        Morphologic examination by phase‑contrast microscopy revealed a markedly damaging effect of MeHg at concentrations exceeding 500 mu M. The cytotoxic effect of MeHg on DNA synthesis was also concentration‑dependent. These results suggest that HVE cells are susceptible to concentration‑dependent MeHg cytotoxicity and that MeHg could induce vascular endothelial injury, which may be involved in the pathogenesis of arteriosclerosis. (C) 1993 Wiley‑Liss, Inc. [References: 34]

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   I have seen several abstracts related to eye degeneration and mercury , due to my friends father's eye degeneration, I researched abstracts for  my friend to give to his father.     I do not have any of them handy yet anymore, but I found 1‑2 from Sam Queen's Chronic Mercury Toxicity book(see anotated bibliog.) , and I found quite a few more when I researched glutathione and lipoic acid, in addition to mercury, and it has been proven that mercury depletes glutathione and lipoate by binding to the thiols in these 2 as well as inhibiting various important glutathione system enzymes.

   I found the abstracts from Medline, additionally, some where in the Life Extension Foundation Magazine abstract sections, and the same can be found also from Medline.    I am sorry that these days I do not have enough time to go fetch the abstracts for you.  But, what I found from tbe abstracts, lipoate, NAC, GSH, E‑vitamin and C‑vitamin have the greatest potential to be used as a protective treatment against mercury also in all eye disease that are due to oxidative damage and thiol‑binding by mercury.

   Plaase go to Medline at www.medscape.com, join them free, and then seach with "mercury" and "macular" or "lipoate" and "macular" or "glutathione" and "macular" and cross all the years down to 1980 at least, and you will fork many abstracst to read.

Hope this helps,Ray

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 From:         "Amy L. Riskedahl, O.D." <ariskedahl@seanet.com>

 Subject:      Re: Vision

Cataracts and macular degeneration are the two eye diseases most often

 attributed  to oxidative damage.  Cataracts can be taken out surgically but macular

 degeneration often can't be helped.  The progression can be slowed with

 large  amounts of certain anti‑oxidants such as lutein.

 The macula is the part of the eye that has the  highest  number of cones and thus the sharpest vision and the best color vision.  Mercury and other things that cause oxidative damage can damge the macula over time.

 Generally what you do to heal the body, heals the eye.  Get rid of the  mercury.     Vit. C, Vit. E, essential fatty acids, proanthocyanadins and several of the  carotenoids are things that have been proven to heal the eye. Keep the  cardiovascular system healthy.  The retinal artery is a branch off of the  carotid  artery so plaques thrown off the carotids can cause strokes in the eye just  as they  do in the brain.

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Cavalleri A, Gobba F.  Reversible color vision loss in occupational exposure to metallic mercury.  Environ Res 1998 May;77(2):173‑7

Sezione di Medicina Preventiva dei Lavoratori, Universita di Pavia, Pavia, Italy.

Color vision was evaluated in twenty‑one mercury exposed workers and referents matched for sex, age, tobacco smoking, and alcohol habits. The Lanthony 15 Hue desaturated panel (D‑15 d) was applied. In the workers, mean urinary Hg (HgU) was 115+/‑61.5 microg/g creatinine; in all but one the values exceeded the biological limit (BEI) proposed by the American Conference of Governmental Industrial Hygienists. A dose‑related subclinical color vision impairment was observed in Hg‑exposed workers compared to the referents. Just after the survey, working

conditions were improved. Twelve months later the workers were reexamined. Mean HgU was 10.0 microg/g creatinine and in no subjects was the BEI exceeded. Color perception was significantly improved compared to the first examination and, furthermore, no differences were observed between exposed workers and referents. The results add evidence that the color vision loss observed during the first part of the study was related to Hg exposure and, moreover, show that this effect is reversible. These data indicate that metallic Hg can induce a reversible impairment in color perception. This suggests that color vision testing should be included in studies on the early effects of Hg. The possibility of applying the D‑15 d as an early effect index in the biological monitoring of Hg exposed workers should also be entertained. Copyright 1998

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I do not know of any direct science references tying mercury with Macular Degeneration.  However, from indirect information there appears to be a connection.

Dr. Johnathon Wright and Alan Gaby have developed a nutritional protocol that is quite

effective.  It is interesting to note that the nutrients are all those that mercury reduces in the body. ie Taurine, Vit E, Selenium, and Zinc.  I am sure most ACAM physicians would be happy to get the formula (if it isn't already included in their data) and administer it.  It is given by IV, except the Vit E.

‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑‑

Sam Ziff

<bpinfo@bioprobe.com>

<http://www.bioprobe.com/>

Myasthenia Gravis

Quite common with mercury poisoned, relates to antibodies against acetylcholine receptors, mercury has major effects of impairing acetylcholine metabolism and neural transmission, and bindind to the receptors. Quite a few abstracts is available of that, so the linking of myastenia gravis to the changes mercury cause is not that great jump to make. I know numerous people that had myastenic

symptoms, and continue to have from amalgams, I am one of those, and Freya on the list has similar, and it was quite frequent when I used to go to amalgam poisoned's meetings in the early part of

the decade, we had meetings of up to 50 poisoned in Tampere Finland and even more in Helsinki, and discussed diagnosises and symptoms each had from amalgams, and myastenia was one fairly common in addition to MS/ALS , autoimmunities, thyroid, prostata, liver, kidney, fibromyalgia, chronic fatique and various other symptoms/ conditions resulting or contributed by the mercury and copper leaking from the amalgams en masse.

Ray Sarela

++++

Washington University Medical School

Neuropothyhttp://www.neuro.wustl.edu/neuromuscular/nother/toxic.htm

>(another source of eye mercury & eye problems)

> Mercury is still used in eye makeup as a preservative. From the FDA  site:

> 

> http://vm.cfsan.fda.gov/~dms/cos-hdb3.html

> 

> Mercury compounds (21 CFR 700.13).

> The use of mercury compounds as cosmetic ingredients is limited to eye

> area cosmetics at concentrations not exceeding 65 parts per million

> (0.0065%) of mercury calculated as the metal (about 100 ppm or 0.01%

> phenylmercuric acetate or nitrate) and provided no other effective and

> safe preservative is available for use.

> 

> Mercury compounds are readily absorbed through the skin on topical

> application and have the tendency to accumulate in the body. They may

> cause allergic reactions, skin irritation, or neurotoxic

> manifestations.

>

> List members may be interested to note that information on this subject

was  published in the American Journal of Clinical Pathology in 1973 (Vol. 59,

> 515-7) by my colleagues in the Department of Forensic Medicine, University

> of Glasgow, Scotland following research in Africa.

> It is surprising that such a toxic metal should continue to be used in

> cosmetics.

> Ian Dale

> Occupational Hygienist

> Glasgow Occupational Health

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 „Conjunctivitis sicca“ or „dry eye study“

_ Conjunctivitis sicca (dry eyes) is a major health problem for about 4 million people in Germany.

The „dry eye study“ with 36 patients has shown that people with heavy metals like amalgam or palladium used in their goldcrowns often have fungi in the large intestine and also food allergies. Patients which have been treated had very good results. Other visual problems (spectacles) have shown to be highly correlated with the number of amalgam fillings as well.

Marburg Amalgam Study. (there also is a published version)

From:         "Dr.B. Weber, Amalgaminformation Marburg,

              http://home,t‑online.de/home/Institut_f._Naturheilverfahren/patinf.htm"

              <b.weber@FIREMAIL.DE>

Subject:    Information about treatment of 3000 patients with amalgam‑problems in german and englisch

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Dr. D.A. Carroll, O.D.& Dr. B.C. Lane,  Preventing mercury related cataracts,

www.medicalvisioncenter.com/prevention.html;    & Alan Thal, MD, Cataract reversal through mercury detox,    www.digitalnaturopath.com/treat/T33633.html;  & Dr, Ben Lane, O.D., Methylmercury in seafood contributes to cataract development, Medical World News, December 20, 1982; &   Dr. Victoria Buntine, Mercury Effects,  Healthinasia Incorporated, 2001, www.healthinasia.com/mercury.html, & Dr. G. E. Poesnecker, Its Only Natural, 2001, www.oneflesh.org/only‑22.html;

Iritis, Inflammation of the Eye, (autoimmune condition, can be caused by mercury)

http://www.hfhut.com/iritis-inflammation-of-the-eye

Syphilitic iritis after treatment with mercury common; likewise use of thimerosal eyedrops

Photophobia often accompanies mercury poisoning,  http://www.causeof.org/sensitivity.htm#TreatIritis

************

Astaxanthin, a natural supplement has been documented to relieve eye fatigue and improve visual acuity and accommodative amplitude. Reduces inflammation.                                                   Life Extension Foundation  Life Extension  Jan 2009

Mercury ‑ inorganic

òToxicity òElemental metal òUsually airborne exposure òOften produces neural disease without systemic disorders òSalts: GI absorption òProduce systemic & neural effects Organic mercurials: Methyl mercury òLittle peripheral nerve toxic toxicity òEarly paresthesias & ataxia related to CNS effects òConverted from inorganic mercury by microorganisms òThen enters food chain Outbreaks of toxicity

Minimata Bay: Spillage of HgCl into sea òIraq: Ethyl Hg fungicide in grain used for baking bread òSubacute: Metallic mercury vapor òNeuropathy òMotor òAxonal òMyokymia ò

Encephalopathy òOther: Mouth inflammation; GI; Fetid breath òChronic ò

CNS: Encephalopathy; Psychosis; Extrapyramidal; Ataxia òNeuropathy:

Sensory & Motor; Pain & paresthesias ò

Children: Acrodynia òEncephalopathy òAutonomic: Tachycardia; Hypertension;

Sweating on trunk òInsomnia; Weight loss; Constipation

òDiagnosis: 24 hour urinary excretion òInorganic toxicity only ò

Treatment: ?Chelation; Spironolactone

 Optic Nerve & Eye

òAtaxias òFriedreich òMitochondrial ‑ NARP Syndrome: (Neuropathy; Ataxia; Retinitis Pigmentosa) òPosterior column ataxia + Retinitis pigmentosa òHMSN VI òToxic òCarbon disulfide òDisulfiram òMercury (Hg) òNutrition: Cuban neuropathy òVernant's disease

3. Cerebellum

òA‑beta‑lipoproteinemia òAtaxia telangectasia òFriedreich Ataxia ò

Paraneoplastic: Hu; CV2 òInfantile Onset Spinocerebellar Ataxia (IOSCA) òMetachromatic Leukodystrophy òRefsum òSCA 2, 3, 4

4. Supratentorial òHereditary òCowchock Syndrome òFabry's òHexosaminidase A (Late Onset) òMulti‑Infarct Dementia (CADASIL) òPorphyria òPrion protein (PrP27‑30)

mutation: Glu200Lys òPolyglucosan body syndromes òFamilial ALS: Higher prevalence of dementia (~15%) than sporadic ALS òInfections òHIV òLyme disease òRabies òSyphilis òInflammatory & Immune òSarcoid òVasculitis òMetabolic òThyroid òVitamin B12 deficiency òHypophosphatemia òMitochondrial: òMELAS (Mitochondrial Encephalomyopathy; Lactic Acidosis; Stroke)

òMERRF (Myoclonic Epilepsy; Ragged Red Fibers

òMNGIE Syndrome (Myopathy and external ophthalmoplegia; Neuropathy; Gastro‑Intestinal; Encephalopathy) òMotor neuron disorders with dementia

(Sporadic) òWestern Pacific ALS òFrontal Dementia followed by motor system disease òUpper motor neuron: Especially bulbar òLower motor neuron: Fasciculations; Less prominent weakness ò? Atypical Creutzfeld‑Jacob syndromes òNeoplastic: Lymphoma (angiotropic large‑cell); Carcinomatous meningitis òParaneoplastic (anti‑Hu) òToxic: Alcohol; Anticholinergic; Arsenic; Lead; Mercury; Podophyllin; Thallium; Vacor

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