Scientists at the University of Calgary have demonstrated that trace amounts of mercury can cause the type of damage to nerves that is characteristic of the damage found in Alzheimer's Disease (AD). The level of mercury exposure used was well below those levels found in humans with mercury/silver amalgam dental fillings. [Leong, CCW; Syed, NI; Lorscheider, FL. Retrograde Degeneration of Neurite Membrane Structural Integrity of Nerve Growth Cones Following In Vitro Exposure to Mercury. NeuroReport, 12(4):733-737, 2001.]

The exposure to mercury caused the formation of "neurofibrillar tangles," which are one of the two diagnostic markers for AD. The scientists found that a number of other materials, including aluminum, did not cause the characteristic damage.

The research, published in a peer-reviewed medical journal, is accompanied by a dramatic video visual presentation. Utilizing digital time-lapse photography, this video shows the rapid damage to the nerve cells after the introduction of minute amounts of mercury.

Upon introduction of the mercury, the stripping away of the protein tubulin from the nerve can be seen. The tubulin forms the skeletal structure for the nerve. When the tubulin is stripped away, the bare nerve fiber is left unsupported, resulting in the "neurofibrillar tangles" characteristic of Alzheimer's Disease. The video also contains an animated description of this process.

It is important to the public health that the information from this study is widely revealed through the media. An addendum to this newsletter provides the details for members of the media to obtain the video for use in their outlet. This new study provides a dramatic culmination of years of research investigating a possible connection between mercury and Alzheimer's Disease. Abstracts of the following studies are provided in the "Science" section of this newsletter.

Scientists at the University of Kentucky began a series of autopsy studies in the 1980's. They conducted autopsy studies on AD victims and compared the levels of various heavy metals and other elements in the brain tissue to that of controls.

In the first study, bulk gray- and white-matter specimens were investigated. [Ehmann, WD et al. 1986.] The most significant differences between AD victims and controls were large elevations of mercury and bromine and depletion of rubidium in the AD brain.

Next, the scientists determined the element levels in the specific brain areas involved in AD. [Thompson, CM et al, 1988.] These were the hippocampus, amygdala, and the nucleus basalis of Meynert (nbM). The elevation of mercury in AD nbM as compared to controls was the largest element imbalance found. Mercury levels in the amygdala of AD brain were also much higher. The authors stated (page 5): "The source of the Hg in brain is not known, although environmental pollution and dental amalgams have been widely suggested."

Finally, element levels in subcellular fractions (nuclei, mitochondria, microsomes) were examined. [Wenstrup, D et al, 1990.] Again, elevations of mercury and bromine and depletion of rubidium were found. The mercury elevation was found in all fractions of AD brain, although it was significantly elevated in the microsomal fraction. Again, the authors stated (page 130): "The source of the brain Hg in AD is not known although dental amalgams and environmental sources such as seafoods are potential sources."

Another team of researchers at the University of Kentucky and other scientists at the University of Calgary, then began investigating the pathology of Alzheimer's Disease at the molecular level. It had been previously demonstrated that the formation of neurofibrillar tangles in Alzheimer's Disease (AD) was a result of an interruption of tubulin polymerization.

Molecular experimentation at the University of Kentucky on rats found that this same type of lesion could be produced by exposure to mercury, and that this damage was irreversible. [Duhr, EF et al, 1991; Duhr, EF et al, 1993.]

Next, scientists at the University of Calgary conducted an in vitro and in vivo (rats) study that confirmed the findings that mercury inhibited the neuronal proteins tubulin and actin. This resulted in loss of the skeletal structure of the neurons, which is the characteristic of neurofibrillar tangles. [Palkiewicz, P; Zwiers, H; Lorscheider, FL, 1994.]

To date, the research had utilized ionic mercury. Now the two groups of scientists joined together to investigate the effects of inhaled mercury vapor (the major exposure route of dental amalgam mercury). [Pendergrass, JC et al, 1997.] The mercury vapor exposure levels used were consistent with the levels experienced by many humans with mercury/silver amalgam dental fillings.

The effect on the tubulin of nerve structure was even more dramatic. The average mercury concentrations in rat brains increased 11-47 fold with the duration of exposure to mercury vapor. These levels were similar to the levels found in human AD victims. The identical neural lesion to that found in human AD victims was seen in the rat brains, at an occurrence of 41-74% compared to control tissues.

Alzheimer's Disease (AD) cannot be accurately diagnosed in the living human. AD can only be distinguished from other dementia disorders on autopsy, with the finding of the two characteristic AD markers - neurofibrillar tangles and amyloid plaques. There is considerable controversy in the scientific community as to which of these two markers is the more significant.

Further indication of a relation between mercury and AD was provided by a study published in 1998. [Hock, D et al, 1998.] The study found that victims of AD had blood mercury levels more than two-fold higher than did controls. In early onset AD patients, the blood mercury levels were almost three-fold higher than in controls. The blood mercury levels were significantly correlated to the levels of amyloid beta-peptide in the cerebrospinal fluid.

In 2000, scientists in Switzerland published a study that demonstrated that extremely low levels of mercury could cause the formation of amyloid plaques on nerve tissue. [Olivieri, G et al, 2000.] The authors concluded (abstract): "These results indicate that mercury may play a role in pathophysiological mechanisms of AD."

In the face of all of this published research, the dental profession continues to try to contradict a connection between dental amalgam mercury and Alzheimer's Disease.

One study, published in the journal General Dentistry, compared mercury urine concentrations from AD victims to controls. [Fung, YK et al, 1996.] They concluded that AD victims do not have a greater body burden of mercury than controls. Of course, they failed to mention that even the American Dental Association has formally acknowledged that "the distribution of mercury into body tissues is highly variable and there appears to be little correlation between levels in urine, blood or hair, and toxic effects." [JADA, 109, page 470, Sep 1984.]

Two additional studies were published in the Journal of the American Dental Association. [Saxe, SR et al, 1995; Saxe, SR et al, 1999.] These studies both concluded that mercury from amalgam dental fillings are not connected to AD. Actually, the latter study even concluded that there was no correlation between the presence of amalgam fillings and brain mercury levels in the subjects, a conclusion that is contradicted by a number of other published studies.

It should be noted that all three of these studies, commonly referred to by organized dentistry as "The Nun Study," were published in dental journals. Their findings and conclusions are contradictory to studies published in peer-reviewed medical scientific journals.

Alzheimer's Disease is a devastating disorder that has an immeasurable impact on the lives of its victims and their loved ones. Nobody that has encountered the disease can deny its horror.

Presently, the cause of Alzheimer's Disease is "unknown" and, worse yet, there is no cure. Diagnosis of the condition cannot be accurately made on the living. On autopsy, two diagnostic markers are characteristic of the disease; 1) neurofibrillar tangles, and 2) amyloid plaques. The medical community is uncertain as to which of these two is more significant if, indeed, either is more significant than the other.

Research conducted by reputable medical scientists and published in valid peer-reviewed medical scientific journals has demonstrated that mercury, in extremely small quantities, can cause both of these characteristics.

Several facts are acknowledged by all involved in the controversy over the safety of mercury/silver amalgam dental filling; 1) the fillings are circa 50% mercury, 2) the amalgam mercury exits the fillings continuously, 3) stimulation of the fillings (chewing, heat, brushing, etc.) greatly increases the release of mercury from the fillings, 4) dental amalgam mercury enters the body of the patient and builds up with time, 5) amalgam mercury from mothers has been scientifically traced to the brain tissues of unborn babies and into newborns from nursing mothers, and 6) the amount of human exposure to mercury vapor that is without harm is unknown.

The amount of published research demonstrating that mercury can cause the type of damage found in Alzheimer's Disease is absolutely compelling. The three studies in contradiction were all published in dental journals, rather than appropriate medical scientific journals.

Action on this issue must NOT be delayed any longer! Every congressman in the United States and Member of Parliament in Canada must be made aware of this evidence, and urged to take immediate action to protect their citizens!

Source: BioProbe Newsletter

Also make sure to read these books: Poison in Your Teeth: Mercury Amalgam (Silver) Fillings...Hazardous to Your Health! and Mercury Detoxification by Tom McGuire