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Alzheimer's Disease

Alzheimer’s disease (AD) is considered a disease of unknown etiology. However, it is widely accepted that most AD is not directly genetically inherited and that some external vector, such as a toxicant exposure or an infection, must be involved for the disease to progress into a clinically observable condition. In the USA the rate of AD is very similar for rural versus urban peoples and it does not vary appreciably from state to state. Therefore, if a toxicant is involved then this toxicant must be of a very personal nature, like what we eat or what is placed into our bodies through other sources such as dental fillings, vaccines, etc.

The involvement of infectious agents, such as bacteria, virus or yeasts, while possible at this time seems not to be directly involved. This is based on the huge amount of U.S. National Institutes of Health and other world-wide funds spent on AD to identify the causal factors and they have not detected a consistent microbial vector. If an infectious agent were involved (like in AIDS and polio) it seems as if it would have been identified by now. However, focal infections caused by microbes in the oral cavity (root canals) must still be considered as these microbes are known to produce toxicants such as hydrogen sulfide, methyl-mercaptan, gliatoxin and other compounds that inhibit thiol-sensitive enzymes.

A distinguished university professor, speaking before a gathering of an international doctors group, said he believes a buildup of the toxic mineral mercury is the leading cause of Alzheimer’s disease, the debilitating illness that afflicts older people and leads to memory loss, confusion and general mental deterioration.

“Mercury and only mercury, causes all the diagnostic hallmarks of Alzheimer’s disease,” said Dr. Boyd Haley, chairman of the University of Kentucky ’s Department of Chemistry, at the June 2004 meeting of Doctors for Disaster Preparedness in San Diego , California . Haley is a biochemist. Some of his publications can be found in The Proceedings of the National Academy of Science. Haley also said that this element causes all the abnormal biochemical reactions that kill neurons and cause the disease.

The National Institutes of Aging, however, claim there is no known cause.

According to Dr. Haley, Mercury(II) or Hg²⁺, is neurotoxic and when exposed to normal brain tissue homogenates, is capable of causing many of the same biochemical aberrancies found in Alzheimer’s diseased brain. Also, rats exposed to mercury vapor show some of these same aberrancies in their brain tissue. Specifically, the rapid inactivation of the brain thiol-sensitive enzymes tubulin, creatine kinase and glutamine synthetase occurs on the addition of low micromolar levels of Hg²⁺ or exposure to mercury vapor, and these same enzymes are significantly inhibited in AD brain. Further, extended Hg²⁺ exposure to neurons in culture has been shown to produce three of the widely accepted pathological diagnostic hallmarks of AD. These are elevated amyloid protein, hyper-phosphorylation of Tau, and formation of neurofibillary tangles.

The hypothesis is that mercury and other blood-brain permeable toxicants that have enhanced specificity for thiol-sensitive enzymes are the etiological source of AD. Included in this category are other heavy metals such as lead and cadmium that act synergistically to enhance to toxicity of mercury and organic-mercury compounds, like thimerosal that is found in vaccines and other medicines. This hypothesis is also able to explain the genetic susceptibility to AD that is expressed through the APO-E gene family. Specifically, a reduction of APO-E gene types carrying cysteines decreases the ability to remove mercury and other thiol-reactive toxicants from the cerebrospinal fluid. This increases brain exposure to thiol-reactive toxicants and the risk of AD.

Haley found that laboratory cultures of neurons, when treated with mercury, form the tangles and deposits observed when the brains of people with AD are autopsied. Structures, called microtubulin, inside neurons degenerate to form tangles. A soluble protein, called tubulin, becomes insoluble to form the deposits. Both tubulin and creatine kinase are proteins that bind the nucleotides GTP (guanosine-5’-triphosphate) and ATP (adenosine-5’-triphosphate), respectively.

Mercury poisons an enzyme that converts glutamate to glutamine in the brain. Unconverted glutamate kills brain cells. According to Haley, mercury poisons more enzymes than any other toxic metal. Released into Minamata Bay in Japan in the 1950s, mercury contamination has been blamed for a disastrous outbreak of neurological diseases there.

Haley’s group’s first finding was simple and straight-forward. After testing numerous heavy metals they observed that only Hg²⁺ could mimic the AD effect in homogenates of normal brain at concentrations that might be expected to be found in brain. The observation was that Hg²⁺ at very low micromolar levels (@ 1 micromolar) could rapidly and selectively abolish the GTP binding activity of tubulin (M_r = 55,000 daltons) without any noticeable effect on the other GTP binding proteins observed at an M_r of about 42,000 daltons, that are present in both control and AD brain at approximately equal levels.

Therefore, concerning heavy metals the addition of only mercury at low micromolar levels to control brain homogenates gave a GTP binding profile that was identical to that observed in AD brain and that chelation of Hg²⁺ by EDTA did not prevent but enhanced this effect. Further, additional results have shown that the addition of Hg²⁺ to control brain homogenates not only caused the decrease in nucleotide interaction but could also support the abnormal partitioning of tubulin into the particulate fraction as observed in AD brain. This was especially effective in the presence of other divalent metals, such as zinc, which is elevated in AD brain.

For any toxicant, or class of toxicants, to be proposed as involved in the etiology of AD they must be available equally to individuals living in markedly different locations. The toxicant proposed must explain the genetic susceptibility concept of AD. Further, under experimental conditions the toxicants must be able to cause the exacerbation of the many biochemical aberrancies found in AD brain. Based on Haley's research and a literature review, mercury and mercury containing compounds from dental amalgams, vaccines, other medicinals and preservatives used in paints, seed grains, etc. represent a class of compounds that fill this requirement.

Mercury and organic mercurials are neurotoxicants. Further, the enzyme inhibitory effects of mercury are synergistically enhanced by exposures to other toxicants such as lead and cadmium (smokers). Even the simultaneous presence of EDTA (ethylene-diamine-tetraacetic acid, a common food additive) or metal binding antibiotics such as tetracycline can enhance mercury toxicity. Therefore, any determination of a safe level of mercury exposure using rats in a cage being feed carefully monitored food and water is not reliable for determination of a "safe level of exposure to mercury" for humans. The fact is that science does not know what the combined toxic effects of many toxicants or enhancers of toxicity would be if present with mercury and therefore cannot identify a safe level of exposure.

Therefore, thiol-reactive toxicants such as mercury, cadmium, lead and certain organics are rational suggestions as being exacerbating factors for AD, or possibly even causal. However, mercury is the one toxicant that has been shown to reproduce many of the biochemical aberrancies and diagnostic hallmarks of AD. Also, mercury exposure is readily available to most humans. It is reasonable to propose that exposure to mercury is one of the major toxic factors involved in early onset AD. Further, that simultaneous exposures to other toxicants or factors enhance the toxicity of mercury and hasten the onset of AD, especially in those individuals who are genetically susceptible.

The fact that mercury has inhibitory effects on tubulin, CK and GS and that these proteins are proven to be aberrantly inhibited in AD does not alone conclusively prove that mercury exposure causes AD. However, it definitely proves that chronic, daily exposure to mercury would at least exacerbate the clinical conditions of AD. Is such an exposure to mercury likely? The answer is yes, and this makes mercury involvement in AD plausible.

First, the question must be addressed if there is enough mercury in an amalgam filling to continue a low chronic level exposure for years? The answer is yes. For example, if a single large amalgam filling contained 1 gram of mercury (1 million micrograms) and lost a significantly toxic 10 micrograms per day there would be enough mercury for 100,000 days or about 274 years of exposure. A small, one-tenth gram mercury filling would last 27 years. So enough mercury is within amalgam fillings to provide a consistent chronic toxic exposure for the life of most fillings. Dental amalgams, or "silver fillings" as organized dentistry calls them, are approximately 50% mercury by weight and it is quite easy to demonstrate that mercury vapors readily emit from these fillings. The actual amount can only be determined with the amalgam in a closed container and the amount of mercury released being determined using solid, time proven chemical techniques and instrumentation. The accurate level of mercury released cannot be accomplished on amalgams in the mouth. In a carefully designed study in a sealed container Chew et al. tested the "long term dissolution of mercury from a non-mercury-releasing amalgam (trade name Composil)." Their results demonstrated "that the overall mean release of mercury was 43.5 +/-3.2 micrograms/cm²/24hr, and the amount of mercury released remained fairly constant during the duration of the experiment (2 years)."

In Haley’s opinion, this 43.5 micrograms/cm²/day is not an insignificant amount of mercury exposure if one considers the number of years a 70 year old individual living today may have been exposed to chronic mercury levels from his amalgams. Additionally, 43.5 micrograms/cm²/day is the level released without galvanism, excess heat, or pressure from chewing, all factors that increase mercury release from amalgams in the mouth. Brushing with a toothbrush causes10 times more vaporization, and drinking hot liquids, like coffee, causes another 10-fold increase in emission.Furthermore, soaking amalgams in water produces a solution that kills neurons in culture.

A great deal of the research on which Haley bases his conclusions has been accomplished in other countries. There have been numerous published reports of increased tissue mercury levels in subjects and the relationship to increased number of amalgams fillings. Also, the World Health Organization Scientific Panel found ranges of mercury exposures from 3 to 70 micrograms/day with the bulk being from amalgam fillings. However, the dispensers of money for research in the United States , like the FDA, the NIH and the Alzheimer’s Research Foundation, generally refuse to support research on toxic metals as a cause of disease. The Institute of Medicine of the National Academy of Science also discourages such research. Hundreds of millions of dollars are spent yearly on AD research.

AD has devastating effects not only on the victims, but also on their families; it involves a heavy financial burden. Total direct and indirect costs have been estimated to be at least $100 billion annually. These are expected to increase, not only because of inflation, but also because of increasing numbers of AD patients. In 2000 there were about 4.5 million of them. In 2050 there may be 11 million to 16 million.

Average cost of care for the eight- to 20-year duration of this illness has been estimated to be $174,000. Nursing homes chare $42,000 to $70,000 a year. For the 70 percent who are cared for at home, supplemental care runs about $12,000 annually.

The Alzheimer’s Association claims that the best available scientific evidence shows no relation between these fillings, which typically contain 50 percent mercury that, in certain forms, is known to be toxic to the brain and other organs. The group says amalgam fillings emit small amounts of mercury vapor when they are installed or removed and as they wear. The organization also says that mercury affects some of the biochemical processes implicated in AD. But they add that an FDA panel concluded in 1991 that there was no evidence that amalgam fillings pose any danger.

Haley says that research by people in his department and the AD research department at Kentucky showed that AD brains contained mercury and that the concentration of mercury in patient’s fingernails decreased as the disease progressed. This indicated increasing difficulty in excreting this substance. After Haley’s report was issued, his grant was terminated. NIH then funded a study by Dr. Stanley R. Saxe, a dentist at the university. His research, published in the Journal of the American Dental Association, stated that there was no significant association between AD and any aspect of amalgam fillings and no correlation between AD and levels of mercury in AD brains.

Critics have disputed Saxe’s findings noting that Saxe must be a very unusual dentist. Very few dentists are experts in neurological diseases. Saxe’s research and a review of the health effects of mercury published in The New England Journal of Medicine in October 2003, underpin the endorsement of amalgam fillings as safe by the FDA, the Public Health Service and the World Health Organization. The American Dental Association informs dentists that amalgam fillings are safe. On the other hand, Haley claims that there are no studies in the scientific literature proving that mercury does not vaporize from amalgam fillings. The FDA has no data to refute his claims, nor have they funded any studies to show that amalgam fillings are safe.

People also acquire this metal from coal-fired power plants, preservatives in vaccines and fish. People used to be exposed by handling liquid mercury and by breathing air in rooms where mercury from broken thermometers had spilled on the floor. Gold miners still use mercury to recover gold, and large quantities are said to get into rivers in Brazil from this source.

Our bodies have a protein that protects us from toxic metals. About 67 percent of this is located in our digestive systems, so mercury in fish is probably not as bad as that from other sources. Each dose of influenza vaccine contains 25 micrograms of mercury in thimerosal, a preservative. Given to someone weighing 220 pounds, this amounts to 2.5 times the amount of mercury the FDA and EPA say is safe to take in a day by mouth. Given to a 110-pound person this is five times the amount. This does not enter our digestive system, where the bulk of our protection against mercury is located. Therefore you might expect it to have an even more toxic effect.

It would be interesting to know why the Institute of Medicine is discouraging research on the relationship between toxic metals and disease. Is it possible that, where lots of money is involved, as Haley suggests, conflicts of interest can arise that impact people’s health?