Following are some extracts from the Amalgam mailing list group - which provide both pointers to causes and treatments for the illness.

The "apoE4" link?

This part of the document has some technical discussions on related questions - including the possiblility of a genetic predisposition to mercury poisioning - people with a certain gene (apoE4) are less able to naturally "scavange" mercury and are thus sensitive to much lower doses than other people. This is a very SPECULATIVE line of discussion that I find very interesting...

* From: "David C. Kennedy, DDS" <dkennedy@chem.ucsd.edu>

.....it has been shown for some time that mercury in all its forms is present in the human body when only one form is ingested. The form of mercury coming off amalgam is Hg0 which is soluble in fat. The blood brain barrier is fat (lipid) barrier and thus Hgo will transfer across this membrane. Inside the brain the common enzyme catylase will oxidize it to Hg++ which cannot egress across the polar sensitive blood brain barrier. The Alzheimer's disease is now linked to a gene which transports unneeded cholesterol out of the brain (APO-E 2,3 & 4). If the gene does not produce a transport molecule with sulfur containing amino acid binding sights some AD victims develop the disease as early as 40 years of age. On the other hand if the gene makes a molecule with sulfur binding sights the disease of AD is rarely seen even in advanced age.

The dentists have always claimed that if mercury is poisoning us we would see it in everyone. This would not necessarily be true when multiple risk factors are applied to a single event such mercury vapor exposure when a second and third factor (selenium intake and genetic predisposition) are corrected for.

... In Otzenhausen, Dr. Boyd Haley discussed in detail his research into Alzheimer's disease and how mercury is intimately involved in the process. Mercury at extremely low levels interferes with the formation of a critical protein called tubulin. Without tubulin the nerves grow into neurofibril tangles and new memory and thought ceases. That condition renders its victims senile or worse. Research at the University of Calgary has discovered the mechanism that causes this injury. The introduction of minute amounts of mercury into nerve cells causes damage to the ADP ribosilation cycle. ADP is essential to the production of the tubulin protein.

Researchers at the University of Kentucky have concluded that mercury is associated with Alzheimer's disease and dental amalgam is the most likely source. Their work has been further expanded to investigate similar neurological disorders and look specifically for the role of heavy metals in their etiology. They have found similarities in Amyotrophic Lateral Sclerosis (ALS), Parkinson's and Multiple Sclerosis (MS). One theory is that all of these diseases are essentially the same disease and genetic predisposition makes the clinical symptoms vary from patient to patient. They also stated that a third genetic factor is involved.

Mercury attaches to sulfur. In the body it is found not in free form but attached to tissue ligands or protein containing sulfur. This is how it exerts its toxic effect. The brain is high in these types of sulfur bonds and is, apparently, a slowly releasing long term reservoir for mercury. Elemental mercury vapor rapidly absorbs across the blood brain barrier.

Mercury comes off the fillings in the uncharged fat soluble state of Hg0. It readily diffuses into the blood stream and circulates several times before diffusing into the bodily tissues. Once it diffuses into the brain it will contact a family of enzymes called catylase. They reduce the Hg0 to Hg++. The charged form of mercury cannot diffuse across the blood brain barrier. It is estimated that the half life for mercury in the brain is approximately 27 years.

Dr. Boyd Haley at the University of Kentucky College of Pharmacy made another discovery. The AD brain many times has tubulin which is almost totally devoid of normal ability to bind important regulatory compounds. Tubulin is a critical protein which is found in every cell. Nerve cells contain even more than most cells. He cannot find even minute traces of tubulin with normal binding properties in the advanced AD brain.

AD brain has been studied to find out where the mercury has accumulated. It is collected in the mitochondrias well as other cell fractions. These tiny organelles are inside the nerve cells and have as their main function the production of high energy biochemical compounds used in every metabolic pathway. In nerve cell cultures mercury is an effective toxin at extremely low levels. Dr. Haley's laboratory has shown that EDTA and mercury together are much more toxic than mercury alone. Mercury II prechelated with EDTA when added to normal human brain homogenates specifically abolishes the normal binding properties of tubulin. This is the identical situation seen in AD brain homogenates with no added mercury.

I asked Dr. Haley to explain what possible role the Apo-E genes associated with AD had to do with the onset of the disease. He remarked that some people with a certain genetic make up have begun to develop AD as young as 40 years old. First one must understand the brain is protected by a system that limits the in and out molecules which is called the blood brain barrier.

The Apo-E gene regulates the production of a protein which is an active transport mechanism for cholesterol out of the brain. The function of this protein is to transport cholesterol out of the brain. Dr. Haley explained the Apo-E gene produces 3 different alliles called E-2, E-3, E-4. Each person gets two copies which may consist of two copies of each gene or any mixture such as E-2 + E4, etc. Having two copies of Apo-E 4 is indicative of early AD. Having two copies of Apo-E 2 seems to prevent early AD. Apo-E 3 seems intermediate. The difference between Apo-E2, E3 and E4 is that E2 has two cysteines, in E3 one Cysteine is replaced by an arginine, in E4 both cysteines are replaced by arginine. He explained that unlike cysteine the arginine does not pick up mercury since it contains no sulfur. Sulfur is called a mercaptan (Latin for mercury capture). Mercury loves sulfur more than other molecules. It will drop whatever it is attached to and bind with sulfur. So with the E2 people, who are less likely to get AD have a protein that carries mercury as well as cholesterol out of the brain by binding mercury with sulfur seats.

Those with Apo-E3 are intermediate AD have a lesser number of sulfur seats. Those who are more likely to develop AD have less seats available. Once mercury gets into their brains it cannot get out. I have a young lady in my practice who had all of her fillings out in 1987. She insisted that her neurologist who was treating her for multiple sclerosis test to see what her cerebral spinal fluid level of mercury was in 1994. Seven years after her last filling was removed. She says she never eats fish. Her brain fluid was 13 times higher than an ordinary person. Once mercury gets into the brain it is very difficult to remove.

Some chelating agents have been administered to try and mobilize mercury from the brain. The results clearly show that the most common medications, in fact, make the problems worse. Some new medications are now being introduced which hold the promise of better therapy for mercury poisoning. The best approach is to avoid exposure.

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