* I am preparing a memo on the connection between AD and amalgams for a physician who is doing research on Alzheimer's Disease (AD) here in the Twin Cities. He doesn't know me, and I have no way to know whether he'll give my memo more than two seconds. I'm hoping that he will be intrigued enough about the amalgam-AD connection that he will persuade some of his AD patients to have my dentist take their amalgams out. I find the Boyd Haley theory you have explained quite exciting. It helps me tie up a lot of data on amalgams and AD into a single hypothesis. Here's what I think we know:

* From: Kip Sullivan <kiprs@IX.NETCOM.COM>

(1) According to a 1993 study at Duke U., three in four AD victims carry the ApoE4 gene (due to a defect on chromosome 19), which causes the body to make a particular type of blood protein -- apolipoprotein E type 4 (apoE4). The July 13 Minneapolis Star Tribune carries a story about the latest Duke study, published last week in the British Medical Journal, showing that the presence of the apoE4 gene is a near-perfect predictor of AD. Specifically, the study's authors "performed genetic tests on the brain samples from 67 suspected Alzheimer's patients and found that every patient who tested positive for the gene had autopsy-confirmed Alzheimer's." A recent study in Lancet, also described in the Star Tribune story, found that every subject in the study with the apoE4 gene was confirmed to have AD while none of the people without AD had the gene.

(2) The protein made by the apoE4 gene (according to David Kennedy's explanation of Haley's thesis on this list on 2-28) cannot scavenge mercury from the brain (and other body parts?) because it "has two arginines" (I have no idea what that phrase means, but I roll with it); arginine can't lock onto mercury because it has no sulphur (mercury loves sulphur and binds to it). On the other hand, apolipoprotein type 2 has two cysteines, which do contain sulphur, while apoE3 has one cysteine and one arginine. Thus, apoE2 is a good mercury scavenger, apoE2 is a poor mercury scavenger, and apE3 is somewhere in between.

(3) At least two studies indicate ApoE2 appears to offer protection against AD (Corder et al., "Protective effect of apolipoprotein E type 2 allele for late-onset Alzheimer's disease," Nat Genet 7:180-184 [1994]; and Talbot et al., "Protection against Alzheimer's disease with APOE E 2," Lancet 343:1432-1433 [1994]).

(4) The Duke researchers found that "the information-carrying microtubules [in the brain] were more likely to break down faster in people with E4 versions of apo E, compared with people with the E3 gene" (Richard Golden, "Dementia and Alzheimer's Disease," Minnesota Medicine 78: 25-29 [1995], p. 26).

(5) Haley and colleagues have demonstrated that mercury blocks the uptake of proteins (beta-tubulin is one) which are essential to the construction and maintenance of microtubules (their studies are the ones I need help interpreting).

(6) Haley and colleagues have shown that people with AD have much more mercury in their brains than people who die without AD.

(7) Now dig this: At least one study shows that AD victims have significantly lower concentrations of mercury in their nails than non-AD victims (Vance et al, "Trace element imbalances in hair and nails of Alzheimer's Disease patients," Neurotoxicol 9: 197-208 [1988], cited in G. Mark Richardson, Assessment of Mercury Exposure and Risks from Dental Amalgam, Health Canada, Ottowa, August 18, 1995, p. 80). If your blood can't scavenge mercury, isn't it likely that you will show low levels of mercury in your nails, not to mention blood, urine, and hair? Hal Huggins is the only researcher I know who talks about "retention toxicity." The all-knowing Judge Nancy Connick said that theory was nuts. Seems to me that theory is quite insightful.

All of this suggests that researchers should check out the correlation between apoE4 and other diseases, such as Parkinson's and MS. After all, if blood cannot clean the brain of mercury, it is probably equally incapable of cleaning up other parts of the central nervous system and other body parts. If "poor excretors," to use Hal's term, are particularly prone to AD, they may well be prone to a lot of other nasty diseases.

" My only original submission to the Hg and AD connection involves cholecystectomies. I asked an Alzheimers support group how many of their family members had underwent gall-bladder surgery prior to the onset of AD. One-half replied affirmative. Bile contains the stuff filtered by the liver--like trace elements e.g. Hg, Al, Zn.... The liver excretes bile into the GB where it is held until it is deposited on passing stool (about to be eliminated from the body). When the gall-bladder is removed, the bile is dumped into the colon where it may be reabsorbed.

My "theory" is that cholecystectomy exacerbates a preexisting problem like in those with an impaired means of removing trace-elements (Apoe4). IMHO cholecystectomy is one more step beyond the threshold of what the body will bare--in those individuals with a high-load of (for instance) Hg, the inability to efficiently eliminate bile aggravates the situation. I can find no studies regarding any disease etiology and cholecystectomy--perhaps "acceptable risk" again.There are studies that show ApoE effects gall stone composition."

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