From: 23x11.5c@gmail.com   
      
   What Doctors Don't Tell You: ALZHEIMER'S DISEASE - METAL FATIGUE	    
      
   What Doctors Don't Tell You © (Volume 5, Issue 12)   
      
      
   In the search for a magic bullet, orthodox medicine ignores preliminary   
   evidence suggesting that some forms of dementia may be caused by metallic   
   poisoning.   
   In the US around four million men and women suffer from Alzheimer's disease   
   (AD), and in the UK over 600,000, mostly over the age of 65 years. As the   
   world elderly population increases, so too does the incidence of AD. The   
   disease is ultimately fatal in    
   every case, with an average seven years from onset to death.   
      
   Despite over 30 years of research, mainstream medicine has come up with   
   neither a cause nor a cure for AD. In doing so, the establishment is ignoring   
   startling new evidence that AD could be, to a large extent, an environmental   
   disease. Although AD is an    
   umbrella term, now used to characterize all sorts of dementias in the elderly,   
   recent, preliminary evidence suggests that classic Alzheimer's may have   
   something to do with poisoning from toxic metals.   
      
   Aluminium an established neurotoxin has long been linked to AD; high levels of   
   both metallic elements have been found in the brains of people with AD.   
      
   However, recent attention has focused on research published last year that   
   claims there is no connection whatsoever between aluminium and AD (Nature,   
   November 1994).   
      
   This study found no trace of aluminium in the brains of dead Alzheimer's   
   patients, and suggested that previous studies that had, did so as a result of   
   laboratory contamination, possibly through dyes used to stain the tissue for   
   analysis. This does not    
   explain why aluminium was not found in the brain tissue taken from control   
   groups, though.   
      
   It has also been suggested that the nuclear microscope the team used to   
   examine brain tissue may not have been as sensitive to aluminium as the   
   chemical method used in previous studies.   
      
   It is difficult to dismiss the many previous studies which have made a   
   connection between aluminium and AD, the latest also published only last year,   
   which concluded that their findings "are consistent with a role for aluminium   
   in the development of AD-   
   like pathology in patients subjected to prolonged aluminium exposure" (The   
   Lancet, April 23, 1994).   
      
   This lends itself to the argument that, rather than being a cause of AD,   
   aluminium may accumulate in the brain because of the disease processes. Dr   
   John Growdon stated that aluminium may act as a neurotoxin in AD, or might   
   just accumulate in dying nerve    
   cells (New England Journal of Medicine, March 18, 1993), and a 1993 study   
   concluded that aluminium and other metallic elements may gain increased access   
   to the brain through alterations in the brain and other organs (Experimental   
   Gerontology, July-Oct    
   1993).   
      
   An earlier study suggested that rather than being a cause of AD per se, high   
   levels of aluminium in the brain may cause an AD-type dementia (Ciba   
   Foundation Symposium, 1992; 169: 142-54). This is supported by high levels of   
   aluminium having been found in    
   the brains of people suffering from a brain disease known as dialysis dementia   
   (The Lancet, March 21, 1992). High levels of aluminium have also been found in   
   the brains of people with Down's syndrome, which has similar neurochemical   
   features to Alzheimer'   
   s disease. People with Down's also have a predisposition to AD (The Lancet,   
   March 31, 1990).   
      
   As well as drinking water, in which aluminium levels vary from area to area,   
   aluminium is found in foodstuffs, cosmetics, deodorants and pharmaceuticals,   
   particularly some antacids. Aluminium utensils and drink cans have also been   
   touted as a possible    
   danger.   
      
   One study found that aluminium concentration was far higher in several   
   commercially available brands of fresh and reconstituted orange juice, and   
   concluded that drinking most brands of so called fresh and pure orange juice   
   might result in far greater    
   exposure to aluminium than drinking a similar volume of tap water (The Lancet,   
   May 16, 1992).   
      
   Silicic acid and fluoride are said to protect against excess accumulation of   
   aluminium, although increased accumulation in lung, bone and brain does occur   
   with age (The Lancet, March 21, 1992).   
      
   But the most damning new research points the finger at mercury, a substance   
   rated among the most toxic known to man, particularly that present in amalgam   
   fillings.   
      
   A medical research team at the University of Kentucky in Lexington, Kentucky,   
   who have been investigating the possible link between mercury and AD, found   
   high levels of the element in the brain tissue of AD victims (Neurotoxicology,   
   1986; 7: 197-206;    
   Biol Trace Element Res, 1987; 13: 19-23), and WR Markesbery and his team found   
   that the highest trace element in the brains of 10 autopsied AD patients was   
   mercury (Brain Research, 1990; 533: 125-31).   
      
   As with aluminium, however, the Markesbery study noted that whether mercury   
   was a possible cause of AD, or simply a deposit on a degenerating brain,   
   remained to be determined. They concluded: "This and our previous studies   
   suggest that mercury toxicity    
   could play a role in neuronal degeneration in AD."   
      
   The link between mercury and AD was strengthened by Haley et al, who found   
   that mercury fed rats developed a diminished tubulin level similar to people   
   with AD. Tubulin is a protein needed for the healthy formation of nerve tissue   
   in the brain, and a    
   lack of tubulin will result in messages in the brain not connecting properly.   
   When fed aluminium, the rats displayed no change in tubulin levels (Federation   
   of American Societies for Experimental Biology, 75th Annual Meeting, 21-25   
   April 1991).   
      
   Markesbery and his team also found diminished levels of zinc and selenium in   
   the 10 AD-affected brains they examined. This is significant in that zinc and   
   selenium are known to have a protective role against heavy metal poisoning in   
   tissue.   
      
   It has also been suggested that low levels of zinc, coupled with high levels   
   of mercury, could make the brain more susceptible to aluminium deposits. Or   
   that mercury and aluminium both contribute to AD.   
      
   The Markesbery team noted that "the source of brain mercury in AD is not   
   known, although dental amalgams and environmental sources such as seafood are   
   potential sources". However, even the World Health Organization concedes that   
   the public's highest    
   daily exposure to mercury comes from dental amalgam fillings. (For a more   
   detailed analysis of the potential dangers associated with amalgam, see The   
   WDDTY Dental Handbook).   
      
      
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