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With a heavy heart, we share the news of Dr. John McDougall’s passing. A visionary physician and author, beloved husband, father, grandfather, brother, mentor and friend, Dr. McDougall died peacefully at his home on Saturday, June 22nd, at the age of 77.
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Alzheimer's Disease

The fundamentals of the McDougall Program are simple yet often difficult to implement. Learn about the 12-Day McDougall Program - a life-saving medical program that empowers participants with the knowledge and practical steps needed to live a vibrant, long life. For questions on whether a change in diet can help your ailment, learn more about our consultations.
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In patients having Alzheimer’s disease the brain is somewhat shrunken and, on postmortum examination, a definite loss of nervous tissue is noted. Examination of the brain tissues under a microscope reveals small bundles of material called senile plaques, scattered throughout the tissues. The more plaques that are present, the worse is the mental condition of the patient. Chemical analysis reveals the presence of the metal aluminum at the core of each plaque and within many of the cells found in the plaques. Evidence is accumulating to indicate that aluminum may be involved in the formation of the plaques, and it is therefore a prime suspect as the initial cause of the disease.

Five population studies now link Alzheimer’s disease to aluminum in drinking water. As early as 1885, aluminum was shown to be toxic to the nervous tissues of animals. Aluminum can also produce a degeneration of the nervous tissues in cats and rabbits that resembles in some ways that seen in the brains of human patients with Alzheimer’s disease. Patients with diseased kidneys accumulate large amounts of aluminum in their bodies from medications and from kidney-machine solutions that have been used until recently. This accumulation results in a severe mental deterioration.

Aluminum is the third most common element in the earth’s crust. “Normal” dietary intake of aluminum is about 3 to 5 mg per day, of which only a very small amount is absorbed by the body’s tissues. The aluminum to which we are exposed comes from many sources, and most of these are under our control. Dust, water, and even unprocessed foods contain aluminum that may be difficult to avoid. But aluminum in cosmetics, many medicines, food additives (for example, some brands of baking powders, and highly absorbable aluminum maltol used in instant chocolate mixes), cans, kitchenware, and utensils can be easily avoided. A very popular antacid, Amphojel, consists of aluminum hydroxide.

Most of this daily intake is eliminated by healthy kidneys. However, some individuals seem to absorb aluminum more readily, or are less able to eliminate it; these people, who cannot be identified before symptoms begin, are most likely to suffer from Alzheimer’s disease. Certainly not every one of the multitudes of us who have been fed for a lifetime on foods cooked in aluminum pots and pans will end our days in this world as severely mentally deficient patients. Aluminum is only one strongly suspected culprit. Scientists believe that other factors, yet to be identified, are involved in the interactions that allow the body to suffer this form of degeneration.

Some scientists are particularily worried about inhaled aluminum because autopsy studies have shown a high proportion of senile plaques in the olfactory (smelling) lobes of the brain. Spray antiperspirants would be a likely product for this concern.

Your choice of cookware is important. Glass and porcelain are relatively nonreactive with foods. Metal cookware does react with the acids in foods and the metal ions thereby released gain access to your body. In the case of copper, iron, and stainless steel cookware the metals are actually essential trace elements, and therefore make a valuable nutritional contribution if they are not absorbed in excess. Aluminum, on the other hand, not only has no recognized function in the body, but is toxic.


  • Recommendations
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    Based on present information prudent action would be to avoid all sources of ingestable and inhaled aluminum. Those who fail to heed this advice will serve as “guinea pigs” for the human experiments that may eventually prove the presence or absence of serious health effects of aluminum.

    Two years of investigation were reported in the Lancet in 1991 using an aluminum chelating agent, desferrioxamine, to slow the progress of Alzheimer’s disease. Between 1979 and 1987 there has been a thirteen-fold increase in the number of deaths from Alzheimer’s disease in the United States. To me this represents the increase in exposure to aluminum that has happened to people in our society.


  • References
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    Krishnan, S. Aluminum toxicity to the brain. Sci Total Environ 71:59, 1988

    Bertholf, R. Aluminum and Alzheimer’s disease: prospectives for a cytoskeletal mechanism. CRC-Crit Rev Clin Lab Sci 25:195, 1987

    Candy, J. Aluminosilicates and senile plaque formation in Alzheimer’s disease. Lancet 1:354, 1986

    Perl, D. Aluminum neurotoxicity–potential role in the pathogenesis of neurofibrillary tangle formation. Can J Neurol Sci 13(4 suppl):441, 1986

    Edwardson, J. Aluminosilicates and the ageing brain: implications for the pathogesesis of Alzheimer’s disease. Ciba Found Symp 121:160, 1986

    Martyn, C. Geographical relationship between Alzheimer’s disease and aluminum in drinking water. Lancet 1:59, 1989

    Birchall, J. Aluminum, chemical physiology, and Alzheimer’s disease. Lancet 2:1008, 1988

    Shore, D. Aluminum and Alzheimer’s disease. J Nervous and Mental Disease 171:553, 1983

    Perl, D. Uptake of aluminum into the central nervous system along nasal-olfactory pathways (letter). Lancet 1:1028, 1987

    Cowburn, J. Aluminum chelator (transferrin) reverses biochemical deficiency in Alzheimer brain preparations (letter). Lancet 1:99, 1989

    Greger, J. Aluminum content of the American diet. Food Technol 39:73, 1985

    McLachlan D. Intramuscular desferioxamine in patients with Alzheimer’s disease. Lancet 337:1304, 1991.

    Increase in incidence of Alzheimer’s disease. JAMA 265:313, 1991.