Alzheimer's disease (AD) is a chronic, degenerative condition that affects over five million Americans. It was first described by the German physician Alois Alzheimer 80 years ago.
Alzheimer's disease is characterized by progressive memory loss and deterioration of intellect and judgment. This is followed by loss of coordination and ability to perform motor functions. Incontinence of urine and feces occurs and there is a loss of ability for self-care. Actual diagnosis is only possible at autopsy, where senile plaques and neurofibrillary tangles are visible in brain specimens viewed under the microscope.
Although Alzheimer's disease is only one cause of dementia, it is responsible for at least half the senile dementia in America.
A number of hypotheses have been advanced for the cause of Alzheimer's disease, including genetic factors, neurotoxins (aluminum), acetylcholine deficiency and deficiency of calcium, magnesium, zinc, copper and iron.
Alzheimer's disease is more prevalent in certain families. This could be due to a genetic factor. However, there could be other reasons for the familial tendency. Nutritional imbalances and toxic metals are passed on from one generation to the next. This could cause an increased incidence in some families. People living together are also exposed to environmental toxins, water pollutants, etc., which could account for familial patterns of the disease.
Individuals with Down's Syndrome, a genetic disorder, who survive to age 40 almost invariably develop the neuropathology of Alzheimer's disease. This has suggested a genetic link between these two conditions.
Aluminum is unquestionably toxic to the nervous system. Although there appears to be a link between aluminum and Alzheimer's disease, it is not certain that aluminum is the causative agent. The following is known:
We have found that high aluminum in the hair is not present in all Alzheimer's patients. However, it is possible that aluminum is present in brain tissues even though it is not revealed on the hair test. This possibility exists because the hair mineral tests may not detect a metal if it is not concentrated in the hair tissue.
Also, it is postulated that aluminum may have a particular affinity with damaged neurons. It is thus possible that excessive aluminum may be present in brain tissue, but will not be revealed on a hair mineral analysis.
The majority of the toxic metals, including lead, mercury and cadmium, are known to be neurotoxic. W. D. Ehmann, W. R. Marksbery, M. Alauddin, T. I. M. Hossain and E. H. Brubaker reported in Neurotoxicology 7(1):197-206 (1986) that levels of bromine and mercury were elevated in AD brains and the mineral rubidium was depleted.
D. E. Vance, W. D. Ehmann and W. R. Marksbery reported in Neurotoxicology 9(2):197-208 (1988) that bromine and zinc was elevated in AD hair tissue, while calcium and cobalt levels were reduced.
These and other studies indicate that several toxic metals may play a role in the development of Alzheimer's disease. A complicating factor is that perhaps several metals play a role, but no single toxic metal is responsible for all cases. In cases such as these, studies would be inconclusive if only a single toxic metal is studied.
Serious deficiencies of the neurotransmitters acetylcholine, norepinephrine and serotonin have been observed in the brains of Alzheimer's patients. Most research has focused on the deficiency of acetylcholine. A deficiency of acetylcholine could help explain symptoms of Alzheimer's such as memory loss and loss of motor functions.
Acetylcholine is produced at nerve synapses from choline and acetyl Coenzyme A. The reaction is catalyzed by the enzyme choline acetyltransferase. Although studies are underway to help restore acetylcholine activity by supplying precursors, as of this writing, results have not been encouraging.
A possible connection exists between aluminum and acetylcholine deficiency. Research shows that aluminum inhibits cholinergic activity. Compounds used in antiperspirants may inhibit synaptic uptake of dopamine, norepinephrine and 5 hydroxytryptamine. Aluminum has also been shown to inhibit Na-K-ATPase and hexokinase. These are critical enzymes for energy metabolism.
A calcium deficiency may directly cause symptoms in Alzheimer's disease, or may be important indirectly by allowing aluminum to accumulate in brain cells.
Parkinsonism dementia and amyotrophic lateral sclerosis are neurodegenerative diseases that are endemic among Guamanian and Kii Peninsula Chamorro Indians and are characterized by neurofibrillary tangles. These endemic diseases have epidemiological features that strongly indicate that environmental factors may play an important role. The soils of these areas are particularly rich in aluminum and iron, while deficient in calcium and magnesium.
There are indications that aluminum increases parathyroid activity that reduces calcium levels and causes calcium to be withdrawn from brain tissue. The loss of brain calcium may be the major cause of Alzheimer's disease.
Mayor and coworkers reported that increased parathyroid hormone activity can increase intestine and brain absorption of aluminum.
Dialysis patients, in particular, display increased fractures when their drinking water is high in aluminum and low in calcium. The exact mechanism for the mineralization problem is unknown. It appears that aluminum affects the activity of alkaline and acid phosphatase and modifies the response of these enzymes to parathyroid hormone and vitamin D.
The calcium/aluminum connection could help explain why other biochemical imbalances which interfere with calcium metabolism - lead poisoning, phosphates in soda pop, copper imbalance, manganese deficiency which affects thyroid function, etc., could contribute to the causation of Alzheimer's disease.
A principal way that aluminum appears to express toxicity is that it replaces magnesium ions at critical target sites in the cell.
"...chemically, aluminum is quite similar to magnesium... aluminum can compete effectively for magnesium binding sites in biological systems... aluminum binding to ATP is 7 to 10 times stronger than magnesium, so even at very low concentrations (nanmolar) aluminum can potentially interfere with magnesium-dependent systems..." Berthoff, pp 250
"The relative binding strengths of the ligands will determine the pathway of aluminum in vivo and its competition with other metal ions such as Mg2. For example, the hexokinase reaction is the first step in the metabolism of glucose in which ATP-Mg is involved in the formation of glucose-6-phosphate. In vitro, aluminum inhibits this reaction by binding to ATP 10 times more strongly than Mg2, forming inactive ATP-Al. However, activity is restored in the presence of citrate because citrate binds aluminum 20 times more strongly than ATP. (The Lancet, Oct. 29, 1988, p.1008)
Garruto et al. have suggested that hyperparathyroidism secondary to calcium and magnesium deficiency may enhance aluminum absorption. The role of parathyroid status in aluminum accumulation in dialysis patients has been much debated, but no consistent relationship has emerged from the data.
R. J. Boegman and L. A. Bates reported that the effect of aluminum on catecholamine balance appears to depend on copper, zinc, iron and magnesium in the diet. (Can. J. Physio. Pharmacol. 62:1010 1014, 1984). Diets low in these minerals cause enzyme deficiencies which are restored to normal activity by the addition of aluminum.
This is of interest because it is known that most of the enzymes concerned with DNA replication and repair are zinc-dependent. Zinc and magnesium are commonly deficient in modern diets. Perhaps dietary modifications or supplementation could help prevent replacement of vital metals by aluminum and thus prevent the onset of Alzheimer's disease.
The ionic radius of aluminum closely resembles that of iron and the hydrolysis behavior of Al3 and Fe3 in aqueous solution are also very similar. Aluminum follows the iron pathway in the extracellular environment in being bound to the iron transport proteins transferrin and lactoferrin. (The Lancet, October 29, 1988, P. 1008)
In our research, we have repeatedly noted a direct correlation between iron and aluminum levels on tissue mineral tests. If aluminum can displace iron, this may impair critical iron-bearing enzyme systems, including the catalase system and the electron transport system. Defects in either system could cause cellular dysfunction and destruction.
Therapeutic attempts to remove aluminum from brain tissue by the administration of chelating agents has, thus far, been unsuccessful in improving the clinical signs of Alzheimer's disease. Aluminum chelation with desferrioxamine, a chelating agent, has been quite effective in reversing dialysis dementia. It is possible that the intranuclear binding of aluminum in Alzheimer's disease precludes removal by chelation.
A recent newspaper headline stated, "Scientists in southern California have found the first compelling evidence that the brain fights back while under attack by Alzheimer's disease, a major cause of early senility in the elderly. " Studies of tissue taken from the brains of deceased Alzheimer's victims showed that even as the disease destroyed nerve cells, others begin creating connections, desperately trying to rebuild brain circuitry.
This is, of course, a compensatory action, not a clinical reversal of the destructive process involved in Alzheimer's disease. It does however indicate, that some degree of reversal may be possible.
Our clinical experiences are those early signs of memory loss and decreased mental function can often be reversed through specific nutritional therapy. Our approach is non-specific, meaning that we attempt to correct the entire body chemistry. We feel this is always a superior approach, especially since no single causative agent has been identified.
The hair analysis is used as a guide to improving body chemistry. A specific diet of natural foods is important. Individualized supplemental vitamins and minerals are given to enhance cellular energy production. This facilitates healing and cellular regeneration at all levels. It also improves the body's ability to eliminate toxic metals. Energy is enhanced by supplying basic nutrients required for the energy cycles and by nutritionally balancing mineral ratios that in turn improve the efficiency of energy production.
Supplementary choline may be given, although results have been mixed. Substances that enhance cerebral circulation including vitamin E, niacin and the herb Gingko Biloba, may also be helpful.
Late-stage Alzheimer's disease does not respond well to therapy in our experience.
Today Alzheimer's disease remains a challenging problem that affects many Americans. Several theories exist regarding its cause, including genetics, nutritional deficiencies and toxic metal poisoning.
A natural food diet, avoidance of aluminum exposure and an individualized supplementary nutrition program may be helpful for prevention of Alzheimer's disease. In early cases, these measures may be able to arrest or even reverse the course of the disease.
We are confident that as research on Alzheimer's disease progresses, the nutritional aspects of this illness will become clear and their importance appreciated.