The first study linking aluminum and Alzheimers disease was conducted by a group led by Klatzo. In the 31 years proceeding their initial conclusion, countless dollars have been gone towards research attempting to find a possible linkage between Alzheimers and aluminum, resulting in a wide range of conclusions.
One of the researches shows that autopsies performed on persons who have died of Alzheimer's disease have revealed accumulation of up to 4 times the normal amount of aluminum in the nerve cells in the brain. Especially high concentrations of aluminum have been found in the region of the hippocampus, which plays a role in memory.
British researchers concluded that the risk of contracting Alzheimer's disease was 50 percent higher in regions of Great Britain where drinking water contained elevated levels of aluminum. The threat from aluminum may be increased by chronic calcium deficiency, which may change the way in which the body uses minerals and result in greater accumulations of aluminum.
While the British populations must contend with the threat of aluminum-tainted water, Americans can ingest aluminum through a wide variety of products. While there is still a great deal of controversy as to whether the accumulation of aluminum in the neurons is the cause or a result of neuronal dysfunction, there is wide-spread opinion among scientists and general population, that it is best to avoid aluminum as much as possible as a preventive measure.
Elevated Aluminum Levels in the Brains of Alzheimers Disease Patients?
One of the most fundamental arguments in this debate is the presence of elevated aluminum levels in the brain tissue and the surrounding cerebralspinal fluid (CSF). Collectively, a majority of all the reviewed studies concurrred with the conclusion that the concentration of aluminum was greater in the brains of AD patients than those not afflicted with the disease. For example, a study led by M. Hollosi showed that the aluminum levels in AD patients ranged between 6 and 12 parts per million (ppm) in lesion containing areas and between 0 and 15 ppm in areas that had not gone through any noticeable degeneration, which is much higher than the amount found in non-Alzheimer disease brains.
Another study, led by P. Evans, states that, "of the various environmental factors that have been implicated, the one with the greatest amount of supportive evidence is aluminum". In the studies found that opposed the majority's consensus, methodological practices were cited as the major cause of discrepancies between the two conclusions, such as not taking into account the taclum powder inside latex examination gloves. M. Lovell and his group showed that samples analyzed and corrected for multiple substances that interfered with the measurement of the aluminum level reflected a nonexistent to minimal elevation in the concentration of aluminum in AD patients, also citing other groups that had failed to find a difference in aluminum amounts.
Also contradicting the norm is a study focusing on the concentration of aluminum in the CSF, led by E.
Kopaki. This group pointed out the controversial argument dealing with poor sampling and handling of samples and inferior analysis procedures for the level of aluminum present in previous studies of CSF. Being careful to follow a strict procedure to avoid contamination of samples and a control group with which to compare the results, the Kopaki group concluded that any possible increase in the aluminum concentration level in the brain is not evident in the CSF.
Can Aluminum Pass the Blood Brain Barrier?
An additional area dealing with aluminum in the brain that is currently in question is the extent to which aluminum present in the bloodstream is able to cross into the brain tissue. Aluminum is thought to cross the blood-brain barrier (BBB) by using the iron transport and storage systems because the solution chemistries of aluminum and iron are very similar. The hypothesis is supported by the gradual buildup of aluminum in bone and brain tissue.
A possible mechanism for crossing the BBB has been suggested as a "Trojan horse" method of transport for aluminum, where aluminum is mistaken for iron, once again because of their similar properties, and brought into the brain from the bloodstream by hematogenous macrophages and monocytes. It has also been hypothesized that the increased absorption of aluminum in the brain is enhanced by the possible increase in permeability of the BBB as a result of the development of AD.
The Effect of Aluminum on Neurofibrillary Tangles
Involved in the ongoing debate is the speculation that aluminum somehow affects neurofibrillary tangles. Initially, the scientific community believed that the high concentration of aluminum in NFTs was an irreparable event in a dying neuron. Presently, it is believed that aluminum plays a role in NFT formation by acting on the tau protein, the major component of NFTs.
Because tau contains multiple phosphorylation sites, aluminum acts as a catalyst for the nonenzymatic covalent shift of the triphosphate group from adenosine triphosphate (ATP) to tau. Aluminum, having a positive charge of three, bonds with three phosphates of ATP, each having a negative charge, because the triphosphates have a higher affinity for aluminum than the adenosine. From there, the phosphates, having a greater affinity for the tau protein than the aluminum, are transferred to the protein, causing its precipitation. When this occurs, the entire triphosphate group is transferred to the protein and results in the aggregation of tau.
Also, evidence of aluminum induced NFT formation in animals has been provided as support that aluminum does affect neurofibrillary tangles. In 1965, Klatzo and coworkers reported that the injections of aluminum salts in the brains of rabbits caused NFT formation. Later, it was found that in cultured rat neurons, aluminum treatment prompts the formation of NFTs. In opposition, Lovell et al. argued that no significant differences in aluminum levels were found in "NFT-bearing neurons compared with NFT- free neurons" in AD patients. In a study performed by M.P. Mattson and colleagues, data indicated that neuronal damage and an alteration of tau did not occur with increases in aluminum. The data collected in this same study indicated that the collection of aluminum alone in neurons cannot perpetuate NFTs, the tell-tale features of Alzheimers disease.
The Effect of Aluminum on Senile Plaques
A similar argument surrounds the possible involvement of aluminum in the formation of senile plaques. The roles that beta-amyloid protein and aluminum play in this formation has been the subject of many studies. Kuroda and colleagues performed a study on this relationship and concluded that aluminum promoted the aggregation of synthetic beta-amyloid protein. Because the aggregation of beta-amyloid protein results in neurotoxicity, the elevated presence of aluminum in the brain accelerates the aggregation of beta-amyloid protein in the brain tissue, therefore, accelerating the development of senile plaques and AD.
A differing idea relating aluminum to the protein has been presented by M. Clauberg and J.G. Joshi, who speculate that aluminum could have an effect on the production of beta-amyloid protein by suppressing the inhibitor domain, making the cell incapable of suspending the production of the protein when there is an excess amount in the cell. Without anything to hold its level of production within a normal range, the beta-amyloid protein accumulates and increases the rate at which senile plaques are formed. In opposition to both of these ideas are many scientists who have failed to find a considerable elevation in aluminum levels in senile plaques. A group led by H. Jacqmin and associates concurs with the conclusion that there is no reliable evidence for aluminum in senile plaques.
Drinking Water Studies on the Effects of Aluminum
An area in which myriad studies have been conducted regarding aluminum as an environmental factor is the correlation between the number of diagnosed AD cases and the aluminum levels in public drinking water. The reason aluminum is added to drinking water is most commonly as a clearing agent. The amount of aluminum present in drinking water has been recommended to be below 200 micrograms per liter by the World Health Organization.
In a study conducted by D.R.C. McLachlan and colleagues, it was found that a relationship did exist between the number of diagnosed AD cases and the level of aluminum present in the drinking water supply. This study concluded that between 15,180 and 26,910 of the estimated 66,000 to 117,000 cases of AD might have been prevented if the aluminum concentration in the municipal water supply had been kept below 100 micrograms per liter. A similar study performed by H. Jacqmin and associates using different variables showed no significant effect for aluminum in drinking water when pH was not included in the experiment model, but showed a small relationship between aluminum and AD when pH was also taken into consideration.
Several other studies have shown no relationship to exist between AD and aluminum, for example, those lead by DJ Wood and A. Wettstein. Their conclusion, that the silicon in the water reacted with the aluminum to reduce the neurotoxicity presented by aluminum, concurs with the previous conclusion by Birchell et al.. Birchell suggested in his report that the inverse relationship between soluble aluminum and soluble silicon shows that maintaining a constant level of approximately 3 milligrams per liter of soluble silicon in drinking water would be enough to protect the population against neurotoxic effects of the absorption of all forms of aluminum in the diet.
Is There Treatment For Excess Aluminum?
Possibilities for treatments of excess aluminum in the body have been suggested by a number of different researchers. D.R.C. McLachlan and colleagues suggest decreasing the amount of the aluminum with the trivalent chelating agent desferrioxamine (DFO). The results of tests monitoring a group of AD patients taking DFO and one without showed that the rate of cognitive decline of the no DFO patients was twice that of the group receiving the DFO. Another study using chelating agents as a method to slow the progression of AD was one led by G. Fasman, concluding that the use of silicates to chelate the aluminum in the body could possibly be used to help slow the buildup of aluminum in the brain. Progress in this area of research could play an important role in the possible treatment and even prevention of AD.
Other Possible Health Issues with Aluminum
Exposure to aluminum can cause many more health problems than just Alzheimer's Disease.
The MedicineNet.com website says aluminum toxicity occurs in people with renal insufficiency. This generally applies to people who are treated by dialysis with aluminum-contaminated solutions or oral agents that contain aluminum, however today many people have weak kidneys from being overstressed by other environmental toxins. It is likely that most people today have some degree of renal insufficiency--not to the point of needing dialysis, but enough that their kidneys are probably not working optimally to flush the aluminum out of the body.
MedicineNet.com notes "The clinical manifestations of aluminum toxicity include anemia, bone disease, and progressive dementia with increased concentrations of aluminum in the brain. Prolonged intravenous feeding of preterm infants with solutions containing aluminum is associated with impaired neurologic development."
Sources of Aluminum
If you want to reduce your exposure to aluminum, cookware is not at the top of the list either.
According to
Food and Drug Administration FDA, "in a worst-case scenario, a person using uncoated aluminum pans for all cooking and food storage every day would take in an estimated 3.5 milligrams of aluminum daily." By contrast, "one antacid tablet can contain 50 milligrams of aluminum or more, and it is not unusual for a person with an upset stomach to consume more than 1,000 milligrams, or 1 gram, of aluminum per day. A buffered aspirin tablet may contain about 10 to 20 milligrams of aluminum." If you use these products, look for aluminum-free antacids and plain, non-buffered aspirin.
Other sources of aluminum exposure include:
- table salt which is industrial sodium chloride--use a natural salt instead
- baking powder 5 to 70 milligrams of sodium aluminum sulfate per teaspoon and baked goods and packaged baking mixes containing baking powder check your natural food store for aluminum-free baking powder and natural baking mixes and baked goods made with aluminum-free baking powder
- antipersirants containing aluminum chlorohydrate again, check your natural food store for aluminum-free deodorants
- aluminum beverage cans
- aluminum foil
- anti-dandruff preparations magnesium aluminum silicate or aluminum lauryl sulfate
- feminime douches aluminum salts
Summary
So far most of the mainstream studies have failed to document a clear role for aluminum in causing Alzheimer’s. Every perspective from which researchers have explored the question has yielded contradictory data. For virtually every study suggesting that aluminum may be linked to Alzheimer’s, there is another study failing to confirm those results.
The vast majority of the scientists now believe that if aluminum plays any role at all in Alzheimer’s, that role is small. If aluminum exposure had a major impact on risk, scientists would have gained a clearer picture of its involvement over the decades that they have been studying the issue, even though certain factors hamper research. One such issue lies in the widespread occurrence of both aluminum and Alzheimer’s, which complicates the effort to characterize their relationship. Aluminum is Earth’s third most common element after oxygen and silicon, and Alzheimer’s occurs frequently in older adults. Another factor is the lack of an animal model in which to study aluminum’s effects. The best animal models of Alzheimer’s disease are mice that are genetically engineered to mimic human Alzheimer pathology, but mice lack sensitivity to aluminum. Rabbits have the necessary sensitivity, but there is no transgenic Alzheimer rabbit model.
Although research into the Alzheimer’s/aluminum connection continues, most mainstream health professionals believe, based on current knowledge, that exposure to aluminum is not a significant risk factor. Public health bodies sharing this conviction include the World Health Organization (WHO), the U.S. National Institutes of Health (NIH), the U.S. Environmental Protection Agency (EPA), and Health Canada. Further, it is unlikely that people can significantly reduce their exposure to aluminum through such measures as avoiding aluminum-containing cookware, foil, beverage cans, medications, or other products. Even if aluminum were clearly implicated in Alzheimer’s, these routes of exposure account for only a small percentage of the average person’s intake. Most experts encourage people to focus their wellness efforts on measures with a proven impact on health or quality of life—avoiding smoking, exercising regularly, eating moderately, maintaining social connections, and remaining intellectually active.
The following points summarize some of the conflicting findings about aluminum and Alzheimer’s disease:
- Aluminum is known to be toxic to the nervous system, but its effects differ from those of Alzheimer’s disease.
- Some studies show elevated aluminum levels in the Alzheimer brain, but others do not. These studies include both “bulk” investigations measuring amounts of aluminum by weight and advanced analysis using laser microprobes.
- There is some evidence that in laboratory cultures of nerve cells, aluminum promotes aggregation of the protein fragment beta-amyloid into the amyloid plaques that are a hallmark Alzheimer abnormality. However, efforts to correlate aluminum levels with plaque density in people with Alzheimer’s have been inconclusive.
- Research has failed to document a clear elevation of Alzheimer risk in individuals with occupational exposure to aluminum.
- Studies finding the most consistent link have examined elevated levels of aluminum in drinking water and increased incidence of Alzheimer’s. However, there is no evidence that Alzheimer’s disease is more prevalent in cultures that traditionally drink large amounts of tea, even though tea is one of the few plants whose leaves accumulate large amounts of aluminum that may leach into the brewed beverage.
Even as there is no sufficient proof that there is connection between normal Aluminum exposure with Alzheimer’s Disease, you may want to reconsider your consumer’s habits, trying to avoid the unnecessary exposure to Aluminum. Better be safe than sorry.
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