Aluminum and the Brain

During the early 1970s, doctors working in the dialysis units of several hospitals noticed that a growing number of their patients were developing rather unusual symptoms, such as jerking muscles, hallucinations, and rapid-onset dementia. Several of these patients died before the culprit was discovered: high concentrations of aluminum in the water being used for dialysis. Ironically, this was ordinary tap water. Once aluminum was removed from the water, the dialysis dementia syndrome disappeared and patients improved significantly when chelated with a substance called deferoxamine, a medication that removes aluminum from body tissues. This was the first human demonstration that aluminum could cause dementia, somewhat similar to Alzheimer's dementia.

Like most of the toxic metals thus far discussed, aluminum is a significant brain toxin. It can reach the brain by several routes. Aluminum gases and dust can enter by way of the olfactory tracts in the mucous membranes of the nasal passages, pass directly along these tiny nerve filaments, and enter the olfactory parts of the brain where it is then distributed to other vital areas of the nervous system. There is also evidence that aluminum can pass along nerves in the limbs and travel to the spinal cord, in much the same way that mercury does.

When ingested—in medications, foods and beverages—aluminum is readily absorbed. Once in the blood stream, it is tightly bound by a special transport protein called transferrin, which is also the main carrier for iron and manganese. The brain cells themselves have special transferrin receptors that allow the aluminum to enter the cells easily. Recent evidence indicates that aluminum can also enter the body by other mechanisms as well.

Interestingly, some are of the opinion that when aluminum enters a neuron, the metal itself causes very little damage.179 It appears that most of the damage is actually caused by increasing the concentration of iron within the cell. Remember that iron is a very powerful free-radical generator, and elevated levels of cellular iron have been observed in all neurodegenerative diseases. Aluminum can also increase the oxidation power of several other pro-oxidant metals, including copper and chromium.180 This means that elevated tissue aluminum levels will increase the destructive power of other types of metals.

You may recall that in chapter one I discussed the oxidative destruction of the fatty parts of cells (lipids), a process called lipid peroxidation. It is known that aluminum and iron both can significantly increase brain lipid peroxidation.181 Studies have also indicated that aluminum has a special affinity for myelin, the fatty lining of nerve pathways. In one study, the presence of aluminum increased lipid peroxidation in myelin 72 percent.182 This is especially important to persons with multiple sclerosis or any other myelin disorder. Both iron and aluminum can increase the oxidation of other parts of the cell, resulting in protein oxidation and/or DNA oxidation as well as lipid peroxidation. This can severely disrupt the function of the cells, and can eventually lead to their death.

Aluminum also acts on cell membrane function by binding to the parts of the membrane responsible for transduction, the relay of information signals within the cell. We know that calcium normally plays a vital part in this signaling process and that aluminum competes with calcium for its information receptors. When calcium levels are low, aluminum becomes significantly more toxic. The same is true for low magnesium levels.

Another way aluminum causes problems is by interfering with metal-dependent enzymes. Certain enzymes require the presence of a particular metal—such as zinc, iron, manganese, or magnesium—to work properly. Aluminum can displace these metals and cause those enzymes to function poorly or not at all.183 Combined with citrate or malate, aluminum produces fewer adverse effects. This is how plants protect themselves from aluminum toxicity. Unfortunately, while citrate may block aluminum's ability to damage metal-dependent enzymes, it also significantly increases aluminum absorption and distribution.

Of equal concern is the enormous body of evidence collected over the past twenty years connecting glutamate accumulation to most of the neurodegenerative diseases, as well as to all other types of central nervous system injuries. The problem thus far has been determining how glutamate accumulates and why the brain's normal removal system cannot protect the brain from this excess glutamate. We may now have an answer.

Several studies have shown that aluminum forms a highly absorbable chemical complex with glutamate in the gastrointestinal tract. Not only will the aluminum-glutamate complex enter the blood stream in much higher concentrations than normal, it can also easily pass through the blood-brain barrier. These actions increase brain levels of aluminum, as well as glutamate levels in discrete areas of the brain. Several of these areas are involved in Alzheimer's disease and Parkinson's disease.

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