IDENTIFICATION AND USE: Aluminum is established as a neurotoxin, although the basis for its toxicity is unknown. It recently has been shown to alter the function of the blood-brain barrier, which regulates exchanges between the central nervous system and peripheral circulation. The blood-brain barrier owes its unique properties to the integrity of cell membranes that comprise it. Aluminum affects some of the membrane like functions of the blood-brain barrier. It increases the rate of transmembrane diffusion and selectively changes saturable transport systems without disrupting the integrity of the membranes or altering CNS hemodynamics. Such alterations in the access to the brain of nutrients, hormones, toxins, and drugs could be the basis of CNS dysfunction. Aluminum is capable of altering membrane function at the blood-brain barrier; many of its effects on the CNS a well a peripheral tissues can be explained by its actions as a membrane toxin.


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ANIMAL EXPOSURE/TOXICITY: Excessive dietary aluminum has been proposed to be a factor contributing to several neurological disorders in humans. Six 8 week old female Swiss Webster mice were fed for 10 weeks purified diets containing 100 (control, 100 aluminum, 500 (500 aluminum) or 1000 (1000 aluminum) ug aluminum/g diet.

Brain and liver lipid peroxidation was determined by evaluating the production of 2-thiobarbituric acid reactive substances in brain and liver homogenates in the presence or absence of 50 mM ferrous iron. 2-Thiobarbituric acid reactive substances production in the absence of iron in brain homogenates from mice fed the 1000 aluminum diet was higher (30%) than that in the 100 aluminum control group (3.1 versus 2.4 nmol 2-thiobarbituric acid reactive substances/mg protein).

The additional of ferrous iron increased 2-thiobarbituric acid reactive substances production in-brain homogenates from all 3 dietary group. The iron induced 2-thiobarbituric acid reactive substances production was 26% higher in the 1000 aluminum brain homogenates than in the 100 aluminum group (4.9 vs. 3.9 nmol 2-thiobarbituric acid reactive subtances/mg protein). Brain 2-Thiobarbituric acid reactive substances production in the presence and absence of iron was similar between the 100 and 500 aluminum groups. 2-Thiobarbituric acid reactive substances production in liver homogenates measured either with or without iron was similar for the 3 groups.

These results show that, in mice, dietary aluminum intoxication leads to increased brain 2-thiobarbituric acid reactive substance production, suggesting that enhanced lipid peroxidation may be one possible mechanism underlying the neurological damage associated with increased tissue aluminum.

HUMAN EXPOSURE/TOXICITY: evidence is presented indicating that dementias are associated with a relative insufficiency of magnesium in the brain. Such insufficiency may be attributable to low intake or retention of magnesium; high intake of a neurotoxic metal, such a aluminum, which inhibits activity of magnesium requiring enzymes; or impaired transport of magnesium and/or enhanced transport of the neurotoxic metal into brain tissue.

It is proposed that Alzheimer’s disease involves a defective transport process, characterized by both an abnormally high incorporation of aluminum and an abnormally low incorporation that an altered serum protein contributes to the progression of Alzheimer’s disease by having a greater affinity for aluminum than for magnesium, in contrast to the normal protein, which binds magnesium better than aluminum.

The altered protein crosses the blood-brain barrier more efficiently than the normal protein and competes with the normal protein in binding to brain neurons. Binding of the altered protein to the target neurons would both facilitate aluminum uptake and impede magnesium uptake. Evidence suggests that albumin is the serum protein that is altered.

A new case study from Keele University in the UK1 unequivocally shows high levels of aluminum in the brain of an individual exposed to aluminum at work, who later died from Alzheimer’s disease. While aluminum exposure has been implicated in Alzheimer’s and a number of other neurological diseases, this case claims to be “the first direct link” between Alzheimer’s disease and elevated brain aluminum following occupational exposure. Vaccines present a particularly problematic source of toxic metal exposure.

Aluminum is the most commonly used vaccine adjuvant and is considered “safe” even though research shows it may induce serious immunological disorders and neurological complications in humans. In the video above, Dr. David Ayoub discusses how the aluminum in vaccines may be even more dangerous than mercury. The number of aluminum-containing vaccines children receive today has quadrupled over the past 30 years. In the 1970s, children got only four aluminum-containing vaccines in their first 18 months of life, but now they typically receive 17.

As children’s aluminum burden has increased, so has the prevalence of childhood neurological disorders. In one school, 90 percent of the children developed ADHD during the course of a single school year, and their toxicity profiles all revealed massive amounts of aluminum. Aluminum is also in vaccines and is used as an adjuvant. If you go by the aluminum content on vaccine labels, the amount kids are getting is excessive, but if you add in the aluminum NOT listed on the labels—”accidental exposure” due to contamination—it’s a much more serious problem.

Dr. Ayoub cites one study that found five to six times more aluminum in vaccines than what was actually listed on the labels. When you review the signs and symptoms of aluminum toxicity, they are shockingly similar to the symptoms of autism, ADHD, Alzheimer’s, Parkinson’s, and other neurological diseases. Vaccine adjuvants can cause serious chronic brain inflammation.

ADVERSE EFFECTS: aluminum targets your cerebellum and autonomic nervous system—the part responsible for biological processes over which you have no conscious control (breathing, blood pressure, balance, coordination, etc.). When you look at the MSDS sheet for aluminum, you will see symptoms strikingly similar to those in common neurological diseases, including memory problems, speech impairments and aphasia, dementia, depression, muscle weakness, motor disturbances, and other neurological difficulties.