"From the earliest days of food regulation, the use of alum (aluminum sulphate) in foods has been condemned. It is universally acknowledged as a poison in all countries. If the Bureau of Chemistry had been permitted to enforce the law ... no food product in the country would have any trace of ... any aluminum or saccarin. No soft drink would contain caffeine or hebromin; no bleached flour would be in interstate commerce. Our food and drugs would be wholly without adulteration ... and the health of our people would be vastly improved and their life greatly extended."

From History of crime against the Food Laws (1929) by Dr. Wiley, the prime mover behind the original Pure Food Law and Director of the FDA. He resigned in disgust in 1912 over exceptions granted to the law and lack of enforcement.

Aluminum has been exempted from tesitng for safety by the FDA under a convoluted logic wherein it is classified as GRAS. (Generally Regarded As Safe.) It has never been tested by the FDA on its safety and there are NO restrictions whatever on the amount or use of aluminum.

There are over 2000 references in the National Library of Medicine on adverse effects of alumium. The following were extracted to provide a small sample of the range of toxicity of aluminum.

Chemical Registry
Aluminum toxicity has been recognized in many settings where exposure is heavy or prolonged, where renal function is limited, or where apreviously accumulated bone burden is released in stress or illness. Toxicity may include: encephalopathy (stuttering, gait disturbance, myoclonic jerks, seizures, coma, abnormal EEG) osteomalacia or aplastic bone disease ( associated with painful spontaneous fractures, hypercalcemia, tumorous calcinosis ) proximal myopathy, increased risk of infection, increased left ventricular mass and decreased myocardial function microcytic anemia with very high levels, sudden death.

Aluminum is ubiquitous in our environment; it is the third most prevalent element in the earth's crust. The gastrointestinal tract is relatively impervious to aluminum, absorption normally being only about 2%. Aluminum is absorbed by a mechanism related to that for calcium. Gastric acidity and oral citrate favors absorption, and H2-blockers reduce absorption. As is true for several trace elements, transferrin is the primary protein binder and carrier for aluminum in the plasma, where 80% is protein bound and 20% is free or complexed to small molecules such as citrate.

Cells appear to take up aluminum from transferrin rather than from citrate. Purified preparations of ferritin from brain and liver have been found to contain aluminum.

It is not known if ferritin has a specific binding site for aluminum. Factors regulating the migration of aluminum across the blood–brain barrier are not well understood.

Serum aluminum correlates with encephalopathy; red cell aluminum correlates with microcytic anemia, and bone aluminum correlates with aluminum bone disease.

Basal PTH when elevated appears to protect bone and thereby favor CNS toxicity.

Other factors favoring one form of toxicity over another are not well understood.

Aluminum toxicity has been reported to impair the formation and release of parathyroid hormone. The parathyroid glands concentrate aluminum above levels in surrounding tissues. Treatment of aluminum toxicity in renal failure patients often reactivates hyperparathyroidism, which to a certain extent is helpful for bone remodeling and healing.