Aluminum levels were measured in a variety of tissues obtained from 36 control subjects, 30 nondialyzed uremic patients, 57 dialyzed uremic patients dying of a variety of different causes, and 38 dialyzed uremic patients dying of dialysis encephalopathy. The low aluminum levels consistently found in the control tissues support the fact that in health aluminum is largely excluded from the body. However, this ability to prevent aluminum accumulation is overcome with renal failure. Bone and liver aluminum levels were found to be significantly increased in 82% and 56% respectively in nondialyzed uremic patients and in 100% of the tissues examined from dialyzed uremic patients. In patients dying of dialysis encephalopathy, tissue aluminum levels were not only the highest but also affected in a different manner than that found in other dialyzed patients. It is suggested that dialysis encephalopathy occurs as a result of such rapid aluminum loading during dialysis that bone's ability to sequester this element is overcome, and it is shunted to liver and brain with resulting toxicity.

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The onset and progression of symptomatology in patients with anorexia nervosa and bulimia nervosa is complex. It is unlikely that dysregulation of a single neurotransmitter system would be sufficient to explain the pathophysiology of these disorders. The studies reviewed above provide preliminary evidence that decreased central serotonin function may contribute to the onset or persistence of binge eating episodes in patients with bulimia nervosa, including low weight anorexic patients with bulimic symptoms. Future clinical studies will benefit from the availability of selective serotonin receptor agonists and antagonists. Longitudinal studies through progressive phases of treatment and clinical remission will be important to clarify the contribution of dietary and body weight changes to results of neurotransmitter studies with eating disorder patients.

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