Zinc and Manganese in the Schizophrenias

The essential trace elements zinc and manganese have been noted as factors in brain disease since the 1920s. The combined use of zinc and manganese in schizophrenia is based on: 1) Increased urinary excretion of copper when both zinc and manganese are given orally; 2) Zinc alone causes a decrease in blood manganese; 3) The double deficiency of zinc and manganese frequently is found in patients with excess copper. The mauve factor (Kryptopyrrole) is known to increase the excretion of zinc and vitamin B6 (pyridoxine). In children, insufficient levels of zinc and manganese have been associated with lowered learning ability, apathy, lethargy and mental retardation. Hyperactive children may be deficient in zinc, manganese and vitamin B6 and have an excess of lead and copper. Alcoholism, schizophrenia, Wilson’s disease, and Pick’s disease are brain disorders dynamically related to zinc and manganese levels. Zinc has been employed with success to treat Wilson’s disease, achrodermatitis enteropathica, and specific types of schizophrenia. Manganese is important in the building and breakdown cycles of protein and nucleic acid. For RNA chain initiation, manganese was found to be a better effector than magnesium. Manganese stimulates adenylate cyclase activity in brain tissue. Because cyclic-AMP plays a regulatory role in the action of several brain neurotransmitters, manganese is important in brain function. Owing to the fact that zinc is well absorbed from the gut but manganese is poorly absorbed all diagnostic categories may be harmed by large prolonged oral doses of zinc without manganese. In oral doses manganese occasionally elevates blood pressure in patients over 40 years of age. Zinc alone can lower blood pressure in some hypertensive patients. Chronic use of hydralazine (a manganese chelator) in rats produced manganese deficiency which resulted in convulsions. Low blood and serum manganese levels may play a role in epilepsy possibly by interfering with membrane stability. Prolonged use of pheno-thiazines causes tardive dyskinesia. Phenothiazines might chelate manganese making it unavailable for some presumed function as an enzyme activator.

Carl C. Pfeiffer, Ph.D., M.D. and Scott LaMola, B.S (Journal of Orthomolecular Medicine, 1999)