Contrast between Vitamin-Responsive Inherited Metabolic Diseases and Vitamin Use in Schizophrenia

  • Leon E. Rosenberg
Part of the Advances in Behavioral Biology book series (ABBI, volume 14)


I am not a psychiatrist. I am an internist and a medical geneticist who has become interested in the question of the use of large doses of vitamins in the therapy of schizophrenia because of my involvement with a number of inherited metabolic diseases which I would like to tell you about briefly. In 1954, Hunt and his colleagues described two female siblings with neonatal convulsions whose seizure disorder was not controlled by the usually prescribed anticonvulsants or by physiologic doses of pyridoxine. When these girls were given 10 to 20 times the physiologic requirement, however, seizures stopped abruptly and recurred only after cessation of the pyridoxine supplements. This pattern of seizure control by large amounts of pyridoxine followed by exacerbation after vitamin withdrawal led Hunt to propose that these children were “dependent” on increased amounts of pyridoxine to prevent central nervous system hyperactivity. Thus, the concept of vitamin-dependent metabolic disorders was born. It is interesting, I think, to note that Hunt’s study was reported at about the same time that Dr. Osmond first suggested that nicotinic acid was beneficial in schizophrenia. Since these early observations, the two fields of “vitamin-responsive” or “vitamin-dependent” inborn metabolic disorders and so-called “megavitamin-responsive” schizophrenia have followed very divergent courses. I shall underscore this divergence by first summarizing the pattern of investigation followed in the vitamin-responsive inborn errors of metabolism.


Nicotinic Acid Glutamic Acid Decarboxylase Pyridoxal Phosphate Physiologic Dose Vitamin Therapy 


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Copyright information

© Plenum Press, New York 1975

Authors and Affiliations

  • Leon E. Rosenberg
    • 1
  1. 1.Department of Human GeneticsYale University School of MedicineNew HavenUSA

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