The Search for an Endogenous Schizogen: The Strange Case of Taraxein

Abstract

In 1956, Dr. Robert Galbraith Heath, Chair of Psychiatry and Neurology at Tulane University School of Medicine in New Orleans, announced that he and colleagues had discovered a protein they called taraxein in the blood of schizophrenic patients that caused symptoms of schizophrenia when injected into healthy volunteers. Heath's claim received wide public and professional attention. Researchers quickly tried to confirm the discovery. These efforts, which were rigorous and in some cases conducted in consultation with the Tulane researchers, failed. Nevertheless, for the next four decades Heath continued to defend his claim. This article recounts the scientific developments that led up to Heath's putative discovery and it explores the scientific findings for and against the taraxein theory of schizophrenia. ^{1 1}The neologism “schizogen” refers to a substance that produces schizophrenia. Although use of the term is uncommon, it is not without precedent. Hoffer (1981) Hoffer, A . 1981. The adrenochrome hypothesis of schizophrenia revisited. Orthomolecular Psychiat, 10: 98–118. [Google Scholar] uses it in his review of the Adrenochrome Hypothesis of schizophrenia (p. 100). More widely use alternatives include schizophrenogenic compound, psychotomimetic, or endogenous schizophrenia-inducing agent. Schizogen is used in this article for its brevity. View all notes