Abstract

The author presents a hypothesis relating prostaglandin E1 (PGE1) deficiency to schizophrenia. The hypothesis is consistent with the importance of prolactin-stimulating properties in currently used antipsychotic drugs, the effect of prolactin on PGE1 synthesis, and the deficiency of PGE1 regulation in schizophrenic platelets. The author relates the PGE1 deficiency hypothesis to theories implicating dopamine and endorphins in the etiology of schizophrenia. A clinical trial in chronic schizophrenics has suggested the possible therapeutic efficacy of penicillin, a drug without dopamine-blocking actions which can stimulate PGE1 synthesis directly.