Abstract

In recent years it has been suggested that the biological defect in schizophrenia may be related to excess dopamine activity, to production of an abnormal opioid or a normal opioid in excess, to a prostaglandin deficiency, to a hypersensitivity to wheat proteins, to an allergic phenomenon, to a defect in zinc metabolism, or to a pineal deficiency. The present hypothesis proposes that the various concepts are not mutually exclusive but represent different aspects of the same problem. The final common path in schizophrenia may be a failure of formation and action of prostaglandins of the 1 series.