Schizophrenia as a prostaglandin deficiency disease.
Evidence that schizophrenia may be a prostaglandin deficiency disease comes from three main sources: (1) all effective antischizophrenic drugs stimulate prolactin secretion and prolactin is a potent stimulator of prostaglandin synthesis; (2) schizophrenics are resistant to pain and inflammation and are free of rheumatoid arthritis and there is increasing evidence that prostaglandins play important roles in pain, inflammation, and rheumatoid arthritis; (3) high doses of drugs recently shown to be prostaglandin antagonists cause schizophrenia-like syndromes. The hypothesis is not necessarily inconsistent with current transmitter theories of schizophrenia since prostaglandins modify transmitter secretion and action. It does indicate radically new approaches to investigation, treatment, and drug design not suggested by the transmitter concepts.
D014150:Antipsychotic Agents / Q000494:pharmacology; D005228:Fatty Acids, Essential / Q000378:metabolism*; D006801:Humans; D008052:Lipid Metabolism, Inborn Errors / Q000150:complications*; D011388:Prolactin / Q000378:metabolism / Q000502:physiology; D011448:Prostaglandin Antagonists / Q000009:adverse effects; D011453:Prostaglandins / Q000096:biosynthesis / Q000172:deficiency*; D012559:Schizophrenia / Q000139:chemically induced / Q000188:drug therapy / Q000209:etiology*; D013268:Stimulation, Chemical
D014150:Antipsychotic Agents; D005228:Fatty Acids, Essential; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011388:Prolactin