Horrobin D F
Lancet. 1979 Mar 10;1(8115):529-31. doi: 10.1016/s0140-6736(79)90948-6.
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.
近年来,有人提出精神分裂症的生物学缺陷可能与多巴胺活性过高、异常阿片类物质或过量正常阿片类物质的产生、前列腺素缺乏、对小麦蛋白过敏、过敏现象、锌代谢缺陷或松果体缺乏有关。目前的假说认为,这些不同的观点并非相互排斥,而是同一问题的不同方面。精神分裂症的最终共同途径可能是1系列前列腺素的形成和作用出现障碍。