缩小精神病生物学模型与社会心理学模型研究间的差距（英文）

Bridging the gap between research into biological and psychosocial models of psychosis

Paul Bebbington最近发表的专题文章对精神病的社会心理学研究的最新进展做了一个极好的综述。然而,我们对一个仅仅基于社会流行病学和认知理论的模型可以完全描述精神病持有疑虑,并且公平地说,Bebbington也不认为这个模型可以完全描述。一个完整的模型必须纳入我们从非社会流行病学、神经科学和遗传学中汲取的经验教训。有证据表明,Bebbington感兴趣的社会风险因素,和诸如滥用兴奋剂和大麻之类的生物危险因素都可以通过纹状体多巴胺失调而激发精神病症状。在精神分裂症样精神病的病因学中,我们也需要考虑神经发育异常。此外,我们对精神病的遗传学理解上的惊人进展为研究探讨基因-环境相关性和基因-环境相互作用打开一扇令人兴奋的大门。总之,Bebbington阐述了认知领域的学者与社会研究者互相交流的价值,但偶尔更倾向于生物学方面的角度可能发展出一个更全面的模型。

Paul Bebbington＇s recent Special Article provides an excellent synthesis of recent advances in psychosocial research on psychosis. However, we doubt that a model based solely on social epidemiology and cognitive theory can totally describe psychosis, and to be fair, Bebbington does not suggest that it does. A complete model must also incorporate what we have learned from non-social epidemiology, neuroscience, and genetics. Evidence indicates that both the social risk factors that interest Bebbington and biological risk factors, such as abuse of stimulants and cannabis, can provoke psychotic symptoms by dysregulating striatal dopamine. The role of neurodevelopmental deviance also needs to be considered in the etiology of schizophrenia-like psychosis. Moreover, the striking advances in our understanding of the genetic architecture of psychosis open an exciting door into studies examining gene-environment correlation and gene-environment interaction. In short, Bebbington demonstrates the value of cognitive and social researchers talking to each other, but the occasional chat with the more biologically inclined could produce a more comprehensive model.