Paquin Vincent, Lapierre Mylène, Veru Franz, King Suzanne
Department of Psychiatry, McGill University, Montréal, Québec H3A 1A1, Canada; email:
Douglas Research Centre, Montréal, Québec H4H 1R3, Canada.
Annu Rev Clin Psychol. 2021 May 7;17:285-311. doi: 10.1146/annurev-clinpsy-081219-103805. Epub 2021 Feb 5.
Why does prenatal exposure to wars, natural disasters, urbanicity, or winter increase the risk for schizophrenia? Research from the last two decades has provided rich insight about the underlying chains of causation at play during environmental upheaval, from conception to early infancy. In this review, we appraise the evidence linking schizophrenia spectrum disorder to prenatal maternal stress, obstetric complications, early infections, and maternal nutrition and other lifestyle factors. We discuss putative mechanisms, including the maternal stress system, perinatal hypoxia, and maternal-offspring immune activation. We propose that gene-environment interactions, timing during development, and sex differentiate the neuropsychiatric outcomes. Future research should pursue the translation of animal studies to humans and the longitudinal associations between early exposures, intermediate phenotypes, and psychiatric disorders. Finally, to paint a comprehensive model of risk and to harness targets for prevention, we argue that risk factors should be situated within the individual's personal ecosystem.
为什么孕期暴露于战争、自然灾害、城市化环境或冬季会增加精神分裂症的风险？过去二十年的研究为从受孕到婴儿早期环境动荡期间起作用的潜在因果链提供了丰富的见解。在这篇综述中，我们评估了将精神分裂症谱系障碍与孕期母亲压力、产科并发症、早期感染、母亲营养及其他生活方式因素联系起来的证据。我们讨论了可能的机制，包括母亲应激系统、围产期缺氧和母婴免疫激活。我们提出，基因-环境相互作用、发育时期以及性别会使神经精神结果产生差异。未来的研究应致力于将动物研究成果转化到人类研究中，并探索早期暴露、中间表型和精神障碍之间的纵向关联。最后，为了构建一个全面的风险模型并确定预防靶点，我们认为风险因素应置于个体的个人生态系统中。
