Environmental Risk Factors for Schizophrenia and Bipolar Disorder and Their Relationship to Genetic Risk: Current Knowledge and Future Directions.
Environmental Risk Factors for Schizophrenia and Bipolar Disorder and Their Relationship to Genetic Risk: Current Knowledge and Future Directions.
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DOI：
10.3389/fgene.2021.686666
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发表时间：
2021
影响因子：
3.7
通讯作者：
Bergen SE
中科院分区：
文献类型：
--
作者：
Robinson N;Bergen SE
精神分裂症（SZ）和双相情感障碍（BD）是遗传和环境因素复杂相互作用的严重精神疾病。众所周知，它们是高度遗传性疾病，在确定其共同和独特的遗传风险因素方面取得了相当大的进展。然而，来自环境来源的15-40%的风险尚不明确。与SZ相关的环境因素包括：产科并发症、感染、冬季或春季出生、移民、城市生活、童年逆境和大麻使用。有证据表明，童年逆境和某些类型的感染也与双相障碍有关。由于研究较少，通常样本量较小，双相障碍中其他危险因素的证据较弱。对SZ或BD的环境暴露进行的检查相对较少，可能还会发现更多的环境暴露。要全面了解遗传和环境风险因素如何导致这些疾病的风险，就需要了解它们是如何相互作用的。早期对SZ和BD的基因与环境相互作用的研究通常涉及候选基因，而且研究力度不足。现在，具有全基因组数据和多基因风险评分的更大样本提供了更好的前景，以揭示遗传与环境暴露之间的相互作用，从而导致这些疾病的风险。总的来说，虽然已经确定了一些与SZ有关的环境风险因素，但与BD有关的环境风险因素却很少，而且这些因素在多大程度上占环境来源的总风险仍然未知。对于这两种疾病，遗传和环境风险因素之间的相互作用也没有得到很好的理解，值得进一步研究。关于风险因素发挥作用的机制，以及环境因素因性别而异的方式，问题仍然存在。我们需要同时对SZ和BD的环境和遗传风险因素进行调查，以更全面地了解这些疾病的发生方式。
Schizophrenia (SZ) and bipolar disorder (BD) are severe psychiatric disorders which result from complex interplay between genetic and environmental factors. It is well-established that they are highly heritable disorders, and considerable progress has been made identifying their shared and distinct genetic risk factors. However, the 15–40% of risk that is derived from environmental sources is less definitively known. Environmental factors that have been repeatedly investigated and often associated with SZ include: obstetric complications, infections, winter or spring birth, migration, urban living, childhood adversity, and cannabis use. There is evidence that childhood adversity and some types of infections are also associated with BD. Evidence for other risk factors in BD is weaker due to fewer studies and often smaller sample sizes. Relatively few environmental exposures have ever been examined for SZ or BD, and additional ones likely remain to be discovered. A complete picture of how genetic and environmental risk factors confer risk for these disorders requires an understanding of how they interact. Early gene-by-environment interaction studies for both SZ and BD often involved candidate genes and were underpowered. Larger samples with genome-wide data and polygenic risk scores now offer enhanced prospects to reveal genetic interactions with environmental exposures that contribute to risk for these disorders. Overall, although some environmental risk factors have been identified for SZ, few have been for BD, and the extent to which these account for the total risk from environmental sources remains unknown. For both disorders, interactions between genetic and environmental risk factors are also not well understood and merit further investigation. Questions remain regarding the mechanisms by which risk factors exert their effects, and the ways in which environmental factors differ by sex. Concurrent investigations of environmental and genetic risk factors in SZ and BD are needed as we work toward a more comprehensive understanding of the ways in which these disorders arise.
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