Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses.

Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses.
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DOI:
10.1186/s13229-017-0121-4
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发表时间:
2017
期刊:
影响因子:
6.2
通讯作者:
Reichenberg A
Reichenberg A
中科院分区:
医学1区
文献类型:
--
作者:
Modabbernia A;Velthorst E;Reichenberg A

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被引文献

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根据最近的证据,高达40-50%的自闭症谱系障碍(ASD)易感性的变化可能是由环境因素决定的。在本文中,我们进行了系统的审查和荟萃分析的ASD的环境危险因素的审查。我们评估了每一篇综述的证据质量,并简要概述了ASD环境风险因素的假定机制。目前的证据表明,几个环境因素,包括疫苗接种,母亲吸烟,硫柳汞暴露,以及最有可能的辅助生殖技术与ASD的风险无关。相反,父母年龄越大,患ASD的风险越高。与创伤或缺血和缺氧相关的出生并发症也显示出与ASD的密切联系,而其他妊娠相关因素,如母亲肥胖,母亲糖尿病和剖腹产与ASD风险的相关性较低(但显着)。关于营养元素的评论对叶酸和欧米茄3缺乏的有害影响尚无定论,但维生素D似乎在ASD患者中缺乏。对有毒元素的研究在很大程度上受到其设计的限制,但有足够的证据表明,一些重金属(最重要的无机汞和铅)和ASD之间的关联,值得进一步研究。环境因素和ASD之间的关联机制存在争议,但可能包括非因果关联(包括混杂),基因相关效应,氧化应激,炎症,缺氧/缺血,内分泌干扰,神经递质改变和干扰信号通路。与ASD的遗传学研究相比,环境危险因素的研究处于起步阶段,具有显著的方法学局限性。ASD危险因素的未来研究将受益于发展心理病理学方法,前瞻性设计,精确的暴露测量,与关键发育期相关的可靠暴露时间,并应考虑到基因和环境之间的动态相互作用,通过使用遗传信息设计。本文的在线版本(doi:10.1186/s13229-017-0121-4)包含补充材料,可供授权用户使用。
According to recent evidence, up to 40–50% of variance in autism spectrum disorder (ASD) liability might be determined by environmental factors. In the present paper, we conducted a review of systematic reviews and meta-analyses of environmental risk factors for ASD. We assessed each review for quality of evidence and provided a brief overview of putative mechanisms of environmental risk factors for ASD. Current evidence suggests that several environmental factors including vaccination, maternal smoking, thimerosal exposure, and most likely assisted reproductive technologies are unrelated to risk of ASD. On the contrary, advanced parental age is associated with higher risk of ASD. Birth complications that are associated with trauma or ischemia and hypoxia have also shown strong links to ASD, whereas other pregnancy-related factors such as maternal obesity, maternal diabetes, and caesarian section have shown a less strong (but significant) association with risk of ASD. The reviews on nutritional elements have been inconclusive about the detrimental effects of deficiency in folic acid and omega 3, but vitamin D seems to be deficient in patients with ASD. The studies on toxic elements have been largely limited by their design, but there is enough evidence for the association between some heavy metals (most important inorganic mercury and lead) and ASD that warrants further investigation. Mechanisms of the association between environmental factors and ASD are debated but might include non-causative association (including confounding), gene-related effect, oxidative stress, inflammation, hypoxia/ischemia, endocrine disruption, neurotransmitter alterations, and interference with signaling pathways. Compared to genetic studies of ASD, studies of environmental risk factors are in their infancy and have significant methodological limitations. Future studies of ASD risk factors would benefit from a developmental psychopathology approach, prospective design, precise exposure measurement, reliable timing of exposure in relation to critical developmental periods and should take into account the dynamic interplay between gene and environment by using genetically informed designs. The online version of this article (doi:10.1186/s13229-017-0121-4) contains supplementary material, which is available to authorized users.