Asthma UK Centre for Applied Research, Centre for Medical Informatics, Usher Institute of Population Health Sciences and Informatics, The University of Edinburgh, Edinburgh, UK.
Department of Paediatrics and Child Health, Cork University Hospital, Cork City, Ireland.
Clin Exp Allergy. 2018 Apr;48(4):403-414. doi: 10.1111/cea.13091. Epub 2018 Feb 8.
Prenatal maternal stress may influence offspring's atopic risk through sustained cortisol secretion resulting from activation of the hypothalamic-pituitary axis (HPA), leading to Th2-biased cell differentiation in the foetus. We undertook a systematic review and meta-analysis investigating the relationship between prenatal maternal psychosocial stress and risk of asthma and allergy in the offspring.
We searched 11 electronic databases from 1960 to 2016, searched the grey literature and contacted experts in the field. Type of stress indicator included mood disorders, anxiety, exposure to violence, bereavement and socio-economic problems occurring during pregnancy, both objectively and subjectively measured. We included all possible asthma and IgE-mediated allergy outcomes. We conducted random-effects meta-analyses to synthesize the data.
We identified 9779 papers of which 30 studies (enrolling >6 million participants) satisfied inclusion criteria. The quality of 25 studies was moderate, 4 were strong, and one was weak. Maternal exposure to any type of stressors was associated with an increased risk of offspring atopic eczema/dermatitis (OR 1.34, 95% CI 1.22-1.47), allergic rhinitis (OR 1.30, 95% CI 1.04-1.62), wheeze (OR 1.34, 95% CI 1.16-1.54) and asthma (OR 1.15, 95% CI 1.04-1.27). Exposure to anxiety and depression had strongest effect compared to other stressors. Exposure during the third trimester had the greatest impact compared to first and second trimesters. The increased risk was stronger for early-onset and persistent than for late-onset wheeze. Bereavement of a child (HR 1.28, 95% CI 1.10-1.48) or a spouse (HR 1.40, 95% CI 1.03-1.90) increased the risk of offspring asthma.
Exposure to prenatal maternal psychosocial stress was associated with increased risk, albeit modestly, of asthma and allergy in the offspring. The pronounced risk during the third trimester may represent cumulative stress exposure throughout pregnancy rather than trimester-specific effect. Our findings may represent a causal effect or a result of inherent biases in studies, particularly residual confounding.
产前母体应激可能通过激活下丘脑-垂体轴（HPA）导致持续的皮质醇分泌，从而影响后代的特应性风险，导致胎儿中 Th2 偏向的细胞分化。我们进行了一项系统评价和荟萃分析，调查了产前母体心理社会应激与后代哮喘和过敏风险之间的关系。
我们从 1960 年到 2016 年搜索了 11 个电子数据库，搜索了灰色文献，并联系了该领域的专家。应激指标的类型包括怀孕期间出现的情绪障碍、焦虑、暴露于暴力、丧亲之痛和社会经济问题，这些指标可以客观和主观地测量。我们包括了所有可能的哮喘和 IgE 介导的过敏结果。我们进行了随机效应荟萃分析来综合数据。
我们确定了 9779 篇论文，其中 30 项研究（纳入了超过 600 万名参与者）符合纳入标准。25 项研究的质量为中等，4 项为强，1 项为弱。母体暴露于任何类型的应激源与后代特应性湿疹/皮炎（OR 1.34，95%CI 1.22-1.47）、过敏性鼻炎（OR 1.30，95%CI 1.04-1.62）、喘息（OR 1.34，95%CI 1.16-1.54）和哮喘（OR 1.15，95%CI 1.04-1.27）的风险增加相关。与其他应激源相比，焦虑和抑郁的暴露具有最强的影响。与第一和第二孕期相比，第三孕期的影响最大。与晚发和持续喘息相比，早发和持续喘息的风险增加更强。孩子（HR 1.28，95%CI 1.10-1.48）或配偶（HR 1.40，95%CI 1.03-1.90）的丧亡增加了后代哮喘的风险。
产前母体心理社会应激的暴露与后代哮喘和过敏的风险增加相关，尽管幅度不大。第三孕期的显著风险可能代表整个孕期累积的应激暴露，而不是特定于孕期的影响。我们的研究结果可能代表了研究中固有的偏差或因果效应，特别是残余混杂。
