Maternal Traumatic Stress, Oxidative Stress, Antioxidant Exposures, and Child Asthma and Lung Function

项目总结 儿童呼吸道和特应性疾病占相当大的发病率和不成比例的负担 城市贫困的少数民族儿童。儿童呼吸道健康的起源始于子宫，并受到 可改变的因素，如母亲的心理压力和饮食。虽然研究表明有必要研究 母亲的饮食和心理压力结合在一起，到目前为止还没有在儿童方面做到这一点 呼吸结果。此外，创伤应激在低收入人群中尤其重要，因为 更高的暴露流行率。越来越多的证据表明，产前应激与哮喘和肺功能有关； 然而，机制仍然鲜为人知。尽管心理压力通过以下途径影响健康 在许多途径中，氧化应激总是被认为是一个中心成分。产前应激可能 破坏胎盘，从而破坏胎儿的氧化剂/抗氧化剂平衡，这可能在压力中发挥作用- 诱发程序的喘息/哮喘风险和肺生长受损。相反，更高的胎儿期 抗氧化剂/抗炎摄入量(如维生素E、n-3多不饱和脂肪酸[PUFAs])减少 胎盘氧化应激，并与减少儿童喘息和哮喘有关。这将是第一次 探讨母体创伤应激、氧化应激、抗氧化剂之间关系的前瞻性研究 状况和儿童哮喘及肺功能。我们将测量产前创伤应激和饮食，以前瞻性地 检验新的中心假设，即产前母体创伤应激导致喘息/哮喘 儿童的风险和肺功能降低，氧化应激起着关键作用，而且这种联系将是 通过产前营养暴露，降低胎儿对氧化应激的易感性。我们会研究 母体产前创伤应激、以F2-异前列腺素为指标的氧化应激与儿童的关系 哮喘/喘息(目标1)、肺功能(目标2)以及母亲的营养暴露(维生素E，n-3多不饱和脂肪酸) 可以修改关系(目标3)。影响儿童神经认知发育和学习的条件 早期儿童(蜡烛)队列是主要由城市低收入非裔美国人组成的产前队列 母子二胎，据我们所知，这是唯一有产前暴露数据并存入银行的队列 解决我们的目标所需的样本。这项研究利用了现有的产前和产后心理社会 评估，产前饮食评估，储存生物检疫，并提出前瞻性后续行动 在9岁时确定喘息/哮喘/特应性疾病和肺功能。这项研究将告诉我们如何饮食 干预可能有助于缓解社会心理压力引发的氧化剂失衡以及由此产生的影响 呼吸系统疾病的发展规划。研究结果有可能影响临床政策和 实践和告知饮食干预试验，以减少对肺功能的压力影响。

PROJECT SUMMARY Childhood respiratory and atopic disease accounts for substantial morbidity and disproportionately burdens urban, poor minority children. The origins of child respiratory health begin in utero and are influenced by modifiable factors, such as maternal psychological stress and diet. While research points to the need to study both maternal diet and psychological stress together, this has not been done to date in regards to child respiratory outcomes. Also, traumatic stress is of particular importance in lower income populations given a higher prevalence of exposure. Evidence linking prenatal stress to asthma and lung function is growing; however, mechanisms remain poorly understood. Although psychological stress impacts health through numerous pathways, oxidative stress is invariably identified as a central component. Prenatal stress may disrupt placental, and consequently fetal, oxidant/antioxidant balance, which likely plays a role in stress- induced programming of wheeze/asthma risk and impaired lung growth. Conversely, higher prenatal antioxidant/anti-inflammatory intakes (e.g., vitamin E, n-3 polyunsaturated fatty acids [PUFAs]) reduce placental oxidative stress and are linked with decreased child wheezing and asthma. This will be the first prospective study to examine associations between maternal traumatic stress, oxidative stress, antioxidant status and child asthma and lung function. We will measure prenatal traumatic stress and diet to prospectively examine the novel central hypothesis that prenatal maternal traumatic stress contributes to wheeze/asthma risk and reduced lung function in childhood, that oxidative stress plays a key role, and that associations will be modified by prenatal nutritional exposures that reduce fetal vulnerability to oxidative stress. We will study associations among maternal prenatal traumatic stress, oxidative stress indexed by F2-Isoprostanes, and child asthma/wheeze (Aim 1), lung function (Aim 2), and how maternal nutritional exposures (Vitamin E, n-3 PUFAs) may modify relationships (Aim 3). The Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) cohort is a prenatal cohort of largely urban, low-income, African-American mother-child dyads, which, to our knowledge, is the only cohort with the prenatal exposure data and banked samples needed to address our aims. The study leverages existing prenatal and postpartum psychosocial assessments, prenatal dietary assessments, banked biospecimens, and proposes prospective follow-up to ascertain wheeze/asthma/atopic disease and lung function at age 9 years. This study will inform how dietary interventions may help mitigate psychosocial stress-elicited oxidant imbalance and consequent effects on developmental programming of respiratory disorders. Findings have the potential to impact clinical policy and practice and inform trials of dietary interventions to reduce stress effects on lung function.