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

母亲创伤应激、氧化应激、抗氧化剂暴露以及儿童哮喘和肺功能

• 批准号: 9263527
• 负责人: KECIA Nicole CARROLL
• 金额: $ 81.86万
• 依托单位: VANDERBILT UNIVERSITY MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2017
• 资助国家: 美国
• 起止时间: 2017-04-01 至 2021-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9263527
• 关键词: 9 year old; Address; Affect; African American; Anti-Inflammatory Agents; Anti-inflammatory; Antioxidants; Ascorbic Acid; Asthma; Attenuated; Biological; Child; Childhood; Chronic; Clinical; Comorbidity; Data; Databases; Development; Diet; Dietary Assessment; Dietary Factors; Dietary Intervention; Dietary intake; Disease; Disease Outcome; Enrollment; Equilibrium; Event; Extrinsic asthma; F2-Isoprostanes; Failure; Forced expiratory volume function; Growth; Health; High Prevalence; Impairment; Infant; Intake; Intervention; Learning; Life; Link; Low Income Population; Low income; Lung; Lung diseases; Measures; Mediating; Minority; Morbidity - disease rate; Mothers; N-3 polyunsaturated fatty acid; Neurocognitive; Nutritional; Outcome; Oxidants; Oxidative Stress; Pathway interactions; Physiological; Play; Policies; Polyunsaturated Fatty Acids; Population; Positioning Attribute; Postpartum Period; Prospective Studies; Psychological Stress; Psychophysiology; Psychosocial Assessment and Care; Psychosocial Stress; Pulmonary Function Test/Forced Expiratory Volume 1; Questionnaires; Research; Respiration Disorders; Respiratory physiology; Risk; Role; Sampling; Serum; Smoking; Stress; Trauma; Umbilical Cord Blood; Urine; Vital capacity; Vitamin E; Wheezing; Woman; alpha Tocopherol; cohort; cost; disease phenotype; disorder risk; early childhood; experience; fetal; follow-up; in utero; indexing; intergenerational; maternal stress; minority children; neurobehavior; novel; postnatal; prenatal; prenatal exposure; prenatal stress; prospective; respiratory; respiratory health; transmission process

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.

项目摘要 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。儿童呼吸系统健康的起源开始在子宫内，并受到 可改变的因素，如产妇的心理压力和饮食。虽然研究表明有必要研究 母亲的饮食和心理压力一起，这还没有做到这一点，迄今为止，关于儿童 呼吸结果。此外，创伤性压力在低收入人群中特别重要， 暴露率较高。越来越多的证据表明，产前压力与哮喘和肺功能有关; 然而，对机制仍然知之甚少。虽然心理压力通过以下方式影响健康 在众多的途径中，氧化应激总是被确定为核心成分。产前压力可能 破坏胎盘，因此胎儿，氧化剂/抗氧化剂平衡，这可能在压力中发挥作用- 诱发哮鸣/哮喘风险和肺生长受损。相反，较高的产前 抗氧化剂/抗炎剂摄入（例如，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 一项前瞻性研究，旨在研究母体创伤应激、氧化应激、抗氧化剂 儿童哮喘和肺功能。我们将测量产前创伤压力和饮食， 检验产前母体创伤应激导致喘息/哮喘的新中心假设 风险和降低肺功能在儿童时期，氧化应激起着关键作用， 通过产前营养暴露来改变，从而降低胎儿对氧化应激的脆弱性。我们将研究 母体产前创伤性应激、F2-异前列腺素标记的氧化应激和儿童 哮喘/喘息（目标1）、肺功能（目标2）以及母体营养暴露（维生素E、n-3 PUFA） 可以修改关系（目标3）。影响儿童神经认知发展和学习的条件 早期儿童（CANDLE）队列是一个产前队列，主要是城市，低收入，非洲裔美国人， 据我们所知，这是唯一一个有产前暴露数据的队列， 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学 评估，产前饮食评估，库存生物标本，并提出前瞻性随访， 在9岁时确定喘息/哮喘/特应性疾病和肺功能。这项研究将告知饮食如何 干预措施可能有助于减轻心理社会压力引起的氧化剂不平衡和随之而来的影响， 呼吸系统疾病的发展规划。研究结果有可能影响临床政策， 实践并告知饮食干预试验，以减少对肺功能的压力影响。