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

基本信息

批准号：
10094068
负责人：
KECIA Nicole CARROLL
金额：
$ 50.48万
依托单位：
VANDERBILT UNIVERSITY MEDICAL CENTER
依托单位国家：
美国
项目类别：
财政年份：
2017
资助国家：
美国
起止时间：
2017-04-01 至 2021-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10094068
关键词：
9 year old Address Affect African American Anti-Inflammatory Agents Antioxidants Ascorbic Acid Asthma Attenuated Biological Biological Specimen Banks Child Childhood Chronic Clinical Data 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 Risk Role Sampling Serum Smoking Stress Trauma Umbilical Cord Blood Urine Vital capacity Vitamin E Wheezing Woman alpha Tocopherol cohort comorbidity cost data repository dietary disease phenotype disorder risk early childhood experience fetal follow-up in utero indexing intergenerational maternal stress minority children mother nutrition neurobehavior novel postnatal prenatal prenatal exposure prenatal stress prospective pulmonary function respiratory respiratory health transmission process traumatic stress

项目摘要

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.

项目摘要儿童期呼吸道和特应性疾病造成了巨大的发病率和不成比例的负担城市，贫穷的少数民族儿童。儿童呼吸健康的起源从子宫开始，受到可修改的因素，例如母体心理压力和饮食。研究表明需要学习孕产妇饮食和心理压力都在一起，迄今为止尚未做到这一点呼吸结果。同样，在低收入人群中，创伤压力特别重要暴露率更高。将产前应激与哮喘和肺功能联系起来的证据正在增长。但是，机制仍然很少理解。尽管心理压力通过众多途径，氧化应激总是被识别为中心成分。产前压力可能破坏胎盘，因此是胎儿，氧化剂/抗氧化剂平衡，可能在应力中起作用诱发喘息/哮喘风险的编程和肺部生长受损。相反，产前更高抗氧化剂/抗炎摄入量（例如，维生素E，N-3多不饱和脂肪酸[PUFAS]）降低胎盘氧化应激，与儿童喘息和哮喘的减少有关。这将是第一个前瞻性研究以检查母体外伤应激，氧化应激，抗氧化剂之间的关联状态和儿童哮喘和肺功能。我们将测量产前创伤压力和饮食检查新的中心假设，即产前母体外伤应激有助于喘息/哮喘风险和儿童期肺功能降低，氧化应激起着关键作用，而关联将是通过产前营养暴露来改变胎儿易受氧化应激的脆弱性。我们将学习母体产前创伤应力之间的关联，F2-异前列腺指数和儿童指数的氧化应激哮喘/喘息（AIM 1），肺功能（AIM 2）以及母体营养暴露（维生素E，N-3 PUFAS）可以修改关系（AIM 3）。影响神经认知发展和学习的条件幼儿（蜡烛）队列是一个城市，低收入，非裔美国人的产前队列据我们所知，母子二元组是唯一具有产前暴露数据并储存的队列样本需要解决我们的目标。该研究利用现有的产前和产后社会心理评估，产前饮食评估，生物测量的存放，并提出了前瞻性后续行动确定9岁时的喘息/哮喘/特应性疾病和肺功能。这项研究将告知饮食干预措施可能有助于减轻心理压力引起的氧化剂失衡，从而对呼吸系统疾病的发展节目。调查结果有可能影响临床政策和实践并告知饮食干预措施的试验，以减少压力对肺功能的影响。