Dietary Behaviors, The Food Environment and Sleep Duration Changes in Urban Children with Asthma

城市哮喘儿童饮食行为、食物环境和睡眠时间的变化

• 批准号: 10842648
• 负责人: Daphne Koinis Mitchell
• 金额: $ 22.06万
• 依托单位: RHODE ISLAND HOSPITAL
• 依托单位国家: 美国
• 财政年份: 2021
• 资助国家: 美国
• 起止时间: 2021-08-15 至 2026-07-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10842648
• 关键词: Address; Adipose tissue; Adult; Affect; Age; Asthma; Beds; Behavior; Behavioral; Biological Process; Body fat; Body mass index; Child; Childhood Asthma; Chronic; Clinic Visits; Clinical; Data; Development; Diet; Dietary Assessment; Disease; Eating; Enrollment; Environment; Epidemiology; Equilibrium; Experimental Designs; Extrinsic asthma; Faculty; Fatty acid glycerol esters; Food; Future; Goals; Guidelines; Health Food; Height; Home; Household; Immune; Immunologic Markers; Impulsivity; Individual Differences; Inflammation; Inflammatory; Intake; Interferon Type II; Interferons; Interleukin-13; Interleukin-4; Interleukin-5; Interleukin-6; Interleukins; Intervention; Life Style; Link; Measurement; Mediating; Modeling; Morbidity - disease rate; Obesity; Outcome; Parents; Pharmaceutical Preparations; Plasma; Play; Polysomnography; Populations at Risk; Prevention; Protocols documentation; Pulmonary Function Test/Forced Expiratory Volume 1; Recovery; Reduce health disparities; Research; Research Training; Sampling; Schedule; Self-control as a personality trait; Sleep; Sleep Deprivation; Spirometry; Symptoms; Testing; Time; Underserved Population; Unhealthy Diet; Visceral; Weight; Work; actigraphy; adequate sleep; asthma inhaler; career; clinical care; comorbidity; cytokine; design; dietary; emotional eating; ethnic minority; experience; food environment; food insecurity; high risk; immune function; improved; indexing; minority children; modifiable behavior; multi-component intervention; obesity in children; obesity risk; obesity treatment; obesogenic; overweight child; parent grant; pulmonary function; response; skills; sleep health; urban children; urban minority; urban setting; Address; Adipose tissue; Adult; Affect; Age; Asthma; Beds; Behavior; Behavioral; Biological Process; Body fat; Body mass index; Child; Childhood Asthma; Chronic; Clinic Visits; Clinical; Data; Development; Diet; Dietary Assessment; Disease; Eating; Enrollment; Environment; Epidemiology; Equilibrium; Experimental Designs; Extrinsic asthma; Faculty; Fatty acid glycerol esters; Food; Future; Goals; Guidelines; Health Food; Height; Home; Household; Immune; Immunologic Markers; Impulsivity; Individual Differences; Inflammation; Inflammatory; Intake; Interferon Type II; Interferons; Interleukin-13; Interleukin-4; Interleukin-5; Interleukin-6; Interleukins; Intervention; Life Style; Link; Measurement; Mediating; Modeling; Morbidity - disease rate; Obesity; Outcome; Parents; Pharmaceutical Preparations; Plasma; Play; Polysomnography; Populations at Risk; Prevention; Protocols documentation; Pulmonary Function Test/Forced Expiratory Volume 1; Recovery; Reduce health disparities; Research; Research Training; Sampling; Schedule; Self-control as a personality trait; Sleep; Sleep Deprivation; Spirometry; Symptoms; Testing; Time; Underserved Population; Unhealthy Diet; Visceral; Weight; Work; actigraphy; adequate sleep; asthma inhaler; career; clinical care; comorbidity; cytokine; design; dietary; emotional eating; ethnic minority; experience; food environment; food insecurity; high risk; immune function; improved; indexing; minority children; modifiable behavior; multi-component intervention; obesity in children; obesity risk; obesity treatment; obesogenic; overweight child; parent grant; pulmonary function; response; skills; sleep health; urban children; urban minority; urban setting

Project Summary / Abstract Urban children with asthma are at high risk for short sleep, due to an environment that jeopardizes sleep and asthma management. Further, this group suffers from altered immune balance, a key biological process contributing to individual differences in asthma morbidity and sleep health. Allergic asthma is a chronic inflammatory disorder driven primarily by disturbed T helper 1 (Th1)/ 2 (Th2) cytokine balance marked by Th2 cytokine (IL-4, IL-5 and/or IL-13) predominance. Experimental findings in healthy adults show that shortened sleep increases inflammatory cytokine (e.g., IL-6) and certain Th2 cytokine levels and that recovery sleep following sleep restriction promotes a return to immune balance. Whether sleep duration plays a key role in immune function and associated asthma activity in urban children with asthma remains a scientific gap. We will use an experimental design that targets sleep duration, because (1) the urban environment and asthma symptoms interact to shorten sleep, (2) sleep duration is a modifiable behavior overlooked in clinical care of urban children with asthma, and (3) experimental data are critical to test a causal link for sleep duration as a mechanism underlying immune balance and asthma. We will enroll urban children (N=204; ages 8-9 years) with persistent allergic asthma and adequate sleep duration (9-11 h) who will complete a 4-week within-subjects protocol that includes 3 scheduled experimental sleep conditions: (1) 1 week stabilized sleep (individualized; 9-11 h time in bed), (2) 1 week shortened sleep (1.5 h decrease in time in bed), and (3) 2 weeks recovery sleep (1.5 h increase in time in bed). We will monitor sleep duration (actigraphy) and lung function (home spirometry) daily and assess immune biomarkers weekly and at the midpoint of shortened sleep. To control time-in-study effects, 1/3 of our sample will receive only the stabilized sleep schedule across the 4-week protocol. In this project, we will study only urban children with allergic asthma who obtain sufficient sleep (9-11 h, within national guidelines). Our shortened sleep protocol will model the sleep loss that urban children with asthma can experience due to asthma and/or urban context. Additionally, our recovery sleep protocol simulates a sleep optimization intervention following shortened sleep in a well-controlled approach. The first aim of the study is to examine the effects of shortened sleep on immune balance [e.g., Th1 (Interferon-IFNγ)/Th2 (Interleukin-IL-4, IL-5, IL-13)R and plasma IL-6 levels]. The second aim involves determining the effects of recovery sleep on immune balance. The third aim involves examining the extent to which changes in immune balance are associated with changes in asthma-related lung function (changes in FEV1) under conditions of shortened and recovery sleep. Results from this study ultimately will support the development feasible, ecologically valid, and clinically meaningful interventions to optimize sleep duration, immune balance, and asthma in this at-risk group.

项目摘要 /摘要 由于环境危害睡眠和 哮喘管理。此外，该组患有改变的免疫平衡，这是一个关键的生物学过程 导致哮喘发病率和睡眠健康的个体差异。过敏性哮喘是慢性 炎症性疾病主要由受干扰的T辅助器1（TH1）/ 2（TH2）的细胞因子平衡驱动。 细胞因子（IL-4，IL-5和/或IL-13）优势。健康成年人的实验发现表明缩短 睡眠增加炎性细胞因子（例如IL-6）和某些TH2细胞因子水平，恢复睡眠 在睡眠限制后，促进了免疫平衡的回报。睡眠持续时间在 哮喘的城市儿童的免疫功能和相关的哮喘活性仍然是科学差距。我们将 使用针对睡眠持续时间的实验设计，因为（1）城市环境和哮喘 症状相互作用以缩短睡眠，（2）睡眠时间是一种可修改的行为，在临床护理中忽略了 哮喘的城市儿童和（3）实验数据对于测试睡眠时间的因果关系至关重要 免疫平衡和哮喘的基础机制。 我们将注册城市儿童（n = 204； 8-9岁），持续过敏和足够的睡眠 持续时间（9-11 h）将完成为期4周的受试者内部协议，其中包括3个计划的实验 睡眠条件：（1）1周稳定睡眠（个性化；床上9-11小时），（2）1周缩短睡眠 （卧床时间减少1.5 h），（3）2周恢复睡眠（床上的时间增加1.5 h）。我们将监视 每天的睡眠持续时间（行动学）和肺功能（家用肺活量法）和评估免疫生物标志物每周 在睡眠缩短的中点。为了控制成熟时间的效果，我们的样本中的1/3只会收到 跨4周协议稳定睡眠时间表。在这个项目中，我们将仅研究城市儿童 过敏性哮喘患有足够的睡眠（在国家准则中9-11小时）。我们缩短的睡眠协议 将模拟由于哮喘和/或城市环境，患有哮喘的城市儿童可能会遭受的睡眠损失。 此外，我们的恢复睡眠协议模拟睡眠缩短后的睡眠优化干预措施 以良好的控制方法。 该研究的第一个目的是检查睡眠缩短对免疫平衡的影响[例如，Th1 （Interferon-IFNγ）/Th2（介体-IL-4，IL-5，IL-13）R和血浆IL-6水平]。第二个目标涉及 确定恢复睡眠对免疫平衡的影响。第三个目的涉及检查范围 免疫平衡的变化与哮喘相关肺功能的变化有关（变化 FEV1）在缩短和恢复睡眠条件下。这项研究的结果最终将支持 开发可行的，生态上有效且具有临床意义的干预措施，以优化睡眠持续时间， 该高危组的免疫平衡和哮喘。