Stress-induced poor sleep: Sex differences, vulnerability & resilience factors

压力引起的睡眠不佳：性别差异、脆弱性

• 批准号: 8522230
• 负责人: Elissa S. Epel
• 金额: $ 22.48万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2012
• 资助国家: 美国
• 起止时间: 2012-08-01 至 2015-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8522230
• 关键词: Accounting; Arousal; Basic Science; Behavior; Biological; Biological Aging; Biological Markers; Biological Process; Buffers; Caregivers; Caring; Cell Aging; Child; Chronic stress; Circadian Rhythms; Cognitive; Conflict (Psychology); Cost Savings; Couples; Disease; Emotional; Emotions; Feedback; Fostering; Funding; Goals; Health; Hydrocortisone; Individual; Intervention; Lead; Length; Leukocytes; Link; Measurement; Measures; Mediating; Modeling; Mothers; Neurodevelopmental Disorder; Parents; Pathway interactions; Pattern; Personal Satisfaction; Persons; Physiological; Process; Psychological Stress; Recruitment Activity; Regulation; Reporting; Research; Risk; Sampling; Severities; Sex Characteristics; Shame; Sleep; Sleep Disorders; Social Environment; Source; Spouses; Stress; Testing; Vacuum; Woman; actigraphy; age related; autism spectrum disorder; awake; biological adaptation to stress; caregiving; cell age; design; emotion regulation; male; men; novel; psychobiologic; psychologic; public health relevance; resilience; response; sex; sleep onset; social stress; stress management; stressor; telomere; vigilance

DESCRIPTION (provided by applicant): Stress-induced poor sleep: Sex differences, vulnerability & resilience factors Caring for a child with a neurodevelopmental disorder is a source of chronic stress that can impair sleep, but not for all parents. There is little understanding of the exact psychological or biological mechanisms linking stress and sleep behavior, or the vulnerability and resiliency factors that promote or dampen the stress-sleep relationship. One plausible vulnerability factor is being high in stress sensitivity-certain psychological and biological processes that promote vigilance and arousal. The goal of the proposed project is to unpack the sleep-stress cycle, by examining: 1) stress-sensitivity related psychobiological predictors (emotional and cognitive reactivity and regulation and daily cortisol) of daily sleep (delayed onset, short duration, low efficiency, poor subjective quality); and 2) the ensuing effects of sleep on stress sensitivity variables. Individuals do not exist in a vacuum, and, if partnered, supportive or conflict-laden interactions within a partner dyad can dampen or exacerbate psychological and biological stress responses, further impacting sleep patterns. Therefore, our third goal is to examine if spousal/partner interactions compound or mitigate the effects of stress sensitivity on sleep. To this end, we propose to examine stress and sleep in a sample stratified on chronic stress, with 50 high stress couples (parents of children with Autism Spectrum Disorder or ASD) and 50 low stress couples, demographically similar parents of typically developing children (100 pairs total). We will efficiently piggyback the design and measures onto an already-funded R01 study on stress- induced cell aging that is currently following the sample of mothers. In the proposed project we will recruit their partners and add measures of objective sleep actigraphy, subjective sleep quality, daily psychological stress processes, and diurnal measures of cortisol over 10 consecutive days. The aims of the study are: 1) To assess whether daily stress sensitivity predicts poorer night to night sleep parameters within subjects and across the sample and explains the poorer sleep of the parents of children with ASD compared to control parents; 2) To assess whether supportive vs. strained partner interactions moderate the stress sensitivity-sleep relationship; and 3) To determine whether sex differences exist in the stress-sleep relationships in the above aims. Secondarily, using the R01-funded measures of stress-related biological aging, we will be able to test whether poor sleep, averaged across the 10 days of measurement, is associated with marked changes in biomarkers of chronic stress -- lower vagal tone, dysregulation of the HPA axis negative feedback loop, and shorter leukocyte telomere length. The proposed study answers unique and novel questions about the stress- sleep cycle with remarkable cost savings and efficiency by piggybacking onto the large longitudinal R01 study. Identifying the stress-related influences on nightly sleep within the parent dyads, and the resulting impact of sleep on stress markers, will have implications for both basic research and interventions.

描述（由申请人提供）：压力引起的睡眠不良：性别差异，脆弱性和弹性因素照顾患有神经发育障碍的儿童是慢性压力的来源，可能会损害睡眠，但并非所有父母。人们对压力和睡眠行为之间的确切心理或生物机制，或者促进或抑制压力-睡眠关系的脆弱性和弹性因素知之甚少。一个可能的脆弱因素是对压力的敏感性高，这种心理和生物过程会促进警觉和觉醒。该项目的目标是通过检查以下内容来解开睡眠-压力周期：1）与压力敏感性相关的心理生物学预测因素（情绪和认知反应和调节以及每日皮质醇）（延迟开始，持续时间短，效率低，主观质量差）;以及2） 睡眠对压力敏感性变量的影响。个人并不存在于真空中，如果伴侣在一对伴侣中相互支持或充满冲突，会抑制或加剧心理和生物压力反应，进一步影响睡眠模式。因此，我们的第三个目标是检查配偶/伴侣的互动是否会复合或减轻压力敏感性对睡眠的影响。为此，我们建议在一个按慢性压力分层的样本中检查压力和睡眠，其中有50对高压力夫妇（自闭症谱系障碍或ASD儿童的父母）和50对低压力夫妇，人口统计学上相似的典型发育儿童的父母（共100对）。我们将有效地将设计和措施搭载到已经资助的R 01研究中，该研究是关于压力诱导的细胞衰老，目前正在跟踪母亲的样本。在拟议的项目中，我们将招募他们的合作伙伴，并增加客观睡眠活动记录，主观睡眠质量，每日心理压力过程和连续10天的皮质醇昼夜测量的措施。这项研究的目的是：1）评估日常压力敏感性是否预测受试者和样本中夜间睡眠参数较差，并解释与对照父母相比，ASD儿童父母的睡眠较差; 2）评估支持性与紧张性伴侣互动是否调节压力敏感性-睡眠关系; 3）确定上述目标中的压力-睡眠关系是否存在性别差异。其次，使用R 01资助的与压力相关的生物衰老的测量，我们将能够测试在10天的测量中平均的睡眠不佳是否与慢性压力的生物标志物的显著变化相关-较低的迷走神经张力，HPA轴负反馈回路的失调，以及较短的白细胞端粒长度。拟议的研究回答了关于压力-睡眠周期的独特和新颖的问题，通过搭载大型纵向R 01研究，节省了显着的成本和效率。确定父母二人组中与压力相关的夜间睡眠影响，以及睡眠对压力标记物的影响，将对基础研究和干预措施产生影响。