Childhood Adversity, Biopsychosocial Pathways, and Telomere Length in Adolescence

童年逆境、生物心理社会途径和青春期端粒长度

基本信息

批准号：
10066463
负责人：
Jodi Ford
金额：
$ 37.67万
依托单位：
OHIO STATE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-09-10 至 2023-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10066463
关键词：
11 year old Accounting Adolescence Adolescent Adolescent Development Adult Affect Area Biological Biological Markers Biological Testing Birth Caregivers Cell Aging Cellular Phone Cellular Stress Censuses Characteristics Child Childhood Chromosomes Chronic Disease Cohort Studies Communities Data Data Analyses Development Disease Exposure to Family Funding Future Geography Hair Health Home environment Hydrocortisone Individual Intervention Length Life Life Cycle Stages Linear Regressions Location Longevity Measures Mediating Mental Health Mission Modeling Neighborhoods Normalcy Parents Pathway interactions Pattern Personal Satisfaction Psychological Stress Reporting Research Research Personnel Risk Safety Saliva Sampling Schools Source Stress Structure Subgroup Telomere Shortening Testing Time United States National Institutes of Health Violence Youth adolescent health adverse childhood events aged anxiety symptoms biopsychosocial childhood adversity data space depressive symptoms early childhood epigenetic regulation experience high risk hypothalamic-pituitary-adrenal axis indexing middle childhood novel peer physical conditioning prevent psychologic psychological distress psychological symptom secondary analysis sex socioeconomic disadvantage statistics suburb telomere therapy development

项目摘要

Summary Both adverse childhood experiences (ACEs) and shorter telomere length (TL) have been associated with chronic disease in adulthood, however, few researchers have examined effects of ACEs on TL early in the life course or at sensitive periods in development, limiting opportunities for earlier and/or developmentally timed intervention. Additionally, studies focused on hypothesized biological and psychological mechanisms through which ACEs contribute to shortening of telomeres are limited. Moreover, the effect of contextual exposures outside of adolescents' neighborhood on TL has not been examined. In our previous research, we found that adolescents spend 35% of their waking time outside of their residential census tract, thus the effect of contextual exposures encompassing adolescents' neighborhood and other routine locations (e.g. school, peers, activities, etc.), known as their “activity space,” on TL has not been examined. Our study will add to the evidence on the relationship between ACEs and TL in adolescence by examining ACEs occurring at specific developmental periods (birth, early childhood, middle childhood, and adolescence) as well as cumulatively. We will also investigate biological (HPA axis; hair cortisol) and psychological (depressive and anxious symptoms) stress pathways through which ACEs may affect TL. Moreover, we will also use novel activity space data to examine relationships between adolescents' exposure to contemporary individual and sociospatial adversity and TL. Our specific aims are to examine: patterns of ACEs occurring across childhood and adolescence (birth, 0-5 years, 6-10 years, and 11 to 17 years) and their effect on adolescent biological stress, psychological distress, and TL; relationships between biological stress and TL and psychological distress and TL; the extent to which biological stress and psychological distress mediate the relationship between patterns of child/adolescent ACEs and adolescent TL; patterns of contemporary individual and activity space ACEs during adolescence and their effect on adolescent biological stress, psychological distress, and TL, accounting for ACEs prior to age 11 years; and the extent to which biological stress and psychological distress mediate the relationship between patterns of contemporary individual and activity space ACEs and adolescent TL, accounting for ACEs prior to age 11 years. In the analysis of each aim we will explore sex as a moderator of the hypothesized relationships. The study is a secondary analysis of data collected from two NIH funded studies of 1,018 adolescents. Study variables will be constructed from existing data and analyzed using descriptive statistics for data distribution, identify outliers, conduct data transformation if needed to achieve normality, and summarize subject characteristics. We will use latent class analysis and multiple linear regressions models for hypothesis testing. Our approach will identify sub-groups of ACEs across childhood and adolescence that increase adolescents' risk for shorter TL as well as the extent to which biological and psychological stress pathways explain these relationships. The findings will inform the development of interventions targeted to specific exposure patterns and the effects of stress on TL.

概括不良的童年经历（ACE）和较短的端粒长度（TL）都与慢性然而，很少有研究人员研究过 ACEs 对生命历程早期或 TL 的影响。在发育的敏感时期，限制早期和/或发育定时干预的机会。此外，研究的重点是探索 ACE 的生物和心理机制。此外，环境暴露对端粒缩短的影响是有限的。在我们之前的研究中，我们发现青少年对 TL 的邻里关系没有得到检验。 35% 的醒着时间都在居住人口普查区之外度过，因此受到环境暴露的影响涵盖青少年的社区和其他日常地点（例如学校、同伴、活动等），已知作为他们的“活动空间”，TL 尚未得到检验，我们的研究将增加这种关系的证据。通过检查发生在特定发育时期（出生、出生、幼儿期、童年中期和青春期）以及累积性的研究。（HPA 轴；头发皮质醇）和心理（抑郁和焦虑症状）压力途径此外，ACE 可能会影响 TL。此外，我们还将使用新颖的活动空间数据来检查之间的关系。青少年面临当代个人和社会空间逆境和 TL 我们的具体目标是检查：儿童期和青春期（出生、0-5 岁、6-10 岁和 11 岁至 11 岁）发生的 ACE 模式 17 岁）及其对青少年生物压力、心理困扰和 TL 关系的影响；生物应激和 TL 以及心理困扰和 TL；生物应激和 TL 的程度；心理困扰介导儿童/青少年 ACE 模式与青少年 TL 之间的关系；当代青少年个体和活动空间ACE模式及其对青少年的影响生物压力、心理困扰和 TL，解释 11 岁之前的 ACE 及其程度；生物压力和心理困扰调解当代模式之间的关系个人和活动空间 ACE 和青少年 TL，在分析中考虑了 11 岁之前的 ACE。对于每个目标，我们都将探索性作为所探索的关系的调节因素。将对 NIH 资助的两项针对 1,018 名青少年的研究收集的数据进行分析，构建研究变量。根据现有数据并使用数据分布的描述性统计进行分析，识别异常值，进行数据处理如果需要实现常态化，并总结主题特征，我们将使用潜在类。用于假设检验的分析和多元线性回归模型将识别子组。整个童年和青春期的 ACE 会增加青少年 TL 较短的风险以及哪些生物和心理途径强调解释了这些关系。针对特定暴露模式和压力对 TL 的影响制定干预措施。