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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：
10454285
负责人：
Jodi Ford
金额：
$ 36.7万
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 2024-07-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10454285
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 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 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.

摘要不良童年经历(ACE)和较短的端粒长度(TL)都与慢性成年期的疾病，然而，很少有研究人员研究ACE对生命过程早期或在发展的敏感时期，限制早期和/或发展时机干预的机会。此外，研究集中于假想的生物和心理机制，通过这些机制导致端粒缩短的因素是有限的。此外，外部背景暴露的影响青少年在TL上的邻居还没有被检查。在我们之前的研究中，我们发现青少年他们醒着的35%的时间都在他们居住的人口普查区域之外，因此背景暴露的影响包括青少年社区和其他常规场所(如学校、同龄人、活动等)，已知作为他们的“活动空间”，TL还没有被考察过。我们的研究将增加关于这种关系的证据通过检测发生在特定发育阶段(出生、出生、儿童早期、儿童中期和青春期)以及累积。我们还将调查生物 (HPA轴；头发皮质醇)和心理(抑郁和焦虑症状)应激途径 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青少年暴露在当代个人和社会空间逆境和TL中。我们的具体目标是检查：发生在儿童和青春期(出生、0-5岁、6-10岁和11-10岁)的ACEs模式 17岁)及其对青春期生物压力、心理困扰和TL的影响；生物应激与TL、心理困扰与TL；生物应激与TL之间的关系心理困扰在儿童/青少年王牌类型与青少年目标语言之间的关系中起中介作用；青春期当代个体和活动空间王牌模式及其对青少年的影响生物压力、心理困扰和TL，占11岁之前的A；以及哪种生物压力和心理痛苦调节了当代生活方式之间的关系个人和活动空间ACES和青少年TL，占11岁之前的ACES。在分析中在每个目标中，我们都将探索性作为假想关系的调节因素。这项研究是次要的分析了从NIH资助的两项研究中收集的数据，这些研究涉及1018名青少年。将构建研究变量从现有数据并使用描述性统计分析数据分布，识别离群值，管理数据如果需要进行转化以实现常态化，并总结学科特点。我们将使用潜班级用于假设检验的分析和多元线性回归模型。我们的方法将确定以下子组儿童和青春期的ACE增加了青少年患较短TL的风险，以及哪些生理和心理压力途径可以解释这些关系。调查结果将向针对特定暴露模式和应激对TL的影响制定干预措施。