Contextual and Health Behavior Effects on Epigenetic Aging Among African Americans

背景和健康行为对非裔美国人表观遗传衰老的影响

• 批准号: 9754796
• 负责人: Steven R Beach
• 金额: $ 63.45万
• 依托单位: UNIVERSITY OF CONNECTICUT STORRS
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-08-02 至 2023-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9754796
• 关键词: Acceleration; Accounting; Address; Adolescence; Adolescent; Adolescent and Young Adult; Adult; Affect; African American; Age; Aging; Alcohol consumption; Alcohol or Other Drugs use; Behavior; Biological; Biological Assay; Biological Markers; Blood; Blood specimen; Buffers; Censuses; Characteristics; Childhood; Chronic Disease; Chronology; Collaborations; Collection; Communities; Conscious; Cytokine Gene; DNA Methylation; Data; Data Set; Development; Diet; Discrimination; Disease; Economics; Environment; Epigenetic Process; Ethnic group; Event; Exposure to; Family; Family and Community Health Study; Family member; Funding; Future; Gene Expression; Glucocorticoids; Goals; Health; Health Status; Health behavior; Individual; Inflammation; Inflammatory; Intervention Studies; Investigation; Life; Life Style; Link; Marijuana; Measures; Mediating; Mediator of activation protein; Methylation; Modeling; Morbidity - disease rate; Outcome; Parents; Participant; Pathway interactions; Patient Self-Report; Positioning Attribute; Prevention; Prevention program; Preventive Intervention; Process; Race; Reaction; Reporting; Research; Research Personnel; Resources; Risk; Role; Sampling; Scientist; Smoking; Societies; Source; Stress; System; Testing; Time; Toxic Environmental Substances; Toxic effect; Translations; Variant; Weather; Work; Youth; age related; base; behavior influence; cohort; coping; design; drinking; early childhood; early life stress; epigenetic marker; epigenetic variation; experience; genome wide methylation; healthy aging; heuristics; improved; indexing; inflammatory marker; longitudinal dataset; marijuana use; mortality; primary caregiver; prospective; protective factors; racial and ethnic; response; social; stressor; young adult

ABSTRACT: Considerable evidence exists linking early stress to accelerated aging, but potential mechanisms (mediators) accounting for this effect are poorly understood. Likewise, the impact of continuing stress in young adulthood on accelerated aging is largely unknown. Compounding the lack of information regarding mechanisms and timing of effects, available research is limited because it has focused mostly on White samples -- in spite of the fact that Blacks have significantly higher rates than other racial/ethnic groups of almost every type of chronic illness, as well as most markers of inflammation, and epigenetic aging (epi-A) —i.e., the difference between chronological age, and biological age, based on epigenetic changes in DNA methylation. The proposed research is designed to examine: a) factors that affect accelerated aging in Blacks, especially economic and race- related stress; and b) the role of mediators and moderators that may be useful targets for preventive interventions, such as substance use and poor diet, and also protective factors. A focus of the current investigation is testing alternative pathways to accelerated aging attributable to early and later stressors. One pathway focuses on stressor effects on potentially unhealthy behavior (e.g., substance use, diet) that may, in turn, give rise to chronic diseases of aging. This possibility is supported by evidence that stressful life events, especially those linked to discrimination, predict life style choices. Conversely, stress effects may also accelerate aging by altering functioning of the glucocorticoid system. Or, the two pathways may be interrelated. In addition, we focus on expanding what is known about the range of stressors within a given developmental period that are most critical, and the extent to which protective factors affect epi-A. Addressing an important limitation of prior research, we will have reliable, sensitive biomarkers of smoking, marijuana, alcohol use, and diet available at two time points as well as census track and parent report indices of stressors at multiple time points, allowing and us to supplement self-report measures and examine models more rigorously and with greater precision than has previously been possible. The proposed research will focus on 470 young adults who are part of a larger (N=889) panel study of Black families, the Family and Community Health Study. FACHS has followed a cohort of “target” participants from ages 10 to 28, along with their parents and family members. By characterizing methylation using the Illumina Epic array for two time points in young adulthood (28 and 33), we will be able to determine change in epi-A; i.e., the extent to which accelerated aging continues to be malleable in young adulthood. Using existing self- and parental reports of a variety of stressors-- from 8 waves of data, along with well-validated epigenetic biomarkers of epi-A, smoking, and drinking, we will be able to leverage the exceedingly rich existing prospective FACHS dataset, including its information on stress, protective factors, substance use, and coping, with the goal of informing preventive intervention research that can address the sources of disparities in healthy aging.

摘要：已有大量证据表明早期应激与加速衰老有关，但存在潜在的机制