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.
As the public impact of age-related diseases has grown over time, it has become apparent that improving the quality of longer lives requires further exploration of the causes of accelerated epigenetic aging (epi-A), which forecasts heightened risk for all-cause morbidity and mortality. This proposal seeks funding to conduct new assays on existing blood samples from members of the Family and Community Health Study (FACHS), and to collect another wave of blood from these individuals, in order to assess the impact of various stressors and supports on epi-A (at age 28) and changes in epi-A from age 28 to age 33.
