||5R01CA220254-02 Interpret this number
||University Of Connecticut Storrs
||Contextual and Health Behavior Effects on Epigenetic Aging Among African Americans
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.
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