Monday, Nov 3
a PSC Research Project
Investigators: Arline T. Geronimus, Amy Jo Schulz
We are conducting the first community-based study of racial differences in telomere length and allostatic load in adults of broad age range and their association with urban stressors. We hypothesize that chronic stressors experienced by black urban residents accelerate biological aging and chronic disease onset.
Evidence suggests that leukocyte telomere length (TL) may be an indicator of biological age that can be affected by stress; and that allostatic load is an indicator of stress-mediated wear on important body systems. We have a unique opportunity to supplement survey data scheduled to be collected by the Healthy Environments Partnership (HEP) – a partnership between the University of Michigan and community-based organizations and health service agencies in Detroit – with blood collection and lab analyses of TL, telomere-related compounds, and allostatic load, including measures of the biological stress response, inflammation, and cardiovascular and metabolic risk. By appending a venous blood draw to the HEP survey, we can construct a data set including these biomeasures and detailed psychosocial and physical environmental measures in a cost-effective way; enhance access to a hard-to-reach population; and facilitate dissemination of study results to improve community health.
We will estimate a series of regressions of TL and allostatic load on race, controlling for the confounding effects of age, gender, and socioeconomic characteristics and exploring the extent to which psychosocial or environmental stressors mediate remaining racial differences. To ensure findings are not driven by functional form we will reanalyze the data using matching methods. We will also model disease outcomes, conditional on telomere length, on high oxidative stress or low telomerase activity to explore biological mechanistic pathways between telomere length and chronic disease.
We expect study findings to shed light on the plausibility of cumulative stress hypotheses to explain the social patterning of disease; the viability of telomere length as a biomeasure of aging; and the mechanistic pathways through which stressors may be linked to telomere length and disease processes. If findings from this interdisciplinary collaborative effort support study hypotheses, this could constitute a significant advance in the understanding of the biological mechanisms that underlie racial inequality in health.
|Funding:||National Institute on Aging (1 R01 AG032632)|
Funding Period: 09/01/2008 to 06/30/2014
Country of Focus: USA