A large body of evidence links low socioeconomic status (SES) to the development of age- related diseases and to earlier mortality. The biological mechanisms are not well elucidated, although it appears to be in part through chronic exposure to stressful conditions and stress-mediated damage. The maintenance of telomeres (the DNA caps at the ends of chromosomes) may be mechanistically involved in disease processes and premature mortality. Leukocyte telomere length generally shortens with chronological age and with chronic stress, and predicts mortality independent of age. Further, a recent study found shorter telomeres in people with low socioeconomic status (SES). Leukocyte telomere length thus may link social disadvantage to earlier mortality, and is the focus of this study. Methods: Using data from the National Health and Nutrition Examination Survey (NHANES) 1999- 2002, the proposed study will be the first to examine telomere length in a nationally representative sample, allowing us to expand on past findings linking SES to shorter telomere length, and telomere length to mortality. We will be able to examine these relationships in a racially and ethnically diverse sample, and examine moderating effects of genetic vulnerabilities, as well as mediating effects of health behaviors and mental health. Our interdisciplinary team represents epidemiology, genetics, biostatistics, psychology, and sociology. We will measure telomere length and polymorphisms in three genes (TERT, TERC, PINX1) that regulate telomere length from archived DNA in approximately 7,200 men and women, aged 20 to 85+, who participated in the NHANES 1999-2002 study. We will examine whether SES predicts telomere length and whether this is mediated by health behaviors and mental health. We will also examine gene-environment interactions, specifically whether low SES interacts with polymorphisms in these 3 genes to predict telomere length. Lastly, in the sample over 50 years of age, we will examine whether telomere length predicts mortality 8 years later, and whether telomere length mediates the well-established relationship between SES and mortality. For all analyses, we will examine whether relationships exist across the entire sample and within three racial/ethnic groups (i.e., Mexican-Americans, African-Americans, and non-Hispanic Whites). Relevance: This study will help determine if social disadvantage is linked to telomere shortening;the behavioral and mental health mediators and genetic moderators of the association between SES and telomere length;and if telomere length mediates the relationship between low SES and early mortality. It will thus help determine whether telomere length might become a useful risk factor to monitor and target of intervention. Understanding the aging process is central to preventing premature morbidity and mortality and to lengthening the healthy lifespan.

Public Health Relevance

This study will inform possible interventions and policies to help the nation to achieve the Healthy People 2010 goal of eliminating health disparities, which necessitates understanding the mechanisms by which disparities develop. Findings from the proposed research will shed light on cellular aging as a biological pathway through which social disadvantage may increase vulnerability to premature mortality. Using a nationally representative sample, it will provide data on the role of socioeconomic status within and across racial/ethnic groups and the interaction with genetic vulnerabilities in determining cell aging, and in turn, how cell aging predicts mortality.

National Institute of Health (NIH)
National Institute on Aging (NIA)
Research Project (R01)
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Behavioral Genetics and Epidemiology Study Section (BGES)
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Nielsen, Lisbeth
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University of California San Francisco
Schools of Medicine
San Francisco
United States
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