We hypothesize that black women experience accelerated biological aging in response to repeated or prolonged adaptation to subjective and objective stressors. Drawing on stress physiology and ethnographic, social science, and public health literature, we lay out the rationale for this hypothesis. We also perform a first population-based test of its plausibility, focusing on telomere length, a biomeasure of aging that may be shortened by stressors. Analyzing data from the Study of Women’s Health Across the Nation (SWAN), we estimate that at ages 49–55, black women are 7.5 years biologically “older” than white women. Indicators of perceived stress and poverty account for 27% of this difference. Data limitations preclude assessing objective stressors and also result in imprecise estimates, limiting our ability to draw firm inferences. Further investigation of black-white differences in telomere length using large-population-based samples of broad age range and with detailed measures of environmental stressors is merited.
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Excessive prevalence of stress-related diseases of aging among nonelderly black women calls for better understanding and reversal, per se. In addition, life history theory suggests that local population health and life expectancy play a role in the development of life history traits such as reproductive strategies and risk-taking behavior (Chisholm 1993, 1999; Wilson and Daly 1997). Chisholm (1993, 1999) theorizes that the chronic risk and uncertainty suffered by adults of reproductive and working age who face chronic, multiple stressors could compromise their ability to invest in or buffer their children from risk through the development of secure attachments, with potentially lifelong implications. Stressful life experiences in childhood can also result in lifelong inefficiency in one’s physiological adaptation to stressors or in a conditioned predisposition to overreact to challenges to homeostasis, with adverse health implications (McEwen 1998).
In the most recent decades, gendered aspects of US public sentiment on race may have severely limited black men’s role in providing social and economic security for their families, while raising expectations of black women, especially in high poverty populations. For example, young, less-educated black men have experienced a long secular decline in employment rates, continuing even through the labor market expansion of the 1990s (Holzer et al. 2005). At the same time, incarceration rates of young, less-educated black men soared (Western 2006), dramatically disrupting their potential to contribute to family support, while “welfare to work” requirements heightened the demands on black women (Geronimus and Thompson 2004; Jarrett and Burton 1999).
For example, 30-year-old Francine was the primary caregiver of both her 6-year-old severely asthmatic son and her mother, who, during the course of the ethnography, suffered a stroke, a heart attack, and underwent tumor surgery. Francine herself developed stomach cancer. Yet, Burton and Whitfield note, “like many of the mothers in the ethnography, Francine endured tremendous physical pain, going to the doctor only when the pain was unbearable and when she ‘didn’t have other folks to take care of’” (2003:17). Another example was Barbara, who at age 37 suffered from multiple chronic health problems, including diabetes, back injury, kidney problems, migraines, hernias, depression, and anxiety. She was not unusual among the study participants.
Unhealthy behaviors can also be enabled or facilitated by environmental triggers, such as ethnically targeted cigarette advertising or the presence of many liquor stores and fast-food restaurants in central-city neighborhoods, whose residents also often lack spatial accessibility to healthy diets (LaViest and Wallace 2002; Stoddard et al. 1998; Zenk et al. 2005, 2006).
Telomere length in women around this age range is about 7,000 base pairs; thus, crudely, there is a loss of about 6–7% of telomere length per year in midlife.
As a robustness test, we also estimated models using the mean of the triplicate qPCR amplifications and obtained similar results.
In fact, depending on the length of interval between DNA sample collections, this short-term longitudinal approach would not always provide a reliable test of our hypothesis, which concerns the accumulated impact of stressors over a span of 30 or more years.
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Study analyses were supported by the National Institute on Aging (NIA), grants R01 AG032632 and T32 AG000221, and, through the Michigan Center on the Demography of Aging, grant AG012846. Support was also provided by the Center for Advanced Study in the Behavioral Sciences at Stanford University through a fellowship to Dr. Geronimus. The authors are also indebted to the SWAN Core Study and the SWAN Repository for collecting and providing access to study data, and to their sponsors, NIA, the National Institute of Nursing Research (NINR), the National Institutes of Health (NIH), Office of Research on Women’s Health, and the National Center for Complementary and Alternative Medicine. We are grateful for helpful comments from Drs. John Bound, Oliver Smithies, and MaryFran Sowers, from four anonymous reviewers, and from participants at the 2007 Chicago Biomeasures Workshop sponsored by CCBAR and The MacLean Center for Clinical Medical Ethics at The University of Chicago, in collaboration with the National Institute on Aging. We thank Diane Laviolette for help with preparation of the manuscript.
Telomere Length Measurement
The telomere amplification reaction for each sample included 35 ng of sample DNA, 25 μl of Power SYBR® Green PCR Master Mix (Applied Biosystems, Foster City, CA), 40 ng of E. Coli DNA, and the telomere primers, which have been specifically designed to prevent the formation of primer dimmers (Cawthon 2002). Final reaction volume was 50 μl. Telomere primer sequences were tel 1b 5′-CGGTTTGTTTGGGTTTGGGTTTGGGTTTGGGTTTGGGTT-3′ (final concentration of 100 nM) and tel 2b 5′-GGCTTGCCTTACCCTTACCCTTACCCTTACCCTTACCCT-3′ (final concentration of 900 nM) (Gil and Coetzer 2004). The single copy gene amplification reaction for each sample included 35 ng of sample DNA, 25 μl of Power SYBR® Green PCR Master Mix, 36B4 primers, and deionized, distilled water to a final volume of 50 μl. The 36B4 primer sequences are 36B4u 5′-CAGCAAGTGGGAAGGTGTAATCC-3′ (final concentration of 300 nM) and 36B4d 5′- CCCATTCTATCATCAACGGGTACAA-3′ (final concentration of 500 nM). All amplification runs were prepared in MicroAmp Optical 96-well reaction plates (Applied Biosystems, Foster City, CA). For each amplification run, known standards from a single DNA reference sample were also amplified (as described above) to ensure that the amplification was functioning as expected. Following the addition of all sample or standard DNA and reagents, the plates were sealed with a MicroAmp Optical Adhesive film (Applied Biosystems, Foster City, CA) and centrifuged at 3,000 rpm for approximately 20 s.
All reactions were performed on the ABI 7500 Real-Time qPCR system. Both amplifications (telomere and 36B4) included a heat-activation step at 9°C for 10 min. For the telomere amplification, this was followed by 25 cycles of 95°C for 15 s and 54°C for 1 min. For the 36B4 amplification, this was followed by 30 cycles of 95°C for 15 s, 58°C for 1 min. Fluorescence data was collected during the annealing/extension steps of both reactions. The instrument was set to run in 9600 emulation mode with auto ramping. Resulting data was analyzed with ABI’s SDS v1.2 software package using a manual Ct of 0.06 and the auto baseline setting. Telomere: 36B4 Ct ratios and telomere length were calculated using Cawthon’s (2002) formula.
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Geronimus, A.T., Hicken, M.T., Pearson, J.A. et al. Do US Black Women Experience Stress-Related Accelerated Biological Aging?. Hum Nat 21, 19–38 (2010). https://doi.org/10.1007/s12110-010-9078-0