Article

Socioeconomic Status, Financial Strain, and Leukocyte Telomere Length in a Sample of African American Midlife Men

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Abstract

Background: African American men in the USA experience poorer aging-related health outcomes compared to their White counterparts, partially due to socioeconomic disparities along racial lines. Greater exposure to socioeconomic strains among African American men may adversely impact health and aging at the cellular level, as indexed by shorter leukocyte telomere length (LTL). This study examined associations between socioeconomic factors and LTL among African American men in midlife, a life course stage when heterogeneity in both health and socioeconomic status are particularly pronounced. Methods: Using multinomial logistic regression, we examined associations between multiple measures of SES and tertiles of LTL in a sample of 92 African American men between 30 to 50 years of age. Results: Reports of greater financial strain were associated with higher odds of short versus medium LTL (odds ratio (OR)=2.21, p = 0.03). Higher income was associated with lower odds of short versus medium telomeres (OR=0.97, p = 0.04). Exploratory analyses revealed a significant interaction between educational attainment and employment status (χ (2) = 4.07, p = 0.04), with greater education associated with lower odds of short versus long telomeres only among those not employed (OR=0.10, p = 0.040). Conclusion: Cellular aging associated with multiple dimensions of socioeconomic adversity may contribute to poor aging-related health outcomes among African American men. Subjective appraisal of financial difficulty may impact LTL independently of objective dimensions of SES. Self-appraised success in fulfilling traditionally masculine gender roles, including being an economic provider, may be a particularly salient aspect of identity for African American men and have implications for cellular aging in this population.

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... The most common assessment of SSS asks the individual to place themselves on a ten-rung ladder, where the top rung represents the highest socioeconomic status (e.g., the most income, education, and prestigious occupations) and the bottom rung the lowest status (e.g., the least income, education and least desirable occupations) (Adler et al., 2000). Individuals make this determination based on the factors they deem most important for status, which allows for a more nuanced determination of social status in that respondents may factor in debt or wealth as well as income, or quality of their education as well as years of schooling (Schrock et al., 2018). Meta-analyses support that SSS is associated with physical health, even after accounting for objective SES (Cundiff and Matthews, 2017;Zell et al., 2018). ...
... Limited work has linked SSS to aging-related biomarkers. SSS has been associated with inflammation in young adults (Freeman et al., 2016) and the subjective assessment of finances was associated with leukocyte telomere length (Schrock et al., 2018). To our knowledge, the current study is the first to examine whether SSS is associated with epigenetic aging, in women in early middle age. ...
... The current study was the first to find subjective social status (SSS) at the national level (i.e., comparison of self to others in the United States) to be a robust predictor of epigenetic age acceleration, independently of objective SES, for both Black and White women. These findings are in line with evidence (Schrock et al., 2018) that suggests SSS may impact cellular aging independently of SES, and that when both objective SES and SSS have been considered, SSS remains significantly associated with indices of health (Singh-Manoux et al., 2005). ...
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Objective Subjective social status (SSS), an individual’s assessment of their own social status in relation to others, is associated with health and mortality independently of objective SES; however, no studies have tested whether SSS influences epigenetic aging. The current study examines if SSS is associated with epigenetic age acceleration in both Black and White women, independently of objective SES measured during both childhood and adulthood. Method For 9- and 10-year-old Black and White girls, parental education and annual household income was obtained. At ages 39 - 42, 361 participants (175 Black, 186 White) reported their current education, household income, and SSS, and provided saliva to assess age acceleration using the GrimAge epigenetic clock. Linear regression estimated the association of SSS with epigenetic age acceleration, controlling for objective SES (current education, current income, parents’ education, income during childhood), smoking, and counts of cell types. Results When all objective SES variables were included in the model, SSS remained significantly associated with epigenetic age acceleration, b = -0.31, p =.003, ß = -.15. Black women had significantly greater age acceleration than White women, (t(359) = 5.20, p >.001, d = 0.55) but race did not moderate the association between SSS and epigenetic age acceleration. Conclusions Women who rated themselves lower in SSS had greater epigenetic age acceleration, regardless of income and education. There was no difference by race for this association.
... In addition to discrimination, chronic stress stemming from differences in SES is often investigated as a possible explanation for disparities in rates of telomere shortening between African Americans and European Americans (Gebreab et al., 2016;Geronimus et al., 2015;Needham et al., 2013;Theall, Brett, Shirtcliff, Dunn, & Drury, 2013). Financial strain, education years completed, and household income are some of the most commonly tested SES measures, and all have been associated with either shorter TL or increased telomere attrition in African American cohort studies (Needham et al., 2013;Schrock et al., 2018;Shiels et al., 2011). Thus, we decided to use these three measures of SES as covariates. ...
... Low SES is believed to increase stress levels, and differences in SES are commonly cited as a possible explanation for differences in TL between African Americans and European Americans (eg, Gebreab et al., 2016;Geronimus et al., 2015;Needham et al., 2013;Theall et al., 2013). While many of these studies have found inverse associations between measures of SES and both TL and rate of telomere shortening in African Americans (eg, Needham et al., 2013;Schrock et al., 2018), others have failed to do so, while simultaneously reporting associations that link TL with discrimination (Chae et al., 2016;Lee et al., 2017;this study). We also did not observe any associations between SES and TL, either with or without the unfair treatment data. ...
Article
Objectives: Experiences of interpersonal discrimination are pervasive stressors in the lives of African Americans. Increased discrimination stress may cause premature aging. Telomere length (TL) is a plastic genetic trait that is an emerging indicator of cellular health and aging. Short TL is a risk factor for the earlier onset of disease. TL shortens with age, a process that may be accelerated by psychosocial stress. Our study explores the relationship between TL and experiences of discrimination in the form of self-reported unfair treatment (UT). Methods: Using a qPCR-based method, we measured TL in DNA from saliva samples provided by 135 African American adults from Tallahassee, FL. We developed discrimination measures using a modified survey that explores nine social domains of self-reported unfair treatment experienced both directly and indirectly. We used multiple regression to examine associations between UT and TL. Results: We found that racial discrimination in the form of self-reported unfair treatment attributed to race (UT-Race-Self) is inversely associated with TL. Conclusions: The significant association between increased UT-Race-Self and shorter telomeres supports the hypothesis that psychosocial stress stemming from racial discrimination may affect TL. The potential impact of discrimination on TL may contribute to premature biological aging and racial health inequalities seen in African Americans.
... However, in these cohorts, the African American participants were mostly of higher socioeconomic status, and one cohort included only women. Given that low socioeconomic status can influence both optimism levels and telomere length (Alexeeff et al., 2019;Robertson et al., 2013;Schrock et al., 2018), the relationship between optimism and telomere length in a more socioeconomically diverse group of African Americans might differ from associations observed in prior work. ...
Article
Background Optimism is linked with greater longevity in both White and African American populations. Optimism may enhance longevity by slowing cellular aging, for which leukocyte telomere shortening is a biomarker. However, limited studies have examined the association of optimism with leukocyte telomere length among African Americans. Methods Data are from 723 men and 1,244 women participating in the Jackson Heart Study (age=21-93 years). We used multivariable linear regression models to conduct cross-sectional analyses examining whether higher optimism was associated with longer mean absolute leukocyte telomere length (assayed with Southern blot analysis). Models adjusted for sociodemographic characteristics, depressive symptomatology, health conditions, and health behavior-related factors. We also considered potential effect modification by key factors. Results In the age-adjusted model, optimism, measured as a continuous variable, was not associated with leukocyte telomere length (β=0.01, 95%CI: -0.02, 0.04). This association remained null in the fully-adjusted model (β=0.02, 95%CI: -0.02, 0.05) and was also null when considering optimism as a binary measure (higher vs. lower optimism). We found no evidence of effect modification by sex, age, body mass index, income, or chronic conditions. Conclusions Optimism was not associated with leukocyte telomere length among African American adults. Future studies should investigate alternate biological and behavioral mechanisms that may explain the optimism-health association.
... Como señala un trabajo de la misma autora, este mismo acortamiento del telómero se ha observado en hombres afroamericanos estadounidenses, grupo social que suele presentar peores resultados de salud que sus homólogos anglosajones. Así, en este grupo étnico se observó que el mayor estrés económico y los peores niveles educativos y laborales se vinculaban a una mayor probabilidad de acortamiento del telómero, y este envejecimiento celular acelerado podría contribuir a peores resultados de salud (Schrock et al., 2018). De hecho, uno de los peores resultados de salud sería la pérdida de rendimiento cognitivo, como demuestra otro trabajo reciente que correlaciona el mayor acortamiento del telómero con una mayor pérdida de volumen del hipocampo y del cerebelo. ...
... Longitudinal changes in financial strain have been associated with changes in ambulatory systolic blood pressure; however, improvements in chronic financial strain may result in improved cardiovascular and neuroendocrine functioning among men [49]. Among African American men, financial strain has been associated with shorter leukocyte telomere length, an indicator of cellular aging [50]. Drivers may also find gender rolebased expectations to be a source of financial stress; NYC South Asian taxi drivers have reported stressors around fulfilling familial obligations to be the sole or main providers [1]. ...
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Taxi and for-hire vehicle (FHV) drivers are a predominantly immigrant population facing a range of occupational stressors, including lack of workplace benefits and increasing financial strain from tumultuous industry changes and now COVID-19’s devastating impact. Bilingual research staff surveyed 422 New York City taxi/FHV drivers using a stratified sampling approach in driver-frequented locations to examine drivers’ health and financial planning behaviors for the first time. Drivers lacked health insurance at double the NYC rate (20% vs. 10%). Life insurance and retirement savings rates were lower than U.S. averages (20% vs. 60%, 25% vs. 58%, respectively). Vehicle ownership was a significant predictor of health insurance, life insurance, and retirement savings. Compared to South Asian drivers, Sub-Saharan African drivers were significantly less likely to have health insurance and North African, and Middle Eastern drivers were significantly less likely to have retirement savings. Although most drivers indicated the importance of insurance and benefits, < 50% understood how to use them. Drivers felt primary care coverage to be most important followed by other health-related coverage, retirement benefits, and life insurance. Results reveal compelling addressable gaps in insurance and benefits coverage and the need to implement accessible financial literacy with navigation and advising services and programs.
... For instance, data from the National Health and Nutrition Examination Survey (NHANES) demonstrated that less education was associated with shorter telomeres in African American and Whites, but no associations were observed with income. However, less income has been associated with shorter telomeres in midlife African American men (Schrock et al., 2018). Taken together, these data demonstrate variations in telomere length by social category, some of which are inconsistent with established health disparities. ...
Article
Objective: Studies have linked self-reported discrimination to telomere attrition, a biological marker of accelerated cellular aging. However, it is unknown whether intersections between social categories-race, socioeconomic status (SES), sex, and age-influence the association of varying forms of discrimination with telomere length. We examined these associations in a socioeconomically and racially/ethnically diverse urban sample. Methods: Cross-sectional data were from 341 middle-aged (30-64 years) African American and White, community participants in the Healthy Aging in Neighborhoods of Diversity across the Life Span Study (HANDLS). Multiple regression models examined up to 3-way interactions between a discrimination measure (i.e., everyday, racial, gender, lifetime burden, and frequency of discrimination across sources) and two social categories. Results: After adjusting for depressive symptoms, waist circumference, and lifetime substance use, two themes emerged: 1) among women with higher SES, a) greater lifetime discrimination burden (b = -0.23, p = .011), gender discrimination (b = -0.29, p = .040), and racial discrimination (b = -0.24, p = 0.023) and 2) among younger adults, irrespective of race and sex, greater frequency of discrimination across sources (b = 0.002, p = .008) was associated with shorter telomeres. Conclusions: Irrespective of race, women with higher SES and younger adults reporting greater discrimination may be at particular risk for accelerated aging. Telomere attrition promotes and accelerates chronic health conditions for which there are health disparities. Future research explicating intersections among specific discrimination indices and social categories is warranted.
... Using a life course approach, we have previously reported that three types of chronic social stress (poverty, violence and caregiving of a dependent person) are associated with telomere erosion [5]. Lower socioeconomic status (SES) is generally associated with shorter telomeres [6,7], but results are not consistent across ethnic groups [7], or in older adults who have exceeded their life expectancy at birth and who can be considered survivors of their birth cohorts [8]. ...
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This study assessed whether telomere length is related to chronic conditions, cardiovascular risk factors, and inflammation in women aged 65 to 74 from Northeast Brazil. Participants were selected from two sources, a representative sample of the International Mobility in Aging Study (n = 57) and a convenience sample (n = 49) recruited at senior centers. Leukocyte telomere length was measured by quantitative polymerase chain reaction from blood samples in 83 women. Natural log-transformed telomere/single copy gene ratio was used as the dependent variable in the analysis. Blood analyses included inflammatory markers (high-sensitivity C-reactive protein and interleukin-6), total, low-density lipoprotein and high-density lipoprotein cholesterol, triglycerides, glucose and glycosylated hemoglobin. Self-rated health, chronic conditions, cardiovascular risk factors and inflammatory markers were not associated with telomere length. No significant independent association was found between telomere length and anthropometric measures or blood markers, even after adjusting for age, education and adverse childhood events among these older women in Northeast Brazil. Our results did not confirm the hypothesis that chronic conditions, cardiovascular risk factors or inflammation are associated with shorter telomere length in these women who have exceptional survival relative to the life expectancy of their birth cohort.
... Home ownership, not commonly studied, seems to have a fairly consistent relationship with longer TL, yet lack of home ownership is likely itself a correlate or outcome of some other more fundamental cause of stress. Across socioeconomic stressors, age and race emerge as potentially important moderators-a finding consistent with work published after the search date for this review (Flannagan et al., 2017;Schrock et al., 2017). While financial and educational resources are fairly consistently unrelated to TL among young and middle-aged adults, they may have a more complex relationship with TL for older adults. ...
Article
Numerous studies examine the relationship between social stressors and telomere length (TL). Beyond considering methods and major findings, this scoping systematic review takes a novel approach as it groups studies according to the types of social stressor considered and by age groups. Following PRISMA guidelines, we searched PubMed, Web of Science, Embase, and Scopus. We included all English-language human subject research articles that modeled any measure of TL as a dependent variable and exposure to a social stressor as an independent variable. For the sample of 105 articles, we summarized methods and findings by type of social stressor (socioeconomic stressors, stressful life events, work-related stressors, and neighborhood stressors) and by age of the study population (infants/children, middle-aged adults, older adults, and mixed samples of middle-aged and older adults). We found more variation in TL measurement methodology in studies of infants/children and older adults than in studies focusing on middle-aged adults. The most consistent finding was a relationship between early-life stressors and shorter TL. Work and neighborhood stressors, and older populations, are currently understudied. Across all stressors, limited evidence suggests that the stress-TL relationship may be moderated by characteristics such as age, sex, and race/ethnicity. We conclude with specific suggestions for future research.
... In humans, telomere length and telomerase expression and activity is associated with a host of socio-demographic, biophysical, clinical, biological, behavioural and psychosocial states and conditions, including age, sex, socio-economic status, race/ethnicity, body mass index, infection, diet/nutrition, physical activity, sleep, stress and social relationships. A detailed description is outside the purview of the current paper, but see [74][75][76][77][78][79][80][81][82][83][84][85] for recent studies and reviews. ...
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Research on mechanisms underlying fetal programming of health and disease risk has focused primarily on processes that are specific to cell types, organs or phenotypes of interest. However, the observation that developmental conditions concomitantly influence a diverse set of phenotypes, the majority of which are implicated in age-related disorders, raises the possibility that such developmental conditions may additionally exert effects via a common underlying mechanism that involves cellular/molecular ageing–related processes. In this context, we submit that telomere biology represents a process of particular interest in humans because, firstly, this system represents among the most salient antecedent cellular phenotypes for common age-related disorders; secondly, its initial (newborn) setting appears to be particularly important for its long-term effects; and thirdly, its initial setting appears to be plastic and under developmental regulation. We propose that the effects of suboptimal intrauterine conditions on the initial setting of telomere length and telomerase expression/activity capacity may be mediated by the programming actions of stress-related maternal–placental–fetal oxidative, immune, endocrine and metabolic pathways in a manner that may ultimately accelerate cellular dysfunction, ageing and disease susceptibility over the lifespan. This perspectives paper provides an overview of each of the elements underlying this hypothesis, with an emphasis on recent developments, findings and future directions. This article is part of the theme issue ‘Understanding diversity in telomere dynamics’.
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Background: Psychosocial stressors, such as perceived discrimination and depressive symptoms, may shorten telomeres and exacerbate aging-related illnesses. Methods: Participants from the Jackson Heart Study at visit 1 (2000-2004) with LTL data and Center for Epidemiological Studies-Depression (CES-D) scores (n = 580 men, n = 910 women) were utilized. The dimensions of discrimination scores (everyday, lifetime, burden of lifetime, and stress from lifetime discrimination) were standardized and categorized as low, moderate, and high. Coping responses to everyday and lifetime discrimination were categorized as passive and active coping. Multivariable linear regression analyses were performed to estimate the mean difference (standard errors-SEs) in LTL by dimensions of discrimination and coping responses stratified by CES-D scores < 16 (low) and ≥ 16 (high) and sex. Covariates were age, education, waist circumference, smoking and CVD status. Results: Neither everyday nor lifetime discrimination was associated with mean differences in LTL for men or women by levels of depressive symptoms. Burden of lifetime discrimination was marginally associated with LTL among women who reported low depressive symptoms after full adjustment (b = 0.11, SE = 0.06, p = 0.08). Passive coping with lifetime discrimination was associated with longer LTL among men who reported low depressive symptoms after full adjustment (b = 0.18, SE = 0.09, p < 0.05); and active coping with lifetime discrimination was associated with longer LTL among men who reported high depressive symptoms after full adjustment (b = 1.18, SE = 0.35, p < 0.05). Conclusions: The intersection of perceived discrimination and depressive symptomatology may be related to LTL, and the effects may vary by sex.
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Accelerated telomere length attrition has been associated with psychological stress and early adversity in adults; however, no studies have examined whether telomere length in childhood is associated with early experiences. The Bucharest Early Intervention Project is a unique randomized controlled trial of foster care placement compared with continued care in institutions. As a result of the study design, participants were exposed to a quantified range of time in institutional care, and represented an ideal population in which to examine the association between a specific early adversity, institutional care and telomere length. We examined the association between average relative telomere length, telomere repeat copy number to single gene copy number (T/S) ratio and exposure to institutional care quantified as the percent of time at baseline (mean age 22 months) and at 54 months of age that each child lived in the institution. A significant negative correlation between T/S ratio and percentage of time was observed. Children with greater exposure to institutional care had significantly shorter relative telomere length in middle childhood. Gender modified this main effect. The percentage of time in institutional care at baseline significantly predicted telomere length in females, whereas the percentage of institutional care at 54 months was strongly predictive of telomere length in males. This is the first study to demonstrate an association between telomere length and institutionalization, the first study to find an association between adversity and telomere length in children, and contributes to the growing literature linking telomere length and early adversity.
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Background: Depression is associated with an unusually high rate of aging-related illnesses and early mortality. One aspect of "accelerated aging" in depression may be shortened leukocyte telomeres. When telomeres critically shorten, as often occurs with repeated mitoses or in response to oxidation and inflammation, cells may die. Indeed, leukocyte telomere shortening predicts early mortality and medical illnesses in non-depressed populations. We sought to determine if leukocyte telomeres are shortened in Major Depressive Disorder (MDD), whether this is a function of lifetime depression exposure and whether this is related to putative mediators, oxidation and inflammation. Methodology: Leukocyte telomere length was compared between 18 unmedicated MDD subjects and 17 controls and was correlated with lifetime depression chronicity and peripheral markers of oxidation (F2-isoprostane/Vitamin C ratio) and inflammation (IL-6). Analyses were controlled for age and sex. Principal findings: The depressed group, as a whole, did not differ from the controls in telomere length. However, telomere length was significantly inversely correlated with lifetime depression exposure, even after controlling for age (p<0.05). Average telomere length in the depressed subjects who were above the median of lifetime depression exposure (≥9.2 years' cumulative duration) was 281 base pairs shorter than that in controls (p<0.05), corresponding to approximately seven years of "accelerated cell aging." Telomere length was inversely correlated with oxidative stress in the depressed subjects (p<0.01) and in the controls (p<0.05) and with inflammation in the depressed subjects (p<0.05). Conclusions: These preliminary data indicate that accelerated aging at the level of leukocyte telomeres is proportional to lifetime exposure to MDD. This might be related to cumulative exposure to oxidative stress and inflammation in MDD. This suggest that telomere shortening does not antedate depression and is not an intrinsic feature. Rather, telomere shortening may progress in proportion to lifetime depression exposure.
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It has been hypothesised that socioeconomically deprived people age more rapidly than their more advantaged counterparts and this is biologically manifest in shorter telomeres. However, in the very few studies conducted, substantial uncertainty exists regarding this relationship. In the present investigation, 1542 men in the West of Scotland Coronary Prevention Study responded to a series of enquiries about their socioeconomic position (educational attainment, employment status, area-based deprivation), had their physical stature measured (a proxy for early life social circumstances) and provided a blood specimen from which leucocyte DNA was extracted and telomere length derived. There was no strong evidence that any of these four indices of socioeconomic position was robustly related to telomere length. The only exception was employment status: men who reported being out of work had significantly shorter telomeres than those who were employed (p = 0.007). In this cross-sectional study-the largest to date to examine the relationship-we found little evidence of an association between socioeconomic status and telomere length.
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Achieving the Healthy People 2010 goal of reducing health disparities has been challenging. Disparity in life expectancy by socioeconomic status (SES) has been increasing.1 Much of this disparity is attributable to higher cardiovascular, particularly coronary heart disease (CHD), mortality among persons of lower SES. Disparities in CHD mortality result from multiple factors, including early life environment and material disadvantage,2 social and behavioral risk factors,3 access to care,4 and systematic underestimation of risk among persons with lower SES in clinical care. This Commentary addresses the importance of SES in CHD risk assessment. Current risk-based intervention strategies ignore the independent contribution of SES to CHD and thus may contribute to increasing SES disparities. If CHD risk is better estimated among the poor, it could lead to increased statin use for cholesterol reduction and aspirin use for CHD prevention among this population, which may reduce CHD disparities.
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Dementia takes decades to develop, and effective prevention will likely require early intervention. Thus, it is critical to identify biomarkers of preclinical disease, allowing targeting of high-risk subjects for preventive efforts. Since telomeres shorten with age and oxidative stress, both of which are important contributors to the onset of dementia, telomere length might be a valuable biomarker. Among 62 participants of the Nurses' Health Study, we conducted neurologic evaluations, including patient and caregiver interviews, physical exam, neurologic exam, and neuropsychologic testing. We also conducted magnetic resonance imaging (MRI) in a sample of 29 of these women. In these preliminary data, after adjustment for numerous health and lifestyle factors, we found that truncated telomeres in peripheral blood leukocytes segregate with preclinical dementia states, including mild cognitive impairment (MCI); the odds of MCI were 12-fold higher (odds ratio = 12.00, 95% confidence interval 1.24-116.5) for those with shorter telomere length compared to longer telomere length. In addition, decreasing telomere length was strongly related to decreasing hippocampal volume (p = 0.038). These preliminary data suggest that telomere length may be a possible early marker of dementia risk, and merits further study in large, prospective investigations.
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It has long been presumed impossible to measure telomeres in vertebrate DNA by PCR amplification with oligonucleotide primers designed to hybridize to the TTAGGG and CCCTAA repeats, because only primer dimer-derived products are expected. Here we present a primer pair that eliminates this problem, allowing simple and rapid measurement of telomeres in a closed tube, fluorescence-based assay. This assay will facilitate investigations of the biology of telomeres and the roles they play in the molecular pathophysiology of diseases and aging.
Conference Paper
This paper focuses on financial strain across the life course as a condition underlying health inequalities observed in later life. The analysis is based on data from 1,167 adults 65 years and older collected as part of the 'Aging, Stress and Health Study." Relying on retrospective data about hardship experienced over the life course, we find that long-term financial hardship is reflected in a range of health outcomes at late life, even after controlling for the effects of current financial circumstances. Moreover the sheer persistence of hardship matters more than its episodic occurrence or timing, so that the health effects of early hardship may be obviated if followed by no further hardship. This pattern of findings is consistent with the notion of allostatic load, the cumulative damage done to health and well-being under the but-den of an unrelenting stressor in a critically important life domain.
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I have summarized in this article data on the magnitude of health challenges faced by men in the United States. Across a broad range of indicators, men report poorer health than women. Although men in all socioeconomic groups are doing poorly in terms of health, some especially high-risk groups include men of low socioeconomic status (SES) of all racial/ethnic backgrounds, low-SES minority men, and middle-class Black men. Multiple factors contribute to the elevated health risks of men. These include economic marginality, adverse working conditions, and gendered coping responses to stress, each of which can lead to high levels of substance use, other health-damaging behaviors, and an aversion to health-protective behaviors. The forces that adversely affect men's health are interrelated, unfold over the life course, and are amenable to change.
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There has been a growing interest in African American men’s health and health disparities over the past two decades, but African American men’s health consistently ranks lowest across all groups in the U.S. Existing evidence on health and social causes of morbidity and mortality of African American men has been narrowly concentrated on public health problems such as violence, prostate cancer, and HIV/AIDS and determinants of health such as education and male socialization. This limited focus omits other age-specific leading causes of death such as cardiovascular disease and other determinants of health such as discrimination, segregation, access to health care, employment and income. This review will offer a discussion about the leading causes of death for African American men and their associated risk factors; discuss gaps in the literature; and present a race and gendered framework to address the growing inequities in health for African American men.
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Inflammatory processes are implicated in a number of diseases for which there are known socioeconomic status (SES) disparities, including heart disease and diabetes. Growing evidence also suggests SES gradients in levels of peripheral blood markers of inflammation. However, we know little about potential gender and racial/ethnic differences in associations between SES and inflammation, despite the fact that the burden of inflammation-related diseases varies by gender and race. The present study examines SES (education and income) gradients in levels of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6), in a biethnic (White and Black) sample of men and women (n = 3,549, aged 37–55 years) in the USA from the CARDIA Study. Health status, behavioral and psychosocial variables that may underlie SES differences in inflammatory biomarker levels were also examined. Age-adjusted CRP and IL-6 levels were inversely associated with education level in each race/gender group except Black males. Income gradients were also observed in each race/gender group for IL-6 and in White females and males for CRP. In general, differences in CRP and IL-6 levels between low and high SES groups were reduced in magnitude and significance with the addition of health status, behavioral, and psychosocial variables, although the impact of the addition of model covariates varied across race/gender groups and different SES-inflammation models. Overall, findings indicate SES gradients in levels of inflammation burden in middle-aged White and Black males and females.
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Leukocyte telomere length (LTL) is an indicator of general systemic aging, with shorter LTL being associated with several chronic diseases of aging and earlier mortality. Identifying factors related to LTL among African Americans may yield insights into mechanisms underlying racial disparities in health. To test whether the combination of more frequent reports of racial discrimination and holding a greater implicit anti-black racial bias is associated with shorter LTL among African-American men. Cross-sectional study of a community sample of 92 African-American men aged between 30 and 50 years. Participants were recruited from February to May 2010. Ordinary least squares regressions were used to examine LTL in kilobase pairs in relation to racial discrimination and implicit racial bias. Data analysis was completed in July 2013. After controlling for chronologic age and socioeconomic and health-related characteristics, the interaction between racial discrimination and implicit racial bias was significantly associated with LTL (b=-0.10, SE=0.04, p=0.02). Those demonstrating a stronger implicit anti-black bias and reporting higher levels of racial discrimination had the shortest LTL. Household income-to-poverty threshold ratio was also associated with LTL (b=0.05, SE=0.02, p<0.01). Results suggest that multiple levels of racism, including interpersonal experiences of racial discrimination and the internalization of negative racial bias, operate jointly to accelerate biological aging among African-American men. Societal efforts to address racial discrimination in concert with efforts to promote positive in-group racial attitudes may protect against premature biological aging in this population.
Article
The purpose of this study was to examine the association between socioeconomic status (SES) and leukocyte telomere length (LTL) - a marker of cell aging that has been linked to stressful life circumstances - in a nationally representative, socioeconomically and ethnically diverse sample of US adults aged 20-84. Using data from the National Health and Nutrition Examination Survey (NHANES), 1999-2002, we found that respondents who completed less than a high school education had significantly shorter telomeres than those who graduated from college. Income was not associated with LTL. African-Americans had significantly longer telomeres than whites, but there were no significant racial/ethnic differences in the association between education and telomere length. Finally, we found that the association between education and LTL was partially mediated by smoking and body mass index but not by drinking or sedentary behavior.
Article
While the American Dream remains a unifying cultural tenet for an increasingly diverse society, it may be showing signs of wear. Growing income inequality and slower growth suggest that now is an important moment to review the facts about opportunity and mobility in America and to attempt to answer the basic question: Is the American Dream alive and well? This report summarizes research and provides new evidence on both the extent of intergenerational mobility in the United States and the factors that influence it. In sum, the research reviewed herein leads us to the view that the glass is half empty and half full. The American Dream is alive if somewhat frayed. Chapter I of this report provides new data on how today's families are faring relative to their parents. Most of the historical analysis, detailed in Chapter II, reveals that there has been no strong trend in relative mobility since about 1970, although a few studies suggest that relative mobility may have declined. The international comparisons analyzed in Chapter III reveal that there is less relative mobility in the United States than in many other rich countries. Chapter IV, which reviews the current data on wealth and its effects on intergenerational mobility, concludes that parent-child wealth correlations are similar to parent-child income correlations but that each generation does have a reasonable shot at accumulating assets. Finally, chapters V, VI, and VII look beyond the story for all families to examine how mobility may have varied for men and women, for blacks and whites, and for immigrants and native-born Americans. Appended are: (1) The PSID Sample and Family Income; (2) Non-Cash Contributions to Family Economic Well-Being; (3) Four-Part Typology of Economic Mobility of Sons and Daughters; (4) Four-Part Typology: Economic Mobility of White and Black Families; and (5) Research Literature on Black-White Differences in Intergenerational Income Mobility. (Each chapter contains tables, figures, notes, and resources.)
Article
Previous findings have linked lower socioeconomic status (SES) with elevated morbidity and mortality. Leukocyte telomere length (LTL), which also has been associated with age-related disease morbidity and mortality, is a marker of aging at the cellular level, making it a valuable early biomarker of risk and an indicator of biological age. It is hypothesized that SES will be associated with LTL, indicating that SES influences disease risk by accelerating biological aging. In the present sample we test for associations of childhood SES and adult SES (i.e. education, income, home ownership) with LTL, and examine whether these associations vary by racial/ethnic group. Analyses on 963 subjects (18.7% White, 53% Hispanics, and 28.5% African American) from the Stress ancillary study of the Multi-Ethnic Study of Atherosclerosis revealed a significant difference in LTL between home owners and renters in Hispanic and White participants (p < .05), but not amongst African Americans (p = .98). There were no linear associations of adult education or family income with LTL, however, there was an inverse association between father's education and LTL (p = .03). These findings suggest that for Whites and Hispanics renting vs. owning a home is associated with an older biological age; however we did not replicate previous findings linking education with LTL.
Article
Objectives Empirical findings on racial discrimination and hypertension risk have been inconsistent. Some studies have found no association between self-reported experiences of discrimination and cardiovascular health outcomes, whereas others have found moderated or curvilinear relationships. The current cross-sectional study examined whether the association between racial discrimination and hypertension is moderated by implicit racial bias among African American midlife men.Methods This study examined the data on 91 African American men between 30 and 50 years of age. Primary variables were self-reported experiences of racial discrimination and unconscious racial bias as measured by the Black-White Implicit Association Test. Modified Poisson regression models were specified, examining hypertension, defined as a mean resting systolic level of at least 140 mm Hg or diastolic level of at least 90 mm Hg, or self-reported history of cardiovascular medication use with a physician diagnosis of hypertension.ResultsNo main effects for discrimination or implicit racial bias were found, but the interaction of the two variables was significantly related to hypertension (χ(2)(1) = 4.89, p < .05). Among participants with an implicit antiblack bias, more frequent reports of discrimination were associated with a higher probability of hypertension, whereas among those with an implicit problack bias, it was associated with lower risk.Conclusions The combination of experiencing racial discrimination and holding an antiblack bias may have particularly detrimental consequences on hypertension among African American midlife men, whereas holding an implicit problack bias may buffer the effects of racial discrimination. Efforts to address both internalized racial bias and racial discrimination may lower cardiovascular risk in this population.
Article
Morbidity and mortality are greater among socially disadvantaged racial/ethnic groups and those of lower socioeconomic status (SES). Greater chronic stress exposure in disadvantaged groups may contribute to this by accelerating cellular aging, indexed by shorter age-adjusted telomere length. While studies consistently relate shorter leukocyte telomere length (LTL) to stress, the few studies, mostly from the UK, examining associations of LTL with SES have been mixed. The current study examined associations between educational attainment and LTL among 2599 high-functioning black and white adults age 70-79 from the Health, Aging and Body Composition Study. Multiple regression analyses tested associations of race/ethnicity, educational attainment and income with LTL, adjusting for potential confounders. Those with only a high school education had significantly shorter mean LTL (4806basepairs) than those with post-high school education (4926basepairs; B=125, SE=47.6, p=.009). A significant interaction of race and education (B=207.8, SE=98.7, p=.035) revealed more beneficial effects of post-high school education for blacks than for whites. Smokers had shorter LTL than non-smokers, but the association of education and LTL remained significant when smoking was covaried (B=119.7, SE=47.6, p=.012). While higher income was associated with longer LTL, the effect was not significant (p>.10). This study provides the first demonstration of an association between educational attainment and LTL in a US population where higher education appears to have a protective effect against telomere shortening, particularly in blacks.
Article
Physical activity and financial strain are independent, and opposite, predictors of disease. This study examines whether physical activity modifies the concurrent and prospective relation between financial strain and impaired fasting glucose. Participants were part of the Coronary Artery Risk Development in Young Adults study, a prospective study examining the development of disease. Participants were recruited in 1985 to 1986 and followed up for 20 years. The outcome measures were fasting glucose (FG) levels at Years 7 and 20. FG was available at Years 7 and 20 from 3991 and 3500 participants, respectively. The effects of financial strain on elevated glucose levels differed by physical activity levels as indicated by the significant interaction terms for the analyses of covariance at Year 7 (p = .02) and Year 20 (p = .04). Planned contrast comparisons demonstrated that FG levels in financially strained participants who were physically inactive were significantly different from financially strained participants who were active, and all participants with low financial strain. Specifically, in less active participants, the adjusted mean FG levels were higher in financially strained participants (2.27 mg/dL at Year 7 and 5.86 mg/dL at Year 20). In active participants, these differences were -1.78 mg/dL at Year 7 and negligible at Year 20. In adults burdened by financial strain, physical activity is associated with a reduced risk of developing impaired FG up to 13 years later. This adds to a growing literature showing the potential of physical activity to moderate stress-related disease processes.
Article
Studies of racial health gaps often find that disparities persist even after adjusting for socioeconomic status (SES). We contend that the persistent residual variation may, in part, be the result of conceptual and methodological problems in the operationalization of SES. These include inadequate attention to the content validity of SES measures and insufficient adjustments for SES differences across racial groups. Using data from the 1997-2007 U.S. Panel Study of Income Dynamics (N = 9932), we use longitudinal and multi-level measures of SES and apply a propensity score adjustment strategy to examine the black/white disparity in self-rated health. Compared to conventional regression estimates that yield unexplained racial health gaps, propensity score adjustment accounts for the entire racial disparity in self-rated health. Results suggest that previous studies may have inadequately adjusted for differences in SES across racial groups, that social factors should be carefully and conscientiously considered, and that acknowledgment of the possibility of incomplete SES adjustments should be weighed before any inferences to non-SES etiology can be made.
Article
This investigation explored the relationship of socioeconomic status (SES) to physical and mental health in two nationally representative samples of whites and African-Americans. We examined the interrelations among SES variables and assessed their contribution to health for the two racial groups. Throughout, we assessed the contribution of a less traditional indicator of SES-wealth-in the SES-health relationship. As we expected, African-Americans had lower levels of education, household income, and wealth than whites. Unexpectedly, however, the strength of the interrelationships among the three SES indicators did not differ for African-Americans and whites. In addition, we found that SES operated to affect health in a very similar fashion for African-Americans and whites. We found that wealth, in addition to more traditional indicators of SES (education and household income), made a unique and significant contribution to explaining both physical and mental health. Examining relations of different SES indicators to health across groups is critical to eliminating persistent social inequalities in health.
Article
Little research has focused on the social patterning of diabetes among African Americans. We examined the relationship between socioeconomic status (SES) and the prevalence, awareness, treatment, and control of diabetes among African Americans. Education, income and occupation were examined among 4,303 participants (2,726 women and 1,577 men). Poisson regression estimated relative probabilities (RP) of diabetes outcomes by SES. The prevalence of diabetes was 19.6% in women and 15.9% in men. Diabetes awareness, treatment, and control were 90.0%, 86.8%, and 39.2% in women, respectively, and 88.2%, 84.4%, and 35.9% in men, respectively. In adjusted models, low-income men and women had greater probabilities of diabetes than high-income men and women (RP, 1.94; 95% confidence interval [CI], 1.28-2.92; and RP, 1.35; 95% CI, 1.04-1.74, respectively). Lack of awareness was associated with low education and low occupation in women (RP, 2.28; 95%CI 1.01-5.18; and RP, 2.62; 95% CI, 1.08-6.33, respectively) but not in men. Lack of treatment was associated with low education in women. Diabetes control was not patterned by SES. Diabetes prevalence is patterned by SES, and awareness and treatment are patterned by SES in women but not men. Efforts to prevent diabetes in African Americans need to address the factors that place those of low SES at higher risk.
Article
The association between education and good health is well established, but whether the strength of the association depends on other social statuses is not. We test a theory of resource substitution which predicts a larger correlation between education and health (measured for physical impairment) for people who grew up in families with poorly-educated parents than for those whose parents were well educated. This is supported in the Aging, Status, and Sense of control (ASOC) survey, a representative national U.S. sample with data collected in 1995, 1998, and 2001. The reason that parental education matters more to people who are poorly educated themselves is due to an unhealthy lifestyle, specifically to smoking and being overweight. Finally, as the poorly educated age, the negative health effects of their parents' low educational attainment get worse.
Article
To address the question of whether childhood abuse and other adversities have lasting, detectable consequences for inflammation and cell aging late in life, and whether the effects are large enough to be discernible beyond that of a major chronic stressor, dementia family caregiving. Previous research on the physical health consequences of childhood abuse and other adversities has been based on data from young or middle-aged adults. In this community sample of 132 healthy older adults (mean age = 69.70 years; standard deviation = 10.14), including 58 dementia family caregivers and 74 non-caregivers, blood samples were analyzed for interleukin (IL)-6, tumor necrosis factor (TNF)-α, and telomere length, a measure of cell aging. Depressive symptoms were assessed by the Center for Epidemiological Studies Depression Scale. After controlling for age, caregiving status, gender, body mass index, exercise, and sleep, the presence of multiple childhood adversities was related to both heightened IL-6 (0.37 ± 0.03 log10 pg/mL versus 0.44 ± 0.03 log10 pg/mL) and shorter telomeres (6.51 ± 0.17 Kb versus 5.87 ± 0.20 Kb), compared with the absence of adversity; the telomere difference could translate into a 7- to 15-year difference in life span. Abuse was associated with heightened IL-6 and TNF-α levels; for TNF-α, this relationship was magnified in caregivers compared with controls. Moreover, abuse and caregiving status were associated significantly and independently with higher levels of depressive symptoms. Adverse childhood events are related to continued vulnerability among older adults, enhancing the impact of chronic stressors. Childhood adversities cast a very long shadow.
Article
Persistent racial inequality in employment, housing, and a wide range of other social domains has renewed interest in the possible role of discrimination. And yet, unlike in the pre-civil rights era, when racial prejudice and discrimination were overt and widespread, today discrimination is less readily identifiable, posing problems for social scientific conceptualization and measurement. This article reviews the relevant literature on discrimination, with an emphasis on racial discrimination in employment, housing, credit markets, and consumer interactions. We begin by defining discrimination and discussing relevant methods of measurement. We then provide an overview of major findings from studies of discrimination in each of the four domains; and, finally, we turn to a discussion of the individual, organizational, and structural mechanisms that may underlie contemporary forms of discrimination. This discussion seeks to orient readers to some of the key debates in the study of discrimination and to provide a roadmap for those interested in building upon this long and important line of research.
Article
To determine the association between leukocyte telomere length (TL) and atherosclerosis and its clinical sequelae stroke and myocardial infarction. Within the scope of the prospective population-based Bruneck Study, leukocyte TL was measured by quantitative polymerase chain reaction in 800 women and men aged 45 to 84 years (in 1995). The manifestation of cardiovascular disease (CVD) (1995-2005) and the progression of atherosclerosis (1995-2000) were carefully assessed. The TL was shorter in men than in women (age-adjusted mean [95% CI], 1.41 [1.33 to 1.49] versus 1.55 [1.47 to 1.62]; P=0.02) and inversely correlated to age (r=-0.22, P<0.001) and family history of CVD (P=0.03). Participants with CVD events during follow-up (n=88) had significantly shorter telomeres (age- and sex-adjusted mean [95% CI], 1.25 [1.08 to 1.42] versus 1.51 [1.45 to 1.57]; P<0.001). In multivariable Cox models, baseline TL emerged as a significant and independent risk predictor for the composite CVD end point and its individual components (myocardial infarction and stroke); however, this was not the case for de novo stable angina and intermittent claudication. Subjects in the top and bottom TL tertile group differed in their CVD risk by a factor of 2.72 (95% CI, 1.41 to 5.28), which is the risk ratio attributable to a 13.9-year difference in chronological age. Remarkably, in our atherosclerosis progression model, TL was strongly associated with advanced, but not early, atherogenesis. All findings were consistent in women and men. Our findings indicate a differential role of telomere shortening in the various stages of atherosclerosis, with preferential involvement in advanced vessel pathology and acute vascular syndromes.
Article
Differential exposure to financial strain may explain some differences in population health. However, few studies have examined the cumulative health effect of financial strain across the life-course. Studies that have are limited to self-reported health measures. Our objective was to examine the associations between childhood, adulthood, and life-course, or cumulative, financial strain with disability, lung function, cognition, and depression. In a population-based cross-sectional cohort study of adult African-American twins enrolled in the US Carolina African American Twin Study of Aging (CAATSA), we found that participants who reported financial strain as children and as adults are more likely to be physically disabled, and report more depressive symptoms than their unstrained counterparts. Participants who reported childhood financial strain had lower cognitive functioning than those with no childhood financial strain. We were unable to detect a difference in lung function beyond the effect of actual income and education in those who reported financial strain compared to those who did not. Financial strain in adulthood was more consistently associated with poor health than was childhood financial strain, a finding that suggests targeting adult financial strain could help prevent disability and depression among African-American adults.
Article
The brain is the key organ of stress reactivity, coping, and recovery processes. Within the brain, a distributed neural circuitry determines what is threatening and thus stressful to the individual. Instrumental brain systems of this circuitry include the hippocampus, amygdala, and areas of the prefrontal cortex. Together, these systems regulate physiological and behavioral stress processes, which can be adaptive in the short-term and maladaptive in the long-term. Importantly, such stress processes arise from bidirectional patterns of communication between the brain and the autonomic, cardiovascular, and immune systems via neural and endocrine mechanisms underpinning cognition, experience, and behavior. In one respect, these bidirectional stress mechanisms are protective in that they promote short-term adaptation (allostasis). In another respect, however, these stress mechanisms can lead to a long-term dysregulation of allostasis in that they promote maladaptive wear-and-tear on the body and brain under chronically stressful conditions (allostatic load), compromising stress resiliency and health. This review focuses specifically on the links between stress-related processes embedded within the social environment and embodied within the brain, which is viewed as the central mediator and target of allostasis and allostatic load.
Article
Over the past two decades, exponential growth of empirical research has fueled markedly increased concern about health disparities. In this paper, we show the progression of research on socioeconomic status (SES) and health through several eras. The first era reflected an implicit threshold model of the association of poverty and health. The second era produced evidence for a graded association between SES and health where each improvement in education, income, occupation, or wealth is associated with better health outcomes. Moving from description of the association to exploration of pathways, the third era focused on mechanisms linking SES and health, whereas the fourth era expanded on mechanisms to consider multilevel influences, and a fifth era added a focus on interactions among factors, not just their main effects or contributions as mediators. Questions from earlier eras remain active areas of research, while later eras add depth and complexity.
Article
Telomere shortening is a marker of cellular aging and has been associated with risk of Alzheimer's disease. Few studies have determined if telomere length is associated with cognitive decline in non-demented elders. We prospectively studied 2734 non-demented elders (mean age: 74 years). We measured cognition with the Modified Mini-Mental State Exam (3MS) and Digit Symbol Substitution Test (DSST) repeatedly over 7 years. Baseline telomere length was measured in blood leukocytes and classified by tertile as "short", "medium", or "long". At baseline, longer telomere length was associated with better DSST score (36.4, 34.9 and 34.4 points for long, medium and short, p<0.01) but not for change in score. However, 7-year 3MS change scores were less among those with longer telomere length (-1.7 points vs. -2.5 and -2.9, p=0.01). Findings were similar after multivariable adjustment for age, gender, race, education, assay batch, and baseline score. There was a borderline statistically significant interaction for telomere length and APOE e4 on 3MS change score (p=0.06). Thus, telomere length may serve as a biomarker for cognitive aging.
Article
Telomeres are the DNA-protein complexes that protect the ends of eukaryotic chromosomes. The cellular enzyme telomerase counteracts telomere shortening by adding telomeric DNA. A growing body of literature links shorter telomere length and lower telomerase activity with various age-related diseases and earlier mortality. Thus, leukocyte telomere length (LTL) and telomerase activity are emerging both as biomarkers and contributing factors for age-related diseases. However, no clinical study has directly examined telomerase activity and telomere length in different lymphocyte subtypes isolated from the same donors, which could offer insight into the summary measure of leukocyte telomere maintenance. We report the first quantitative data in humans examining both levels of telomerase activity and telomere length in four lymphocyte subpopulations from the same donors-CD4+, CD8+CD28+ and CD8+CD28- T cells and B cells, as well as total PBMCs-in a cohort of healthy women. We found that B cells had the highest telomerase activity and longest telomere length; CD4+ T cells had slightly higher telomerase activity than CD8+CD28+ T cells, and similar telomere length. Consistent with earlier reports that CD8+CD28- T cells are replicatively senescent cells, they had the lowest telomerase activity and shortest telomere length. In addition, a higher percentage of CD8+CD28- T cells correlated with shorter total PBMC TL (r=-0.26, p=0.05). Interestingly, telomerase activities of CD4+ and CD8+CD28+ T cells from the same individual were strongly correlated (r=0.55, r<0.001), indicating possible common mechanisms for telomerase activity regulation in these two cell subtypes. These data will facilitate the understanding of leukocyte aging and its relationship to human health.
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In the Whitehall study, 17 530 civil servants were classified according to employment grade, and their mortality was recorded over 10 years. There was a steep inverse relation between grade and mortality. Compared with the highest grade (administrators), men in the lowest grade had 3 times the mortality rate from coronary heart disease, from a range of other causes, and from all causes combined. This is larger than the mortality differences, nationally, between classes I and V. Smoking and other coronary risk factors are more common in the lowest grades, but these differences account for only part of the mortality difference. The similarity of the risk gradient from a range of specific diseases could indicate the operation of factors affecting general susceptibility. The inverse relation between height and mortality suggests that factors operating from early life may influence adult death rates.
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It has long been presumed impossible to measure telomeres in vertebrate DNA by PCR amplification with oligonucleotide primers designed to hybridize to the TTAGGG and CCCTAA repeats, because only primer dimer-derived products are expected. Here we present a primer pair that eliminates this problem, allowing simple and rapid measurement of telomeres in a closed tube, fluorescence-based assay. This assay will facilitate investigations of the biology of telomeres and the roles they play in the molecular pathophysiology of diseases and aging.