Added: Billy Holcombe - Date: 12.11.2021 02:22 - Views: 16012 - Clicks: 641
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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.
Data limitations preclude assessing objective stressors and also result in imprecise estimates, limiting our ability to draw Older Paterson women into younger black guys 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.
Despite overall gains in active life expectancy and efforts to reduce health disparities in the United States, black-white and socioeconomic inequalities in life expectancy and the prevalence of chronic disease persist Flegal et al. These health disadvantages are severe among African Americans. More troubling still, some evidence suggests that black health disadvantages worsened after the early s, especially among women.
In some high-poverty localities, excess mortality rates increased among black women residents between andlargely due to deaths attributed to chronic disease Geronimus et al. Yet another example, estimates using data from the National Health and Nutrition Examination Surveys III — and IV — show that hypertension prevalence rates grew in nonelderly black adults nationwide between the two survey waves, both absolutely and relative to whites Geronimus et al. The entrenchment and, in some cases, worsening of black health disadvantages occurred across a wide range of health outcomes and during a period when the reduction or elimination of health disparities was identified as a high-priority national health objective.
The clear failure to meet this objective suggests that future success may require new conceptual models and deepening understandings of the sources and mechanisms leading to health disparities. The age dimension of black-white health disadvantages may provide key insights. For example, in the case cited above, black women in young through middle adulthood experienced the steepest increase with age in the probability of being hypertensive, even net of excess obesity rates among US black relative to white women.
More broadly, the most pronounced differences in health between US black and white women are seen in middle age, suggesting, at least metaphorically, an accelerated aging process Geronimus Geronimus hypothesized that this age pattern of US black health disadvantage reflects a process of biological weathering Geronimus That is, US blacks may be biologically older than whites of the same chronological age due to the cumulative impact of repeated exposure to and high-effort coping with stressors.
Stress physiology Sapolsky ; Selyeincluding the concept of allostatic load, or that overexposure to stress hormones can cause wear and tear on important body systems McEwen and Seeman ; Seeman et al. Our bodies are deed to respond to stressors through the cooperative effects of the primary stress response systems—the sympathetic nervous system SNS and hypothalamic-pituitary-adrenal HPA axis.
However, with exposure to chronic stress and repeated activation of the stress response systems, these stress responses become inefficient, resulting in an allostatic load on the body's systems McEwen For example, continued SNS activation with chronic stress coupled with HPA dysfunction in the form of the loss of cortisol's anti-inflammatory effects would result in an increase in inflammation and oxidative stress.
In turn, inflammatory processes result in increased risk of cardiovascular, immune, and metabolic dysfunction Khansari et al. Through such mechanisms, allostatic load may then take a toll throughout the body and contribute to the development or progression of a broad range of clinical and preclinical pathological processes, including cardiovascular disease, obesity, diabetes, susceptibility to infection, carcinogenesis, and accelerated aging.
Large literatures in sociology, economics, anthropology, and public health document that US blacks are more likely to experience stressful situations, such as material hardship Charles and Guryan ; Mayer and Jencksinterpersonal discrimination Barnes et al. Ambient stressors in residential or work environments—such as noise, crowding, decaying housing, danger, or extremes of temperature; regular disruption of diurnal rhythms; hunger; infection; or sustained cognitive or emotional engagement with stressful life experiences—are further examples of stressors that can pose ificant physiological challenge and to which US blacks are disproportionately exposed, not only with greater frequency but, plausibly, also with greater duration or intensity than whites Almeida et al.
Indeed, researchers report black-white differences in the hypothesized stress-mediated pathways to poor health, whereby black adults exhibit a blunted diurnal cortisol rhythm and higher levels of general inflammation compared with white adults Cohen et al. Geronimus et al. Moreover, by age 30, black women exhibit greater risk of having high allostatic load scores than black men or than white men or women.
This risk gap increases through midlife and is most severe among black women who are poor. Stress-mediated health impacts may be felt especially by black women in poverty because they often bear central responsibility for the social and economic survival of their families and communities, 2 and thus, perhaps, the wear and tear on biological systems of repeated adaptation to related stressors Burton and Whitfield ; Dilworth-Anderson and Rhoden ; Geronimus et al.
Recruited to the study as primary caregivers of children, many were also the primary caregivers of their ailing or disabled mothers. A ificant of their mothers died prematurely—by age 55—and of cardiovascular disease, strokes, or cancer. This source of distress for adult daughters was also a window into their own future. Prolonged psychosocial or physical challenge to metabolic homeostasis contributes to poor health outcomes and may also accelerate aging McEwen and Seeman Older Paterson women into younger black guys Sapolsky et al. Thus, the concept of weathering, related empirical findings showing the steepest age-gradient increase in the probability of chronic disease onset to be among black women, and ethnographic findings providing thick description of why this may be so raise the question of whether US black women may experience accelerated biological aging.
The possibility that black women weather to the degree that they experience accelerated biological aging sets an ambitious research agenda requiring the identification of a measure of biological aging and, ultimately, a well-specified set of measurable environmental, material, and psychosocial stressors that have the potential to impact it, and can be studied across populations of blacks and whites. In this paper we take a modest empirical first step toward this end by considering a leading candidate biomeasure of aging—telomere length in a subset of leukocytes called peripheral blood mononuclear cells PBMC —as a potentially appropriate outcome variable for continued study.
Telomeres, the stabilizing caps on chromosomes, shorten with cell division until a certain point, at which the chromosomes are no longer stable and the cell either dies or enters senescence Allsopp et al. Research also indicates that, because breaks in the DNA structure due to oxidative stress are not easily repaired in telomeres, oxidative stress is an important mechanism by which telomeres are shortened von Zglinicki ; von Zglinicki et al. Since oxidative stress is an important mechanism linking aging, psychosocial stress, biological stress activation, inflammation, and disease development, PBMC telomeres may serve as a powerful marker of overall biological, versus chronological, age Bauer et al.
We propose that the excess morbidity and mortality experienced by black relative to white adults stems fundamentally from the persistent and multifactorial stressors—subjective and objective—experienced by black adults. This stress le to greater activation of the biological stress processes, which in turn le to a greater allostatic load and greater levels of inflammation and oxidative stress. Early inflammatory processes and oxidative stress then contribute to the black-white disparities in the development and progression of disease and subsequent mortality, with PBMC telomere length marking this process.
Because the wear and tear of stress on the body accumulates over the lifespan, telomeres shorten with age and serve as an indicator of the resultant aging- Older Paterson women into younger black guys stress-related increase in inflammation and oxidative stress over the lifespan. Research using samples of white adults provide support for our proposed mechanism linking black-white disparities in stress, disease, and PBMC telomere length Houben et al. Telomere length is inversely related to age Benetos et al. Furthermore, research suggests that telomere length is also inversely related to stress biomarkers, including cortisol, epinephrine, and norepinephrine Epel et al.
Finally, shorter telomeres have been associated with many chronic diseases known to have marked black-white disparities Taylorsuch as hypertension Aviv ; Demissie et al. Researchers have reported no racial differences in telomere length at birth Okuda et al. Although individual variation in telomere length has a strong genetic component Graakjaer et al. If PBMC telomere length marks the increase in oxidative stress due to biological stress activation, and if weathering is produced by persistent high-effort coping with and physiologic adaptation to stressors, then black adults would experience a faster rate of PBMC telomere shortening through the lifespan, since they experience a greater accumulation of allostatic load.
Thus, we hypothesize that by middle age, black women have shorter average telomere length than white women owing to a lifetime of repeated adaptation to material, psychosocial, and environmental stressors posing ificant challenge to homeostasis. We note that we are forwarding a fundamentally different understanding and more unified theory of black-white health disparities than more common ones that explain them by socioeconomic differences alone, or interpret racial differences in health as expressions of behavioral or genetic difference, or that focus on the epidemiology of a single disease outcome.
An enduring puzzle in social epidemiology is that race coefficients remain sizeable and statistically ificant, even after socioeconomic indicators are controlled Schoendorf et al. Indeed, while weathering appears marked for African Americans in poverty, it is evident to varying degrees at all socioeconomic levels Geronimus Since US blacks across the socioeconomic spectrum engage with some degree of race-related stress Colen et al. Although unhealthy behaviors are more prevalent among the socioeconomically disadvantaged black or whitethey do not fully explain disparities that persist net of socioeconomic characteristics Lantz et al.
To the extent that unhealthy behaviors contribute to health disparities, they can sometimes be coping responses to psychosocial or environmental stressors Bennett et al. Moreover, some unhealthy behaviors may themselves reflect neuroendocrine effects Brunner et al. For example, chronically high levels of glucocorticoids are thought to increase compulsive activities and the appeal of drugs, sugar, and fats. Based on such action of chronic stress hormone exposure, Dallman et al. This may contribute to obesity, central adiposity, and related diseases in populations facing chronic stress.
Most would agree that environmental contributions are important Wallace Still, biological mechanisms must link social and environmental forces to population health. For this initial test of the plausibility of our broader hypothesis and of the viability of telomere length as a candidate outcome measure for further study, we report on black-white differences in telomere length in a population-based sample of middle-aged women from the Study of Women's Health Across the Nation SWAN.
SWAN is a multi-site, multi-ethnic, population-based, observational cohort study deed to examine the health of women during their middle years. Recruitment procedures and the study de have been described elsewhere Sowers et al. Briefly, at baseline —women were screened from defined sampling frames at seven US sites. Women between 42 and 52 years of age at baseline, who reported having had a menstrual period and no use of hormone therapy in the three months prior to recruitment, were invited to participate in a longitudinal study of natural menopause.
The cohort participated in a baseline clinical examination and annual follow-up examinations. Participants also completed an annual questionnaire that included select demographic, economic, and psychometric characteristics. DNA samples from PBMCs were collected in year 7, when the youngest sample Older Paterson women into younger black guys were 49 years of age, and immortalized for storage in the SWAN specimen repository, applying an approach which maintains the integrity of the genetic structure Neitzel ; Wall et al.
We analyzed DNA samples on a randomly selected subsample of SWAN respondents who were recruited from sites that included both blacks and whites. We also drew on data associated with these samples, including race, age, study site, estradiol, perceived stress, income category, smoking status, and waist-to-hip ratio WHR.
Initially, our sample included whites and blacks aged 49 through 55 at year 7. After excluding women who had missing information for key variables, our final sample size was white and black. Chi-square and t -test analyses comparing differences between the women included and women omitted indicated that there were no statistically ificant differences in the distribution of perceived stress, income, or WHR variables. We measured telomere length by a ratio of telomere repeat copy to a known single copy gene 36B4.
Laboratory personnel conducting the telomere length measurements were completely blinded to all known characteristics of the SWAN participants. We measured telomere length using real-time qPCR Cawthon with the several modifications. The ratio of telomere repeat copy to 36B4 was compared to samples whose telomere lengths were known, as measured by the traditional Southern Blot method Cawthon ; Slagboom et al.
Separate amplification reactions were prepared for analysis of the telomeric repeat units and the 36B4 gene; all samples were analyzed in triplicate. See the Appendix for more complete details of our telomere length measurement process. The dependent variable used in this study is the median of the triplicate qPCR amplifications. Confirming the qPCR assay performed well and the DNA samples were high quality, the average coefficient of variation of the three measures was low, at 0. We report telomere length differences in terms of base pairs, calculated from the qPCR information Cawthonbecause of our interest in interpreting them with reference to cellular aging.
Others report an average annual loss of 41 base pairs for middle-aged and older women Iwama et al. In line with this estimate, we find that telomeres shortened in our sample at a rate of approximately 49 base pairs per year. We controlled for estradiol in all models to ensure that variation in telomere length is not simply due to individual variation in estradiol, as estrogen has been shown to lengthen telomeres through its actions on telomerase Bayne et al.
Furthermore, estradiol is a general antioxidant that is associated with decreased cardiovascular disease risk, evidenced by the increase in heart disease risk with menopause in women Barrett-Connor and Bush Because our sample includes women of perimenopausal age range, we wanted to for the possible explanation that black-white estrogen differences were responsible for telomere length differences Lee et al.
Self-reported race was coded as black or white. Self-reported age was measured in single years. Smoking is associated with telomere length Valdes et al. Smoking status was measured as two dummy variables, one indicating whether or not the respondent was a current smoker at the time of DNA data collection, and the other indicating whether or not the respondent ever smoked. WHR measures central adiposity and was calculated from waist and hip circumference measurements in centimeters. Given volatility of single-year weight measures, we averaged all available measurements for each respondent. We chose to use a measure of central adiposity WHR rather than of obesity BMI because research suggests that stress is more closely linked to central fat distribution Epel et al.
Some have hypothesized a link between stress and central adiposity through hypothalamic dysregulation Bjorntorp and inflammatory processes associated with chronic diseases showing marked black-white disparities e. Using ordinary least squares regression, median telomere length was regressed on race, perceived stress, poverty, smoking, and WHR in a series of models that all include the control variables of age at year 7, estradiol at year 7, SWAN study site, and qPCR batch.
To test our primary hypothesis that black SWAN respondents experience accelerated cellular aging relative to their white counterparts, we regress telomere length on race and the control variables only. Our theoretical model predicts that we will find that, on average, black respondents have shorter telomere length a smaller of base pairs than white respondents.
We further hypothesize that this difference is mediated by experience with stressors. Thus, our theory predicts that the magnitude of the estimated black-white difference in base pairs will be reduced when the remaining study variables are controlled.Older Paterson women into younger black guys
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