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The effects of social status on biological aging as measured by white-blood-cell telomere length

Twin Research & Genetic Epidemiology Unit, St Thomas' Hospital, London, UK, and The Center of Human Development and Aging, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103-2714, USA.
Aging Cell (Impact Factor: 5.94). 11/2006; 5(5):361-5. DOI: 10.1111/j.1474-9726.2006.00222.x
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ABSTRACT Low socio-economic status (SES) is associated with a shortened life expectancy, but its effect on aging is unknown. The rate of white-blood-cell (WBC) telomere attrition may be a biological indicator of human aging. We tested the hypothesis that SES is associated with telomere attrition independent of known risk factors influencing the aging process. We studied 1552 female twins. A venous blood sample was taken from each twin and isolated WBCs used for extraction of DNA. Terminal restriction fragment length (TRFL) was measured. Questionnaire data were collected on occupation, education, income, smoking, exercise, height and weight. Standard multiple linear regression and multivariate analyses of variance tested for associations between SES and TRFL, adjusting for covariates. A discordant twin analysis was conducted on a subset to verify findings. WBC telomere length was highly variable but significantly shorter in lower SES groups. The mean difference in TRFL between nonmanual and manual SES groups was 163.2 base pairs (bp) of which 22.9 bp (approximately 14%) was accounted for by body mass index, smoking and exercise. Comparison of TRFL in the 17 most discordant SES twin pairs confirmed this difference. Low SES, in addition to the harmful effects of smoking, obesity and lack of exercise, appears to have an impact on telomere length.

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    • "Stigma increases risk for deleterious mental and physical health outcomes across multiple groups, including racial/ethnic minorities (Paradies, 2006; Williams, 1999), sexual minorities (i.e., individuals who identify as lesbian, gay, or bisexual) (Meyer, 1995), individuals who are overweight/obese (Muennig, 2008), and those with mental illness (Link & Phelan, 2006). Stigma serves as a chronic source of psychological stress (Clark, Anderson, Clark, & Williams, 1999; Link & Phelan, 2006; Major & O'Brien, 2005; Meyer, 2003a; Pachankis, 2007), which in turn contributes to the development of psychopathology (Brown, 1993; Dohrenwend, 2000) and disrupts physiological pathways that increase vulnerability to disease (Cherkas et al., 2006; Epel et al., 2004; McEwen, 1998). As substantive evidence emerges that stigma represents an important social determinant of health (Hatzenbuehler, Phelan, & Link, 2013), researchers have begun to focus on the appropriate measurement and conceptualization of stigma and related constructs (Clark et al., 1999; Krieger et al., 2010; Lauderdale, 2006; Meyer, 2003b; Quinn & Chaudoir, 2009; Williams, Neighbors, & Jackson, 2008). "
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    • "It is noteworthy that some TERT polymorphisms correlated to telomere length but did not affect longevity or the parameters of healthy aging (Soerensen et al., 2012). This is probably due to the great environmental component affecting telomere length; oxidative stress, depression and uncertainty for the future have been found to significantly correlate with shorter telomeres (Cherkas et al., 2006; Epel et al., 2004; Lung et al., 2007; Yen and Lung, 2013). Thus, environmental factors Fig. 2. Mean LTL expressed as T/S ratio among the three age classes studied. "
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    ABSTRACT: BACKGROUND: Telomerase, encoded by TERT, is the ribonucleoprotein polymerase that maintains telomere ends and it plays a crucial role in cellular senescence. TERT single nucleotide polymorphisms (SNPs) have been associated both with various malignancies and telomere length (TL). The association of TERT SNPs with longevity remains uncertain and varies with ethnicity. Aim of this study was to investigate whether the functional variable number of tandem repeat (VNTR) MNS16A of TERT is associated with longevity. METHODS: MNS16A genotypes have been determined for 1072 unrelated healthy individuals from Central Italy (18-106 years old) divided into three gender-specific age classes defined according to demographic information and accounting for the different survivals between sexes: for men (women), the first class consists of individuals <66 years old (<73 years old), the second class of individuals 66-88 years old (73-91 years old), and the third class of individuals >88 years old (>91 years old). TL was assessed using genomic DNA from whole blood of 72 selected individuals by a multiplex real-time PCR assay. RESULTS: MNS16A appears associated to longevity, showing significant associations in Comparison 2 (Age Class 3 vs. Age Class 2) under both additive (odds ratio [OR] 0.749; p=0.019) and dominant (OR 0.579; p=0.011) models. The MNS16A*L allele is significantly underrepresented in Age Class 3 (OR 0.759; p=0.020) compared to Age Class 2. A significant telomere attrition is reported along the three age classes (p=0.0001), that remains significant only in L*/L* genotype carriers (p=0.002) when the analysis was conducted according to MNS16A genotype. CONCLUSIONS: The TERT MNS16A*L allele appears negatively associated with longevity. The concomitant significant telomere cross sectional attrition rate observed for L*/L* genotype suggests that this polymorphism could influences human longevity by affecting TL.
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    • "Other studies have similarly shown associations between current objective and perceived stress with telomere length (Damjanovic et al., 2007; Parks et al., 2009; Puterman et al., 2010). Additionally, past or current psychiatric disorders, including depression, posttraumatic stress disorder, and schizophrenia, are linked to short telomeres (Elvsashagen et al., 2011; Fernandez-Egea et al., 2009; Hartmann, Boehner, Groenen, & Kalb, 2010; Hoen et al., 2011; O'Donovan, Epel, et al., 2011; Simon et al., 2006; Wikgren et al., 2012; Wolkowitz et al., 2011) as is lower socioeconomic position in several studies (Batty et al., 2009; Cherkas et al., 2006; Diez-Roux et al., 2009; Shiels et al., 2011; Steptoe et al., 2011; Surtees et al., 2012). "
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    ABSTRACT: Accumulation of life stressors predicts accelerated development and progression of diseases of aging. Telomere length, the DNA-based biomarker indicating cellular aging, is a mechanism of disease development, and is shortened in a dose response fashion by duration and severity of life stressor exposures. Telomere length captures the interplay between genetics, life experiences and psychosocial and behavioral factors. Over the past several years, psychological stress resilience, healthy lifestyle factors, and social connections have been associated with longer telomere length and it appears that these factors can protect individuals from stress-induced telomere shortening. In the current review, we highlight these findings, and illustrate that combining these `multisystem resiliency' factors may strengthen our understanding of aging, as these powerful factors are often neglected in studies of aging. In naturalistic studies, the effects of chronic stress exposure on biological pathways are rarely main effects, but rather a complex interplay between adversity and resiliency factors. We suggest that chronic stress effects can be best understood by directly testing if the deleterious effects of stress on biological aging processes, in this case the cell allostasis measure of telomere shortening, are mitigated in individuals with high levels of multisystem resiliency. Without attending to such interactions, stress effects are often masked and missed. Taking account of the cluster of positive buffering factors that operate across the lifespan will take us a step further in understanding healthy aging. While these ideas are applied to the telomere length literature for illustration, the concept of multisystem resiliency might apply to aging broadly, from cellular to systemic health.
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