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      Leukocyte telomeres are longer in African Americans than in whites: the National Heart, Lung, and Blood Institute Family Heart Study and the Bogalusa Heart Study

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          Abstract

          Leukocyte telomere length (LTL) is ostensibly a bio-indicator of human aging. Here we report that African Americans have longer LTL than whites. We studied cross-sectionally 2453 individuals from the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study (age = 30–93 years) and the Bogalusa Heart Study (age = 19–37 years), comprising 1742 whites and 711 African Americans. We measured LTL by Southern blots of the terminal restriction fragments length. In 234 participants, telomere repeats were also measured by quantitative polymerase chain reaction (qPCR). Adjusted for age and body mass index (BMI), the respective leukocyte telomere lengths (mean ± SEM) were considerably longer in African Americans than in whites both in the Family Heart Study (7.004 ± 0.033 kb vs. 6.735 ± 0.024 kb, p < 0.0001) and the Bogalusa Heart Study (7.923 ± 0.063 kb vs. 7.296 ± 0.039 kb, p < 0.0001). We confirmed the racial effect on LTL by qPCR (3.038 ± 0.565 T/S units for African Americans vs. 2.714 ± 0.487 T/S units for whites, p < 0.001). Cross-sectionally, sex- and BMI-adjusted LTL became shorter with age (range 19–93 years) at a steeper slope in African Americans than in whites (0.029 kb year −1 vs. 0.020 kb year −1, respectively, p = 0.0001). We suggest that racial difference in LTL arises from a host of interacting biological factors, including replication rates of hematopoietic stem cells.

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          Obesity, cigarette smoking, and telomere length in women.

          Obesity and smoking are important risk factors for many age-related diseases. Both are states of heightened oxidative stress, which increases the rate of telomere erosion per replication, and inflammation, which enhances white blood cell turnover. Together, these processes might accelerate telomere erosion with age. We therefore tested the hypothesis that increased body mass and smoking are associated with shortened telomere length in white blood cells. We investigated 1122 white women aged 18-76 years and found that telomere length decreased steadily with age at a mean rate of 27 bp per year. Telomeres of obese women were 240 bp shorter than those of lean women (p=0.026). A dose-dependent relation with smoking was recorded (p=0.017), and each pack-year smoked was equivalent to an additional 5 bp of telomere length lost (18%) compared with the rate in the overall cohort. Our results emphasise the pro-ageing effects of obesity and cigarette smoking.
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            Telomere length, risk of coronary heart disease, and statin treatment in the West of Scotland Primary Prevention Study: a nested case-control study.

            Inter-individual differences in biological ageing could affect susceptibility to coronary heart disease. Our aim was to determine whether mean leucocyte telomere length is a predictor of the development of coronary heart disease. We compared telomere lengths at recruitment in 484 individuals in the West of Scotland Primary Prevention Study (WOSCOPS) who went on to develop coronary heart disease events with those from 1058 matched controls who remained event free. We also investigated whether there was any association between telomere length and observed clinical benefit of statin treatment in WOSCOPS. Mean telomere length decreased with age by 9% per decade (95% CI 3.6-14.1; p=0.001) in controls; much the same trend was seen in cases (-5.9% per decade, -3.1 to 14.1; p=0.1902). Individuals in the middle and the lowest tertiles of telomere length were more at risk of developing a coronary heart disease event than were individuals in the highest tertile (odds ratio [OR] for coronary heart disease: 1.51, 95% CI 1.15-1.98; p=0.0029 in the middle tertile; 1.44, 1.10-1.90, p=0.0090 in the lowest). In placebo-treated patients, the risk of coronary heart disease was almost double in those in the lower two tertiles of telomere length compared with those in the highest tertile (1.93, 1.33-2.80, p=0.0005 in the middle tertile; 1.94, 1.33-2.84, p=0.0006 in the lowest). By contrast, in patients treated with pravastatin, the increased risk with shorter telomeres was substantially attenuated (1.12, 0.75-1.69, p=0.5755 in the middle tertile; 1.02, 0.68-1.52, p=0.9380 in the lowest). Mean leucocyte telomere length is a predictor of future coronary heart disease events in middle-aged, high-risk men and could identify individuals who would benefit most from statin treatment. Our findings lend support to the hypothesis that differences in biological ageing might contribute to the risk--and variability in age of onset--of coronary heart disease.
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              Inflammatory exposure and historical changes in human life-spans.

              Most explanations of the increase in life expectancy at older ages over history emphasize the importance of medical and public health factors of a particular historical period. We propose that the reduction in lifetime exposure to infectious diseases and other sources of inflammation--a cohort mechanism--has also made an important contribution to the historical decline in old-age mortality. Analysis of birth cohorts across the life-span since 1751 in Sweden reveals strong associations between early-age mortality and subsequent mortality in the same cohorts. We propose that a "cohort morbidity phenotype" represents inflammatory processes that persist from early age into adult life.
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                Author and article information

                Journal
                Aging Cell
                acel
                Aging Cell
                Blackwell Publishing Ltd
                1474-9718
                1474-9726
                August 2008
                : 7
                : 4
                : 451-458
                Affiliations
                [1 ]simpleCardiovascular Genetics Division, University of Utah School of Medicine Salt Lake City, UT, USA (NHLBI Family Heart Study)
                [2 ]simpleTulane Center for Cardiovascular Health, Tulane University Health Sciences Center New Orleans, LA, USA (The Bogalusa Heart Study)
                [3 ]simpleCenter of Human Development and Aging, University of Medicine and Dentistry of New Jersey, New Jersey Medical School Newark, NJ, USA
                [4 ]simpleDepartment of Laboratory Medicine and Pathology, University of Minnesota Minneapolis, MN, USA (NHLBI Family Heart Study)
                Author notes

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2·5, which does not permit commercial exploitation.

                Correspondence Abraham Aviv, Center of Human Development and Aging, Room F-464, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, 185 South Orange Ave., Newark, NJ 07103, USA, Tel.: 973 972 5280; fax: 973 972 5576; e-mail: avivab@ 123456umdnj.edu
                Article
                10.1111/j.1474-9726.2008.00397.x
                2810865
                18462274
                18df9cac-98b6-489b-ad6c-c4ea18970372
                Journal compilation © 2008 Blackwell Publishing Ltd/The Anatomical Society of Great Britain and Ireland

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

                History
                : 01 March 2008
                Categories
                Original Articles

                Cell biology
                age,demography,race,leukocyte,gender,telomere
                Cell biology
                age, demography, race, leukocyte, gender, telomere

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