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      Depressive Symptoms Are Not Associated with Leukocyte Telomere Length: Findings from the Nova Scotia Health Survey (NSHS95), a Population-Based Study

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          Abstract

          Background

          Premature shortening of leukocyte telomere length has been proposed as a novel mechanism by which depression may confer increased risk of adverse cardiovascular events. Prior studies demonstrating associations of depression and depressive symptoms with shorter leukocyte telomere length were small, included selected psychiatric outpatients, were based on convenience samples, and/or adjusted for a limited number of possible confounding factors.

          Methods and Findings

          We examined the associations of depressive symptoms, probable depressive disorder, and specific depressive symptom clusters, as assessed by the Center for Epidemiological Studies—Depression (CES-D) scale, with leukocyte telomere length, measured by using a real-time PCR method, in 2,225 apparently healthy participants from the 1995 Nova Scotia Health Survey population-based study. The mean age was 48.2±18.9 years; 49.9% of participants were female; and the mean CES-D score was 7.4±7.9. The mean telomere length was 5,301±587 base pairs. In an unadjusted model, depressive symptoms were significantly associated with longer leukocyte telomere length (B = 27.6 base pairs per standard deviation increase in CES-D, 95% confidence interval [CI] = 3.1–52.1, p = 0.027). This association was no longer significant after adjustment for age and sex (B = 9.5, 95% CI = −14.6–33.6, p = 0.44) or after further adjustment for body mass index, Framingham risk score and previous history of ischemic heart disease (all p's≥0.37). Neither probable depressive disorder nor specific depressive symptom clusters were independently associated with leukocyte telomere length.

          Conclusions

          Concurrent depressive symptoms were not associated with leukocyte telomere length in a large, representative, population-based study.

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          Most cited references28

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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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            Depression as an aetiologic and prognostic factor in coronary heart disease: a meta-analysis of 6362 events among 146 538 participants in 54 observational studies.

            With negative treatment trials, the role of depression as an aetiological or prognostic factor in coronary heart disease (CHD) remains controversial. We quantified the effect of depression on CHD, assessing the extent of confounding by coronary risk factors and disease severity. Meta-analysis of cohort studies measuring depression with follow-up for fatal CHD/incident myocardial infarction (aetiological) or all-cause mortality/fatal CHD (prognostic). We searched MEDLINE and Science Citation Index until December 2003. In 21 aetiological studies, the pooled relative risk of future CHD associated with depression was 1.81 (95% CI 1.53-2.15). Adjusted results were included for 11 studies, with adjustment reducing the crude effect marginally from 2.08 (1.69-2.55) to 1.90 (1.49-2.42). In 34 prognostic studies, the pooled relative risk was 1.80 (1.50-2.15). Results adjusted for left ventricular function result were available in only eight studies; and this attenuated the relative risk from 2.18 to 1.53 (1.11-2.10), a 48% reduction. Both aetiological and prognostic studies without adjusted results had lower unadjusted effect sizes than studies from which adjusted results were included (P<0.01). Depression has yet to be established as an independent risk factor for CHD because of incomplete and biased availability of adjustment for conventional risk factors and severity of coronary disease.
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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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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS One
                PLoS ONE
                plos
                plosone
                PLoS ONE
                Public Library of Science (San Francisco, USA )
                1932-6203
                2012
                25 October 2012
                : 7
                : 10
                : e48318
                Affiliations
                [1 ]Center for Behavioral Cardiovascular Health, Columbia University, New York, New York, United States of America
                [2 ]Department of Psychiatry, University of California San Francisco, San Francisco, California, United States of America
                [3 ]Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York, United States of America
                [4 ]Department of Psychiatry and Behavioral Science, Stony Brook University, Stony Brook, New York, United States of America
                [5 ]Department of Community Health and Epidemiology, Dalhousie University, Halifax, Nova Scotia, Canada
                [6 ]Gertrude H. Sergievsky Center, Columbia University, New York, New York, United States of America
                [7 ]Department of Neurology, Columbia University, New York, New York, United States of America
                University of Medicine and Dentistry of New Jersey, United States of America
                Author notes

                Competing Interests: Dr. Elissa Epel’s competing interest as a co-founder of Telomere Health, Inc., which offers commercial telomere length measurement, does not alter the authors' adherence to any of the PLOS ONE policies on sharing data and materials.

                Conceived and designed the experiments: KWD SK JES DS. Performed the experiments: MSK LH. Analyzed the data: JAS JES. Contributed reagents/materials/analysis tools: MSK LH. Wrote the paper: JAS. Made critical intellectual contributions to the development of the manuscript: EE SY JES KWD LH DS.

                Article
                PONE-D-12-20073
                10.1371/journal.pone.0048318
                3485011
                23133583
                79a1bd1a-8295-4ab2-afb1-16deb6627106
                Copyright @ 2012

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 27 June 2012
                : 24 September 2012
                Page count
                Pages: 7
                Funding
                This research was supported by grants HL-091099 and HL-084034 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland. Additional support was provided by National Health and Welfare of Canada, Ottawa, Ontario; the Nova Scotia Department of Health, Halifax, Nova Scotia; and the Heart and Stroke Foundation of New Brunswick, St. John, New Brunswick. Dr. Shaffer is supported by grants 12CRP8870004 of the American Heart Association and T32 HP10260 from the Health Services and Research Administration. Dr. Ye is supported by an American College of Cardiology/Merck Foundation Fellowship Award and by National Institute of Health Grant T32HL007854-16. Dr. Honig receives support from the Alzheimer's Association, the Alzheimer's Drug Discovery Foundation, the National Institute on Aging (grant P50AG008702), the Henry Panasci Fund, and the Taub Institute. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Research Article
                Biology
                Genomics
                Chromosome Biology
                Telomeres
                Molecular Cell Biology
                Chromosome Biology
                Telomeres
                Medicine
                Clinical Research Design
                Epidemiology
                Epidemiology
                Clinical Epidemiology
                Mental Health
                Psychiatry
                Mood Disorders

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                Uncategorized

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