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Basal cortisol, cortisol reactivity, and telomere length: A systematic review and meta-analysis.

ABSTRACT: The objective of the present study is to synthesize the existing empirical literature and perform a meta-analysis of published data on the relationship between cortisol and telomere length. We systematically searched studies that examined the relationship between cortisol and telomere length in humans on electronic databases and screened reference sections of included articles. Fourteen studies were included in the meta-analysis, with effect sizes being extracted for two cortisol measures: basal cortisol levels and cortisol reactivity to acute psychological stress. Results from random effects models showed that basal cortisol levels (13 effect sizes from 12 cross-sectional studies, N?=?3675 participants) were not significantly correlated with telomere length (r =-0.05, 95% CI [-0.11, 0.02]). Further, results stratified by the specimen type for cortisol measurement (i.e., saliva, urine, blood) showed that none of the three basal cortisol level measures were correlated with telomere length. However, we found a statistically significant correlation between salivary cortisol reactivity to acute psychosocial stress (6 cross-sectional studies, N?=?958 participants) and telomere length (r = -0.13, 95% CI [-0.23, -0.03]). Subgroup analyses revealed that correlations between salivary cortisol reactivity and telomere length were more evident in studies conducted among children (vs. adults) and in studies that included female participants only (vs. both genders). However, the small number of available studies limits the conclusions derived from subgroup analyses, and more studies are needed before moderator effects can be properly established. Overall, findings of this study support the existence of a relationship between cortisol reactivity and telomere shortening.

SUBMITTER: Jiang Y

PROVIDER: S-EPMC6450740 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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Basal cortisol, cortisol reactivity, and telomere length: A systematic review and meta-analysis.

Jiang Yanping Y Da Wendi W Qiao Shan S Zhang Quan Q Li Xiaoming X Ivey Grace G Zilioli Samuele S

Psychoneuroendocrinology 20190122

The objective of the present study is to synthesize the existing empirical literature and perform a meta-analysis of published data on the relationship between cortisol and telomere length. We systematically searched studies that examined the relationship between cortisol and telomere length in humans on electronic databases and screened reference sections of included articles. Fourteen studies were included in the meta-analysis, with effect sizes being extracted for two cortisol measures: basal ...[more]

PMID: 30695740

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Project description:ObjectiveTo assess the association between leucocyte telomere length and risk of cardiovascular disease.DesignSystematic review and meta-analysis.Data sourcesStudies published up to March 2014 identified through searches of Medline, Web of Science, and Embase.Eligibility criteriaProspective and retrospective studies that reported on associations between leucocyte telomere length and coronary heart disease (defined as non-fatal myocardial infarction, coronary heart disease death, or coronary revascularisation) or cerebrovascular disease (defined as non-fatal stroke or death from cerebrovascular disease) and were broadly representative of general populations--that is, they did not select cohort or control participants on the basis of pre-existing cardiovascular disease or diabetes.ResultsTwenty four studies involving 43,725 participants and 8400 patients with cardiovascular disease (5566 with coronary heart disease and 2834 with cerebrovascular disease) were found to be eligible. In a comparison of the shortest versus longest third of leucocyte telomere length, the pooled relative risk for coronary heart disease was 1.54 (95% confidence interval 1.30 to 1.83) in all studies, 1.40 (1.15 to 1.70) in prospective studies, and 1.80 (1.32 to 2.44) in retrospective studies. Heterogeneity between studies was moderate (I(2) = 64%, 41% to 77%, Phet<0.001) and was not significantly explained by mean age of participants (P = 0.23), the proportion of male participants (P = 0.45), or distinction between retrospective versus prospective studies (P = 0.32). Findings for coronary heart disease were similar in meta-analyses restricted to studies that adjusted for conventional vascular risk factors (relative risk 1.42, 95% confidence interval 1.17 to 1.73); studies with ≥ 200 cases (1.44, 1.20 to 1.74); studies with a high quality score (1.53, 1.22 to 1.92); and in analyses that corrected for publication bias (1.34, 1.12 to 1.60). The pooled relative risk for cerebrovascular disease was 1.42 (1.11 to 1.81), with no significant heterogeneity between studies (I(2) = 41%, 0% to 72%, Phet = 0.08). Shorter telomeres were not significantly associated with cerebrovascular disease risk in prospective studies (1.14, 0.85 to 1.54) or in studies with a high quality score (1.21, 0.83 to 1.76).ConclusionAvailable observational data show an inverse association between leucocyte telomere length and risk of coronary heart disease independent of conventional vascular risk factors. The association with cerebrovascular disease is less certain.

Project description:BACKGROUND:The present protocol was designed for a systematic review and meta-analysis aimed at determining the association of telomere length with substance use disorders with the exclusion of nicotine addiction, and to identify potential moderators of the effect of telomere length. Such methodological information may provide guidance to improve the quality of future research on this important topic. METHODS:Potential studies will be identified through electronic databases (PubMed/MEDLINE, EMBASE, PsycINFO, and Web of Science) up from inception onwards. The inclusion criteria will include published or unpublished observational studies (cohort, case-control, and cross-sectional studies) reporting telomere length in adult patients with substance use disorder compared with a control group. Non-human studies or other study designs such as reviews, case-only, family-based, and/or population studies with only healthy participants will be excluded, as well as those focused solely on nicotine addiction. The main outcome will be telomere length in adults with substance use disorder (primary) and, specifically, in those with alcohol use disorder (secondary). Two investigators will independently evaluate the preselected studies for possible inclusion and will extract data following a standardized protocol. Disagreements will be resolved by consensus. The risk of bias of all included studies will be assessed using the Newcastle-Ottawa Quality Assessment Scale for non-randomized studies. Data will be converted into standardized mean differences as effect size index, and random-effects models will be used for the meta-analysis. Cochran's Q statistic, I2 index, and visual inspection of the forest plot will be used to verify study heterogeneity. Subgroup analyses and meta-regressions will be conducted to ascertain heterogeneity. Several sensitivity analyses will be conducted to address the influence of potential confounding factors. Publication bias will be examined using the "funnel plot" method with Duval and Tweedie's trim-and-fill method and Egger test. DISCUSSION:This systematic review will assess the association of telomere length with substance use disorders aside from nicotine addiction. SYSTEMATIC REVIEW REGISTRATION:PROSPERO registration number CRD42019119785.

Project description:IMPORTANCE:Psychological stress contributes to numerous diseases and may do so in part through damage to telomeres, protective non-coding segments on the ends of chromosomes. OBJECTIVE:We conducted a systematic review and meta-analysis to determine the association between self-reported, perceived psychological stress (PS) and telomere length (TL). DATA SOURCES:We searched 3 databases (PubMed, PsycInfo, and Scopus), completed manual searches of published and unpublished studies, and contacted all study authors to obtain potentially relevant data. STUDY SELECTION:Two independent reviewers assessed studies for original research measuring (but not necessarily reporting the correlation between) PS and TL in human subjects. 23 studies met inclusion criteria; 22 (totaling 8948 subjects) could be meta-analyzed. DATA EXTRACTION AND SYNTHESIS:We assessed study quality using modified MINORS criteria. Since not all included studies reported PS-TL correlations, we obtained them via direct calculation from author-provided data (7 studies), contact with authors (14 studies), or extraction from the published article (1 study). MAIN OUTCOMES AND MEASURES:We conducted random-effects meta-analysis on our primary outcome, the age-adjusted PS-TL correlation. We investigated potential confounders and moderators (sex, life stress exposure, and PS measure validation) via post hoc subset analyses and meta-regression. RESULTS:Increased PS was associated with a very small decrease in TL (n=8724 total; r=-0.06; 95% CI: -0.10, -0.008; p=0.01; ?=0.025), adjusting for age. This relationship was similar between sexes and within studies using validated measures of PS, and marginally (nonsignificantly) stronger among samples recruited for stress exposure (r=-0.13; vs. general samples: b=-0.11; 95% CI: -0.27, 0.01; p=0.05; ?=0.013). Publication bias may exist; correcting for its effects attenuated the relationship. CONCLUSIONS AND RELEVANCE:Our analysis finds a very small, statistically significant relationship between increased PS (as measured over the past month) and decreased TL that may reflect publication bias, although fully parsing the effects of publication bias from other sample-size correlates is challenging, as discussed. The association may be stronger with known major stressors and is similar in magnitude to that noted between obesity and TL. All included studies used single measures of short-term stress; the literature suggests long-term chronic stress may have a larger cumulative effect. Future research should assess for potential confounders and use longitudinal, multidimensional models of stress.

Dataset Information

Basal cortisol, cortisol reactivity, and telomere length: A systematic review and meta-analysis.

Publications

Basal cortisol, cortisol reactivity, and telomere length: A systematic review and meta-analysis.

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