title: Perceived stress and telomere length: A systematic review, meta-analysis, and methodologic considerations for advancing the field.
abstract: OBJECTIVE
  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).
  
  
  METHODS
  We searched 3 databases (PubMed, PsycInfo, and Scopus), completed manual searches of published and unpublished studies, and contacted all study authors to obtain potentially relevant data.
  
  
  METHODS
  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.
  
  
  METHODS
  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).
  
  
  METHODS
  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; α=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; α=0.013). Publication bias may exist; correcting for its effects attenuated the relationship.
  
  
  CONCLUSIONS
  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.
authors: Quantitative Sciences Unit, Stanford University, Palo Alto, CA, USA. Electronic address: mmathur@stanford.edu.
authors: Maya B
authors: MB
authors: Mathur
authors: Department of Psychiatry, University of California, San Francisco, CA, USA.
authors: Elissa
authors: E
authors: Epel
authors: Department of Psychological and Brain Sciences, Boston University, Boston, MA, USA.
authors: Shelley
authors: S
authors: Kind
authors: Quantitative Sciences Unit, Stanford University, Palo Alto, CA, USA.
authors: Manisha
authors: M
authors: Desai
authors: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, USA.
authors: Christine G
authors: CG
authors: Parks
authors: Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC, USA.
authors: Dale P
authors: DP
authors: Sandler
authors: Division of Pulmonary and Critical Care Medicine, Stanford University, Stanford, CA, USA; Center for Health Policy and Center for Primary Care and Outcomes Research, Stanford University, Stanford, CA, USA.
authors: Nayer
authors: N
authors: Khazeni
mesh_terms: D000818:Animals; D006801:Humans; D017594:Publication Bias; D013223:Statistics as Topic; D013315:Stress, Psychological / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D016615:Telomere / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D059506:Telomere Shortening / Q000502:physiology*
keywords: Cellular damage; Meta-analysis; Stress; Telomere