Mathur Maya B, Epel Elissa, Kind Shelley, Desai Manisha, Parks Christine G, Sandler Dale P, Khazeni Nayer
Quantitative Sciences Unit, Stanford University, Palo Alto, CA, USA.
Department of Psychiatry, University of California, San Francisco, CA, USA.
Brain Behav Immun. 2016 May;54:158-169. doi: 10.1016/j.bbi.2016.02.002. Epub 2016 Feb 4.
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.
We conducted a systematic review and meta-analysis to determine the association between self-reported, perceived psychological stress (PS) and telomere length (TL).
We searched 3 databases (PubMed, PsycInfo, and Scopus), completed manual searches of published and unpublished studies, and contacted all study authors to obtain potentially relevant data.
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.
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).
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.
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.
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.
心理压力会引发多种疾病，部分原因可能是对端粒造成损伤，端粒是染色体末端的保护性非编码片段。
我们进行了一项系统综述和荟萃分析，以确定自我报告的感知心理压力（PS）与端粒长度（TL）之间的关联。
我们检索了3个数据库（PubMed、PsycInfo和Scopus），对已发表和未发表的研究进行了手动检索，并联系了所有研究作者以获取潜在的相关数据。
两名独立评审员评估了在人类受试者中测量（但不一定报告相关性）PS和TL的原始研究。23项研究符合纳入标准；其中22项（共8948名受试者）可进行荟萃分析。
我们使用改良的MINORS标准评估研究质量。由于并非所有纳入研究都报告了PS-TL相关性，我们通过直接从作者提供的数据（7项研究）、与作者联系（14项研究）或从已发表文章中提取（1项研究）来获取这些相关性。
我们对主要结局（年龄调整后的PS-TL相关性）进行了随机效应荟萃分析。我们通过事后亚组分析和荟萃回归研究了潜在的混杂因素和调节因素（性别、生活压力暴露和PS测量的验证）。
在调整年龄后，PS增加与TL非常小的下降相关（总共n = 8724；r = -0.06；95% CI：-0.10，-0.008；p = 0.01；α = 0.025）。这种关系在性别之间以及使用经过验证的PS测量方法的研究中相似，并且在因压力暴露而招募的样本中略强（但无统计学意义）（r = -0.13；与一般样本相比：b = -0.11；95% CI：-0.27，0.01；p = 0.05；α = 0.013）。可能存在发表偏倚；校正其影响后减弱了这种关系。
我们的分析发现，过去一个月测量的PS增加与TL下降之间存在非常小的、具有统计学意义的关系，这可能反映了发表偏倚，不过如前所述，将发表偏倚的影响与其他样本量相关因素完全区分开来具有挑战性。这种关联在已知的主要压力源下可能更强，其幅度与肥胖和TL之间的关联相似。所有纳入研究都使用了短期压力的单一测量方法；文献表明长期慢性压力可能具有更大的累积效应。未来的研究应评估潜在的混杂因素，并使用压力的纵向、多维度模型。
