No association between mean telomere length and life stress observed in a 30 year birth cohort

PLoS One. 2014 May 9;9(5):e97102. doi: 10.1371/journal.pone.0097102. eCollection 2014.

Abstract

Telomeres are specialised structures that cap the ends of chromosomes. They shorten with each cell division and have been proposed as a marker of cellular aging. Previous studies suggest that early life stressors increase the rate of telomere shortening with potential impact on disease states and mortality later in life. This study examined the associations between telomere length and exposure to a number of stressors that arise during development from the antenatal/perinatal period through to young adulthood. Participants were from the Christchurch Health and Development Study (CHDS), a New Zealand longitudinal birth cohort which has followed participants from birth until age 30. Telomere length was obtained on DNA from peripheral blood samples collected from consenting participants (n = 677) at age 28-30, using a quantitative PCR assay. These data were assessed for associations with 26 measures of life course adversity or stress which occurred prior to 25 years of age. No associations were found between telomere length measured at age 28-30 years and life course adversity or stress for specific measures and for the summary risk scores for each developmental domain. The correlations were very small ranging from -0.06 to 0.06 with a median of 0.01, and none were statistically significant. Our results in this well-studied birth cohort do not support prior reports of such associations, and underscore the need for more extensive replication of proposed links between stress and telomere biology in larger cohorts with appropriate phenotypic data.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Age Factors
  • Cohort Studies
  • DNA Primers / genetics
  • Humans
  • Longitudinal Studies
  • New Zealand
  • Polymerase Chain Reaction
  • Regression Analysis
  • Stress, Psychological / physiopathology*
  • Telomere Homeostasis / genetics
  • Telomere Homeostasis / physiology*

Substances

  • DNA Primers

Grant support

This research was funded by grants from the Health Research Council of New Zealand (11/792; www.hrc.govt.nz), the New Zealand Lottery Grants Board (http://www.dia.govt.nz/lotterygrantsboard), and the University of Otago (http://www.otago.ac.nz/). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.