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

Jodczyk S, Fergusson DM, Horwood LJ, Pearson JF, Kennedy MA - PLoS ONE (2014)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Gene Structure and Function Laboratory, Department of Pathology, University of Otago, Christchurch, New Zealand.

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.

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Distribution of LTL.The distribution of observed telomere lengths (T/S ratio) for the CHDS cohort (n = 677) is shown as a histogram, a density curve for a normal distribution with the same mean ( = 1.18) and standard deviation (s = 0.37) has been superimposed. The data is not normally distributed (Shapiro-Wilks p<0.001), and is right skewed (skewness 2.3). Telomere length in this cohort ranges from a T/S ratio of 0.50 to 4.35.
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pone-0097102-g001: Distribution of LTL.The distribution of observed telomere lengths (T/S ratio) for the CHDS cohort (n = 677) is shown as a histogram, a density curve for a normal distribution with the same mean ( = 1.18) and standard deviation (s = 0.37) has been superimposed. The data is not normally distributed (Shapiro-Wilks p<0.001), and is right skewed (skewness 2.3). Telomere length in this cohort ranges from a T/S ratio of 0.50 to 4.35.

Mentions: Figure 1 shows the distribution of LTL in the sample. The distribution was leptokurtic (thinner) and skewed to the right in comparison to a normal distribution (skewness = 2.3; kurtosis 12.3, Shapiro-Wilk test of normality p<.001).


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

Jodczyk S, Fergusson DM, Horwood LJ, Pearson JF, Kennedy MA - PLoS ONE (2014)

Distribution of LTL.The distribution of observed telomere lengths (T/S ratio) for the CHDS cohort (n = 677) is shown as a histogram, a density curve for a normal distribution with the same mean ( = 1.18) and standard deviation (s = 0.37) has been superimposed. The data is not normally distributed (Shapiro-Wilks p<0.001), and is right skewed (skewness 2.3). Telomere length in this cohort ranges from a T/S ratio of 0.50 to 4.35.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4016252&req=5

pone-0097102-g001: Distribution of LTL.The distribution of observed telomere lengths (T/S ratio) for the CHDS cohort (n = 677) is shown as a histogram, a density curve for a normal distribution with the same mean ( = 1.18) and standard deviation (s = 0.37) has been superimposed. The data is not normally distributed (Shapiro-Wilks p<0.001), and is right skewed (skewness 2.3). Telomere length in this cohort ranges from a T/S ratio of 0.50 to 4.35.
Mentions: Figure 1 shows the distribution of LTL in the sample. The distribution was leptokurtic (thinner) and skewed to the right in comparison to a normal distribution (skewness = 2.3; kurtosis 12.3, Shapiro-Wilk test of normality p<.001).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Gene Structure and Function Laboratory, Department of Pathology, University of Otago, Christchurch, New Zealand.

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.

Show MeSH
Related in: MedlinePlus