Abstract
Exposure to stressors early in life is associated with faster ageing and reduced longevity. One important mechanism that could underlie these late life effects is increased telomere loss. Telomere length in early post-natal life is an important predictor of subsequent lifespan, but the factors underpinning its variability are poorly understood. Recent human studies have linked stress exposure to increased telomere loss. These studies have of necessity been non-experimental and are consequently subjected to several confounding factors; also, being based on leucocyte populations, where cell composition is variable and some telomere restoration can occur, the extent to which these effects extend beyond the immune system has been questioned. In this study, we experimentally manipulated stress exposure early in post-natal life in nestling European shags (Phalacrocorax aristotelis) in the wild and examined the effect on telomere length in erythrocytes. Our results show that greater stress exposure during early post-natal life increases telomere loss at this life-history stage, and that such an effect is not confined to immune cells. The delayed effects of increased telomere attrition in early life could therefore give rise to a ‘time bomb’ that reduces longevity in the absence of any obvious phenotypic consequences early in life.
Highlights
Exposure to various stressors during early life can have profound fitness consequences [1,2,3]
Longitudinal study of telomere length and longevity covering the entire lifespan of a group of zebra finches, we showed that telomere length early in life is the best predictor of eventual lifespan; the predictive power of telomere length measured later in life was weaker, and largely a consequence of its strong correlation with early life telomere length [15]
At the start of the experiment, telomere length did not differ among individuals allocated to the three treatment groups (F2,49.82 1⁄4 0.55, p 1⁄4 0.581, q-PCR based telomere length: mean + 1 s.e.m.: 1.03 +0.03), though it was shorter in chicks that were slightly older at the time this pre-treatment sample was collected (F1,111.48 1⁄4 6.20, p 1⁄4 0.014)
Summary
Exposure to various stressors during early life can have profound fitness consequences [1,2,3]. On day 30 (30 days after the experiment began when the first hatched chick was approximately 30 days old, age range 1⁄4 26–33 days, mean 1⁄4 29.65, s.e.m. 1⁄4 0.14), all of the chicks within each nest were blood sampled to examine the effect of the treatment on CORT levels and telomere length. We examined the potential effects of the treatment on baseline CORT levels and telomere length at the first sampling point (i.e. when the first hatched chick in the nest was around 10 days old), and on baseline and handling stress-induced CORT levels 4 (sample collected 10 min after capture and restraint) and telomere length at the second sampling point (i.e. at the end of the experiment when the first hatched chick in the nest was around 30 days old) In these models, we included sex and hatching rank as fixed factors, and age, body mass and brood size as covariates. All statistical analyses were performed in IBM SPSS STATISTICS 19
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