Abstract

Early life exposures are important predictors of adult disease risk. Although the underlying mechanisms are largely unknown, telomere maintenance may be involved. This study investigated the relationship between seasonal differences in parental exposures at time of conception and leukocyte telomere length (LTL) in their offspring. LTL was measured in two cohorts of children aged 2 yrs (N = 487) and 7–9 yrs (N = 218). The association between date of conception and LTL was examined using Fourier regression models, adjusted for age, sex, leukocyte cell composition, and other potential confounders. We observed an effect of season in the older children in all models [likelihood ratio test (LRT) χ²2 = 7.1, p = 0.03; fully adjusted model]. LTL was greatest in children conceived in September (in the rainy season), and smallest in those conceived in March (in the dry season), with an effect size (LTL peak–nadir) of 0.60 z-scores. No effect of season was evident in the younger children (LRT χ²2 = 0.87, p = 0.65). The different results obtained for the two cohorts may reflect a delayed effect of season of conception on postnatal telomere maintenance. Alternatively, they may be explained by unmeasured differences in early life exposures, or the increased telomere attrition rate during infancy.

Highlights

  • Life exposures are important predictors of adult disease risk

  • We found no evidence for a seasonal effect on leukocyte telomere length (LTL) when comparing a crude model with seasonality modelled as a single pair of Fourier terms with a baseline model (likelihood ratio test (LRT) χ22 = 4.24, p = 0.12; Table 2, Model 1; Fig. 1a)

  • In subsequent secondary analyses adjusted for additional covariates (Fig. 1b-e and Supplementary Fig. S3), there was weak evidence for a seasonal effect in models adjusted for maternal body mass index (BMI) (LRT χ22 = 5.48, p = 0.06; Table 2, Model 4; Fig. 1d) and birthweight (LRT χ22 = 5.86, p = 0.05; Table 2, Model 5; Fig. 1e)

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Summary

Introduction

Life exposures are important predictors of adult disease risk. the underlying mechanisms are largely unknown, telomere maintenance may be involved. The different results obtained for the two cohorts may reflect a delayed effect of season of conception on postnatal telomere maintenance. They may be explained by unmeasured differences in early life exposures, or the increased telomere attrition rate during infancy. The biological mechanisms underlying associations between the periconceptional environment and future health remain poorly understood, persistent epigenetic changes may play a role[4,5,6,7] Another molecular process through which the effects of early life factors may exert enduring changes to cellular and organismal phenotypes is the maintenance of telomeres: nucleoprotein structures that protect the ends of linear chromosomes.

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