Parental factors, prenatal air exposures, and adolescent trauma are associated with telomere length in early adulthood: evidence from a UK longitudinal birth cohort
Abstract
Leukocyte telomere length (LTL) is a biomarker of biological ageing, with shorter telomeres linked to increased risk of age-related diseases. Although adverse early-life environments have been associated with shorter LTL in later adulthood, it remains unclear whether such differences are already established by early adulthood and which early-life exposures are most influential. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we analysed LTL in 2,014 participants at a mean age of 24.5 years, examining associations with 50 parental, childhood, and adolescent factors assessed predominantly before age 17. In a subset of 893 participants with repeat measurements at ages 17 and 24, we also examined telomere length change across late adolescence. Longer LTL was associated with older parental age at delivery, particularly maternal age, while shorter LTL was associated with maternal passive smoking during pregnancy and greater cumulative trauma exposure during adolescence. Telomere length declined by approximately 1.1% per year between ages 17 and 24, with little evidence that exposures influenced attrition rates. These findings suggest that variation in LTL by early adulthood primarily reflects prenatal and earlier developmental influences, consistent with early biological embedding.
How strong is the evidence?
Evidence Hub reads this as a cohort study, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence. Reported size: 893 participants or records.
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