Cumulative risk exposure and child cellular aging in a Dutch low‐risk community sample. (2nd November 2022)

• Record Type: Journal Article
• Authors: Beijers, Roseriet; ten Thije, Ilse; Bolhuis, Emma; O'Donnell, Kieran J.; Tollenaar, Marieke S.; Shalev, Idan; Hastings, Waylon J.; MacIsaac, Julia L.; Lin, David T. S.; Meaney, Michael; Kobor, Michael S.; Belsky, Jay; de Weerth, Carolina
• Is Part Of: Psychophysiology. Volume 60:Number 4(2023)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2022-11-02
• Subjects: Psychophysiology -- Periodicals; 612.8
• DOI: 10.1111/psyp.14205
• Languages: English
• ISSNs: 0048-5772

Abstract

Abstract: One of the proposed mechanisms linking childhood stressor exposure to negative mental and physical health outcomes in later life is cellular aging. In this prospective, longitudinal, and pre‐registered study, we examined the association between a cumulative pattern of childhood risk exposure from age 6 to age 10 (i.e., poor maternal mental health, parental relationship problems, family/friend death, bullying victimization, poor quality friendships) and change in two biomarkers of cellular aging (i.e., telomere length, epigenetic age) from age 6 to age 10 in a Dutch low‐risk community sample ( n = 193). We further examined the moderating effect of cortisol reactivity at age 6. Ordinary Least Squares regression analyses revealed no significant main effects of childhood risk exposure on change in cellular aging, nor a moderation effect of child cortisol reactivity. Secondary findings showed a positive correlation between telomere length and cortisol reactivity at age 6, warranting further investigation. More research in similar communities is needed before drawing strong conclusions based on the null results. Abstract : Previous research in high‐adversity risk samples suggests an association between childhood stressor exposure and accelerated cellular aging. Our null‐findings from a longitudinal community sample indicate that such link between childhood stressor exposure and accelerated cellular aging might not be present in low‐adversity risk samples. Furthermore, our study uncovers an association between telomere length and cortisol reactivity and supports the notions of a lack of association between different biomarkers of cellular aging and a period of telomere length stability in childhood.