Parental Preconception Posttraumatic Stress Symptoms and Maternal Prenatal Inflammation Prospectively Predict Shorter Telomere Length in Children

Abstract

Objective Parental trauma exposure and trauma-related distress can increase risk for adverse health outcomes in offspring, but the pathways implicated in intergenerational transmission are not fully explicated. Accelerated biological aging may be one mechanism underlying less favorable health in trauma-exposed individuals and their offspring. This study examines associations of preconception maternal and paternal posttraumatic stress disorder (PTSD) symptoms with child telomere length, and maternal prenatal C-reactive protein (CRP) as a biological mechanism. Methods Mothers (n = 127) and a subset of the fathers (n = 84) reported on PTSD symptoms before conception. Mothers provided blood spots in the second and third trimester that were assayed for CRP. At age 4, children provided buccal cells for measurement of telomere length. Models adjusted for parental age, socioeconomic status, maternal pre-pregnancy BMI, child biological sex, and child age. Results Mothers’ PTSD symptoms were significantly associated with shorter child telomere length (β = -0.22, SE = 0.10, p = .023). Fathers’ PTSD symptoms were also inversely associated with child telomere length (β = -0.21, SE = 0.11), though nonsignificant (p = .065). There was no significant indirect effect of mothers’ PTSD symptoms on child telomere length through CRP in pregnancy, but higher second trimester CRP was significantly associated with shorter child telomere length (β = -0.35, SE = 0.18, p = .048). Conclusions Maternal symptoms of PTSD prior to conception and second trimester inflammation were associated with shorter telomere length in offspring in early childhood, independent of covariates. Findings indicate intergenerational transmission of parental trauma may occur in part through accelerated biological aging processes and provide further evidence that prenatal pro-inflammatory processes program child telomere length. Open Science Framework Pre-registration: https://osf.io/7c2d5/?view_only=cd0fb81f48db4b8f9c59fc8bb7b0ef97

Developmental cascades from maternal preconception stress to child behavior problems: Testing multilevel preconception, prenatal, and postnatal influences.

“…Spanning human and nonhuman animal models, other empirical work has found that preconception influences are independent of prenatal factors, suggesting direct effects of preconception factors on offspring outcomes (Class et al, 2013; Guardino et al, 2022; Keenan et al, 2018; Rinne, Carroll, et al, 2023; Swales et al, 2023; Yehuda et al, 2000). For example, experimental manipulation of parental preconception stress among rodents produced altered offspring behavioral and physiological differences characteristic of stress-related disorders (e.g., epigenetic changes; altered stress coping behaviors), independent of pre- and postnatal factors (for reviews, see Chan et al, 2018; Keenan et al, 2018).…”

“…For example, experimental manipulation of parental preconception stress among rodents produced altered offspring behavioral and physiological differences characteristic of stress-related disorders (e.g., epigenetic changes; altered stress coping behaviors), independent of pre- and postnatal factors (for reviews, see Chan et al, 2018; Keenan et al, 2018). In humans, even with control of prenatal factors, parental preconception stress and parental emotional distress were associated with greater negative emotionality, HPA axis dysregulation, altered neurodevelopment, and shorter telomere length during infancy and childhood (e.g., Guardino et al, 2022; Keenan et al, 2018; Rinne, Carroll, et al, 2023; Swales et al, 2023; Yehuda et al, 2000). Collectively, this multimethod evidence converges around the centrality of preconception influences on offspring outcomes that are distinct from prenatal influences, potentially operating through germline epigenetic mechanisms (Chan et al, 2018; Yehuda & Lehrner, 2018).…”