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Investigating Biological Aging and Pubertal Development in Two High-Risk Pediatric Cohorts

Sat, March 25, 10:00 to 11:30am, Salt Palace Convention Center, Floor: 3, Meeting Room 355 D

Abstract

Background: The impact of early life adversity (ELA) on life-course health is well-established. Two notable outcomes associated with ELA are disruptions to pubertal development and biological aging trajectories. The co-occurrence of these two phenomena has been contextualized as an evolutionary adaptation to ELA, wherein reproductive fidelity is prioritized at the cost of long-term survival to maximize the possibility of reproduction in a high-stress environment. However, the timing and tempo of these processes relative to one another has received limited attention in prospective and developmental research.

Cohorts: Integrating these two bodies of research, we examined associations between early-life adversity, pubertal development, and biological aging within two high-risk pediatric cohorts, the ongoing Child Health Study (CHS) and the Bucharest Early Intervention Project (BEIP).
The CHS is a large multidisciplinary study designed to provide prospective, longitudinal data on the health and development of children with a history of maltreatment, defined here as investigated reports of neglect, physical abuse, or sexual abuse, and demographically matched non-maltreated comparison children. We leveraged existing data from Time 1 (baseline, age: 8-13 yrs) of the CHS to conduct cross-sectional analyses examining associations between ELA, pubertal development, and biological age.
The BEIP is a longitudinal randomized controlled trial comparing foster care to care-as-usual for children in Romanian institutions. Children were recruited between 6 and 31 months of age and randomized to a care-as-usual group or foster care group. At later time points a comparison group of never-institutionalized children were also integrated into the study. We leveraged longitudinal data from 8- and 12-year follow-up assessments to test whether biological age mediated associations between ELA and pubertal development.

Methods: Pubertal development was associated via self-reported Tanner Staging. For both cohorts, each participant self-reported their stage (1-5) of pubic hair development and breast (females only) and testis (males only) development. The final pubertal development measure was calculated as the average across these two ratings. Biological age in the CHS cohort was estimated using qPCR and DNA-methylation-based measurements of telomere length (aTL & DNAmTL). Biological age in the BEIP cohort was estimated using a MMqPCR-based measure of telomere length (T/S ratio). The aTL measure in CHS was converted to a T/S ratio (r=0.99) for meta-analytic measurements across cohorts.

Results: Full results will be presented in the symposium. Preliminary findings within the CHS indicate significant associations between chronological age and measures of biological age. Moreover, ELA was associated with significantly accelerated pubertal development irrespective of differences in chronological age. Substantiated maltreatment exposure was associated with shorter DNAmTL. By contrast, unsubstantiated maltreatment exposure was not associated with accelerated biological age. There was no association between biological age and pubertal development in the CHS cohort.

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