Abstract
Psychosocial acceleration theory suggests that early stress accelerates pubertal development. Using half of the baseline Adolescent Brain and Cognitive Development (ABCD) cohort, Thijssen et al. (2020) provide support that accelerated puberty following stressful family environments may promote neurodevelopment. Here, we replicate and extend those analyses using 1) data from the second half of the ABCD sample (n = 3300 +, ages 9-10), and 2) longitudinal imaging data from the original sample (n = 1800 +, ages 11–12). A family environment latent variable was created and related to anterior cingulate cortex (ACC) thickness, area, white matter fractional anisotropy, amygdala volume, and cingulo-opercular network (CON)–amygdala resting-state functional connectivity. Results from the independent sample replicate the mediating effects of family environment through pubertal stage on amygdala-CON functional connectivity. Sex-stratified analyses show indirect effects via pubertal stage in girls; boys show evidence for direct associations. Analyses using wave 2 imaging data or wave 2-wave 1 difference scores from the originally-analyzed sample replicate the resting-state indirect effects. The current paper replicates the mediating role for puberty in the association between family environment and neurodevelopment. As both direct and indirect associations were found, puberty may be one of multiple mechanisms driving accelerated neurodevelopment following environmental stress.
