Developmental Trajectories of Stress Physiology and Subcortical Neurobiology Following Early Caregiving Adversity

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Integrative Statement

Prior research has identified altered stress physiology and neurobiology following early adversity either in childhood or adolescence cross-sectional samples, often with conflicting results (e.g. hypo vs. hyper-cortisol; larger vs. smaller amygdala). In the current study, we use an accelerated longitudinal design to characterize trajectories of diurnal cortisol and subcortical brain development from early childhood to late adolescence following early institutional care. 227 subjects (140 comparisons, 87 Previously Institutionalized [PI]; ages 4-19 years old) participated in 1-3 waves of diurnal cortisol collection and a sub-sample (N = 153; 86 comparisons, 67 PI youth; ages 6-19 years old) completed 1-3 MRI scans at two-year intervals. Using piecewise mixed-effects modeling, we identified non-linear age-effects in diurnal cortisol that interacted with group status (F (1, 792) = 18.78, p < 0.001). The best model fit revealed a breakpoint age of 13.1 years (95% CI: 11.6 = 15.05). Specifically, PI children (4-13 years) exhibited blunted waking cortisol relative to comparisons, t (178) = -2.92, p < 0.01, and PI adolescents (13.1 – 19 years) showed a significant age-related increase in waking cortisol, t (300) = 2.60, p < 0.001, relative to comparisons. Adversity-related amygdala phenotypes also varied by age (linear mixed effects group x age interaction, F (1, 130) = 7.963, p < 0.01, such that group differences emerged by adolescence, with PIs exhibiting smaller amygdala relative to comparisons at 1 SD above the mean age (15.3 years, t (150) = -2.53, p < 0.05). In contrast, group differences in hippocampal volumes were age-invariant, with smaller hippocampi observed in the PI group (t (150) = -3.42, p < 0.001). Together, these data suggest that the neurodevelopmental sequela following early caregiving adversity is age-specific, with dynamic changes across childhood and adolescence. Further analyses will investigate how these adversity-related phenotypes of stress physiology and neurobiology interact across development to predict psychopathology risk in PI youth.

Authors

• Michelle VanTieghem, Columbia University
  Presenting Author

• Marta Korom, University of Delaware
  Non-Presenting Author

• Jessica Flannery, University of Oregon
  Non-Presenting Author

• Liliana Varman, Case Western Reserve University
  Non-Presenting Author

• Tricia Choy, Columbia University
  Non-Presenting Author

• Christina Caldera, University of California, Los Angeles
  Non-Presenting Author

• Laurel Gabard-Durnam, Boston Children's Hospital
  Non-Presenting Author

• Bonnie Goff, University of California, Los Angeles
  Non-Presenting Author

• Dylan Gee, Yale University
  Non-Presenting Author

• Kathryn Humphreys, Vanderbilt University
  Non-Presenting Author

• Eva H. Telzer, University of North Carolina Chapel Hill
  Non-Presenting Author

• Mor Shapiro, Kaiser Permanente Woodland Hills, Los Angeles
  Non-Presenting Author

• Jennifer Louie, Kaiser Permanente Cupertino
  Non-Presenting Author

• Dominic Fareri, Adelphi University
  Non-Presenting Author

• Niall Bolger, Columbia University
  Non-Presenting Author

• Nim Tottenham, Columbia University
  Non-Presenting Author