Causal effects of the early caregiving environment on development of stress response systems in children

Abstract

Disruptions in stress response system functioning are thought to be a central mechanism by which exposure to adverse early-life environments influences human development. Although early-life adversity results in hyperreactivity of the sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal (HPA) axis in rodents, evidence from human studies is inconsistent. We present results from the Bucharest Early Intervention Project examining whether randomized placement into a family caregiving environment alters development of the autonomic nervous system and HPA axis in children exposed to early-life deprivation associated with institutional rearing. Electrocardiogram, impedance cardiograph, and neuroendocrine data were collected during laboratory-based challenge tasks from children (mean age = 12.9 y) raised in deprived institutional settings in Romania randomized to a high-quality foster care intervention (n = 48) or to remain in care as usual (n = 43) and a sample of typically developing Romanian children (n = 47). Children who remained in institutional care exhibited significantly blunted SNS and HPA axis responses to psychosocial stress compared with children randomized to foster care, whose stress responses approximated those of typically developing children. Intervention effects were evident for cortisol and parasympathetic nervous system reactivity only among children placed in foster care before age 24 and 18 months, respectively, providing experimental evidence of a sensitive period in humans during which the environment is particularly likely to alter stress response system development. We provide evidence for a causal link between the early caregiving environment and stress response system reactivity in humans with effects that differ markedly from those observed in rodent models.

Keywords: HPA axis; autonomic nervous system; childhood adversity; early-life stress; stress reactivity.

Fig. 1.

Group differences in ANS reactivity to the TSST. Figure depicts changes in ANS measures from baseline to each portion of the TSST (speech preparation, speech, and math). A depicts changes in heart rate; B depicts changes in systolic blood pressure; C depicts changes in diastolic blood pressure; D depicts changes in pre-ejection period; and E depicts changes in respiratory sinus arrhythmia. *P < 0.05, two-sided test.

Fig. 2.

Group differences in ANS reactivity to peer evaluation. Figure depicts changes in ANS measures from baseline to the peer evaluation task. A depicts changes in heart rate; B depicts changes in systolic blood pressure; C depicts changes in diastolic blood pressure; D depicts changes in pre-ejection period; and E depicts changes in respiratory sinus arrhythmia. *P < 0.05, two-sided test.

Fig. 3.

Group differences in HPA axis reactivity. Figure depicts changes in HPA axis measures across the study session. A depicts changes in cortisol; B depicts changes in DHEA-S.

Fig. 4.

Timing of placement and HPA axis and parasympathetic nervous system reactivity. Figure depicts changes in HPA axis and parasympathetic nervous system measures across the study session for children in the foster care group, separately for children placed into foster care before and after the age of 24 (A) or 18 months (B). A depicts changes in cortisol; B depicts changes in RSA during the TSST.