TY - JOUR
T1 - Blunted cortisol stress reactivity in low–income children relates to lower memory function
AU - Raffington, Laurel
AU - Prindle, John
AU - Keresztes, Attila
AU - Binder, Julia
AU - Heim, Christine
AU - Shing, Yee Lee
N1 - Funding Information:
This work was supported by the Jacobs Foundation [grant 2014-1151 to YLS and CH] and conducted at the Center for Lifespan Psychology, Max Planck Institute for Human Development; Laurel Raffington was supported by the Berlin School of Mind and Brain, Humboldt–Universität zu Berlin, Berlin, Germany . We thank all members of the Jacobs study team for their vital contribution, and all participants and family members for taking part in the study.
Publisher Copyright:
© 2018 Elsevier Ltd
PY - 2018/4
Y1 - 2018/4
N2 - Lower socioeconomic status (SES) environments are marked by higher stress that is hypothesized to alter cortisol secretion in children, thereby damaging hippocampal volume and memory performance. However, empirical evidence demonstrating these putative links is lacking. We assessed the diurnal cortisol awakening response (CAR) on two mornings and cortisol stress reactivity (CSR) with the Trier Social Stress Test for Children in 102 healthy, socio–demographically diverse 6–to–7–year–old children (46% female). Children performed a hippocampal–dependent item–location associative memory task and 60 of these children underwent structural MRI scanning for hippocampal volume. Cortisol values were modeled with latent–change structural equation models to represent overall levels and change. We found lower income is associated with a flatter CAR, blunted reactivity and recovery to acute stress, and smaller hippocampal volume. Furthermore, hyporeactivity in CSR was related to lower memory among lower–income children, whereas there was no reliable association of CSR and memory among higher–income children (an income x cortisol interaction). We found no evidence that smaller hippocampal volume in lower income was associated with poorer memory performance. Notably, hyporeactivity in both CAR and CSR was specific to using income as the SES predictor. The income x cortisol interaction and smaller hippocampal effects, however, were replicated with education and an SES composite score. This suggests that hyporeactivity to acute stress may function as a mediator in SES–cognition associations at the lower end of the SES spectrum, but it does not imply environmental– or genetically–mediated causation.
AB - Lower socioeconomic status (SES) environments are marked by higher stress that is hypothesized to alter cortisol secretion in children, thereby damaging hippocampal volume and memory performance. However, empirical evidence demonstrating these putative links is lacking. We assessed the diurnal cortisol awakening response (CAR) on two mornings and cortisol stress reactivity (CSR) with the Trier Social Stress Test for Children in 102 healthy, socio–demographically diverse 6–to–7–year–old children (46% female). Children performed a hippocampal–dependent item–location associative memory task and 60 of these children underwent structural MRI scanning for hippocampal volume. Cortisol values were modeled with latent–change structural equation models to represent overall levels and change. We found lower income is associated with a flatter CAR, blunted reactivity and recovery to acute stress, and smaller hippocampal volume. Furthermore, hyporeactivity in CSR was related to lower memory among lower–income children, whereas there was no reliable association of CSR and memory among higher–income children (an income x cortisol interaction). We found no evidence that smaller hippocampal volume in lower income was associated with poorer memory performance. Notably, hyporeactivity in both CAR and CSR was specific to using income as the SES predictor. The income x cortisol interaction and smaller hippocampal effects, however, were replicated with education and an SES composite score. This suggests that hyporeactivity to acute stress may function as a mediator in SES–cognition associations at the lower end of the SES spectrum, but it does not imply environmental– or genetically–mediated causation.
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U2 - 10.1016/j.psyneuen.2018.02.002
DO - 10.1016/j.psyneuen.2018.02.002
M3 - Article
C2 - 29482133
AN - SCOPUS:85042509725
SN - 0306-4530
VL - 90
SP - 110
EP - 121
JO - Psychoneuroendocrinology
JF - Psychoneuroendocrinology
ER -