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Enhanced Cortisol Response to Stress in Children in Autism

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Abstract

Children with Autism often show difficulties in adapting to change. Previous studies of cortisol, a neurobiologic stress hormone reflecting hypothalamic–pituitary–adrenal (HPA) axis activity, in children with autism have demonstrated variable results. This study measured cortisol levels in children with and without Autism: (1) at rest; (2) in a novel environment; and (3) in response to a blood draw stressor. A significantly higher serum cortisol response was found in the group of children with autism. Analysis showed significantly higher peak cortisol levels and prolonged duration and recovery of cortisol elevation following the blood-stick stressor in children with autism. This study suggests increased reactivity of the HPA axis to stress and novel stimuli in children with autism.

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Acknowledgments

This research project was supported by Award Number UL1RR029882 from the National Center for Research Resources, as well as Award Number P50 DA016511 from the Office of Research on Women’s Health at the National Institutes of Health. Control participants were from grant K23 NIH/NIMH K23MH064111: Neurodevelopmental Biology of Neglected Children (PI: Eve G. Spratt) and additional resources were obtained from grant NIH/NIDA K24DA00435: Midcareer Investigator Award in Patient-Oriented Research (PI: Kathleen T. Brady). The content of this research is solely the responsibility of the authors and does not necessarily represent the official views of the National Center for Research Resources or the National Institutes of Health. Many thanks to Quest Diagnostics for performing serum cortisol measurements. Thanks to Drs. Lindsay DeVane and Megan Gunnar, as well as research assistants Loriann Uerebroth, Samantha Friedenberg, Lauren English, and Doreen Condon, for assistance and advice with this project.

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Correspondence to Eve G. Spratt.

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Spratt, E.G., Nicholas, J.S., Brady, K.T. et al. Enhanced Cortisol Response to Stress in Children in Autism. J Autism Dev Disord 42, 75–81 (2012). https://doi.org/10.1007/s10803-011-1214-0

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