19235
Stress Regulation in Children with Autism Spectrum Disorders (ASD): A Scoping Review

Thursday, May 14, 2015: 11:30 AM-1:30 PM
Imperial Ballroom (Grand America Hotel)
M. A. Braeken1, L. Van Schuerbeeck1, J. Steyaert2 and M. Vanvuchelen3, (1)Hasselt University, Diepenbeek, Belgium, (2)Leuven Autism Research (LAuRes), University of Leuven (KU Leuven), Leuven, Belgium, (3)Hasselt University Faculty of Medicine and Life Sciences, Diepenbeek, Belgium
Background:  

Autism spectrum disorders (ASD) are characterized by difficulties with social interaction and communication. In addition, individuals with ASD tend to have limited interests and repetitive behaviors, which is often reflected in having trouble adapting to changes in routine or environment. The major neuroendocrine system that modulates our ability to react emotionally and physiologically to change and to the stress caused by a novel or challenging environment, is the hypothalamic-pituitary-adrenal (HPA) axis. 

Objectives:  

The present review aims to investigate the responses of cortisol, a neurobiological stress hormone reflecting HPA axis activity, in children with ASD. 

Methods:  

The review is organized around four main themes: the cortisol awakening response (CAR), diurnal cortisol variation, cortisol responses to stress and interventions affecting cortisol levels in children with ASD.

Results:  

Our analysis of the literature shows strong indications that cortisol levels in children with ASD follow the same pattern as in children without ASD. This means that, similar to typical developing (TD) peers, children with ASD have a diurnal decrease in cortisol, with higher cortisol concentration in the morning than in the evening. Some studies found no differences in the overall level of cortisol in children with ASD compared to children without ASD, while others reported significant higher cortisol levels in children with ASD during the evening or the whole day.

Studies on the evaluation of the CAR in children with ASD are inconsistent. Some suggest that the CAR is mostly absent, while other studies indicate that are no differences in the magnitude, variability or presence of the CAR when compared to typically developing peers.
While children without ASD tend to show an increase in cortisol in response to the child version of the Trier Social Stress Test (TSST-C), children with ASD have been reported to display a reduced cortisol response. There also exists evidence that a playground social stressor or interactions with unfamiliar peers may provoke significantly higher activation when compared to TD children.

Furthermore, children with ASD and TD children potentially also differ in recovery from a social stress environment, as typical developing children showed a significant reduction in cortisol over time, whereas children with ASD maintained an elevated cortisol level. Nonsocial stimuli such as placement in a mock MRI or a blood draw stressor are associated with significantly greater reactivity of the HPA axis in children with ASD as compared to children without ASD.

Physical exercise and relaxation sessions tend to deliver a short-term reduction in levels of cortisol in children with ASD, but long-term significant reductions have not been found. Theatre-based and peer-mediated intervention programs have proven to yield a decline in cortisol by the end of treatment, but also during post-treatment situations.

Conclusions:  

This analysis of the literature shows that altered stress regulation and HPA axis activity as measured by cortisol concentrations could form a promising biomarker for ASD, but more research is needed if we would like to understand the complex relationship between stress regulation and ASD.