What worries parents of a child with Autism? Evidence from a biomarker for chronic stress
Introduction
Parenting a child with Autism Spectrum Disorders (ASD) has been shown to be a stressful experience (Bouma & Schweitzer, 1990; Mugno, Ruta, D'Arrigo, & Mazzone, 2007; Sharpley, Bitsika, & Efremidis, 1997), often elevating parental anxiety and/or depression above levels reported by parents of non-ASD children (Baker-Ericzen, Brookman-Frazee, & Stahmer, 2005; Weiss, 2002). In a meta-analysis of 26 studies, Hayes and Watson (2013) also found that, as well as experiencing higher levels of parenting stress than parents of typical children, parents of ASD children also reported stress levels that were significantly higher than parents of children with other non-ASD disabilities. Those authors commented that the evidence regarding elevated stress among parents of children with ASD was conclusive and that future investigations should focus upon the factors that contribute to, and moderate, that stress.
Section snippets
Sources of parental stress
Several studies have attempted to identify the ASD child-based factors that are most likely to contribute to parental stress, and these have included severity of ASD symptoms, level of functioning, child’s age, and adaptive behaviour (Davis & Carter, 2008; Rivard, Terroux, Parent-Boursier, & Mercier, 2014). There is also some evidence that the children’s externalising (e.g., aggression, tantrums, self-injurious behaviour) and internalising (withdrawal, anxiety, fear) behaviours had significant
Cortisol: a biomarker of chronic parental stress
One such biological measure that has been used to determine the presence of chronic stress is cortisol, which is released from the Hypothamalus-Pituitary-Adrenal (HPA) axis. A cascade of HPA responses commences in the hypothalamus and moves to the pituitary gland and adrenal cortex, from where cortisol is released into the bloodstream about 8 min after the onset of the stressor (Guyton & Hall, 2006) and into saliva about 10 min later (Buono, Yeager, & Hodgdon, 1986). Cortisol is a key
Participants
A sample of 135 mothers and 14 fathers of 149 young males with ASD were recruited for this study from a local parent support group on the Gold Coast, Queensland, Australia so that each participant was the parent of a different child with ASD. The sons (M age = 11.18yr, SD = 3.33yr, range = 6yr to 18yr) of these parents had received their original diagnosis of ASD from a registered paediatrician or psychiatrist. These initial diagnoses were conducted at varying times before this study and so they were
DR status of parents
There were 20 (13.4%) parents who did not show the expected DR decline in cortisol concentrations from morning to afternoon, and 129 (86.6%) who did. Fig. 1 shows the relative mean cortisol concentrations from the morning and afternoon samplings for these two subgroups. It is apparent that these two subgroups represented quite different sets of participant responses, with the different slopes of the DR being obvious. Although there are some drawbacks to performing MANOVA on different sized
Overview of findings
Both exploratory factorial (by subdividing parents into DR-dysregulation present vs DR- dysregulation not present) and regression (using the whole range of DR dysregulation scores) models of data analysis produced the same outcomes—that parents’ perceptions of their sons’ self-harm behaviour was the single significant ‘predictor’ of their chronic stress as measured by the biological indicator of dysregulation to the HPA-axis diurnal rhythm. This finding may therefore be accepted as valid within
Conclusions
Notwithstanding these limitations, these data represent the first report of the effects of ASD-related behaviour of children upon the physiological stress states of their parents. As such, they expand our understanding of the experiences of these parents and the processes they undergo. These findings also raise the important fact that the SIB of their children may (eventually) produce quite harmful stress-related health effects in parents, such as those described by Chrousos (2009) that include
Conflict of interest
Author CFS declares that he has no conflict of interest. Author VB declares that she has no conflict of interest. Author NMA declares that he has no conflict of interest. Author LLA declares that she has no conflict of interest.
Acknowledgements
The authors express their gratitude to the participants of this study.
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
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These authors share senior authorship