Slower cortisol response during ACTH stimulation test in autistic children. Eur Child Adolesc Psychiatry
Autism is a hereditary, pervasive neurodevelopmental disorder that starts early in life. The main characteristics of the autism are impairment in social interactions, difficulties in adapting to novel environmental situations and improper reaction to stress. Since the Hypothalamic-Pituitary-Adrenocortical (HPA) axis plays a key role in the response to stress and because the previous research found abnormalities in HPA system, we conducted a study to test several elements of the HPA axis. Because autism is a heritable disorder, autistic subjects were studied as well as their parents. Cortisol circadian rhythm, cortisol daily secretion and its suppression response to dexamethasone had been measured from saliva or urine samples of the autistic children and their parents. Cortisol secretion response after ACTH stimulation was done with the autistic children only. The cortisol elevation after ACTH stimulation among the autistic individuals was slower (P = 0.017) than in healthy controls. No differences were found in salivary cortisol circadian rhythm or suppression response, as well as in cortisol daily excretion. These data indicate that, compared to healthy subjects, autistic individuals have fine differences in cortisol response to ACTH stimulation or possibly to other types of stress.
Available from: Blythe A Corbett
- "There is a body of published data on the research question of whether diurnal cortisol levels in children with autism are different from typically developing children. There were six studies (Corbett et al. 2006, 2008; Hoshino et al. 1987; Jansen et al. 2003; Marinovic-Curin et al. 2008; Richdale and Prior 1992) that used collection procedures, comparison populations, and settings that were most relevant to the population and question of interest. For children with autism compared to control children, afternoon and evening cortisol levels were higher in the majority of studies (Corbett et al. 2008; Hoshino et al. 1987; Marinovic-Curin et al. 2008; Richdale and Prior 1992). "
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ABSTRACT: We examined daytime salivary cortisol and salivary alpha-amylase (sAA) secretion levels and variability in preschool-aged children with autism (AUT) and typically developing children (TYP). Fifty-two subjects (26 AUT and 26 TYP) were enrolled. Salivary samples were obtained at waking, midday, and bedtime on two consecutive days at three phases (baseline, 3 months later, 6 months later). There were modest increases in waking cortisol and sAA levels in AUT relative to TYP, but the increases were not statistically significant. Important differences were observed in cortisol and sAA variability between AUT and TYP. There was also a graded response among AUT by functional status-cortisol and sAA secretion levels were higher when IQ was lower.
Journal of Autism and Developmental Disorders 04/2012; 42(12). DOI:10.1007/s10803-012-1522-z · 3.06 Impact Factor
Available from: Jerome Carayol
- "PITX1 is a key regulator of hormonal genes in the pituitary-hypothalamic axis. Its putative involvement in autism is supported by evidence documenting abnormal levels of downstream hormones, such as adrenocorticotropic hormone (ACTH), beta-endorphin and cortisol in individuals with autism [51-53]. Deregulation of pro-opiomelanocortin and high levels of beta-endorphin in the morning, for example, have been shown to be involved in certain maladaptive behaviors, such as self-injurious behaviors, which are often seen in individuals with autism . "
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ABSTRACT: Autism is a complex disorder characterized by deficits involving communication, social interaction, and repetitive and restrictive patterns of behavior. Twin studies have shown that autism is strongly heritable, suggesting a strong genetic component. In other disease states with a complex etiology, such as type 2 diabetes, cancer and cardiovascular disease, combined analysis of multiple genetic variants in a genetic score has helped to identify individuals at high risk of disease. Genetic scores are designed to test for association of genetic markers with disease.
The accumulation of multiple risk alleles markedly increases the risk of being affected, and compared with studying polymorphisms individually, it improves the identification of subgroups of individuals at greater risk. In the present study, we show that this approach can be applied to autism by specifically looking at a high-risk population of children who have siblings with autism. A two-sample study design and the generation of a genetic score using multiple independent genes were used to assess the risk of autism in a high-risk population.
In both samples, odds ratios (ORs) increased significantly as a function of the number of risk alleles, with a genetic score of 8 being associated with an OR of 5.54 (95% confidence interval [CI] 2.45 to 12.49). The sensitivities and specificities for each genetic score were similar in both analyses, and the resultant area under the receiver operating characteristic curves were identical (0.59).
These results suggest that the accumulation of multiple risk alleles in a genetic score is a useful strategy for assessing the risk of autism in siblings of affected individuals, and may be better than studying single polymorphisms for identifying subgroups of individuals with significantly greater risk.
Molecular Autism 02/2010; 1(1):4. DOI:10.1186/2040-2392-1-4 · 5.41 Impact Factor
Available from: Jane E Roberts
- "Taken together, our work and others indicate a relationship between HPA function and autistic behavior in boys with FXS that is complex and interactive with environmental factors, including time spent in social interaction and the format and intensity of stressful events. Given that HPA dysfunction has also been implicated in idiopathic autism as reflected in abnormal baseline levels and circadian profiles [52–54] and exaggerated cortisol reactivity to social stresses in young children with ASD [53, 55–57], future studies including samples of children with FXS with and without ASD, as well as with idiopathic autism, would be highly informative about HPA axis function and its relationship with autistic behavior. The latter research should not only address the seemingly contradictory idiopathic ASD [52, 53, 58] and FXS literature [19, 27, 31] on cortisol levels and regulation, but also to advance our understanding of the causal relationship between cortisol (i.e., correlate or modifier) and autistic behavior. "
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ABSTRACT: The primary goal of this study was to examine environmental and neuroendocrine factors that convey increased risk for elevated autistic behavior in boys with Fragile X syndrome (FXS). This study involves three related analyses: (1) examination of multiple dimensions of social approach behaviors and how they vary over time, (2) investigation of mean levels and modulation of salivary cortisol levels in response to social interaction, and (3) examination of the relationship of social approach and autistic behaviors to salivary cortisol. Poor social approach and elevated baseline and regulation cortisol are discernible traits that distinguish boys with FXS and ASD from boys with FXS only and from typically developing boys. In addition, blunted cortisol change is associated with increased severity of autistic behaviors only within the FXS and ASD group. Boys with FXS and ASD have distinct behavioral and neuroendocrine profiles that differentiate them from those with FXS alone and typically developing boys.
Journal of Neurodevelopmental Disorders 12/2009; 1(4):283-91. DOI:10.1007/s11689-009-9028-5 · 3.27 Impact Factor
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