Plasma β‐Endorphin, Adrenocorticotropin Hormone, and Cortisol in Autism

Abstract

Plasma levels of the hypothalamo-pituitary-adrenal axis hormones beta-endorphin (BE), adrenocorticotropin hormone (ACTH), and cortisol were measured in autistic (N = 48), mentally retarded/cognitively impaired (MR/CI, N = 16), and normal control (N = 26) individuals. Comparison of log transformed data from the three groups revealed that levels of BE and ACTH were significantly higher (p < .05) in the autistic individuals than in normal controls. The higher means in the autistic group were due to significantly higher plasma levels of BE and ACTH, indices of acute stress response, in the more severely affected individuals. The data support the idea that individuals with severe autism have a heightened response to acute stressors rather than chronic hyperarousal or elevated basal stress response system functioning.

Differentiation between Autism and Multiple Complex Developmental Disorder in Response to Psychosocial Stress

“…Similarly, the increase in cortisol levels during the control test may be interpreted as an HPA hyper-response to a situation that is not perceived as stressful. This finding of an HPA hyperresponsiveness is consistent with earlier reports of increased HPA responsivity to stress in autistic patients (Tordjman et al, 1998;Maher et al, 1975). On the other hand, the increase in cortisol levels during the control test may also be interpreted as a disturbance of the circadian rhythm of the HPA axis, as has been previously found in autistic subjects (Yamazaki et al, 1975;Hill et al, 1977;Hoshino et al, 1987).…”

“…Thus, it may be hypothesized that autistic children, given the fact that they clinically show more social impairments, may have even further reduced cortisol responses to psychosocial stress. However, the literature on HPA function describes both normal and increased responses to stress in autism (Yamazaki et al, 1975;Maher et al, 1975;Tordjman et al, 1998). It is difficult to compare these studies with our own, since these studies used metabolic stress (Yamazaki et al, 1975;Maher et al, 1975), or a combined physical/psychological stressor like venapunction (Tordjman et al, 1998).…”

“…However, the literature on HPA function describes both normal and increased responses to stress in autism (Yamazaki et al, 1975;Maher et al, 1975;Tordjman et al, 1998). It is difficult to compare these studies with our own, since these studies used metabolic stress (Yamazaki et al, 1975;Maher et al, 1975), or a combined physical/psychological stressor like venapunction (Tordjman et al, 1998). Considering that the main impairments in autistic and MCDD children are found in their responses to the social environment, it would be more informative if both groups are compared in their responses to an actual psychosocial stress situation.…”

Environmental Enrichment Reverses Behavioral Alterations in Rats Prenatally Exposed to Valproic Acid: Issues for a Therapeutic Approach in Autism

“…Similar behavioral abnormalities have been observed in autistic persons (Militerni et al, 2000;Ayres and Tickle, 1980;Allen and Courchesne, 2001;McAlonan et al, 2002;De Moura-Serra, 1990;Pierce and Courchesne, 2001;American Psychiatric Association, 1994). Autistic patients also exhibit enhanced reaction to stress (Tordjman et al, 1997(Tordjman et al, , 1999aMaher et al, 1975;Jansen et al, 2003).…”

Role of the serotonin transporter gene in the behavioral expression of autism

“…The beneficial effects of agents that block neuronal serotonin transport 8 also focus attention on the possible role of the transporter in the pathophysiology of autism. Additionally, the reported association of a HTT promoter polymorphism with anxiety in the general population, 15 coupled with reports of higher stress responsivity in autism and an increased incidence of anxiety disorder in the families of individuals with autism, 16,17 has further stimulated interest in the HTT in autism. Most intriguing have been discrepant studies reporting preferential transmission of different alleles of the biallelic promoter region polymorphism in individuals with autism.…”