Is cortisol associated with poor sleep in autism? A laboratory study in high functioning adults

Abstract

Introduction Higher cortisol output is known to correlate with poor sleep. Sleep in autism is characterized by disorders such as increased awakenings and less slow wave sleep (SWS) compared to typically developed individuals. This study explores the relationship between saliva cortisol levels and sleep in young adults with and without autism. It was predicted that higher salivary cortisol output would be associated with increased signs of poor sleep. Materials and methods Thirteen individuals with high functioning autism (HFA: 12 M, 1F, 22.2 ± 3.7 years) and 12 typically developed individuals (TYP: 11 M, 1F, 21.8 ± 4.2 years) were recorded for two consecutive nights. Saliva cortisol was measured five times in the evening and twice in the morning. The association between cortisol levels and signs of poor sleep was tested in both groups of participants using Pearson correlation coefficients. Results The TYP group and the HFA group showed a comparable salivary cortisol rhythm, with steady low levels in the evening and high levels in the morning. Only the evening cortisol levels showed the expected correlation with signs of poor sleep. The TYP group showed a significant positive correlation between evening cortisol levels and the number and duration of nocturnal awakenings as well as a significant negative correlation with sleep efficiency. The TYP group also showed a negative correlation between evening cortisol and EEG delta activity in SWS over occipital region. In the HFA group, evening cortisol was correlated negatively with the duration of stage 4 SWS and with EEG delta activity over prefrontal and central regions but not with the number and duration of nocturnal awakenings. Sleep spindles and K-complexes, two EEG markers of cortical sleep protective mechanisms, showed no relationships with cortisol in the control group; K-complexes in the ASD group were associated with morning cortisol. Conclusion Young adults with autism showed a significant association between high salivary cortisol output and signs of poor sleep but the relationship pattern is different from that of their typically developed counterpart: less SWS and low levels of slow EEG activity rather than awakening per se were associated with cortisol output. This atypical relationship pattern between sleep markers and cortisol levels possibly reflects an alternative coupling between neuronal and endocrine mechanisms of sleep control in autism. Acknowledgements Canadian Institute for Health Research; ”Fonds de recherche du Quebec”.