Stress reactivity in salivary cortisol and electrocardiogram in adolescents: Investigating sleep disturbances and insomnia

Abstract

This study examined the role of sleep disturbances and insomnia in the context of stress reactivity in adolescence. One-hundred and thirty-five 11-18 year olds (M age = 14.2 years, SD = 1.9, 52% female) completed the Trier Social Stress Test for Children. Salivary cortisol and subjective stress ratings were collected at six time points, and heart rate as well as heart rate variability were measured pre-, during and post-stress induction. Additionally, sleep disturbances and insomnia diagnosis were assessed by a self-report questionnaire and a sleep interview. Robust mixed models investigated if adolescents with compared with adolescents without (a) sleep disturbances and (b) insomnia differ regarding cortisol, heart rate, heart rate variability and psychological stress reactivity considering gender effects. The results indicated that boys with high sleep disturbances showed higher cortisol activity compared with boys with low sleep disturbances, B = 0.88, p < 0.05. Moreover, in boys with insomnia, heart rate and alpha 1 significantly differ less than in boys without insomnia.These findings support the notion of sex differences regarding the association between poor sleep and increased activity of the hypothalamic-pituitary-adrenal axis, and a less adaptable autonomic nervous system in boys in response to an experimental social stress task.

The nature, consequences, mechanisms, and management of sleep disturbances in individuals at-risk for psychosis

“…Other explaining mechanisms for the association between sleep and subsequent psychosis have been identified, such as negative affects (i.e., depression and anxiety) ( 72 – 74 ), endocrine dysfunction due to exposure to psychosocial and biological stress, and cognitive deficits ( 64 ). In this regard, some biological markers have been found to interfere with both psychosis proneness and sleep disturbances through a stress-induced activation of the hypothalamic–pituitary–adrenal (HPA) axis, including elevated cortisol levels ( 75 , 76 ) and pro-inflammatory cytokines ( 77 , 78 ). Interestingly, an increased reactivity to stress has recently been found to directly affect sleep in the UHR stage.…”