The relationship between stress responding in family context and stress sensitivity with sleep dysfunction in individuals at clinical high-risk for psychosis

Abstract

Stress and sleep have been implicated in the etiology of psychosis, and literature suggests they are closely related. Two distinct domains of stress associated with sleep dysfunction in the general population are responsivity to environmental stressors and stress sensitivity. However, to date, no research has examined relationships between these stress domains and sleep dysfunction in individuals at clinical high-risk (CHR) for psychosis. A total of 57 CHR (mean age = 18.89, SD = 1.82) and 61 healthy control (HC; mean age = 18.34, SD = 2.41) adolescents and young adults completed a measure of emerging stress intolerance. A subset of participants (CHR = 50, HC = 49) completed a measure indexing responsivity to family stressors - an integral context for this developmental stage overlapping with the psychosis-risk period. Sleep efficiency, continuity, and duration were objectively assessed by actigraphy (CHR = 38, HC = 36). Partial correlations with age and sex as covariates were conducted in both groups separately to examine relationships between stress and sleep. Results indicated that automatic maladaptive responsivity to family stressors was associated with disrupted sleep in the CHR but not HC group. Specifically, greater involuntary engagement was associated with poorer sleep efficiency (r = −.42) but not sleep continuity (r = 0.31) and duration (r = .-19). Interestingly, both adaptative and maladaptive voluntary responses to stressors (engagement and disengagement coping) were not associated with sleep. Finally, impaired stress tolerance was associated with sleep efficiency (r = −0.47), continuity (r = 0.37), and duration (r = −0.43). Taken together, findings provided important groundwork for understanding the role of the relationship between involuntary maladaptive responsivity to family stressors and stress sensitivity with sleep in psychosis etiology.