Is a blunted cortisol response to stress a premorbid risk for insomnia?

Vulnerability to stress-related sleep disturbances (sleep reactivity) is an established heritable risk factor for insomnia disorder with unclear biological underpinnings. Preliminary research points to a blunted cortisol response to stress as a biological predisposition to familial risk for insomnia, but the role of cortisol response in sleep reactivity is unknown. Therefore, the current studies examined whether sleep reactivity is associated with a blunted cortisol response to two laboratory stressors among participants without insomnia. Two community samples of adults with no lifetime history of insomnia completed the Trier Social Stress Test (N = 35) or the Cold Pressor Task (N = 34). Participants were grouped by insomnia-risk using sleep reactivity scores from the Ford Insomnia Response to Stress Test (FIRST). Physiological responses were measured via markers of the hypothalamic-pituitary-adrenal (HPA) axis (salivary cortisol) and autonomic nervous system (ANS; heart rate, mean arterial pressure, and salivary alpha amylase). Participants with high insomnia-risk (FIRST score > 18) exhibited blunted cortisol responses to both stressors. There were no group differences in ANS responses across stressors. Insomnia-risk as indicated by sleep reactivity is associated with blunted cortisol responses to psychosocial and physical laboratory stressors among premorbid adults without insomnia disorder. This study replicates previous research and supports a blunted cortisol response to stress as a biomarker for insomnia vulnerability that may be detected using the FIRST. Prospective research is needed to elucidate whether a blunted cortisol response to stress is one mechanism by which sleep reactive individuals may be at risk of developing insomnia. •Sleep reactivity is a tendency to have trouble sleeping when stressed.•Sleep reactivity is a robust risk factor for insomnia.•Sleep reactivity was associated with a dampened cortisol stress response.•These results replicate prior findings on familial risk for insomnia.•More work is needed on this biological stress response across insomnia’s evolution.