Omofolarin Debellotte, Amuksha Ravindra Shetty, Yuzhu Wang, Ayesha Amin, Vikdeep Mann, Morolayo Fadayomi, Pranati Gudipati, Haidy Hanna, Libina Karippaparambil, Manju Rai
Suicide remains a leading global cause of preventable mortality, with sleep disturbances, particularly insomnia, nightmares, and circadian disruption, emerging as critical yet underrecognized contributors to suicidal ideation and behavior. This narrative review synthesizes current evidence on the multifaceted links between sleep disorders and suicidality, integrating findings from epidemiological, neurobiological, and interventional studies. Insomnia contributes to suicide risk through pathways of hyperarousal, hopelessness, and impaired emotion regulation, while nightmares are associated with increased risk of suicidal ideation and attempts, potentially exerting an effect distinct from other sleep disorders. Circadian misalignment, including shift work and evening chronotype, further exacerbates vulnerability through neuroendocrine and molecular alterations involving the hypothalamic-pituitary-adrenal axis, serotonergic imbalance, and disrupted clock gene expression. Shared biological mechanisms, such as inflammation, hypothalamic-pituitary-adrenal (HPA) dysregulation, and serotonergic depletion, intersect with cognitive-emotional deficits, compounding risk. Clinically, interventions such as cognitive behavioral therapy for insomnia (CBT-I), imagery rehearsal therapy, and chronotherapeutic approaches have demonstrated efficacy in improving sleep continuity and mitigating suicidality. Routine assessment of sleep quality and circadian patterns should be integrated into suicide risk evaluation across psychiatric and primary care settings. Future research incorporating objective sleep measures, biomarker profiling, and digital monitoring platforms may enable precision risk stratification and early intervention. However, the current evidence base is limited by heterogeneity in study designs, the predominance of observational and cross-sectional studies, and potential confounding from psychiatric comorbidities, warranting cautious interpretation of causal relationships. By addressing sleep as a core modifiable risk factor, clinicians can move toward a holistic, biologically informed, and preventive model of suicide care.