Phenotypic Variability in Slow‐Wave Sleep in Depression: Associations With Clinical Profiles and Disorder Severity

Slow-wave sleep (SWS; stage N3) is often reported as reduced in depression, yet variability across depressive phenotypes remains poorly characterised. This study aimed to determine whether N3 architecture-proportion, duration, and latency-identifies clinically distinct profiles in major depressive episode (MDE). Ninety-seven adults with MDE underwent overnight polysomnography. N3 metrics (latency, duration, % of total sleep period (TSP), % of total sleep time (TST)) were analysed both dimensionally (correlations with clinical measures) and categorically (reduced, normal, or increased N3). Backward stepwise logistic regression identified variables distinguishing N3 categories, and sensitivity analyses assessed psychotropic medication effects. Shorter N3 latency correlated with poorer subjective sleep quality and greater anxiety and depressive severity. Extremes of N3 (%TSP) carried clinical burden: increased N3% associated with earlier hospitalisation, younger age at first suicide attempt, and higher daytime sleepiness; reduced N3% related to more hospitalisations and depressive episodes. Categorical contrasts showed increased N3 duration linked to higher anxiety and depressive symptom severity, reduced N3 (%TST) predicted more hospitalisations, while increased N3 (%TST) aligned with greater seasonality and morning chronotype. Men exhibited higher %N3 TST than women; bipolar depression had lower N3 than unipolar depression. A five-factor model (episode count, chronotype, seasonality, age, sex) distinguished increased %N3 TST from normal levels (AUC = 0.863; sensitivity = 0.957; specificity = 0.714), explaining 30.8% of variance. Medication analyses revealed no major effects. N3 sleep is not a uniform biomarker in depression. Its proportion and duration delineate distinct, clinically meaningful profiles. Sleep-based stratification may guide precision care.