Abstract
<title>Abstract</title> <p>Sleep difficulties are an increasingly recognised cardiovascular risk factor, but two questions remain unresolved: whether the sleep–blood-pressure pathway is mediated through adiposity, and whether transient or sustained sleep disturbance carries the prognostic burden. We analysed 13,519 men free of treated hypertension at baseline in the Ten to Men cohort (Waves 1–5, 2013–2024), linked to Pharmaceutical Benefits Scheme data. Sleep difficulty was assessed at each wave using a single non-validated self-report item without information on duration, impairment, or sleep apnoea. Incident hypertension was defined as antihypertensive initiation over 142,956 person-years (median 11.1 years). Models examined BMI mediation, symptom trajectories, and bias from unmeasured obstructive sleep apnoea. Over 142,956 person-years of follow-up (median 11.1 years), 1,509 men first received an antihypertensive medication. Baseline sleep difficulty predicted hypertension (HR 1.29, 95% CI 1.16–1.43). BMI minimally attenuated the association (1.2% mediated), suggesting adiposity is not the primary pathway. Risk was driven by persistent symptoms: only the sustained trajectory was associated with hypertension, with a dose–response (HR 1.35 per unit increase in reporting waves). Associations emerged after five years. There was no sleep-by-diabetes interaction; differences likely reflected clinical monitoring. Bias analysis indicated plausible levels of unmeasured sleep apnoea could explain much of the excess risk. Sleep difficulties operate through predominantly non-adiposity, time-accumulating pathways, and only chronic burden predicts treated hypertension, supporting universal sleep-health screening as part of cardiovascular risk assessment.</p>