Sleep

Association of Sleep Duration With Intracranial Atherosclerosis and Cerebral Small Vessel Disease: A Mediation by Metabolic Factors.

TL;DR

Aberrant sleep duration may increase the potential risk for intracranial atherosclerosis and cerebral small vessel disease, which can be partially mediated by blood pressure and fasting plasma glucose.

Key Findings

Long sleep duration was associated with higher risk of intracranial atherosclerotic plaque.

  • Long sleep (>9 h) vs. normal sleep (7-9 h): OR 1.40 (95% CI, 1.10-1.78)
  • Association remained after adjustment for covariates
  • Study enrolled 3038 participants (53.5% women; mean age 61.2 ± 6.7 years) from the PRECISE study cross-sectional baseline survey
  • Participants were categorized into short (<7 h), normal (7-9 h), and long (>9 h) sleep groups

Long sleep duration was associated with higher intracranial atherosclerotic burden.

  • Long sleep vs. normal sleep: common OR 1.38 (95% CI, 1.09-1.75)
  • Association was assessed after adjustment for covariates
  • Intracranial atherosclerotic burden was evaluated as an ordinal outcome using common OR

Long sleep duration was associated with higher risk of enlarged perivascular space in the basal ganglia (BG-EPVS).

  • Long sleep vs. normal sleep: OR 1.45 (95% CI, 1.07-1.97)
  • BG-EPVS is one of the cerebral small vessel disease (CSVD) imaging markers evaluated in the study
  • Association remained significant after adjustment for covariates

Short sleep duration was associated with a higher risk of lacunes.

  • Short sleep (<7 h) vs. normal sleep: OR 1.67 (95% CI, 1.06-2.63)
  • Association was significant after adjustment for covariates
  • Lacunes are a CSVD imaging marker evaluated in the study

The association of long sleep duration with intracranial atherosclerotic plaque, intracranial atherosclerotic burden, and BG-EPVS was partially mediated by metabolic factors of blood pressure and fasting plasma glucose.

  • Mediation percentage for intracranial atherosclerotic plaque: 35.4%
  • Mediation percentage for intracranial atherosclerotic burden: 34.0%
  • Mediation percentage for BG-EPVS: 20.3%
  • Blood pressure and fasting plasma glucose were identified as the specific mediating metabolic factors

The study was a cross-sectional analysis using baseline data from the PRECISE (Poly-vascular Evaluation for Cognitive Impairment and Vascular Events) study.

  • 3038 participants were enrolled (53.5% women; mean age 61.2 ± 6.7 years)
  • Outcomes evaluated included intracranial atherosclerotic plaque, intracranial atherosclerotic burden, total CSVD score, and CSVD imaging markers
  • ClinicalTrials.gov identifier: NCT03178448
  • Sleep duration was self-reported and categorized into three groups: short (<7 h), normal (7-9 h), and long (>9 h)

What This Means

This research suggests that sleeping too little or too much is linked to different types of brain blood vessel disease. In a study of over 3,000 middle-aged and older adults in China, people who slept more than 9 hours per night had about 40% higher odds of having fatty plaque buildup inside the brain's arteries and about 45% higher odds of having enlarged spaces around small brain blood vessels (a marker of small vessel disease) compared to those who slept 7-9 hours. People who slept less than 7 hours had about 67% higher odds of having lacunes — tiny areas of damage in the brain caused by small vessel disease — compared to normal sleepers. Importantly, the study found that metabolic factors — specifically blood pressure and blood sugar levels — helped explain part of why long sleep was linked to brain vascular disease. Blood pressure and fasting blood glucose mediated roughly 20-35% of the association between long sleep and these brain vessel outcomes, meaning these metabolic factors act as a pathway through which sleep duration affects brain vascular health. This research suggests that managing blood pressure and blood sugar levels may be particularly important for people who sleep abnormal amounts, as doing so could help reduce their risk of developing brain blood vessel disease. However, because this was a cross-sectional study (a snapshot in time), it cannot prove that abnormal sleep directly causes these brain changes — only that they tend to occur together. Future longitudinal studies are needed to confirm these relationships.

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Citation

Chen H, Zhang A, Chen W, Cai X, Zhou M, Li S, et al.. (2026). Association of Sleep Duration With Intracranial Atherosclerosis and Cerebral Small Vessel Disease: A Mediation by Metabolic Factors.. CNS neuroscience &amp; therapeutics. https://doi.org/10.1002/cns.70797