Smoking disrupts the relationship between cerebrospinal fluid IL-1β and multiple subdimensions of sleep.

Objective: Inflammatory factors and cigarette smoking have been associated with sleep disorders but molecular mechanisms that regulate sleep, specifically the role of interleukin-1β (IL-1β), remain controversial. Individuals' cerebrospinal fluid (CSF) IL-1β, smoking behavior, and sleep data were collected to investigate how smoking may influence the relationship between CSF IL-1β and sleep via moderation analysis.

Methods: A total of 191 Chinese male patients, including 104 non-smokers and 87 active smokers, scheduled for anterior cruciate ligament reconstructive surgery, were recruited. Pittsburgh Sleep Quality Index (PSQI) scores were collected prior to surgery, and CSF samples were obtained during preoperative lumbar puncture.

Results: Active smokers compared to non-smokers exhibited higher scores across various subdimensions of PSQI, specifically poorer sleep quality, increased sleep latency, reduced sleep efficiency, and heightened sleep disturbance (all p < 0.05). Positive correlations were observed between CSF IL-1β levels and PSQI total scores, as well as several subdimensions of sleep (all p < 0.05) in non-smokers. In contrast, a negative correlation was observed between CSF IL-1β levels and sleep efficiency scores (p < 0.05) among active smokers. Moderation analysis revealed that smoking negatively moderated the relationship between CSF IL-1β and sleep, particularly in PSQI total scores (β = -0.95, p < 0.001), sleep latency scores (β = -1.05, p < 0.001), and sleep disturbance scores (β = -0.45, p < 0.05).

Conclusions: The current study found that smoking disrupts multiple subdimensions of sleep and moderates the effect of the neuroinflammatory factor CSF IL-1β on PSQI sleep latency and sleep disturbance scores.