Longitudinal Associations Between Objective Sleep and Lipids: The CARDIA Study

Study Questions:

What is the longitudinal relationship between sleep duration, quality, and lipids among men and women without cardiovascular disease?

Methods:

Data from the Coronary Artery Risk Development in Young Adults (CARDIA) Sleep Study, an observational cohort, were initiated in 1985. Participants in the current study included those who underwent a clinical examination at year 15 (2000). Subjects were excluded for the following: high blood pressure, stroke, transient ischemic attack, deep vein thrombosis, high systolic or diastolic blood pressure (≥140 or ≥90 mm Hg), hypertension, or lipid medication use. The three sleep measures were wrist actigraphy-derived sleep duration, sleep fragmentation, and sleep quality from the global score from the Pittsburgh Sleep Quality Index. Actigraphs were worn for up to 6 days. Sleep duration was the time from sleep onset to final awakening minus the amount of time spent awake during the night. Sleep fragmentation was a measure of the restlessness of the sleep period, from sleep onset to sleep termination, by summing the percentage of time the participant was moving and the percentage of time spent immobile for ≤1 minute to create a sleep fragmentation score.

Results:

Of the original 670 participants, 503 met study qualifications. Baseline mean age was 39.9 years (standard deviation, 3.7; range, 32-51). Women represented 54.9% of the sample (n = 276), and 40.4% were black (n = 203; black women, n = 119; black men, n = 84). The outcome variables were measured at three examinations over 10 years (baseline [2000-01], 5-year [2005-06], and 10-year follow-up [2010-11]). The associations between each sleep parameter and 10-year change in lipids were analyzed with generalized estimating equation models adjusting for relevant confounders. After adjustment, each hour increase in sleep duration was significantly associated with higher total cholesterol (TC) (5.2 mg/dl; 95% confidence interval [CI], 1.7-8.6) and low-density lipoprotein (3.4 mg/dl; 95% CI, 0.2-6.6) in the total sample, a 1.1 mg/dl increase in triglycerides (95% CI, 1.0-1.1) among men, and a borderline significant greater odds for a TC/high-density lipoprotein ratio ≥5 among men (odds ratio, 1.37; 95% CI, 0.99-1.90). Overall, sleep fragmentation and sleep quality scores were not associated with change in lipids.

Conclusions:

The authors concluded that over a 10-year follow-up, longer objective sleep duration was longitudinally and significantly associated with a poorer lipid profile. Greater objective sleep fragmentation and self-reported poor sleep quality were not related to a poorer lipid profile.

Perspective:

Explaining the relationship between loss of sleep and abnormal lipids has been previously reported. What is new in the current study is the association of longer sleep duration and abnormal lipids. Potential mechanistic pathways for this observation are beyond this investigation. Another strength is that the objective sleep parameter measured by actigraphy did predict lipid changes over time; however, self-reported parameters did not. Future studies on this topic are likely to use polysomnography to allow more accurate definition of sleep-disordered breathing not evaluated by actigraphy.

Clinical Topics: Dyslipidemia, Lipid Metabolism, Sleep Apnea

Keywords: Sleep Disorders, Cardia, Lipids, Cardiovascular Diseases, Sleep


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