Delayed Sleep Time in African Americans and Depression in a Community-Based Population.

STUDY OBJECTIVES: Studies have shown racial differences in circadian rhythm in African Americans when compared to non-Hispanic whites, and an association between circadian dyssynchrony and depression. We hypothesized that the prevalence of delayed sleep time is greater in African Americans when compared to whites and that delayed sleep time is associated with depression. METHODS: We analyzed data from the Sleep Heart Health Study (SHHS), a large community-based sample. Delayed sleep time was defined as self-reported weeknight bedtime after midnight. Depression was defined based on participant's response to the question, "In the past 4 weeks have you felt downhearted and blue?" or reported antidepressant use. We performed multivariate linear and logistic regression, adjusting for age, sex, race, body mass index, smoking, apnea-hypopnea index, alcohol use, and caffeine consumption. RESULTS: Adjusted weekday bedtime was 15 ± 7 minutes later in African Americans compared to whites (P < .001). Similarly, weekend bedtime was 18 ± 7 minutes later in African Americans compared to whites (P = .025). The prevalence of delayed sleep time was greater in African Americans (33.3%) compared to whites (18.7%; P < .001). After adjusting for confounders, when compared to whites, a greater proportion of African Americans had delayed sleep time (adjusted odds ratio [aOR] 2.03; 95% confidence interval [95% CI] 1.5, 2.4; P < .0001). Depression was independently associated with delayed sleep time after adjustment (aOR 1.4; 95% CI 1.1, 1.7; P = .007). CONCLUSIONS: African Americans are more likely to have a delayed sleep time compared to whites, and delayed sleep time was independently associated with depression.

Cerebrovascular reactivity in young subjects with sleep apnea.

STUDY OBJECTIVES: Regional brain alterations may be involved in the pathogenesis and adverse consequences of obstructive sleep apnea (OSA). The objectives for the current study were to (1) determine cerebrovascular reactivity in the motor areas that control upper airway musculature in patients with OSA, and (2) determine whether young patients with OSA have decreased cerebrovascular reactivity in response to breath holding. DESIGN: Case-control study. SETTING: Academic center. PARTICIPANTS: Twelve subjects with OSA (age 24-42 y; apnea-hypopnea index 17; interquartile range [IQR] 9, 69 per hour) and control subjects (n = 10; age 29-44 y; AHI 2; IQR 1, 3 per hour). MEASUREMENTS AND RESULTS: Subjects underwent blood oxygen level-dependent functional magnetic resonance imaging (BOLD-fMRI) while awake, swallowing, and breath holding. In subjects with OSA, during swallowing, there was less activity in the brainstem than in controls (P = 0.03) that remained reduced after adjusting for cortical motor strip activity (P = 0.036). In OSA subjects, brain regions of increased cerebrovascular reactivity (38; IQR 17, 96 cm(3)) was smaller than that in controls (199; IQR 5, 423 cm(3); P = 0.01). In OSA subjects, brain regions of decreased cerebrovascular reactivity during breath hold was greater (P = 0.01), and the ratio of increased-to-decreased brain regions was lower than that of controls (P = 0.006). Adjustment for cerebral volumes, body mass index, and white matter lesions did not change these results substantively. CONCLUSIONS: In patients with obstructive sleep apnea (OSA), diminished change in brainstem activity during swallowing and reduced cerebrovascular reactivity may contribute to the etiopathogenesis and adverse cerebrovascular consequences, respectively. We speculate that decreased cerebral auto-regulation may be causative of gray matter loss in OSA.