Self‐Reported Daytime Sleepiness is Associated with Telomere Shortening

Abstract

Traditionally regarded as a consequence of sleep-disordered breathing, excessive daytime sleepiness (EDS) is now recognized as an independent risk factor for cardiovascular disease. Evidence also links the shortening of telomeres, responsible for protecting DNA, with increased cardiovascular disease risk. Interestingly, recent data illustrate telomere lengthening in patients with obstructive sleep apnea (OSA); however, whether EDS is associated with telomere length independently of OSA remains unknown. To examine this potential relationship, we studied 169 subjects with polysomnography assessment who answered “yes” or “no” to experiencing EDS; 70 subjects (41%) reported EDS (59M, 44±12yrs, 30.3±5.5kg/m2) whereas 99 did not (59%, 71M, 40±15yrs, 28.6±7.5kg/m2). Telomere length was quantified via qPCR of genomic DNA isolated from peripheral blood samples and did not differ between individuals reporting EDS compared to those who did not (4,856±280 vs. 4,880±340bp, respectively, P=0.31). However, 50% of subjects reporting EDS had moderate-to-severe OSA (apnea-hypopnea index ≥15events/hr) compared to 28% of the non-EDS group (P<0.01). To account for the confounding effects of OSA on telomere length, we conducted a series of subgroup analyses. Subjects without OSA who reported EDS (n=35, 27M, 39±11yrs, 27.4±5.0kg/m2) had shorter telomeres (4,805±165 vs. 4,875±231bp, P=0.05) than those not reporting EDS (n=71, 47M, 35±11yrs, 26.8±5.4kg/m2). Interestingly, within the OSA subgroup, there were no differences in telomere length (4,897±235 vs. 4,858±251bp, P=0.45) between those with (n=35, 32M, 48±11yrs, 33.2±4.5kg/m2) and without EDS (n=28, 24M, 53±16yrs, 33.1±9.7kg/m2). These effects do not appear to be influenced by subject demographics as no differences were found between compared groups (EDS-OSA vs. nEDS-OSA and OSA+EDS vs. OSA-EDS). Collectively, our data suggest individuals reporting EDS may be at greater risk of developing cardiovascular disease due to accelerated telomere shortening. It also appears OSA and EDS exert differential effects on telomere length.