Poor sleep quality, sleep variability, and some circadian rhythm measures were linked to over 18 months in healthy older adults.
Evidence
An 18-month observational analysis of 124 older adults from the Age-Well trial used device-based sleep measures and actigraphy to test whether baseline sleep and circadian patterns predicted changes in telomere metrics.
Caveat
The results are observational, rely on modest sleep-assessment subsamples, and some associations were limited to Aβ-positive participants.
Simplified
INTRODUCTION: Sleep and circadian rhythm disturbances have been related to cognitive decline and increased risk of Alzheimer's disease (AD). These disruptions are also closely associated with biological ageing processes. , a key marker of cellular ageing, has been implicated in various age-related diseases, including AD. Although sleep disturbances have been linked to shorter telomere length (TL), the effects of sleep, its variability, and circadian rhythms on telomere dynamics (over 18 months) remain unknown. Furthermore, the interplay between these factors and AD risk has yet to be investigated in healthy older adults. Therefore, the objective of this study was to explore how sleep, sleep variability, and circadian rhythms affect telomere dynamics in healthy older adults and the influence of AD risk on these relationships.
METHODS: Data from 124 healthy older adults (mean age ± SD: 69.27 ± 3.73y) from the Age-Well interventional trial (NCT02977819) were analyzed. Blood samples were collected to determine three TL metrics (50th and 20th percentile TL, and percentage of critically short telomeres (%CST) at baseline and after 18-month follow-up). Sleep and its variability were assessed using the Somno-Artdevice over 5 nights (n = 77), and circadian rhythms using actigraphy for 1 week (n = 123). Multiple linear regressions examined whether baseline sleep and circadian rhythm measures predicted TL changes over time. Interaction analyses assessed the modulatory effects of amyloid (Aβ) status, assessed using Forbetapir-PET imaging, and APOE4 status on these relationships. Age, sex, education, BMI, and intervention group were included as covariates. ®
RESULTS: Poor sleep quality (characterized by lower sleep efficiency and higher wake after sleep onset) and greater variability in sleep efficiency predicted an increase in %CST. Greater regularity in sleep/wake patterns was associated with a decrease in 50th and 20th percentile TL and an increase in %CST. In Aβ-positive individuals, longer latency of rapid eye movement sleep predicted a reduction in 20th percentile TL and an increase in %CST.
CONCLUSIONS: This study suggests that poor sleep quality, sleep variability and circadian rhythm disturbances may accelerate cellular ageing through telomere shortening in older adults. Our results highlight the potential value of sleep interventions in mitigating biological ageing and reducing vulnerability to age-related diseases.
Key numbers
0.325
Increase in %CST
Association between poor sleep quality and telomere dynamics.
0.310
Increase in %CST
Link between sleep variability and cellular aging.
−0.272
Shorter telomeres with higher regularity
Unexpected association between sleep regularity and telomere length.
Full Text
We can’t show the full text here under this license.
Circadian Biology