- Library Home /
- Search Collections /
- Open Collections /
- Browse Collections /
- UBC Theses and Dissertations /
- Epigenetic age acceleration as a mechanism underlying...
Open Collections
UBC Theses and Dissertations
UBC Theses and Dissertations
Epigenetic age acceleration as a mechanism underlying increased risks of chronic disease in night shift workers U, Stephanie Rose
Abstract
Background: Understanding the mechanisms underlying the associations between night shift work and increased risks of chronic disease is key to developing effective measures to protect the long-term health of night shift workers. A compelling yet understudied mechanism is accelerated biological aging. Methods: In a cross-sectional study of 112 female night shift workers, 88 female day shift workers, and 136 male night shift workers, genome wide DNA methylation data were used to calculate five measures of epigenetic age, including Hannum, Horvath, GrimAge, PhenoAge, and DunedinPACE. For each measure, except DunedinPACE, which is the ratio of epigenetic age to chronological age, deviations from chronological age were calculated as measures of epigenetic age acceleration (HannumAA, HorvathAA, GrimAA, PhenoAA). Using linear regression models, the age acceleration measures were compared between female night shift and day shift workers. In additional analyses that were restricted to night shift workers, we also evaluated associations of sleep duration, as measured by actigraphy, with the measures of epigenetic age acceleration. Results: When comparing female night shift to female day shift workers, a statistically significant 0.81-year increase (95% CI: 0.22-1.4, p=0.007) in GrimAA and a statistically significant increase of 0.03 years epigenetic age per year of chronological age (95% CI: 0.004-0.05, p=0.02) as measured with DuendinPACE, were observed. As compared to sleeping ≥5 hours per night, sleeping
Item Metadata
Title |
Epigenetic age acceleration as a mechanism underlying increased risks of chronic disease in night shift workers
|
Creator | |
Supervisor | |
Publisher |
University of British Columbia
|
Date Issued |
2024
|
Description |
Background: Understanding the mechanisms underlying the associations between night shift work and increased risks of chronic disease is key to developing effective measures to protect the long-term health of night shift workers. A compelling yet understudied mechanism is accelerated biological aging. Methods: In a cross-sectional study of 112 female night shift workers, 88 female day shift workers, and 136 male night shift workers, genome wide DNA methylation data were used to calculate five measures of epigenetic age, including Hannum, Horvath, GrimAge, PhenoAge, and DunedinPACE. For each measure, except DunedinPACE, which is the ratio of epigenetic age to chronological age, deviations from chronological age were calculated as measures of epigenetic age acceleration (HannumAA, HorvathAA, GrimAA, PhenoAA). Using linear regression models, the age acceleration measures were compared between female night shift and day shift workers. In additional analyses that were restricted to night shift workers, we also evaluated associations of sleep duration, as measured by actigraphy, with the measures of epigenetic age acceleration. Results: When comparing female night shift to female day shift workers, a statistically significant 0.81-year increase (95% CI: 0.22-1.4, p=0.007) in GrimAA and a statistically significant increase of 0.03 years epigenetic age per year of chronological age (95% CI: 0.004-0.05, p=0.02) as measured with DuendinPACE, were observed. As compared to sleeping ≥5 hours per night, sleeping
|
Genre | |
Type | |
Language |
eng
|
Date Available |
2024-10-02
|
Provider |
Vancouver : University of British Columbia Library
|
Rights |
Attribution-NonCommercial-NoDerivatives 4.0 International
|
DOI |
10.14288/1.0445482
|
URI | |
Degree (Theses) | |
Program (Theses) | |
Affiliation | |
Degree Grantor |
University of British Columbia
|
Graduation Date |
2024-11
|
Campus | |
Scholarly Level |
Graduate
|
Rights URI | |
Aggregated Source Repository |
DSpace
|
Item Media
Item Citations and Data
Rights
Attribution-NonCommercial-NoDerivatives 4.0 International