TY - JOUR
T1 - Epigenetic Age Acceleration and Hearing
T2 - Observations From the Baltimore Longitudinal Study of Aging
AU - Kuo, Pei Lun
AU - Moore, Ann Zenobia
AU - Lin, Frank R.
AU - Ferrucci, Luigi
N1 - Funding Information:
This work was supported by the Intramural Research Program of National Institute on Aging, National Institute of Health. FL reports being a consultant to Frequency Therapeutics, receiving speaker honoraria from Caption Call, and being the director of a public health research center funded in part by a philanthropic donation from Cochlear Ltd., to the Johns Hopkins Bloomberg School of Public Health.
Publisher Copyright:
Copyright © 2021 Kuo, Moore, Lin and Ferrucci.
PY - 2021/12/15
Y1 - 2021/12/15
N2 - Objectives: Age-related hearing loss (ARHL) is highly prevalent among older adults, but the potential mechanisms and predictive markers for ARHL are lacking. Epigenetic age acceleration has been shown to be predictive of many age-associated diseases and mortality. However, the association between epigenetic age acceleration and hearing remains unknown. Our study aims to investigate the relationship between epigenetic age acceleration and audiometric hearing in the Baltimore Longitudinal Study of Aging (BLSA). Methods: Participants with both DNA methylation and audiometric hearing measurements were included. The main independent variables are epigenetic age acceleration measures, including intrinsic epigenetic age acceleration—“IEAA,” Hannum age acceleration—“AgeAccelerationResidualHannum,” PhenoAge acceleration—“AgeAccelPheno,” GrimAge acceleration—“AgeAccelGrim,” and methylation-based pace of aging estimation—“DunedinPoAm.” The main dependent variable is speech-frequency pure tone average. Linear regression was used to assess the association between epigenetic age acceleration and hearing. Results: Among the 236 participants (52.5% female), after adjusting for age, sex, race, time difference between measurements, cardiovascular factors, and smoking history, the effect sizes were 0.11 995% CI: (–0.00, 0.23), p = 0.054] for Hannum’s clock, 0.08 [95% CI: (–0.03, 0.19), p = 0.143] for Horvath’s clock, 0.10 [95% CI: (–0.01, 0.21), p = 0.089] for PhenoAge, 0.20 [95% CI: (0.06, 0.33), p = 0.004] for GrimAge, and 0.21 [95% CI: (0.09, 0.33), p = 0.001] for DunedinPoAm. Discussion: The present study suggests that some epigenetic age acceleration measurements are associated with hearing. Future research is needed to study the potential subclinical cardiovascular causes of hearing and to investigate the longitudinal relationship between DNA methylation and hearing.
AB - Objectives: Age-related hearing loss (ARHL) is highly prevalent among older adults, but the potential mechanisms and predictive markers for ARHL are lacking. Epigenetic age acceleration has been shown to be predictive of many age-associated diseases and mortality. However, the association between epigenetic age acceleration and hearing remains unknown. Our study aims to investigate the relationship between epigenetic age acceleration and audiometric hearing in the Baltimore Longitudinal Study of Aging (BLSA). Methods: Participants with both DNA methylation and audiometric hearing measurements were included. The main independent variables are epigenetic age acceleration measures, including intrinsic epigenetic age acceleration—“IEAA,” Hannum age acceleration—“AgeAccelerationResidualHannum,” PhenoAge acceleration—“AgeAccelPheno,” GrimAge acceleration—“AgeAccelGrim,” and methylation-based pace of aging estimation—“DunedinPoAm.” The main dependent variable is speech-frequency pure tone average. Linear regression was used to assess the association between epigenetic age acceleration and hearing. Results: Among the 236 participants (52.5% female), after adjusting for age, sex, race, time difference between measurements, cardiovascular factors, and smoking history, the effect sizes were 0.11 995% CI: (–0.00, 0.23), p = 0.054] for Hannum’s clock, 0.08 [95% CI: (–0.03, 0.19), p = 0.143] for Horvath’s clock, 0.10 [95% CI: (–0.01, 0.21), p = 0.089] for PhenoAge, 0.20 [95% CI: (0.06, 0.33), p = 0.004] for GrimAge, and 0.21 [95% CI: (0.09, 0.33), p = 0.001] for DunedinPoAm. Discussion: The present study suggests that some epigenetic age acceleration measurements are associated with hearing. Future research is needed to study the potential subclinical cardiovascular causes of hearing and to investigate the longitudinal relationship between DNA methylation and hearing.
KW - DNA methylation
KW - age-related hearing loss (ARHL)
KW - aging
KW - epigenetic age acceleration
KW - epigenetic clock
KW - functional aging
KW - pace of aging
KW - phenotypic aging
UR - http://www.scopus.com/inward/record.url?scp=85121986102&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85121986102&partnerID=8YFLogxK
U2 - 10.3389/fnagi.2021.790926
DO - 10.3389/fnagi.2021.790926
M3 - Article
C2 - 34975461
AN - SCOPUS:85121986102
SN - 1663-4365
VL - 13
JO - Frontiers in Aging Neuroscience
JF - Frontiers in Aging Neuroscience
M1 - 790926
ER -