Associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk: the HOME study

Abstract Background Cardiometabolic risk factors among youth are rising. Epigenetic age acceleration, a biomarker for aging and disease-risk, has been associated with adiposity in children, but its association with other cardiometabolic risk markers remains understudied. We employed data from the He...

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Main Authors: Jennifer L. Arzu, Karl T. Kelsey, George D. Papandonatos, Kim M. Cecil, Aimin Chen, Scott M. Langevin, Bruce P. Lanphear, Kimberly Yolton, Jessie P. Buckley, Joseph M. Braun
Format: Article
Language:English
Published: BMC 2024-11-01
Series:Clinical Epigenetics
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Online Access:https://doi.org/10.1186/s13148-024-01779-8
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author Jennifer L. Arzu
Karl T. Kelsey
George D. Papandonatos
Kim M. Cecil
Aimin Chen
Scott M. Langevin
Bruce P. Lanphear
Kimberly Yolton
Jessie P. Buckley
Joseph M. Braun
author_facet Jennifer L. Arzu
Karl T. Kelsey
George D. Papandonatos
Kim M. Cecil
Aimin Chen
Scott M. Langevin
Bruce P. Lanphear
Kimberly Yolton
Jessie P. Buckley
Joseph M. Braun
author_sort Jennifer L. Arzu
collection DOAJ
description Abstract Background Cardiometabolic risk factors among youth are rising. Epigenetic age acceleration, a biomarker for aging and disease-risk, has been associated with adiposity in children, but its association with other cardiometabolic risk markers remains understudied. We employed data from the Health Outcomes and Measures of the Environment (HOME) study, a prospective pregnancy and birth cohort in the greater Cincinnati metropolitan area, to examine whether accelerated epigenetic age at birth as well as accelerated epigenetic age and faster pace of biological aging at age 12 years were associated with higher cardiometabolic risk in adolescents. Results After adjusting for potential confounders, including estimated cell type proportions, epigenetic gestational age acceleration at birth, derived from the Bohlin, Knight, and Haftorn clocks using cord blood DNA methylation data, was not associated with cardiometabolic risk z-scores or individual cardiometabolic risk score components (visceral fat, leptin to adiponectin ratio, HOMA-IR, triglycerides to HDL-C ratio, HbA1c, or systolic blood pressure) at age 12 years. We also did not observe any associations of epigenetic age acceleration, calculated with Horvath’s skin and blood, Hannum’s, and Wu’s epigenetic clocks using peripheral blood at age 12 years, with these same cardiometabolic risk markers. In contrast, faster pace of biological aging was associated with higher cardiometabolic risk [βs (95% CIs)] cardiometabolic risk score 0.25 (0.07, 0.42); visceral fat 0.21 (0.05, 0.38); and hemoglobin A1c 0.23 (0.05, 0.41) per standard deviation increase in pace of biological aging. Faster pace of biological aging was also positively associated with systolic blood pressure, triglycerides to HDL-C ratio, HOMA-IR, and leptin to adiponectin ratio, although these associations were not statistically significant. Conclusions Our findings provide evidence that faster pace of biological aging was associated with higher cardiometabolic risk score, visceral fat, and HbA1c at age 12 years. Further research is needed to determine whether these associations persist from adolescence through adulthood.
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spelling doaj-art-26ac25e29a1b42d7b392705a849ddf5f2024-11-24T12:31:07ZengBMCClinical Epigenetics1868-70832024-11-0116111410.1186/s13148-024-01779-8Associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk: the HOME studyJennifer L. Arzu0Karl T. Kelsey1George D. Papandonatos2Kim M. Cecil3Aimin Chen4Scott M. Langevin5Bruce P. Lanphear6Kimberly Yolton7Jessie P. Buckley8Joseph M. Braun9Department of Epidemiology, School of Public Health, Brown UniversityDepartment of Epidemiology, School of Public Health, Brown UniversityDepartment of Biostatistics, School of Public Health, Brown UniversityDepartment of Environmental and Public Health Sciences, University of Cincinnati College of MedicineDepartment of Biostatistics, Epidemiology and Informatics, University of Pennsylvania Perelman School of MedicineLarner College of Medicine, University of VermontFaculty of Health Sciences, Simon Fraser UniversityDepartment of Environmental and Public Health Sciences, University of Cincinnati College of MedicineDepartment of Epidemiology, University of North Carolina Gillings School of Global Public HealthDepartment of Epidemiology, School of Public Health, Brown UniversityAbstract Background Cardiometabolic risk factors among youth are rising. Epigenetic age acceleration, a biomarker for aging and disease-risk, has been associated with adiposity in children, but its association with other cardiometabolic risk markers remains understudied. We employed data from the Health Outcomes and Measures of the Environment (HOME) study, a prospective pregnancy and birth cohort in the greater Cincinnati metropolitan area, to examine whether accelerated epigenetic age at birth as well as accelerated epigenetic age and faster pace of biological aging at age 12 years were associated with higher cardiometabolic risk in adolescents. Results After adjusting for potential confounders, including estimated cell type proportions, epigenetic gestational age acceleration at birth, derived from the Bohlin, Knight, and Haftorn clocks using cord blood DNA methylation data, was not associated with cardiometabolic risk z-scores or individual cardiometabolic risk score components (visceral fat, leptin to adiponectin ratio, HOMA-IR, triglycerides to HDL-C ratio, HbA1c, or systolic blood pressure) at age 12 years. We also did not observe any associations of epigenetic age acceleration, calculated with Horvath’s skin and blood, Hannum’s, and Wu’s epigenetic clocks using peripheral blood at age 12 years, with these same cardiometabolic risk markers. In contrast, faster pace of biological aging was associated with higher cardiometabolic risk [βs (95% CIs)] cardiometabolic risk score 0.25 (0.07, 0.42); visceral fat 0.21 (0.05, 0.38); and hemoglobin A1c 0.23 (0.05, 0.41) per standard deviation increase in pace of biological aging. Faster pace of biological aging was also positively associated with systolic blood pressure, triglycerides to HDL-C ratio, HOMA-IR, and leptin to adiponectin ratio, although these associations were not statistically significant. Conclusions Our findings provide evidence that faster pace of biological aging was associated with higher cardiometabolic risk score, visceral fat, and HbA1c at age 12 years. Further research is needed to determine whether these associations persist from adolescence through adulthood.https://doi.org/10.1186/s13148-024-01779-8Epigenetic ageCardiometabolic riskAdolescenceDevelopmental origins of health and diseaseEpidemiology
spellingShingle Jennifer L. Arzu
Karl T. Kelsey
George D. Papandonatos
Kim M. Cecil
Aimin Chen
Scott M. Langevin
Bruce P. Lanphear
Kimberly Yolton
Jessie P. Buckley
Joseph M. Braun
Associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk: the HOME study
Clinical Epigenetics
Epigenetic age
Cardiometabolic risk
Adolescence
Developmental origins of health and disease
Epidemiology
title Associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk: the HOME study
title_full Associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk: the HOME study
title_fullStr Associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk: the HOME study
title_full_unstemmed Associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk: the HOME study
title_short Associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk: the HOME study
title_sort associations of epigenetic age acceleration at birth and age 12 years with adolescent cardiometabolic risk the home study
topic Epigenetic age
Cardiometabolic risk
Adolescence
Developmental origins of health and disease
Epidemiology
url https://doi.org/10.1186/s13148-024-01779-8
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