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Epigenetic age acceleration in adolescence associates with BMI, inflammation and risk score for middle age cardiovascular disease


Huang, R-C and Lillycrop, KA and Beilin, LJ and Godfrey, KM and Anderson, D and Mori, TA and Rauschert, S and Craig, JM and Oddy, WH and Ayonrinde, OT and Pennell, CE and Holbrook, JD and Melton, PE, Epigenetic age acceleration in adolescence associates with BMI, inflammation and risk score for middle age cardiovascular disease, Journal of Clinical Endocrinology and Metabolism, 104, (7) pp. 3012-3024. ISSN 0021-972X (2018) [Refereed Article]

Copyright Statement

Copyright 2019 Endocrine Society

DOI: doi:10.1210/jc.2018-02076


Context: "Accelerated aging," assessed by adult DNA methylation, predicts cardiovascular disease (CVD). Adolescent accelerated aging might predict CVD earlier. We investigated whether epigenetic age acceleration (assessed age, 17 years) was associated with adiposity/CVD risk measured (ages 17, 20, and 22 years) and projected CVD by middle age.

Design: DNA methylation measured in peripheral blood provided two estimates of epigenetic age acceleration: intrinsic (IEAA; preserved across cell types) and extrinsic (EEAA; dependent on cell admixture and methylation levels within each cell type). Adiposity was assessed by anthropometry, ultrasound, and dual-energy x-ray absorptiometry (ages 17, 20, and 22 years). CVD risk factors [lipids, homeostatic model assessment of insulin resistance (HOMA-IR), blood pressure, inflammatory markers] were assessed at age 17 years. CVD development by age 47 years was calculated by Framingham algorithms. Results are presented as regression coefficients per 5-year epigenetic age acceleration (IEAA/EEAA) for adiposity, CVD risk factors, and CVD development.

Results: In 995 participants (49.6% female; age, 17.3 0.6 years), EEAA (per 5 years) was associated with increased body mass index (BMI) of 2.4% (95% CI, 1.2% to 3.6%) and 2.4% (0.8% to 3.9%) at 17 and 22 years, respectively. EEAA was associated with increases of 23% (3% to 33%) in high-sensitivity C-reactive protein, 10% (4% to 17%) in interferon-γ-inducible protein of 10 kDa, and 4% (2% to 6%) in soluble TNF receptor 2, adjusted for BMI and HOMA-IR. EEAA (per 5 years) results in a 4% increase in hard endpoints of CVD by 47 years of age and a 3% increase, after adjustment for conventional risk factors.

Conclusions: Accelerated epigenetic age in adolescence was associated with inflammation, BMI measured 5 years later, and probability of middle age CVD. Irrespective of whether this is cause or effect, assessing epigenetic age might refine disease prediction.

Item Details

Item Type:Refereed Article
Research Division:Biomedical and Clinical Sciences
Research Group:Nutrition and dietetics
Research Field:Nutrigenomics and personalised nutrition
Objective Division:Health
Objective Group:Public health (excl. specific population health)
Objective Field:Nutrition
UTAS Author:Oddy, WH (Professor Wendy Oddy)
UTAS Author:Melton, PE (Dr Phillip Melton)
ID Code:131502
Year Published:2018
Web of Science® Times Cited:20
Deposited By:Menzies Institute for Medical Research
Deposited On:2019-03-20
Last Modified:2022-07-06

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