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 2019 Endocrine Society
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 Type:||Refereed Article|
|Research Division:||Biomedical and Clinical Sciences|
|Research Group:||Nutrition and dietetics|
|Research Field:||Nutrigenomics and personalised nutrition|
|Objective Group:||Public health (excl. specific population health)|
|UTAS Author:||Oddy, WH (Professor Wendy Oddy)|
|UTAS Author:||Melton, PE (Dr Phillip Melton)|
|Web of Science® Times Cited:||2|
|Deposited By:||Menzies Institute for Medical Research|
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