Abstract P012: Three Biological Age Estimates May Capture Distinct Aspects of Aging
Background: Biological age (BA) may reflect an individual’s aging process better than chronological age (CA). The objective of our study was to construct BA measures from different types of biomarkers and test their associations with mortality and age-related disease in a community-based sample.
Methods: We selected 6 clinical predictors that capture pulmonary, vascular, atherosclerosis, insulin sensitivity, inflammatory, and kidney domains of aging, and 9 inflammatory biomarkers measured in Framingham Heart Study Offspring cohort participants at exams 7 (1998-2001, N=3539, mean age 62±10) and 8 (2005-2008, N=3021, mean age 67±9). We used the Klemera-Doubal method to calculate a clinical variable BA and an inflammatory marker BA. We computed BA using DNA methylation (DNAm) data at exam 8 using Horvath’s method. For each of the measures we computed the difference (ΔAge) between BA and CA and modeled the effects of ΔAge after accounting for CA. We followed participants through 2014 for all-cause mortality (N=713), cardiovascular disease (CVD, N=412), coronary heart disease (CHD, N=223), stroke (N=129), and cancer (N=509).
Results: Inflammatory and clinical ΔAge were correlated (=0.35, =0.33, for exams 7 and 8 respectively), and also across exams (inflammatory ΔAge exam 7 vs 8: =0.61; clinical ΔAge: =0.76). DNAm ΔAge was not significantly correlated with exam 8 inflammatory or clinical ΔAge. After adjusting for CA and sex, larger inflammatory and clinical ΔAge, corresponding to older BA than CA, was associated with significantly increased hazards of all-cause mortality, CVD, and CHD (Table). The clinical and inflammatory ΔAge were significant (p<0.05) in models containing both measures. DNAm ΔAge was associated with increased hazards of all-cause mortality, CVD, cancer, and stroke, and remained significant in a model for mortality that also included inflammatory ΔAge (p<0.05).
Conclusions: Our findings suggest the three BA measures may be complementary in predicting risk for age-related disease.
Author Disclosures: J.M. Murabito: None. Q. Zhao: None. D. Levy: None. E.J. Benjamin: None. M.G. Larson: None. K.L. Lunetta: None.
- © 2017 by American Heart Association, Inc.