Send to

Choose Destination
Am J Epidemiol. 2018 Jun 1;187(6):1220-1230. doi: 10.1093/aje/kwx346.

Eleven Telomere, Epigenetic Clock, and Biomarker-Composite Quantifications of Biological Aging: Do They Measure the Same Thing?

Author information

Department of Population Health Sciences, Duke University School of Medicine, Durham, North Carolina.
Department of Medicine, Division of Geriatrics, Duke University School of Medicine, Durham, North Carolina.
Social Science Research Institute, Duke University, Durham, North Carolina.
Center for the Study of Aging and Human Development, Duke University, Durham, North Carolina.
Department of Psychology and Neuroscience, Duke University, Durham, North Carolina.
Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Durham, North Carolina.
Center for Genomic and Computational Biology, Duke University, Durham, North Carolina.
MRC Social, Genetic, and Developmental Psychiatry Center, Institute of Psychiatry, Psychology, and Neuroscience, King's College London, London, United Kingdom.
Department of Family Medicine, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, Canada.
Department of Pathology, Yale University School of Medicine, New Haven, Connecticut.
Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.


The geroscience hypothesis posits that therapies to slow biological processes of aging can prevent disease and extend healthy years of life. To test such "geroprotective" therapies in humans, outcome measures are needed that can assess extension of disease-free life span. This need has spurred development of different methods to quantify biological aging. But different methods have not been systematically compared in the same humans. We implemented 7 methods to quantify biological aging using repeated-measures physiological and genomic data in 964 middle-aged humans in the Dunedin Study (New Zealand; persons born 1972-1973). We studied 11 measures in total: telomere-length and erosion, 3 epigenetic-clocks and their ticking rates, and 3 biomarker-composites. Contrary to expectation, we found low agreement between different measures of biological aging. We next compared associations between biological aging measures and outcomes that geroprotective therapies seek to modify: physical functioning, cognitive decline, and subjective signs of aging, including aged facial appearance. The 71-cytosine-phosphate-guanine epigenetic clock and biomarker composites were consistently related to these aging-related outcomes. However, effect sizes were modest. Results suggested that various proposed approaches to quantifying biological aging may not measure the same aspects of the aging process. Further systematic evaluation and refinement of measures of biological aging is needed to furnish outcomes for geroprotector trials.

Supplemental Content

Full text links

Icon for Silverchair Information Systems Icon for PubMed Central
Loading ...
Support Center