Quantification of biological aging in young adults
- Daniel W. Belskya,b,1,
- Avshalom Caspic,d,e,f,
- Renate Houtsc,
- Harvey J. Cohena,
- David L. Corcorane,
- Andrea Danesef,g,
- HonaLee Harringtonc,
- Salomon Israelh,
- Morgan E. Levinei,
- Jonathan D. Schaeferc,
- Karen Sugdenc,
- Ben Williamsc,
- Anatoli I. Yashinb,
- Richie Poultonj, and
- Terrie E. Moffittc,d,e,f
- aDepartment of Medicine, Duke University School of Medicine, Durham, NC 27710;
- bSocial Science Research Institute, Duke University, Durham, NC 27708;
- cDepartment of Psychology & Neuroscience, Duke University, Durham, NC 27708;
- dDepartment of Psychiatry & Behavioral Sciences, Duke University School of Medicine, Durham, NC 27708;
- eCenter for Genomic and Computational Biology, Duke University, Durham, NC 27708;
- fSocial, Genetic, & Developmental Psychiatry Research Centre, Institute of Psychiatry, Kings College London, London SE5 8AF, United Kingdom;
- gDepartment of Child & Adolescent Psychiatry, Institute of Psychiatry, King’s College London, London SE5 8AF, United Kingdom;
- hDepartment of Psychology, The Hebrew University of Jerusalem, Jerusalem 91905, Israel;
- iDepartment of Human Genetics, Gonda Research Center, David Geffen School of Medicine, University of California, Los Angeles, CA 90095;
- jDepartment of Psychology, University of Otago, Dunedin 9016, New Zealand
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Edited by Bruce S. McEwen, The Rockefeller University, New York, NY, and approved June 1, 2015 (received for review March 30, 2015)
Significance
The global population is aging, driving up age-related disease morbidity. Antiaging interventions are needed to reduce the burden of disease and protect population productivity. Young people are the most attractive targets for therapies to extend healthspan (because it is still possible to prevent disease in the young). However, there is skepticism about whether aging processes can be detected in young adults who do not yet have chronic diseases. Our findings indicate that aging processes can be quantified in people still young enough for prevention of age-related disease, opening a new door for antiaging therapies. The science of healthspan extension may be focused on the wrong end of the lifespan; rather than only studying old humans, geroscience should also study the young.
Abstract
Antiaging therapies show promise in model organism research. Translation to humans is needed to address the challenges of an aging global population. Interventions to slow human aging will need to be applied to still-young individuals. However, most human aging research examines older adults, many with chronic disease. As a result, little is known about aging in young humans. We studied aging in 954 young humans, the Dunedin Study birth cohort, tracking multiple biomarkers across three time points spanning their third and fourth decades of life. We developed and validated two methods by which aging can be measured in young adults, one cross-sectional and one longitudinal. Our longitudinal measure allows quantification of the pace of coordinated physiological deterioration across multiple organ systems (e.g., pulmonary, periodontal, cardiovascular, renal, hepatic, and immune function). We applied these methods to assess biological aging in young humans who had not yet developed age-related diseases. Young individuals of the same chronological age varied in their “biological aging” (declining integrity of multiple organ systems). Already, before midlife, individuals who were aging more rapidly were less physically able, showed cognitive decline and brain aging, self-reported worse health, and looked older. Measured biological aging in young adults can be used to identify causes of aging and evaluate rejuvenation therapies.
Footnotes
- ↵1To whom correspondence should be addressed. Email: dbelsky{at}duke.edu.
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Author contributions: D.W.B., A.C., R.P., and T.E.M. designed research; D.W.B., A.C., R.H., H.J.C., D.L.C., A.D., H.H., S.I., M.E.L., J.D.S., K.S., B.W., A.I.Y., R.P., and T.E.M. performed research; M.E.L. contributed new reagents/analytic tools; D.W.B., A.C., R.H., H.H., and T.E.M. analyzed data; and D.W.B., A.C., and T.E.M. wrote the paper.
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The authors declare no conflict of interest.
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This article is a PNAS Direct Submission.
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This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1506264112/-/DCSupplemental.
Freely available online through the PNAS open access option.
