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Disparities in the pace of biological aging among midlife adults of the same chronological age have implications for future frailty risk and policy

Nature Aging volume 1, pages 295–308 (2021)Cite this article

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Abstract

Some humans age faster than others. Variation in biological aging can be measured in midlife, but the implications of this variation are poorly understood. We tested associations between midlife biological aging and indicators of future frailty risk in the Dunedin cohort of 1,037 infants born the same year and followed to age 45. Participants’ ‘Pace of Aging’ was quantified by tracking declining function in 19 biomarkers indexing the cardiovascular, metabolic, renal, immune, dental and pulmonary systems across ages 26, 32, 38 and 45 years. At age 45 in 2019, participants with faster Pace of Aging had more cognitive difficulties, signs of advanced brain aging, diminished sensory–motor functions, older appearances and more pessimistic perceptions of aging. People who are aging more rapidly than same-age peers in midlife may prematurely need supports to sustain independence that are usually reserved for older adults. Chronological age does not adequately identify need for such supports.

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Fig. 1: Study design.
Fig. 2: Biological aging across two decades from age 26 to age 45.
Fig. 3: Study members who were aging faster showed signs of advanced brain aging relative to slower-aging peers.
Fig. 4: Study members who were aging faster were perceived as less healthy and looking older when compared to slower-aging peers.

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Data availability

The Dunedin Study datasets reported in the current Article are not publicly available due to a lack of informed consent and ethical approval for public data sharing. The Dunedin study datasets are available on request by qualified scientists. Requests require a concept paper describing the purpose of data access, ethical approval at the applicant’s university and provision for secure data access (https://moffittcaspi.trinity.duke.edu/research-topics/dunedin). We offer secure access on the Duke, Otago and King’s College campuses.

Code availability

Custom code that supports the findings of this study is available from the corresponding author on request.

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Acknowledgements

This research was supported by the National Institute on Aging (NIA) grant nos. R01AG032282 and R01AG049789, and the UK Medical Research Council grant no. MR/P005918/1. Additional support was provided by the Jacobs Foundation, grant nos. NIA P30 AG028716 and NIA P30 AG034424. The Dunedin Multidisciplinary Health and Development Research Unit was supported by the New Zealand Health Research Council (Project Grant nos. 15-265 and 16-604) and the New Zealand Ministry of Business, Innovation and Employment (MBIE). M.L.E. is supported by the National Science Foundation Graduate Research Fellowship (no. NSF DGE-1644868) and grant no. NIA F99 AG068432-01. We thank members of the Advisory Board for the Dunedin Neuroimaging Study, Dunedin Study members, Unit research staff, Pacific Radiology Group staff and study founder P. Silva.

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Authors and Affiliations

  1. Department of Psychology and Neuroscience, Duke University, Durham, NC, USA

    Maxwell L. Elliott, Avshalom Caspi, Renate M. Houts, HonaLee Harrington, Annchen Knodt, Karen Sugden, Benjamin S. Williams, Ahmad R. Hariri & Terrie E. Moffitt

  2. Center for Genomic and Computational Biology, Duke University, Durham, NC, USA

    Avshalom Caspi & Terrie E. Moffitt

  3. Social, Genetic and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK

    Avshalom Caspi, Antony Ambler & Terrie E. Moffitt

  4. PROMENTA, Department of Psychology, University of Oslo, Oslo, Norway

    Avshalom Caspi & Terrie E. Moffitt

  5. Department of Psychiatry and Behavioral Sciences, Duke University, Durham, NC, USA

    Avshalom Caspi & Terrie E. Moffitt

  6. Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand

    Antony Ambler, Sean Hogan, Sandhya Ramrakha, Graham Wilson & Richie Poulton

  7. Faculty of Dentistry, University of Otago, Dunedin, New Zealand

    Jonathan M. Broadbent & W. Murray Thomson

  8. Department of Preventive and Social Medicine, Otago Medical School, University of Otago, Dunedin, New Zealand

    Robert J. Hancox & Antoinette Righarts

  9. Brain Research New Zealand-Rangahau Roro Aotearoa, Centre of Research Excellence, Universities of Auckland and Otago, Auckland, New Zealand

    Ross Keenan, Tracy R. Melzer, Suzanne C. Purdy & Peter R. Thorne

  10. Christchurch Radiology group, Christchurch, New Zealand

    Ross Keenan

  11. School of Psychology, University of Auckland, Auckland, New Zealand

    Joan H. Leung & Suzanne C. Purdy

  12. Eisdell Moore Centre, University of Auckland, Auckland, New Zealand

    Joan H. Leung, Suzanne C. Purdy & Peter R. Thorne

  13. Department of Medicine, University of Otago, Dunedin, New Zealand

    Tracy R. Melzer

  14. Department of Psychology, University of Michigan, Ann Arbor, MI, USA

    Leah S. Richmond-Rakerd

  15. School of Population Health, University of Auckland, Auckland, New Zealand

    Peter R. Thorne

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  1. Maxwell L. Elliott
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Contributions

M.L.E., A.C., A.R.H., R.P. and T.E.M. designed the research. M.L.E., A.C., R.M.H, A.A., J.M.B., R.J.H., H.L.H., S.H., R.K., A.K., J.H.L., T.R.M., S.C.P., S.R., L.S.R.-R., A.R., K.S., W.M.T., P.R.T., B.S.W., G.W., A.R.H., R.P. and T.E.M. performed the research. M.L.E., R.M.H. and A.K. analyzed data. M.L.E., A.C., A.R.H. and T.E.M. wrote the paper.

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Correspondence to Maxwell L. Elliott.

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Peer review information Nature Aging thanks William Jagust, Juulia Jylhava, Diana Kuh, John Rowe and Thomas Travison for their contribution to the peer review of this work.

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Elliott, M.L., Caspi, A., Houts, R.M. et al. Disparities in the pace of biological aging among midlife adults of the same chronological age have implications for future frailty risk and policy. Nat Aging 1, 295–308 (2021). https://doi.org/10.1038/s43587-021-00044-4

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