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Association of Neurocognitive and Physical Function With Gait Speed in Midlife.
JAMA Netw Open. 2019 10 02; 2(10):e1913123.JN

Abstract

Importance

Gait speed is a well-known indicator of risk of functional decline and mortality in older adults, but little is known about the factors associated with gait speed earlier in life.

Objectives

To test the hypothesis that slow gait speed reflects accelerated biological aging at midlife, as well as poor neurocognitive functioning in childhood and cognitive decline from childhood to midlife.

Design, Setting, and Participants

This cohort study uses data from the Dunedin Multidisciplinary Health and Development Study, a population-based study of a representative 1972 to 1973 birth cohort in New Zealand that observed participants to age 45 years (until April 2019). Data analysis was performed from April to June 2019.

Exposures

Childhood neurocognitive functions and accelerated aging, brain structure, and concurrent physical and cognitive functions in adulthood.

Main Outcomes and Measures

Gait speed at age 45 years, measured under 3 walking conditions: usual, dual task, and maximum gait speeds.

Results

Of the 1037 original participants (91% of eligible births; 535 [51.6%] male), 997 were alive at age 45 years, of whom 904 (90.7%) had gait speed measured (455 [50.3%] male; 93% white). The mean (SD) gait speeds were 1.30 (0.17) m/s for usual gait, 1.16 (0.23) m/s for dual task gait, and 1.99 (0.29) m/s for maximum gait. Adults with more physical limitations (standardized regression coefficient [β], -0.27; 95% CI, -0.34 to -0.21; P < .001), poorer physical functions (ie, weak grip strength [β, 0.36; 95% CI, 0.25 to 0.46], poor balance [β, 0.28; 95% CI, 0.21 to 0.34], poor visual-motor coordination [β, 0.24; 95% CI, 0.17 to 0.30], and poor performance on the chair-stand [β, 0.34; 95% CI, 0.27 to 0.40] or 2-minute step tests [β, 0.33; 95% CI, 0.27 to 0.39]; all P < .001), accelerated biological aging across multiple organ systems (β, -0.33; 95% CI, -0.40 to -0.27; P < .001), older facial appearance (β, -0.25; 95% CI, -0.31 to -0.18; P < .001), smaller brain volume (β, 0.15; 95% CI, 0.06 to 0.23; P < .001), more cortical thinning (β, 0.09; 95% CI, 0.02 to 0.16; P = .01), smaller cortical surface area (β, 0.13; 95% CI, 0.04 to 0.21; P = .003), and more white matter hyperintensities (β, -0.09; 95% CI, -0.15 to -0.02; P = .01) had slower gait speed. Participants with lower IQ in midlife (β, 0.38; 95% CI, 0.32 to 0.44; P < .001) and participants who exhibited cognitive decline from childhood to adulthood (β, 0.10; 95% CI, 0.04 to 0.17; P < .001) had slower gait at age 45 years. Those with poor neurocognitive functioning as early as age 3 years had slower gait in midlife (β, 0.26; 95% CI, 0.20 to 0.32; P < .001).

Conclusions and Relevance

Adults' gait speed is associated with more than geriatric functional status; it is also associated with midlife aging and lifelong brain health.

Authors+Show Affiliations

Department of Psychology and Neuroscience, Duke University, Durham, North Carolina. Clinical Research Centre, Copenhagen University Hospital Amager and Hvidovre, Hvidovre, Denmark.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. Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology, and Neuroscience, King's College London, London, United Kingdom.Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.Department of Oral Sciences, University of Otago, Dunedin, New Zealand.Claude D. Pepper Older Americans Independence Center, Duke University, Durham, North Carolina. Duke Center for the Study of Aging and Human Development, Duke University, Durham, North Carolina. Department of Medicine, Duke University, Durham, North Carolina.Department of Psychology and Neuroscience, Duke University, Durham, North Carolina.Department of Psychology and Neuroscience, Duke University, Durham, North Carolina.Department of Preventive and Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.Department of Psychology and Neuroscience, Duke University, Durham, North Carolina.Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.Department of Psychology and Neuroscience, Duke University, Durham, North Carolina.Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.Department of Psychology and Neuroscience, Duke University, Durham, North Carolina.Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.Claude D. Pepper Older Americans Independence Center, Duke University, Durham, North Carolina. Department of Medicine, Duke University, Durham, North Carolina. Geriatric Research, Education, and Clinical Center, Durham VA Medical Center, Durham, North Carolina.Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.Department of Psychology and Neuroscience, Duke University, Durham, North Carolina. Frank Porter Graham Child Development Institute, University of North Carolina at Chapel Hill, Chapel Hill.Department of Psychology and Neuroscience, Duke University, Durham, North Carolina.Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.Department of Oral Sciences, University of Otago, Dunedin, New Zealand.Department of Psychology and Neuroscience, 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. Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, Psychology, and Neuroscience, King's College London, London, United Kingdom.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

31603488

Citation

Rasmussen, Line Jee Hartmann, et al. "Association of Neurocognitive and Physical Function With Gait Speed in Midlife." JAMA Network Open, vol. 2, no. 10, 2019, pp. e1913123.
Rasmussen LJH, Caspi A, Ambler A, et al. Association of Neurocognitive and Physical Function With Gait Speed in Midlife. JAMA Netw Open. 2019;2(10):e1913123.
Rasmussen, L. J. H., Caspi, A., Ambler, A., Broadbent, J. M., Cohen, H. J., d'Arbeloff, T., Elliott, M., Hancox, R. J., Harrington, H., Hogan, S., Houts, R., Ireland, D., Knodt, A. R., Meredith-Jones, K., Morey, M. C., Morrison, L., Poulton, R., Ramrakha, S., Richmond-Rakerd, L., ... Moffitt, T. E. (2019). Association of Neurocognitive and Physical Function With Gait Speed in Midlife. JAMA Network Open, 2(10), e1913123. https://doi.org/10.1001/jamanetworkopen.2019.13123
Rasmussen LJH, et al. Association of Neurocognitive and Physical Function With Gait Speed in Midlife. JAMA Netw Open. 2019 10 2;2(10):e1913123. PubMed PMID: 31603488.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Association of Neurocognitive and Physical Function With Gait Speed in Midlife. AU - Rasmussen,Line Jee Hartmann, AU - Caspi,Avshalom, AU - Ambler,Antony, AU - Broadbent,Jonathan M, AU - Cohen,Harvey J, AU - d'Arbeloff,Tracy, AU - Elliott,Maxwell, AU - Hancox,Robert J, AU - Harrington,HonaLee, AU - Hogan,Sean, AU - Houts,Renate, AU - Ireland,David, AU - Knodt,Annchen R, AU - Meredith-Jones,Kim, AU - Morey,Miriam C, AU - Morrison,Lynda, AU - Poulton,Richie, AU - Ramrakha,Sandhya, AU - Richmond-Rakerd,Leah, AU - Sison,Maria L, AU - Sneddon,Kate, AU - Thomson,W Murray, AU - Hariri,Ahmad R, AU - Moffitt,Terrie E, Y1 - 2019/10/02/ PY - 2019/10/12/entrez PY - 2019/10/12/pubmed PY - 2020/6/17/medline SP - e1913123 EP - e1913123 JF - JAMA network open JO - JAMA Netw Open VL - 2 IS - 10 N2 - Importance: Gait speed is a well-known indicator of risk of functional decline and mortality in older adults, but little is known about the factors associated with gait speed earlier in life. Objectives: To test the hypothesis that slow gait speed reflects accelerated biological aging at midlife, as well as poor neurocognitive functioning in childhood and cognitive decline from childhood to midlife. Design, Setting, and Participants: This cohort study uses data from the Dunedin Multidisciplinary Health and Development Study, a population-based study of a representative 1972 to 1973 birth cohort in New Zealand that observed participants to age 45 years (until April 2019). Data analysis was performed from April to June 2019. Exposures: Childhood neurocognitive functions and accelerated aging, brain structure, and concurrent physical and cognitive functions in adulthood. Main Outcomes and Measures: Gait speed at age 45 years, measured under 3 walking conditions: usual, dual task, and maximum gait speeds. Results: Of the 1037 original participants (91% of eligible births; 535 [51.6%] male), 997 were alive at age 45 years, of whom 904 (90.7%) had gait speed measured (455 [50.3%] male; 93% white). The mean (SD) gait speeds were 1.30 (0.17) m/s for usual gait, 1.16 (0.23) m/s for dual task gait, and 1.99 (0.29) m/s for maximum gait. Adults with more physical limitations (standardized regression coefficient [β], -0.27; 95% CI, -0.34 to -0.21; P < .001), poorer physical functions (ie, weak grip strength [β, 0.36; 95% CI, 0.25 to 0.46], poor balance [β, 0.28; 95% CI, 0.21 to 0.34], poor visual-motor coordination [β, 0.24; 95% CI, 0.17 to 0.30], and poor performance on the chair-stand [β, 0.34; 95% CI, 0.27 to 0.40] or 2-minute step tests [β, 0.33; 95% CI, 0.27 to 0.39]; all P < .001), accelerated biological aging across multiple organ systems (β, -0.33; 95% CI, -0.40 to -0.27; P < .001), older facial appearance (β, -0.25; 95% CI, -0.31 to -0.18; P < .001), smaller brain volume (β, 0.15; 95% CI, 0.06 to 0.23; P < .001), more cortical thinning (β, 0.09; 95% CI, 0.02 to 0.16; P = .01), smaller cortical surface area (β, 0.13; 95% CI, 0.04 to 0.21; P = .003), and more white matter hyperintensities (β, -0.09; 95% CI, -0.15 to -0.02; P = .01) had slower gait speed. Participants with lower IQ in midlife (β, 0.38; 95% CI, 0.32 to 0.44; P < .001) and participants who exhibited cognitive decline from childhood to adulthood (β, 0.10; 95% CI, 0.04 to 0.17; P < .001) had slower gait at age 45 years. Those with poor neurocognitive functioning as early as age 3 years had slower gait in midlife (β, 0.26; 95% CI, 0.20 to 0.32; P < .001). Conclusions and Relevance: Adults' gait speed is associated with more than geriatric functional status; it is also associated with midlife aging and lifelong brain health. SN - 2574-3805 UR - https://www.unboundmedicine.com/medline/citation/31603488/Association_of_Neurocognitive_and_Physical_Function_With_Gait_Speed_in_Midlife_ L2 - https://jamanetwork.com/journals/jamanetworkopen/fullarticle/10.1001/jamanetworkopen.2019.13123 DB - PRIME DP - Unbound Medicine ER -