Abstract
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. 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. 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. Childhood neurocognitive functions and accelerated aging, brain structure, and concurrent physical and cognitive functions in adulthood. Gait speed at age 45 years, measured under 3 walking conditions: usual, dual task, and maximum gait speeds. 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). Adults' gait speed is associated with more than geriatric functional status; it is also associated with midlife aging and lifelong brain health.
Highlights
The ability to walk and gait speed depend on the function and interplay of the musculoskeletal, visual, central nervous, and peripheral nervous systems, as well as aerobic capacity, cardiorespiratory fitness, and energy production and delivery.[1,2] Reduced gait speed is a sign of advancing age[3]; it is associated with poorer response to rehabilitation, age-related diseases, including cardiovascular disease and dementia, and early mortality.[4,5,6]Gait speed is frequently used in geriatric settings as a quick, simple, and reliable way of estimating older patients’ functional capacity
Adults’ gait speed is associated with more than geriatric functional status; it is associated with midlife aging and lifelong brain health
If gait speed is antedated by early-life central nervous system (CNS) variation, this would point to possibilities for early identification of vulnerability and resilience in functional capacity well before late life and suggest potential targets for early intervention
Summary
The ability to walk and gait speed depend on the function and interplay of the musculoskeletal, visual, central nervous, and peripheral nervous systems, as well as aerobic capacity, cardiorespiratory fitness, and energy production and delivery.[1,2] Reduced gait speed is a sign of advancing age[3]; it is associated with poorer response to rehabilitation, age-related diseases, including cardiovascular disease and dementia, and early mortality.[4,5,6]Gait speed is frequently used in geriatric settings as a quick, simple, and reliable way of estimating older patients’ functional capacity. It is increasingly recognized that gait is associated with musculoskeletal mechanisms and with the central nervous system (CNS).[4,7] To date, longitudinal research on gait and cognitive functioning has primarily focused on older adults, many with neurological diseases.[8] Few studies have integrated cognitive and structural measures of the CNS with gait in healthy midlife adults, and, to our knowledge, none has examined the childhood CNS origins of gait. Filling this information gap is important for understanding the origins of gait speed and for prevention of functional disability. If gait speed is antedated by early-life CNS variation, this would point to possibilities for early identification of vulnerability and resilience in functional capacity well before late life and suggest potential targets for early intervention
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