Population-representative Birth Research Articles

GAIT SPEED AND CHILDHOOD-TO-MIDLIFE BRAIN HEALTH: RETHINKING GAIT

Background: Gait speed is a well-known predictor of functional decline and mortality in older adults, but little is known about the origins of gait speed earlier in life. We tested the hypothesis that slow gait reflects accelerated biological aging already at midlife, as well as poor neurocognitive functioning in childhood and childhood-to-midlife cognitive decline. Methods: Prospective study of the population-representative Dunedin Study birth cohort (n=1,037), followed to age 45 (until April 2019). We measured age-45 gait speed in 904 (90.7%) participants and tested associations with key life course factors. Results: The mean (SD) gait speeds (m/s) were: usual: 1.30 (0.17); dual task: 1.16 (0.23); and maximum: 1.99 (0.29). Among midlife adults, those with more physical limitations (β -0.27; P<.001), poorer physical functions (β 0.24–0.36; all P<.001), accelerated biological aging across multiple organ systems (β -0.33), older facial appearance (β -0.25), smaller brain volume (β 0.15), more cortical thinning (β 0.09), smaller cortical surface area (β 0.13), and more white matter hyperintensities (β -0.09) had slower gait speed, all P<.05. Participants with lower IQ in childhood (β 0.34) and midlife (β 0.38) and who exhibited childhood-to-midlife cognitive decline (β 0.10) had slower gait speed at midlife, all P<.01. Adults with poorer neurocognitive function as early as age 3 had slower gait in midlife (β 0.26; P<.001). Conclusion: Adults’ gait speed is more than an indicator of geriatric functional status, it is also an index of midlife aging and lifelong brain health.

Early-Life Intelligence Predicts Midlife Biological Age.

Early-life intelligence has been shown to predict multiple causes of death in populations around the world. This finding suggests that intelligence might influence mortality through its effects on a general process of physiological deterioration (i.e., individual variation in "biological age"). We examined whether intelligence could predict measures of aging at midlife before the onset of most age-related disease. We tested whether intelligence assessed in early childhood, middle childhood, and midlife predicted midlife biological age in members of the Dunedin Study, a population-representative birth cohort. Lower intelligence predicted more advanced biological age at midlife as captured by perceived facial age, a 10-biomarker algorithm based on data from the National Health and Nutrition Examination Survey (NHANES), and Framingham heart age (r = 0.1-0.2). Correlations between intelligence and telomere length were less consistent. The associations between intelligence and biological age were not explained by differences in childhood health or parental socioeconomic status, and intelligence remained a significant predictor of biological age even when intelligence was assessed before Study members began their formal schooling. These results suggest that accelerated aging may serve as one of the factors linking low early-life intelligence to increased rates of morbidity and mortality.

Early Life Infections and Onset of Puberty: Evidence From Hong Kong's Children of 1997 Birth Cohort

As economic development increases, puberty occurs at younger ages, and this could contribute to an increase in the incidence of cardiovascular diseases and hormone-related cancers. The factors that determine pubertal timing are poorly understood. The growth axis that is active during puberty is active in the first 6 months of life and interacts with the immune system. The authors examined whether prior infections, proxied by number of hospital admissions for infections at different ages, were associated with age at pubertal onset (Tanner stage II) using interval-censored regression in the Children of 1997 cohort, which is a population-representative Chinese birth cohort (n = 7,527). Mediation by growth was also examined. Girls, but not boys, who were hospitalized for infections at least twice in the first 6 months of life experienced pubertal onset about 8 months later (mean = 10.3 years, time ratio = 1.08, 95% confidence interval: 1.04, 1.12) than did those without such hospitalizations (mean = 9.6 years) after adjustment for infant characteristics and socioeconomic position (sex interaction: P = 0.02). There were no such associations for infections at 6 months to ≤8 years of age. Growth did not mediate the association. Early infectious morbidity in girls may be associated with later puberty, perhaps via suppression of the gonadotropic axis. The lowering of the number of infections in early life that accompanies economic development could be an additional factor that contributes to earlier puberty.

Birth Weight, Infant Growth, and Childhood Body Mass Index

To investigate the association between birth weight, infant growth rate, and childhood adiposity as a proxy for adult metabolic or cardiovascular risk in a Chinese population with a history of recent and rapid economic development. Prospective study in a population-representative birth cohort. Hong Kong Chinese population. Six thousand seventy-five term births (77.5% successful follow-up). Main Exposures Birth weight and growth rate (change in the weight z score) at ages 0 to 3 and 3 to 12 months. Main Outcome Measure Body mass index (BMI) (calculated as the weight in kilograms divided by the height in meters squared) z score at about age 7 years. Each unit increase in the weight z score at ages 0 to 3 and 3 to 12 months increased the BMI z score by 0.52 and 0.33, respectively. Children in the highest birth weight and growth rate tertiles had the highest BMI z scores. In the lowest birth weight tertile, increases in the weight z score at ages 0 to 3 months had a larger effect on the BMI z score in boys (mean difference, 0.88; 95% confidence interval 0.69-1.07) than in girls (mean difference, 0.52; 95% confidence interval, 0.33-0.71); these differences by birth weight, growth rate at ages 0 to 3 months, and sex were significant (P = .007). Faster prenatal and postnatal growth were associated with higher childhood BMI in a population with a recent history of rapid economic growth and relatively low birth weight, suggesting that maximal growth may not be optimal for metabolic risk. However, there may be a developmental trade-off between metabolic risk and other outcomes.