
Exploring how the conditions we're exposed to in our first breaths can shape the course of our lives, researchers have shed light on the intricate dance between early-life exposures and our biological clock's pace. Delving into the lives of over 200,000 individuals, the study measured the imprint of factors like birth conditions, breastfeeding, and maternal habits on the aging process, captured through indicators such as KDM-BA and PhenoAge. Intriguingly, the findings revealed a clear link: the more we're nudged by early-life risks, the faster we tread on the path of aging, with frailty waiting as an unwelcome companion. Yet, there's a glimmer of hope. Embracing a healthy lifestyle might just be our shield, slowing down the ticking clock and redefining our golden years.
Article Information
Published in QJM, by Xu Gao et al.
Background: Early-life exposure increases health risks throughout an individual's lifetime. Biological aging is influenced by early-life risks as a key process of disease development, but whether early-life risks could accelerate biological aging and elevate late-life mortality and morbidity risks remains unknown. Knowledge is also limited on the potential moderating role of healthy lifestyle.
Methods: We investigate associations of three early-life risks around birth, breastfeeding, maternal smoking, and birth weight, with biological aging of 202,580 UK Biobank participants (54.9 ± 8.1 year-old). Biological aging was quantified as KDM-BA, PhenoAge, and frailty. Moderate alcohol intake, no current smoking, healthy diet, BMI < 30 kg/m2, and regular physical activity were considered as healthy lifestyles. Mortality and morbidity data was retrieved from health records.
Results: Individual early-life risk factors were robustly associated with accelerated biological aging. A one-unit increase in the "early-life risk score" integrating the three factors was associated with 0.060 (standard error [SE]=0.0019) and 0.036-unit (SE = 0.0027) increase in z-scored KDM-BA acceleration and PhenoAge acceleration, respectively, and with 22.3% higher odds (95% confidence interval: 1.185-1.262) of frailty. Increased chronological age and healthy lifestyles could mitigate the accelerations of KDM-BA and PhenoAge, respectively. Associations of early-life risk score with late-life mortality and morbidity were mediated by biological aging (proportions: 5.66%∼43.12%). KDM-BA and PhenoAge accelerations could significantly mediate the impact on most outcomes except anxiety, and frailty could not mediate the impact on T2D.
Conclusion: Biological aging could capture and mediate the late-life health risks stemming from the early-life risks, and could be potentially targeted for healthy longevity promotion.