April 17, 2024
Article

Early-Life Influences on Aging: Bridging Health Risks from Youth to Old Age

The impact of early-life health factors on aging and longevity has emerged as a pivotal area of scientific inquiry. This study delves into how factors from our earliest days—like birth conditions, breastfeeding, maternal smoking, and birth weight—play a significant role in how quickly we age biologically, which is crucial in understanding our health as we grow older. By analyzing the health data of over 202,000 participants from the UK Biobank, researchers developed a unique score that integrates these early-life risks to predict biological aging, measured through various markers including KDM-BA and PhenoAge.

Researchers found that higher early-life risk scores were strongly linked to faster biological aging. Intriguingly, while certain aspects of biological aging could be mitigated by a healthy lifestyle during adulthood, the foundational effects of early-life conditions still had a significant influence on later-life health risks like frailty and overall mortality. This finding underscores the long arm of childhood conditions in shaping health trajectories well into older age.

The study suggests a nuanced understanding of how the interplay between our earliest health exposures and our lifestyle choices can either compound or alleviate health risks later in life. This highlights the potential of early interventions and sustained healthy practices as a strategy for promoting longevity and reducing late-life health complications. The findings advocate for a holistic approach to health, emphasizing prevention from a young age as a key to better aging.

Article Information

Abstract

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 years 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 were 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 (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% CI: 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.