Accelerated Epigenetic Aging in Diabetes: Socio-Biological Pathways of Health Inequity.

Social Adversity, Systemic Inflammation, and the Ticking of the Biological Aging Clocks in Men and Women

It is found that socioeconomic adversity influences not only inflammatory pathways but also distinct biological aging processes, including metabolomic aging, and that socioeconomic adversity influences not only inflammatory pathways but also distinct biological aging processes.

Sex differences in aging acceleration: higher susceptibility in women, greater preventability in men

Aging acceleration contributes to heterogeneity of chronic disease risk and mortality; however, the sex differences of its risk factors and population attributable fractions (PAFs) remain poorly characterized. We conducted an exposure-wide association analysis (ExWAS) among 236,099 UK Biobank participants and examined sex differences in exposure factors of aging acceleration and corresponding PAFs. Our results indicated that environmental exposures, lifestyles, early-life factors, psychosocial factors, and socioeconomic status were all associated with increased risk of accelerated aging. Additionally, several reproductive factors were found to be associated with aging acceleration in women. Notably, women showed higher risk of aging acceleration than men and were more susceptible to adverse lifestyle effects (OR 1.97 [1.91–2.04], PAF = 5.0%), while the potentially preventable proportion was higher in men (OR 1.87 [1.82–1.93], PAF = 16.8%). Collectively, we mapped the risk factor spectrum for accelerated aging and revealed sex differences in aging acceleration, with variation in risk factor effects and corresponding PAFs between sexes.

Sex-specific aging clocks from a large-scale human phenome reveal distinct aging transitions and circulating signatures.

Epigenetic Clock Trajectories and Brain Health in Midlife

Middle-aged adults with faster 15-year epigenetic aging trajectories demonstrated worse cognitive performance, whereas those with slower biological aging trajectories exhibited cognitive resilience and more favorable AD biomarker profiles.

ACCELERATED BIOLOGICAL AGING: ENVIRONMENTAL, LIFESTYLE, AND SOCIAL DETERMINANTS OF EPIGENETIC AGE ACCELERATION: A SYSTEMATIC REVIEW

Background: A gap between biological and chronological age known as "accelerated aging" has become a quantifiable phenomenon associated with modifiable features of modern urban and industrial environments. Two or more of the following factors linked to premature biological aging, independent of chronological age: environmental pollution and poor air quality, a sedentary lifestyle, circadian rhythm and sleep disorders, chronic psychosocial stressors, ultra-processed diet, and social or digital isolation. Objective: To comprehensively explore the modifiable features of modern society that have been implicated in accelerated biological aging as measured by validated biomarkers (epigenetic clock, telomere length, allostatic load) and to discuss the implications for public health. Methods: A structured narrative systematic literature review conducted in accordance with PRISMA guidelines. All sources identified using iterative keywords. Searches in peer-reviewed databases (PubMed, ScienceDirect, Frontiers, Nature journals and PMC/PubMed Central). Studies reporting associations between validated biological-aging biomarkers and modifiable environmental, behavioural, or psychosocial exposures prioritized for inclusion. Results: The literature search identified six major domains of contemporary life consistently associated with accelerated biological aging, ambient and traffic-related air pollution, sedentary behaviour and physical inactivity, sleep deprivation and circadian disruption, chronic psychosocial stress and allostatic load, consumption of ultra-processed foods, and social isolation and loneliness or problematic digital media use. These exposures share common underlying biological mechanisms such as chronic low-grade inflammation, oxidative stress, telomere attrition, mitochondrial dysfunction and dysregulated DNA methylation patterns, which correspond to known hallmarks of aging. Emerging intervention studies (including dietary, exercise and multi-domain lifestyle programs) suggest that epigenetic age acceleration is at least partially reversible. Conclusion: Accelerated biological aging driven by modifiable aspects of contemporary society represents a novel and unrecognized public health challenge that extends beyond individual disease categories. Population level interventions aim to improving air quality, the built environment, food system and social connectivity could substantially reduce the overall age-related disease burden throughout life.

How education gets under the skin: Pathways linking educational advantage to slower biological aging.

Educational attainment strongly predicts inequalities in accelerated biological aging. These differences are likely due to social and material benefits of education levels, but studies have yet to systematically evaluate how multiple overlapping pathways simultaneously are associated with differences in accelerated biological aging in later life. Using nationally representative data from the 2016 Venous Blood Study from the Health and Retirement Study (n = 9025; mean age = 70) in the United States and structural equation modeling, we investigate multiple adult life pathways between educational attainment and accelerated biological aging through a broad blood chemistry-based indicator of multisystem physiological aging (Expanded Biological Age). We find that economic (wealth), social (social participation), psychological (depression), and behavioral (smoking) pathways combine to explain up to 47% of the educational gradient in biological aging. Economic and social factors emerged as the strongest mediating pathways, explaining 20% and 13%, respectively, whereas psychological and behavioral factors explained a smaller share (7% and 7%, respectively). These findings highlight that multiple domains of adult life may underlie the association between higher educational attainment and slower biological aging. We additionally find that biological aging associations are contingent on level of education, where older adults without a high school diploma had 2.7 times the effect magnitude for social participation compared to those with at least a high school diploma, but no effect of wealth or smoking, demonstrating that pathways may manifest differently at varying levels of social advantage. This study also points to the importance of considering severe social disadvantage that may undermine the potential benefits of otherwise important resources for healthy aging.