From visiting museums and listening to music to regular exercise, researchers found that people who engaged in enriched leisure activities more often showed signs of slower biological aging in peak epigenetic clocks.
Study: Does leisure matter for epigenetic aging? Analyzes of arts engagement and physical activity in the UK Longitudinal Household Study. Image credit: Bangkok Click Studio/Shutterstock.com
A recent one Innovation in Aging The study examines whether leisure activities, such as engaging in the arts and physical activity, may be related to the aging process.
Epigenetic mechanisms, lifestyle factors and measurement of biological aging
The increasing proportion of older adults worldwide has shifted the focus from simply extending lifespan to improving the years lived in good health. Current priorities focus on minimizing illness, maintaining independence and reducing pressure on healthcare systems.
Molecular biology has revealed fundamental mechanisms that drive aging, with epigenetic changes such as DNA methylation, chromatin remodeling, histone modifications, and non-coding RNA activity playing a central role. Environmental stress over time disrupts these epigenetic patterns, increasing the risk of genomic instability, cancer, and cardiovascular disease.
Biohorology uses molecular aging clocks to estimate biological age by analyzing DNA methylation at key CpG sites. While the original clocks measured chronological age, newer versions incorporate phenotypic traits, predictors of lifespan, and rates of aging. Although patterns and causal links remain under debate, aging clocks are widely used to study and guide biological aging interventions.
Lifestyle factors such as avoiding tobacco and excessive alcohol use, maintaining a healthy weight, eating a Mediterranean diet, managing stress, and practicing meditation may slow epigenetic aging, although the evidence remains preliminary and many recreational activities have not been adequately studied.
Arts and cultural engagement (ACEng) are increasingly recognized as health behaviors that enhance mental and physical well-being by providing social, cognitive and sensory stimulation. Experimental studies, particularly involving music, suggest that ACEng can influence gene expression. For example, music has been shown to influence gene pathways related to dopamine signaling, neuroplasticity, neurogenesis, and anti-inflammatory pathways. Despite these findings, there is a lack of population-level evidence linking ACEng to epigenetic aging.
Physical activity (PA) can experimentally alter DNA methylation and reduce epigenetic mutation load, but observational studies linking PA to epigenetic clocks remain few, small, and inconclusive, often missing key confounders. Previous studies have also yielded mixed findings depending on the epigenetic clock examined. Comprehensive, multi-clock and causally robust approaches are needed to elucidate these links.
Assessing the effect of lifestyle on epigenetic aging
The UK Household Longitudinal Study (UKHLS) is a national survey that has followed 40,000 UK households since 2009. This analysis demonstrated DNA methylation (DNAm) in 3,654 white European adults from blood samples collected between 2010 and 2012. After quality control, 3,556 participants with complete data. Over 850,000 methylation sites were evaluated. DNA methylation analysis was limited to participants of white European descent, which may affect the generalizability of the findings.
UKHLS has seven epigenetic clocks from DNAm data spanning three generations. First-generation clocks calculate chronological age, second-generation clocks incorporate mortality and disease risk, and third-generation clocks quantify the rate of biological aging. First and second generation watches report age in years. Third generation watches reflect the rate of aging.
ACEng was measured by self-reported participation in arts, heritage and cultural activities during the past year. Frequency was grouped into four categories: ≤2 times/year, 3–4 times/year, monthly, and weekly. Diversity was calculated as the total number of activities, grouped into quartiles. PA was assessed with reported sports of varying intensity. the most frequently reported activity reflected PA frequency.
Higher levels of leisure activity are associated with slower epigenetic aging
The analytic sample had a mean age of 52.1 years, compared to 47.5 years in the original sample, and included 10.9 % single individuals, compared to 22.5 % in the original. Other demographic and socioeconomic characteristics were similar. Engagement in ACEng was high: 82% of participants participated in three or more activities and 27.9% participated in 11 or more. Over 75% participated in ACEng on a monthly or weekly basis. In contrast, 19.3% of participants reported no PA and less than a third engaged in four or more PA activities, although almost half participated in PA weekly.
Higher frequency and diversity of ACEng and PA were associated with slower epigenetic aging as measured by second- and third-generation clocks (PhenoAge, DunedinPoAm and DunedinPACE), but not by first-generation clocks. Therefore, the associations were mainly seen in newer epigenetic clocks designed to reflect declining health and the rate of aging rather than just chronological age.
For PhenoAge, monthly ACEng was associated with a 0.8-year reduction in epigenetic age, while weekly ACEng was associated with a 1.02-year reduction. More frequent ACEng was also associated with slower rates of biological aging, ranging from 0.01 to 0.04 years per chronological year, in DunedinPoAm and DunedinPACE.
Greater diversity in ACEng was associated with reductions in PhenoAge of up to 0.96 years and slower biological aging rates of 0.02 to 0.04 years per year in DunedinPoAm and DunedinPACE. PA frequency showed no associations with first-generation clocks, while weekly PA was associated with a 0.59-year reduction in PhenoAge. Monthly and weekly PA were also associated with slower epigenetic aging in DunedinPoAm and DunedinPACE by 0.01 to 0.04 years per year.
Greater variation in PA was associated with a 0.76-year decline in PhenoAge and with 0.02 to 0.05 years slower epigenetic aging in DunedinPoAm and DunedinPACE. High PA activity corresponded to a reduction of up to 1.34 years in PhenoAge, and all activity levels were associated with slower epigenetic aging by 0.01 to 0.05 years per year. These associations remained strong after adjustment for behavioral and health factors and were strongest among participants aged 40 years and older. However, the epigenetic measures were derived from blood samples, which may not fully capture the aging-related changes that occur in other tissues, such as muscle.
conclusions
The current study offers preliminary evidence linking ACEng to epigenetic aging, highlighting its potential contribution to healthy biological aging along with other lifestyle factors. Both diversity and frequency of engagement with ACEng appear significant and its effect size is comparable to that of PA. These findings suggest that ACEng could be further explored as part of broader public health strategies for healthy aging.
According to emerging research, epigenetic aging may be modifiable or partially reversible in some cases, and the effect of leisure behaviors on these processes remains unclear. Future intervention studies are warranted to determine whether lifestyle modifications can slow or reverse biological aging.
