From museum visits and music to regular exercise, researchers found that people who engaged more often in enriching leisure activities showed signs of slower biological aging in cutting-edge epigenetic clocks.
Study: Does leisure activity matter for epigenetic ageing? Analyses of arts engagement and physical activity in the UK Household Longitudinal Study. Image credit: Bangkok Click Studio/Shutterstock.com
A recent Innovation in Aging study examines whether leisure activities, such as arts engagement and physical activity, may be associated with the aging process.
Epigenetic mechanisms, lifestyle factors, and the measurement of biological aging
The increasing proportion of older adults worldwide has shifted attention from simply extending lifespan to enhancing years lived in good health. Current priorities focus on minimizing disease, maintaining independence, and reducing strain on healthcare systems.
Molecular biology has revealed fundamental mechanisms driving 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 initial clocks measured chronological age, newer versions incorporate phenotypic traits, lifespan predictors, and aging rates. Although standards and causal links remain debated, aging clocks are widely used to study and guide interventions for biological aging.
Lifestyle factors, such as avoiding tobacco and excessive alcohol use, maintaining a healthy weight, following a Mediterranean diet, managing stress, and practicing meditation, may slow epigenetic aging, although the evidence remains preliminary, and many leisure activities are understudied.
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 ACEng can affect 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 omitting key confounders. Previous studies have also produced mixed findings depending on the epigenetic clock examined. Comprehensive, multi-clock, and causally robust approaches are needed to clarify these links.
Assessing the impact 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 profiled 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 remained. Over 850,000 methylation sites were assessed. The DNA methylation analysis was limited to participants of white European ancestry, which may affect the generalizability of the findings.
UKHLS features seven epigenetic clocks from DNAm data spanning three generations. First-generation clocks estimate chronological age, second-generation clocks integrate mortality and disease risk, and third-generation clocks quantify the rate of biological aging. First- and second-generation clocks report age in years; third-generation clocks reflect the pace of aging.
ACEng was measured by self-reported participation in arts, heritage, and cultural activities over 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 by reported sports of varying intensity; the most frequently reported activity reflected PA frequency.
Higher leisure activity levels are associated with slower epigenetic aging
The analytical 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 engaged in three or more activities, and 27.9 % participated in 11 or more. Over 75 % took part in ACEng on a monthly or weekly basis. In contrast, 19.3 % of participants reported no PA, and fewer than one-third engaged in four or more PA activities, though 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. The associations were therefore observed primarily in newer epigenetic clocks designed to reflect health decline and pace of aging rather than chronological age alone.
For PhenoAge, monthly ACEng was associated with a 0.8-year reduction in epigenetic age, whereas weekly ACEng was associated with a 1.02-year reduction. More frequent ACEng was also associated with slower biological aging rates, 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 with slower biological aging rates of 0.02 to 0.04 years per year in DunedinPoAm and DunedinPACE. PA frequency did not show associations with first-generation clocks, whereas 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 diversity in PA was associated with a 0.76-year reduction in PhenoAge and with slower epigenetic aging by 0.02 to 0.05 years per year in DunedinPoAm and DunedinPACE. High PA activeness corresponded to up to a 1.34-year reduction in PhenoAge, and all levels of activeness were linked to slower epigenetic aging by 0.01 to 0.05 years per year. These associations remained robust after adjustment for behavioral and health factors and were more pronounced among participants aged 40 or older. However, the epigenetic measures were derived from blood samples, which may not fully capture aging-related changes occurring in other tissues, such as muscle.
Conclusions
The current study offers preliminary evidence linking ACEng to epigenetic aging, emphasizing its potential contribution to healthy biological aging alongside other lifestyle factors. Both the diversity and frequency of engagement with ACEng appear important, and its effect size is comparable to that of PA. These findings suggest ACEng could be further explored as part of broader healthy-aging public health strategies.
According to emerging research, epigenetic aging may be modifiable or partially reversible in some cases, and the influence of leisure behaviors on these processes remains unclear. Future intervention studies are warranted to determine whether lifestyle modifications can decelerate or reverse biological aging.
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