People whose everyday habits drifted toward smoking, poor diet, inactivity, heavy drinking, or short sleep showed measurable acceleration in biological aging, according to a prospective cohort study drawing on participants from the Korean Genome and Epidemiology Study. The research, published in Clinical Epigenetics, followed 1020 middle-aged and older adults and tracked how shifts in five modifiable behaviors over multi-year intervals related to DNA methylation-based measures of epigenetic age acceleration and to estimated cardiovascular disease risk. The mean age of participants was 50.1 years, with a standard deviation of 8.2 years, and 52.5 percent were men.
The study team constructed a lifestyle score from five behaviors: alcohol consumption, diet, physical activity, sleep, and smoking. Rather than taking a single snapshot, the researchers classified each participant’s trajectory across 4-year and 8-year intervals into one of four transition categories: stable healthy, improved, worsened, or stable poor. This design allowed them to ask whether the direction of long-term lifestyle change, not just the level at any one moment, tracked with how fast a person’s biology appeared to age.
Two families of healthy aging indices anchored the analysis. The first was epigenetic age acceleration, abbreviated EAA, estimated with three DNA methylation-based measures: PhenoAA, Grim2AA, and DunedinPACE. These clocks compare a person’s methylation patterns against chronological age to estimate whether biological aging is running faster or slower than expected. The second was cardiovascular disease risk, quantified with the Predicting Risk of CVD EVENTs equation, known as the PREVENT score. Associations were tested using multivariable linear regression and generalized estimating equation models, and a mediation analysis examined whether epigenetic age acceleration explained part of the link between lifestyle transitions and future cardiovascular risk.
The central finding was consistent across the transition categories. Compared with participants who remained in the stable healthy group, those with poor or worsening lifestyle patterns showed higher epigenetic age acceleration. The gradient was striking: the worse the trajectory, the larger the acceleration. In the improved group, epigenetic aging remained elevated over the 8-year window, with a Grim2AA difference of 1.54 years (95 percent confidence interval 0.81 to 2.27) and a DunedinPACE difference of 2.20 (95 percent confidence interval 0.38 to 4.02) relative to the stable healthy reference.
Acceleration grew steeper as lifestyle trajectories deteriorated. Participants in the worsened group showed a Grim2AA difference of 2.45 years (95 percent confidence interval 1.42 to 3.47) and a DunedinPACE difference of 2.81 (95 percent confidence interval 0.25 to 5.37). The stable poor group carried the largest burden, with a Grim2AA difference of 3.81 years (95 percent confidence interval 3.11 to 4.52) and a DunedinPACE difference of 5.13 (95 percent confidence interval 3.37 to 6.90). These estimates, adjusted for confounding factors through multivariable modeling, suggest that sustained unhealthy habits impose a persistent epigenetic penalty, while even partial improvement does not immediately erase the accumulated signal within the observation window.
The mediation results add a mechanistic dimension to the association. Epigenetic age acceleration partially mediated the relationship between lifestyle transitions and future cardiovascular disease risk, accounting for 51.5 to 52.9 percent of the effect when measured with Grim2AA and 15.2 to 15.7 percent when measured with DunedinPACE. In practical terms, a meaningful share of the way lifestyle trajectories translate into elevated cardiovascular risk estimates appears to travel through accelerated biological aging captured by DNA methylation clocks, though the mediation was incomplete, leaving other pathways unexplained by these measures.
The authors conclude that unfavorable lifestyle transitions were associated with poorer healthy aging indices and that epigenetic aging partially mediated the association between lifestyle transitions and future cardiovascular disease risk. They frame the findings as underscoring the importance of early intervention and sustained healthy behaviors, since trajectories that worsened or remained poor carried the heaviest epigenetic burden in the cohort.
Several caveats shape how these results should be read. The study used a subset of participants from the Korean Genome and Epidemiology Study, so the findings describe an East Asian cohort of middle-aged and older adults and may not generalize to other populations. The design is observational, meaning the associations capture patterns over time rather than proof that changing habits directly slows or speeds the methylation clocks. The elevated epigenetic aging seen in the improved group also hints that recovery from years of poor habits may lag behind the behavioral change itself, an interpretation the data support only within the 8-year follow-up examined. As an open-access article published on 9 September 2026, the study is citable with a permanent DOI, and the reported version is subject to further edits before the final Version of Record replaces it.
For readers tracking the science of healthy aging, the study’s contribution lies in connecting longitudinal behavior change to molecular aging measures and downstream risk estimates in a single framework. By classifying people by the direction of their lifestyle drift over years rather than a single assessment, the researchers captured the cumulative weight of sustained habits on epigenetic age and on predicted cardiovascular risk, and showed that DNA methylation-based aging measures sit along part of that pathway.
Subject of Research: Long-term lifestyle transitions and their association with epigenetic age acceleration and cardiovascular disease risk in middle-aged and older Korean adults
Article Title: Lifestyle transitions and healthier biological aging in middle-aged and older adults: a prospective study in an East Asian cohort
Article References: Jang, H.-M., Chang, Y., Ryu, S., Lee, D.-E., Park, Y. S., Kim, Y. J., & Kim, K. (2026). Lifestyle transitions and healthier biological aging in middle-aged and older adults: a prospective study in an East Asian cohort. Clinical Epigenetics. https://doi.org/10.1186/s13148-026-02240-8
Image Credits: AI Generated
DOI: 10.1186/s13148-026-02240-8
Keywords: epigenetic age acceleration, lifestyle transitions, healthy aging, Korean Genome and Epidemiology Study, cardiovascular disease risk, DNA methylation, PhenoAA, Grim2AA, DunedinPACE, prospective cohort study, biological aging, PREVENT score
News Source: Phoebe Ingram. (October 30, 2026). Lifestyle changes leave lasting marks on biological aging in Korean cohort study. Scienmag.
