Recently, DNA methylation has emerged as a robust biomarker of biological aging. The methylation level of a large number of genomic sites are highly associated with age, to such a point that methods based on a small number of these sites can predict the chronological age with an average error of only 4 years (Hannum et al., 2013; Horvath, 2013). More precisely, the DNA methylation (DNAm) age can be estimated from the methylation levels of 353 CpG sites of the genome and has been found to highly correlate to chronological age and to be stable across most tissues and cell types (i.e. whole blood, peripheral mononuclear cells, brain cells, breast, kidney, liver, lung and saliva) (Horvath, 2013). The deviation between the DNAm age and the chronological age of an individual provides information regarding his epigenetic aging rate (Chen et al., 2016). Faster-running epigenetic clocks have been negatively associated with longevity (Horvath et al., 2015), and positively associated with chronic diseases (Horvath et al., 2014; Horvath and Ritz, 2015; Levine et al., 2015a, 2015b; Perna et al., 2016), frailty (Breitling et al., 2016), cognitive and physical fitness in the elderly (Marioni et al., 2015b) and all cause mortality even after adjusting for chronological age and a variety of known risk factors (Christiansen et al., 2016; Marioni et al., 2015a; Perna et al., 2016). The epigenetic clock therefore may represent an accurate tool to measure the effectiveness of lifestyle-based interventions for the prevention of age-related diseases. This is a health priority area today as revealed by data from the Centers for Disease Control and Prevention indicating that 78% of adults aged 55 years and over present one or more chronic diseases (www.cdc.gov).

Consistent with previous work describing the noxious impact of psychological stress on health span (Juster et al., 2010), it has recently been shown that cumulative lifetime chronic stress (Zannas et al., 2015) and trauma (Boks et al., 2015) predict accelerated epigenetic aging. Meditation-based stress reduction interventions have increasingly become a focus of scientific interest to promote healthy aging. Recent research suggests that meditation has beneficial effects in stress and age-related neuroplastic changes, and mood and cognitive disorders (Davidson and McEwen, 2012; Acevedo et al., 2016; Luders, 2014). Molecular mechanisms involved in the aging process, such as inflammation, immune and epigenetic pathways (Black and Slavich, 2016; Kaliman et al., 2014), as well as telomere maintenance (Epel et al., 2009; Alda et al., 2016), are also sensitive to contemplative practices. However, it remains unexplored whether meditation experience modulates the rate of the epigenetic aging. Given the well-characterized effect of meditation practice on stress reduction (McEwen, 2016), we tested the hypothesis that long-term practitioners would show slower rates of epigenetic aging than age and sex matched controls. To do so, we analyzed DNA methylome data from blood cells of long-term meditators and meditation-naïve controls.

The current study was designed to determine if the rate of epigenetic aging in long-term meditators was different than in meditationnaïve controls (the meditators recruited for this study had between 5 and 30 years of continuous regular practice). We found no difference in the intrinsic epigenetic aging acceleration (IEAA) between long-term meditators and meditation-naïve controls. However, we found a different IEAA trajectory in controls and meditators as a function of age, with an increase of IEAA with age in controls but not in meditators, suggesting that integrating meditation practice into daily routine may have a protecting effect in terms of epigenetic aging in the long run. Cumulative lifetime stress is one of the factors described to accelerate epigenetic aging (Zannas et al., 2015). Our study suggests that psychological stress reduction in meditators as a result of their regular practice may contribute to the stability of their IEAA across ages compared with controls. Consistent with this hypothesis, we found that in long-term meditators the epigenetic aging rate decreased significantly with the number of years of regular meditation practice. When controls were included in this analysis as “zero meditation experience”, the significant effect of years of meditation on IEAA was only found in subjects aged ≥ 52, indicating that this protective effect of meditation practice is observed mainly in older subjects. As a whole, these findings suggest that the protective effect of meditation on epigenetic age acceleration may be progressive and cumulative.

Data presented here extend previous evidence showing the influence of meditation training on aging biomarkers, notably the presence of longer telomeres in long-term meditators (Alda et al., 2016), the increase in telomerase activity after a 3 months meditation retreat (Jacobs et al., 2011), a yogic meditation training (Lavretsky et al., 2013) and a mindfulness-based stress reduction program (Lengacher et al., 2014). Telomere length and epigenetic aging rate, however, have been shown to be mutually uncorrelated and independently linked to disease and mortality risk, probably through different aging signaling pathways (Marioni et al., 2016). Previous reports on telomere biology, together with our findings on epigenetic aging, suggest that meditation practice may modulate different molecular mechanisms involved in cell aging and may represent a useful preventive strategy for age-related chronic diseases.

Our data may contribute to reveal the benefits of long-term meditation on healthy aging although they present several limitations that warrant further investigation. In particular, longitudinal randomized and controlled trials involving larger samples are required to help disentangle the effect of meditation from pre-existing individual differences and/or from other meditation-associated lifestyle factors on epigenetic aging. It is also critical to explore in future studies the type of practices (i.e. mindfulness-related meditations, compassion-related meditations, breath work, visualizations, body scanning or other mind-body techniques) and the frequency and duration of the trainings that could efficiently decrease the epigenetic aging rate in otherwise meditation-naïve healthy subjects or clinical populations.