آموزش فشرده مدیتیشن، فعالیت آنزیم تلومراز سلول ایمنی بدن و واسطه روانی

Background Telomerase activity is a predictor of long-term cellular viability, which decreases with chronic psychological distress (Epel et al., 2004). Buddhist traditions claim that meditation decreases psychological distress and promotes well-being (e.g., Dalai Lama and Cutler, 2009). Therefore, we investigated the effects of a 3-month meditation retreat on telomerase activity and two major contributors to the experience of stress: Perceived Control (associated with decreased stress) and Neuroticism (associated with increased subjective distress). We used mediation models to test whether changes in Perceived Control and Neuroticism explained meditation retreat effects on telomerase activity. In addition, we investigated whether two qualities developed by meditative practice, increased Mindfulness and Purpose in Life, accounted for retreat-related changes in the two stress-related variables and in telomerase activity. Methods Retreat participants (n = 30) meditated for ∼6 h daily for 3 months and were compared with a wait-list control group (n = 30) matched for age, sex, body mass index, and prior meditation experience. Retreat participants received instruction in concentrative meditation techniques and complementary practices used to cultivate benevolent states of mind ( Wallace, 2006). Psychological measures were assessed pre- and post-retreat. Peripheral blood mononuclear cell samples were collected post-retreat for telomerase activity. Because there were clear, a priori hypotheses, 1-tailed significance criteria were used throughout. Results Telomerase activity was significantly greater in retreat participants than in controls at the end of the retreat (p < 0.05). Increases in Perceived Control, decreases in Neuroticism, and increases in both Mindfulness and Purpose in Life were greater in the retreat group (p < 0.01). Mediation analyses indicated that the effect of the retreat on telomerase was mediated by increased Perceived Control and decreased Neuroticism. In turn, changes in Perceived Control and Neuroticism were both partially mediated by increased Mindfulness and Purpose in Life. Additionally, increases in Purpose in Life directly mediated the telomerase group difference, whereas increases in Mindfulness did not. Conclusions This is the first study to link meditation and positive psychological change with telomerase activity. Although we did not measure baseline telomerase activity, the data suggest that increases in perceived control and decreases in negative affectivity contributed to an increase in telomerase activity, with implications for telomere length and immune cell longevity. Further, Purpose in Life is influenced by meditative practice and directly affects both perceived control and negative emotionality, affecting telomerase activity directly as well as indirectly.

Although relations between psychological functioning and physical health have long been documented, mechanistic links are only beginning to be understood at the cellular level (e.g., Miller et al., 2009). Telomere length has recently been proposed as a useful ‘psychobiomarker’ linking stress and disease (Epel, 2009). Shortened telomere length and reduced telomerase (the cellular enzyme primarily responsible for telomere length and maintenance) predict a host of health risks and diseases (Blackburn, 2000, Serrano and Andres, 2004 and Lin et al., 2009b), and new findings suggest they may be regulated in part by psychological stress, stress appraisals, and well-being (Epel et al., 2004, Epel et al., 2009a and Ornish et al., 2008). The literature on Buddhist traditions has long suggested that meditation can reduce psychological stress and enhance well-being (e.g., Dalai Lama and Cutler, 2009). In the present study, we investigated whether meditative practice is associated with immune cell telomerase activity and whether this association is at least partly explained by changes in two major contributors to the experience of stress: Perceived Control and Neuroticism (see Fig. 1).