Can meditation slow rate of cellular aging? Cognitive stress, mindfulness, and telomeres
Humans; Stress; Adaptation; Meditation; Telomere/genetics; Cell Aging/genetics; Cognition/physiology; Psychological/physiology; Psychological/physiopathology
Understanding the malleable determinants of cellular aging is critical to understanding human longevity. Telomeres may provide a pathway for exploring this question. Telomeres are the protective caps at the ends of chromosomes. The length of telomeres offers insight into mitotic cell and possibly organismal longevity. Telomere length has now been linked to chronic stress exposure and depression. This raises the question of mechanism: How might cellular aging be modulated by psychological functioning? We consider two psychological processes or states that are in opposition to one another-threat cognition and mindfulness-and their effects on cellular aging. Psychological stress cognitions, particularly appraisals of threat and ruminative thoughts, can lead to prolonged states of reactivity. In contrast, mindfulness meditation techniques appear to shift cognitive appraisals from threat to challenge, decrease ruminative thought, and reduce stress arousal. Mindfulness may also directly increase positive arousal states. We review data linking telomere length to cognitive stress and stress arousal and present new data linking cognitive appraisal to telomere length. Given the pattern of associations revealed so far, we propose that some forms of meditation may have salutary effects on telomere length by reducing cognitive stress and stress arousal and increasing positive states of mind and hormonal factors that may promote telomere maintenance. Aspects of this model are currently being tested in ongoing trials of mindfulness meditation.
2009
Epel E; Daubenmier J; Moskowitz JT; Folkman S; Blackburn E
Annals Of The New York Academy Of Sciences
2009
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1111/j.1749-6632.2009.04414.x" target="_blank" rel="noreferrer">10.1111/j.1749-6632.2009.04414.x</a>
Beta-endorphin mediates behavioral despair and the effect of ethanol on the tail suspension test in mice.
Female; Male; Behavior; Animals; Mice; Stress; Adaptation; Models; Sex Characteristics; Animal; Psychological/physiology; Animal/physiology; beta-Endorphin/physiology; beta-Endorphin/genetics; Central Nervous System Depressants/pharmacology; Depression/physiopathology; Ethanol/pharmacology; Hindlimb Suspension/psychology; Psychological/physiopathology; Psychological/psychology; Transgenic
Background: The opioid peptide beta-endorphin (beta-E) is synthesized and released in response to stressful stimuli as well as acute alcohol administration. The release of beta-E following exposure to an inescapable aversive situation may mediate behaviors that contribute to allostasis of the stress response. The present study examines the effects of beta-E on immobility in assays involving inescapable stress, both under basal conditions and after acute administration of EtOH.; Methods: Female and male transgenic mice with varying capacities to translate beta-E were subjected to either the forced swim (FST, Experiment 1) or the tail suspension test (TST, Experiment 2). In Experiment 3, mice were divided into three groups based on hormonal status (male, female-estrous, and female-nonestrous) and injected with either 1 g/kg EtOH or equivolume saline 14 minutes prior to behavioral assessment on the TST.; Results: Experiments 1 and 2 demonstrated a direct relationship between beta-E levels and immobility. There were also sex differences in behavior in these tests, with males displaying more immobility than females. A main effect of genotype in Experiment 3 replicated findings in Experiments 1 and 2. There was also an effect of EtOH (increasing immobility) and a significant interaction reflecting a particularly robust effect of the drug in mice with low beta-E. In addition, there were interactions between beta-E, EtOH effects, and hormonal status.; Conclusions: These findings support the contention that beta-E moderates behavioral responses to stressful stimuli and suggest a role for this peptide in coping behavior. Furthermore, the effects of EtOH on the response to stress may be mediated by beta-E. Sex differences in this influence may contribute to sex differences in disease susceptibility and expression.;
2010-06
Barfield ET; Barry SM; Hodgin HB; Thompson BM; Allen SS; Grisel JE
Alcoholism, Clinical And Experimental Research
2010
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Journal Article
<a href="http://doi.org/10.1111/j.1530-0277.2010.01182.x" target="_blank" rel="noreferrer">10.1111/j.1530-0277.2010.01182.x</a>