Changes in stress, eating, and metabolic factors are related to changes in telomerase activity in a randomized mindfulness intervention pilot study.

Changes in stress, eating, and metabolic factors are related to changes in telomerase activity in a randomized mindfulness intervention pilot study.
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DOI:
10.1016/j.psyneuen.2011.10.008
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发表时间:
2012-07
影响因子:
3.7
通讯作者:
Epel, Elissa
Epel, Elissa
中科院分区:
医学2区
文献类型:
--
作者:
Daubenmier, Jennifer;Lin, Jue;Blackburn, Elizabeth;Hecht, Frederick M.;Kristeller, Jean;Maninger, Nicole;Kuwata, Margaret;Bacchetti, Peter;Havel, Peter J.;Epel, Elissa

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心理压力和代谢失调与加速细胞衰老的标志物有关,包括端粒酶活性降低和端粒长度缩短。我们研究了参与基于正念的干预,以及其次,心理困扰,饮食行为和代谢因素的改善是否与外周血单核细胞(PBMC)中端粒酶活性的增加有关。我们招募了47名超重/肥胖女性参加一项随机等待名单对照的试点试验(n = 47),该试验是一项基于正念的压力饮食干预措施,并检查了干预前后端粒酶活性的变化。在二次分析中,检查了样本中端粒酶活性的变化与心理困扰、饮食行为和代谢因素(体重、血清皮质醇、空腹血糖和胰岛素以及胰岛素抵抗)干预前后变化的关系。在意向治疗和治疗效果分析中,两组的平均端粒酶活性在4个月内均增加(p < 0.001)。非显著性趋势表明,更多的出勤率与端粒酶的增加有关,与对照组相比,“接受治疗”的参与者端粒酶增加了18%。在各组中,慢性压力、焦虑、饮食限制、饮食脂肪摄入、皮质醇和葡萄糖的变化与端粒酶活性的变化呈负相关。在探索性分析中,膳食脂肪摄入量的减少部分介导了饮食限制和端粒酶活性之间的关联,具有边缘意义。虽然干预对端粒酶活性没有明确的影响,但心理困扰、饮食行为和代谢健康的改善与端粒酶活性的增加之间存在显著的相关性。这些发现表明,端粒酶活性可能部分受到心理和代谢应激水平的调节。
Psychological distress and metabolic dysregulation are associated with markers of accelerated cellular aging, including reduced telomerase activity and shortened telomere length. We examined whether participation in a mindfulness-based intervention, and, secondarily, improvements in psychological distress, eating behavior, and metabolic factors are associated with increases in telomerase activity in peripheral blood mononuclear cells (PBMCs). We enrolled 47 overweight/obese women in a randomized waitlist-controlled pilot trial (n = 47) of a mindfulness-based intervention for stress eating and examined changes in telomerase activity from pre- to post-intervention. In secondary analyses, changes in telomerase activity across the sample were examined in relation to pre- to post-intervention changes in psychological distress, eating behavior, and metabolic factors (weight, serum cortisol, fasting glucose and insulin, and insulin resistance). Both groups increased in mean telomerase activity over 4 months in intent-to-treat and treatment efficacy analyses (p < 0.001). Nonsignificant trends showed that greater attendance was associated with increases in telomerase, and telomerase increases were 18% higher among ‘as treated’ participants compared to controls. Across groups, changes in chronic stress, anxiety, dietary restraint, dietary fat intake, cortisol, and glucose were negatively correlated with changes in telomerase activity. In exploratory analyses, decreases in dietary fat intake partially mediated the association between dietary restraint and telomerase activity with marginal significance. While there was no clear effect of the intervention on telomerase activity, there was a striking pattern of correlations between improvements in psychological distress, eating behavior, and metabolic health and increases in telomerase activity. These findings suggest that telomerase activity may be in part regulated by levels of both psychological and metabolic stress.
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