Manipulations to set back biological age and extend lifespan in animal models are well established, and translation to humans has begun. The length of human life makes it impractical to evaluate results by plotting mortality curves, so surrogate markers of age have been suggested and, at present, the best established surrogates are DNA methylation clocks. Herein we report on a randomized, controlled clinical trial designed to be a first step in evaluating the effect of a diet and lifestyle intervention on biological age. Compared to participants in the control group (n=20), participants in the treatment group tested an average 3.23 years younger at the end of the eight-week program according to the Horvath DNAmAge clock (p=0.018). Those in the treatment group (n=18) tested an average 1.96 years younger at the end of the program compared to the same individuals at the beginning with a strong trend towards significance (p=0.066 for within group change). This is the first such trial to demonstrate a potential reversal of biological age. In this study, the intervention was confined to diet and lifestyle changes previously identified as safe to use. The prescribed program included multiple components with documented mechanistic activity on epigenetic pathways, including moderate exercise, breathing exercises for stress, and a diet rich in methyl donor nutrients and polyphenols.

中文翻译：

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在一项随机临床试验中通过饮食和生活方式逆转表观遗传年龄

在动物模型中操纵生物年龄和延长寿命的操作已得到很好的确立，并且已经开始向人类翻译。寿命的长短使得通过绘制死亡率曲线来评估结果不切实际，因此提出了年龄的替代标记，目前，最完善的替代方法是DNA甲基化时钟。在此，我们报告了一项随机，对照的临床试验，旨在作为评估饮食和生活方式干预对生物年龄的影响的第一步。与对照组的参与者（n = 20）相比，治疗组的参与者根据Horvath DNAmAge时钟在八周计划结束时的平均年龄年轻了3.23岁（p = 0.018）。治疗组（n = 18）的受试者平均分为1。与一开始的同一个人相比，该计划结束时年轻96岁，具有显着的显着趋势（组内变化p = 0.066）。这是首次证明生物年龄可能逆转的此类试验。在这项研究中，干预措施仅限于饮食和生活方式的改变，这些改变以前被认为可以安全使用。规定的程序包括在表观遗传途径上具有记录的机械活性的多个组成部分，包括适度运动，压力呼吸运动以及富含甲基供体营养素和多酚的饮食。干预仅限于以前确定可以安全使用的饮食和生活方式的改变。规定的程序包括在表观遗传途径上具有记录的机械活性的多个组成部分，包括适度运动，压力呼吸运动以及富含甲基供体营养素和多酚的饮食。干预仅限于以前确定可以安全使用的饮食和生活方式的改变。规定的程序包括在表观遗传途径上具有记录的机械活性的多个组成部分，包括适度运动，压力呼吸运动以及富含甲基供体营养素和多酚的饮食。