Vitamin D supplementation is associated with slower epigenetic aging.

IF 1.1 3区 社会学 Q2 LAW Icsid Review-Foreign Investment Law Journal Pub Date : 2022-06-01 Epub Date: 2022-05-13 DOI:10.1007/s11357-022-00581-9
Valentin Max Vetter, Yasmine Sommerer, Christian Humberto Kalies, Dominik Spira, Lars Bertram, Ilja Demuth
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Abstract

Adverse effects of low vitamin D level on mortality and morbidity are controversially discussed. Especially older people are at risk for vitamin D deficiency and therefore exposed to its potentially harmful consequences. A way of measuring differences in the biological age is through DNA methylation age (DNAm age) and its deviation from chronological age, DNAm age acceleration (DNAmAA). We previously reported on an association between vitamin D deficiency and higher 7-CpG DNAmAA in participants of the Berlin Aging Study II (BASE-II). In this study, we employ a quasi-interventional study design to assess the relationship between DNAmAA of five epigenetic clocks and vitamin D supplementation. Longitudinal data were available for 1,036 participants of BASE-II that were reexamined on average 7.4 years later in the GendAge study (mean age at follow-up: 75.6 years, SD = 3.8 years, age range: 64.9-94.1 years, 51.9% female). DNAmAA was estimated with the 7-CpG clock, Horvath's clock, Hannum's clock, PhenoAge, and GrimAge. Methylation data were obtained through methylation-sensitive single nucleotide primer extension (MS-SNuPE) or Illumina's Infinium "MethylationEPIC" array. Vitamin D-deficient participants who chose to start vitamin D supplementation after baseline examination showed a 2.6-year lower 7-CpG DNAmAA (p = 0.011) and 1.3-year lower Horvath DNAmAA (p = 0.042) compared to untreated and vitamin D-deficient participants. DNAmAA did not statistically differ between participants with successfully treated vitamin D deficiency and healthy controls (p > 0.16). Therefore, we conclude that intake of vitamin D supplement is associated with lower DNAmAA in participants with vitamin D deficiency.

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补充维生素 D 与延缓表观遗传衰老有关。
低维生素 D 水平对死亡率和发病率的不利影响一直备受争议。尤其是老年人面临维生素 D 缺乏的风险,并因此面临其潜在的有害后果。测量生物年龄差异的一种方法是通过 DNA 甲基化年龄(DNAm 年龄)及其与生理年龄的偏差,即 DNAm 年龄加速度(DNAmAA)。我们曾报道过,在柏林老龄化研究 II(BASE-II)的参与者中,维生素 D 缺乏与较高的 7-CpG DNAmAA 之间存在关联。在本研究中,我们采用了一种准干预研究设计来评估五种表观遗传时钟的 DNAmAA 与维生素 D 补充之间的关系。在平均 7.4 年后的 GendAge 研究中,我们获得了 1036 名 BASE-II 参与者的纵向数据(随访时的平均年龄:75.6 岁,SD = 3.8 岁,年龄范围:64.9-94.1 岁):64.9-94.1岁,51.9%为女性)。DNAmAA通过7-CpG时钟、Horvath时钟、Hannum时钟、PhenoAge和GrimAge进行估算。甲基化数据通过甲基化敏感单核苷酸引物延伸(MS-SNuPE)或 Illumina 的 Infinium "MethylationEPIC "阵列获得。与未经治疗和维生素 D 缺乏的参与者相比,在基线检查后选择开始补充维生素 D 的维生素 D 缺乏参与者的 7-CpG DNAmAA 低 2.6 年(p = 0.011),Horvath DNAmAA 低 1.3 年(p = 0.042)。成功治疗维生素 D 缺乏症的参与者与健康对照组之间的 DNAmAA 没有统计学差异(p > 0.16)。因此,我们得出结论,维生素 D 缺乏症患者摄入维生素 D 补充剂与 DNAmAA 降低有关。
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CiteScore
1.10
自引率
27.30%
发文量
46
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