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本文引用的文献

1
Associations of Body Composition and Physical Activity Level With Multiple Measures of Epigenetic Age Acceleration.体成分和身体活动水平与多种表观遗传年龄加速指标的关联。
Am J Epidemiol. 2021 Jun 1;190(6):984-993. doi: 10.1093/aje/kwaa251.
2
Longitudinal trajectories, correlations and mortality associations of nine biological ages across 20-years follow-up.20 年随访中九种生物年龄的纵向轨迹、相关性和与死亡率的关联。
Elife. 2020 Feb 11;9:e51507. doi: 10.7554/eLife.51507.
3
Prediagnostic Immune Cell Profiles and Breast Cancer.术前免疫细胞图谱与乳腺癌。
JAMA Netw Open. 2020 Jan 3;3(1):e1919536. doi: 10.1001/jamanetworkopen.2019.19536.
4
Epigenetic mortality predictors and incidence of breast cancer.表观遗传死亡预测因素与乳腺癌发病率
Aging (Albany NY). 2019 Dec 17;11(24):11975-11987. doi: 10.18632/aging.102523.
5
Reproduction, DNA methylation and biological age.生殖、DNA甲基化与生物学年龄。
Hum Reprod. 2019 Oct 2;34(10):1965-1973. doi: 10.1093/humrep/dez149.
6
Education and Lifestyle Factors Are Associated with DNA Methylation Clocks in Older African Americans.教育和生活方式因素与老年非裔美国人的 DNA 甲基化时钟相关。
Int J Environ Res Public Health. 2019 Aug 28;16(17):3141. doi: 10.3390/ijerph16173141.
7
Epigenetic aging is accelerated in alcohol use disorder and regulated by genetic variation in APOL2.酒精使用障碍会加速表观遗传衰老,且这种加速受 APOL2 基因变异的调控。
Neuropsychopharmacology. 2020 Jan;45(2):327-336. doi: 10.1038/s41386-019-0500-y. Epub 2019 Aug 29.
8
Socioeconomic position, lifestyle habits and biomarkers of epigenetic aging: a multi-cohort analysis.社会经济地位、生活方式习惯与表观遗传衰老的生物标志物:一项多队列分析。
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9
Methylation-Based Biological Age and Breast Cancer Risk.基于甲基化的生物年龄与乳腺癌风险。
J Natl Cancer Inst. 2019 Oct 1;111(10):1051-1058. doi: 10.1093/jnci/djz020.
10
DNA methylation GrimAge strongly predicts lifespan and healthspan.DNA甲基化GrimAge能有力地预测寿命和健康跨度。
Aging (Albany NY). 2019 Jan 21;11(2):303-327. doi: 10.18632/aging.101684.

饮酒与基于甲基化的生物年龄衡量指标。

Alcohol Consumption and Methylation-Based Measures of Biological Age.

机构信息

Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA.

Wellesley College, Massachusetts, USA.

出版信息

J Gerontol A Biol Sci Med Sci. 2021 Nov 15;76(12):2107-2111. doi: 10.1093/gerona/glab149.

DOI:10.1093/gerona/glab149
PMID:34038541
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8599006/
Abstract

Epigenetic age acceleration is considered a measure of biological aging based on genome-wide patterns of DNA methylation. Although age acceleration has been associated with the incidence of diseases and death, less is known about how it is related to lifestyle behaviors. Among 2316 women, we evaluate associations between self-reported alcohol consumption and various metrics of epigenetic age acceleration. Recent average alcohol consumption was defined as the mean number of drinks consumed per week within the past year; lifetime average consumption was estimated as the mean number of drinks per year drinking. Whole-blood genome-wide DNA methylation was measured with HumanMethylation450 BeadChips and used to assess 4 epigenetic clocks (Hannum, Horvath, PhenoAge, and GrimAge) and their corresponding metrics of epigenetic age acceleration (Hannum AgeAccel, Horvath AgeAccel, PhenoAgeAccel, and GrimAgeAccel). Although alcohol consumption showed little association with most age acceleration metrics, both lifetime and recent average consumption measures were positively associated with GrimAgeAccel (lifetime, per additional 135 drinks/year: β = 0.30 years, 95% confidence interval [CI]: 0.11, 0.48, p = .002; recent, per additional 5 drinks/week: β = 0.19 years, 95% CI: 0.01, 0.37, p = .04). In a mutually adjusted model, only average lifetime alcohol consumption remained associated with GrimAgeAccel (lifetime, per additional 135 drinks/year: β = 0.27 years, 95% CI: 0.04, 0.50, p = .02; recent, per 5 additional drinks/week: β = 0.05 years, 95% CI: -0.16, 0.26, p = .64). Although alcohol use does not appear to be strongly associated with biological age measured by most epigenetic clocks, lifetime average consumption is associated with higher biological age assessed by the GrimAge epigenetic clock.

摘要

表观遗传年龄加速被认为是一种基于全基因组 DNA 甲基化模式的生物年龄衡量标准。尽管年龄加速与疾病和死亡的发生有关,但人们对其与生活方式行为的关系知之甚少。在 2316 名女性中,我们评估了自我报告的饮酒量与各种表观遗传年龄加速指标之间的关联。最近的平均饮酒量定义为过去一年中每周平均饮酒量;终生平均饮酒量估计为每年平均饮酒量。全血全基因组 DNA 甲基化采用 HumanMethylation450 BeadChips 进行测量,并用于评估 4 个表观遗传时钟(Hannum、Horvath、PhenoAge 和 GrimAge)及其相应的表观遗传年龄加速指标(Hannum AgeAccel、Horvath AgeAccel、PhenoAgeAccel 和 GrimAgeAccel)。尽管饮酒与大多数年龄加速指标的关联很小,但终生和近期平均饮酒量均与 GrimAgeAccel 呈正相关(终生,每增加 135 杯/年:β=0.30 岁,95%置信区间[CI]:0.11,0.48,p=0.002;近期,每周每增加 5 杯:β=0.19 岁,95%CI:0.01,0.37,p=0.04)。在相互调整的模型中,只有平均终生饮酒量与 GrimAgeAccel 仍相关(终生,每增加 135 杯/年:β=0.27 岁,95%CI:0.04,0.50,p=0.02;近期,每增加 5 杯/周:β=0.05 岁,95%CI:-0.16,0.26,p=0.64)。尽管饮酒似乎与大多数表观遗传时钟测量的生物年龄没有很强的关联,但终生平均饮酒量与 GrimAge 表观遗传时钟评估的更高生物年龄相关。