School of Public Health, Physiotherapy and Sports Science, University College Dublin, Dublin, Ireland.
School of Public Health, Physiotherapy and Sports Science, University College Dublin, Dublin, Ireland.
J Nutr. 2023 Apr;153(4):1075-1088. doi: 10.1016/j.tjnut.2023.01.028. Epub 2023 Jan 28.
Early-life nutritional exposures may contribute to offspring epigenetic modifications. However, few studies have evaluated parental dietary quality effects on offspring DNA methylation (DNAm).
We aim to fill this gap by elucidating the influence of maternal and paternal whole-diet quality and inflammatory potential on offspring DNAm in the Lifeways Cross-generation cohort.
Families (n = 1124) were recruited around 16 weeks of gestation in the Republic of Ireland between 2001 and 2003. Maternal dietary intake during the first trimester and paternal diet during the 12 previous months were assessed with an FFQ. Parental dietary inflammatory potential and quality were determined using the energy-adjusted Dietary Inflammatory Index (E-DII), the Healthy Eating Index-2015 (HEI-2015), and the maternal DASH score. DNAm in the saliva of 246 children at age nine was measured using the Illumina Infinium HumanMethylationEPIC array. DNAm-derived biomarkers of aging, the Pediatric-Buccal-Epigenetic clock and DNAm estimator of telomere length, were calculated. Parental diet associations with the DNAm concentrations of 850K Cytosine-phosphate-guanine sites (CpG sites) and with DNAm-derived biomarkers of aging were examined using an epigenome-wide association study and linear regressions, respectively.
Maternal HEI-2015 scores were inversely associated with DNAm at CpG site (cg21840035) located near the PLEKHM1 gene, whose functions involve regulation of bone development (β = -0.0036, per 1 point increase in the score; P = 5.6 × 10). Higher paternal HEI-2015 score was related to lower methylation at CpG site (cg22431767), located near cell signaling gene LUZP1 (β = -0.0022, per 1 point increase in the score, P = 4.1 × 10). There were no associations with parental E-DII and DASH scores, and no evidence of major effects on biomarkers of aging.
Parental dietary quality in the prenatal period, evaluated by the HEI-2015, may influence offspring DNAm during childhood. Further research to improve our understanding of parental nutritional programming is warranted.
早期生活中的营养暴露可能导致后代的表观遗传修饰。然而，很少有研究评估父母饮食质量对后代 DNA 甲基化（DNAm）的影响。
我们旨在通过阐明母体和父体全饮食质量和炎症潜能对 Lifeways 跨代队列中后代 DNAm 的影响来填补这一空白。
2001 年至 2003 年，在爱尔兰共和国招募了 1124 个家庭，在妊娠 16 周左右。在妊娠早期用 FFQ 评估母亲的饮食摄入量，在过去 12 个月内评估父亲的饮食摄入量。使用能量调整的饮食炎症指数（E-DII）、健康饮食指数-2015（HEI-2015）和母亲的 DASH 评分来确定父母饮食的炎症潜能和质量。使用 Illumina Infinium HumanMethylationEPIC 阵列测量 246 名 9 岁儿童的唾液中的 DNAm。计算 DNAm 衍生的衰老生物标志物，即儿科口腔表观遗传时钟和 DNAm 估计的端粒长度。使用全基因组关联研究和线性回归分别检查父母饮食与 850K 胞嘧啶磷酸鸟嘌呤位点（CpG 位点）的 DNAm 浓度和 DNAm 衍生的衰老生物标志物之间的关联。
母亲的 HEI-2015 评分与位于 PLEKHM1 基因附近的 CpG 位点（cg21840035）的 DNAm 呈负相关，该基因的功能涉及骨骼发育的调节（β=-0.0036，评分每增加 1 分；P=5.6×10）。较高的父亲 HEI-2015 评分与位于细胞信号基因 LUZP1 附近的 CpG 位点（cg22431767）的甲基化程度较低有关（β=-0.0022，评分每增加 1 分，P=4.1×10）。与父母的 E-DII 和 DASH 评分无关联，且对衰老生物标志物无明显影响。
孕期通过 HEI-2015 评估的父母饮食质量可能会影响儿童期后代的 DNAm。需要进一步研究以提高我们对父母营养编程的理解。
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