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  1. NTU Theses and Dissertations Repository
  2. 公共衛生學院
  3. 流行病學與預防醫學研究所
請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/89642
完整後設資料紀錄
DC 欄位值語言
dc.contributor.advisor簡國龍zh_TW
dc.contributor.advisorKuo-Liong Chienen
dc.contributor.author范掀裕zh_TW
dc.contributor.authorHsien-Yu Fanen
dc.date.accessioned2023-09-13T16:12:25Z-
dc.date.available2023-11-10-
dc.date.copyright2023-09-13-
dc.date.issued2023-
dc.date.submitted2023-05-30-
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dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/89642-
dc.description.abstract背景:近年來,孩童早發育問題日漸突出,已成為小兒科常見的內分泌疾病之一。成長發育時間不只與內分泌系統有關,也可能與心血管代謝疾病風險相關。過去研究證實早發育年齡會增加成人心血管疾病的風險,但還沒有一致的結論,至今還有許多機轉尚未完全了解,像是孩童高血壓、成年時期的代謝中介因子、共同基因位點及蛋白質交互作用的關聯性。因此,本研究旨在(1)確認性早熟與孩童高血壓的關聯性;(2)探討早發育年齡與成年心血管疾病之間可能的代謝中介途徑;(3)探索發育年齡與心血管代謝特徵的共同基因及其分子機轉路徑。
材料與方法:本研究納入臺灣發育長期追蹤研究765位的6-14歲女性,以羅吉斯迴歸分析(Logistic regression)確認性早熟與孩童高血壓(依據年齡與身高定義收縮壓或舒張壓大於95百分位數)的關聯性。透過金山社區心血管疾病世代研究1,589位女性,探討早發育年齡與成年心血管疾病的中介代謝途徑,其中包括身體質量指數、血壓、血脂及血糖。另外,透過臺灣人體生物資料庫71,923位女性的資料,應用觀察性研究及孟德爾隨機定律驗證因果中介效果。由於初經年齡與心血管代謝特徵具有一定的遺傳性,為了避免遺漏遺傳力(missing heritability),我們使用臺灣人體生物資料庫的全基因組關聯分析,篩選出兩個特徵共同常見變異的位點,串聯甲基化數量性狀基因座及表現數量性狀基因座,找出重要的機轉路徑。
結果:孩童研究中,性早熟會增加孩童高血壓的風險(勝算比:2.08,95% 信賴區間:1.14-3.78)。金山社區心血管疾病世代研究中,早初經年齡每提前1個標準差(1.8歲),其成人時期冠狀動脈疾病的風險比為1.75(95%信賴區間:1.12-2.19)。臺灣人體生物資料觀察性研究中,初經年齡每提前1個標準差(1.4歲),其成人時期冠狀動脈疾病的勝算比為1.18(95%信賴區間:1.02-1.21),經過孟德爾隨機化的勝算比為1.02(95% 信賴區間:1.001-1.03)。收縮壓可能是重要的中介因子,其孟德爾隨機化的中介效果比例為29%(95% 信賴區間:26%-32%)。此外,我們透過基因多效性分析,從聯集與交集錯誤發現率(false discovery rate,FDR)的方式,找到27個位點同時與初經年齡和心血管代謝特徵有關,其兩種方法的FDR皆小於0.05。這些位點主要坐落於5個基因序列之內或附近,例如:SEC16B、CSK、CYP1A1、FTO及USB1,這些基因除了影響基因甲基化及表現程度,且彼此之間可能有蛋白質的交互作用。
結論與建議:本研究發現性早熟可能與孩童高血壓有關,而成人研究發現收縮壓是早發育年齡與冠狀動脈疾病的重要中介因子。另外,我們也發現發育年齡與心血管代謝特徵存在著一些共同的基因位點,特別是初經年齡與舒張壓之間有明顯的共同基因網路。建議未來研究除了需要釐清早發育年齡與冠狀動脈疾病是否還有其他分子途徑,也需要透過細胞或動物實驗加以確認這些共同基因位點,以利於性早熟與早期心血管代謝疾病的篩檢與預防。
zh_TW
dc.description.abstractBackground: The prevalence of early puberty has increased in recent decades and has been reported to be associated with endocrine disorders and cardiometabolic diseases. Early puberty leads to the increased risk of cardiovascular diseases in adulthood, but mechanisms in childhood remained unclear. In addition, the risk is suggested to be mediated through intermediate variables and may be caused by early puberty indirectly. Genome-wide association studies have the potential to explain more of the missing heritability of the two complex traits.
Objective: We aim (1) to investigate the association between early puberty and early hypertension; (2) to explore the causal mediation pathways between early menarche and adult cardiovascular diseases using the network Mendelian randomization study; (3) to investigate the shared genetic basis for age at menarche and cardiometabolic traits.
Methods: From the Taiwan Puberty Longitudinal Study (N=765) in the project 1, we investigated the association between early puberty and childhood cardiovascular risk factors. From Chin-Shan community cardiovascular cohort (N=1,589) in the project 2, we first investigated the risk of incident cardiovascular diseases among those with early menarche. We also investigated whether this association is mediated by body mass index, blood pressure, blood lipid, and fasting plasma glucose. The mediation pathways were validated using a network Mendelian randomization study using the Taiwan biobank dataset (N=71,923). In the project 3, we used a genetic pleiotropy-informed false discovery rate method to identify new loci associated with age at menarche and cardiometabolic traits, two highly heritable disorders with significant missing heritability. We further investigated the biological association between the top loci through changes in methylation and expression levels.
Results: Children with early puberty significantly suffered from early hypertension (odds ratio: 2.08; 95% confidence interval: 1.14 to 3.78). Earlier age at menarche was associated with a higher risk of coronary artery disease (hazard ratio: 1.57; 95% CI: 1.12 to 2.19) Chin-Shan community cardiovascular cohort study, a 11% higher risk (odds ratio: 1.11; 95% CI: 1.02 to 1.21) in the Taiwan Biobank study, and a 2% higher risk (odds ratio: 1.02; 95% CI: 1.001 to 1.03) in the Mendelian randomization study. All analysis methods consistently supported the role of systolic blood pressure in mediating this effect. The results indicated that 29% (95% CI: 26% to 32%) of the effect of genetically predicted earlier age at menarche on the risk of coronary artery disease was mediated by genetically predicted systolic blood pressure. In addition, we found 27 novel loci at a false discovery rate of less than 0.05 with overlap between menarcheal timing and cardiometabolic traits, including body fat, blood pressure, cerebrovascular accident, and coronary artery disease. Among the novel genes discovered, SEC16B, CSK, CYP1A1, FTO, and USB1 are within a protein interaction network with known cardiometabolic genes, including traits for obesity and hypertension. The identified novel loci were further proved by significant changes in methylation or expression levels of neighboring genes.
Conclusions: We suggested that early puberty was associated with the increased risk of earlt onset hypertension among girls. Adult research studies highlighted systolic blood pressure as the critical mediator in the association of early menarche with the riks of coronary artery diseases. We also highlighted the shared etiology between age at menarche and diastolic blood pressure. Further studies focusing on the molecular pathways of these blood pressure-shared genes are warranted.
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dc.description.tableofcontents致謝 i
中文摘要 ii
English abstract iv
Abbreviations vi
第一章 研究背景與動機 1
1.1 發育年齡的趨勢 2
1.2 過早發育年齡的病理機轉 5
1.3 發育年齡與心血管疾病之觀察性研究的文獻回顧 7
1.4 初經年齡與心血管疾病相關的代謝中介因子 10
1.5 初經年齡與心血管疾病的孟德爾隨機化分析 11
1.6 初經年齡與心血管疾病的孟德爾隨機化中介因子分析 13
1.7 初經年齡與心血管代謝疾病的基因多效性 15
1.8 研究缺口及重要性 17
第二章 研究目的與假設 18
2.1 研究目的 18
2.2 研究假設 18
第三章 研究方法 20
3.1 研究資料與對象 20
3.2 納入及排除條件 22
3.3 暴露與結果之定義 23
3.4 干擾因子 26
3.5 基因型資料 26
3.6 基因甲基化及表現程度 28
3.7 描述性統計 30
3.8 分析性統計 31
3.9 統計檢定力與樣本大小 38
3.10 統計軟體 39
第四章 結果 41
4.1 基本特徵 41
4.2 發育年齡與孩童時期心血管代謝風險的關聯性 43
4.3 初經年齡與心血管疾病的中介因果關係 44
4.4 德爾隨機化的敏感度分析 48
4.5 初經年齡與心血管疾病的基因多效性 50
4.6 初經年齡與心血管疾病的分子機轉 51
第五章 討論 55
5.1 主要結果 55
5.2 孩童性早熟與早期高血壓 55
5.3 初經年齡與冠狀動脈疾病之中介機轉 57
5.4 初經年齡與心血管代謝特徵的共享基因 58
5.5 臨床應用 61
5.6 研究優勢與限制 62
5.7 結論與建議 65
參考文獻 66
TABLES 78
Table 1.1. Summary results for three pooled analyses of associations between age at menarche and cardiovascular diseases and mortality 78
Table 1.2. The review on mediators between age at menarche and cardiovascular diseases risk factors 79
Table 1.3. Summary results for the three Mendelian randomization analyses of associations between age at menarche and metabolic cardiovascular diseases 81
Table 2.1. Statistical packages used in the mediation analysis 82
Table 3.1. Genetic instruments for age at menarche and metabolic factors 83
Table 3.2. Two-sample Mendelian randomization study performed using summary statistics from large genome-wide association studies 84
Table 4.1. General characteristics of participants in the Taiwan Puberty Longitudinal Study 85
Table 4.2. General characteristics of participants in Chin-Shan Community Cardiovascular Cohort and Taiwan Biobank 86
Table 4.3. General characteristics of participants in the Taiwan Biobank 87
Table 4.3. Effects of central precocious puberty on early onset hypertension and high blood pressure in female children 88
Table 4.4. Effects of one standard deviation earlier age at menarche on the risk of cardiovascular diseases 89
Table 4.5. Effects of one standard deviation earlier age at menarche on metabolic mediators 90
Table 4.6. Effects of one standard deviation mediator on the risk of coronary artery diseases 91
Table 4.7. Mendelian randomization sensitivity analyses and external validation 92
Table 4.8. Summary results of single nucleotide polymorphisms on exposures and outcomes 94
Table 4.9. Summary results of single nucleotide polymorphisms on confounding factors 97
Table 4.10. P-values for interaction between the mediators and age at menarche or genetic risk scores of age at menarche on predicting risk of coronary artery diseases 100
Table 4.11. P-values for interaction between mediators and mediators on predicting risk of coronary artery diseases in Taiwan Biobank 101
Table 4.12. The test for the proportional hazard’s assumption for each covariate 103
Table 4.13. Overall pleiotropic loci in menarcheal timing (Trait 1) and cardiometabolic traits (Trait 2) with conjunction false discovery rates (FDRs) less than 0.05 104
Table 4.14. Twenty-seven independent pleiotropic loci in age at menarche (Trait 1) and cardiometabolic traits (Trait 2) with conjunctional false discovery rates (FDRs) <0.05 107
Table 4.15. Overview of expression quantitative trait loci (eQTL) and methylation effects related to cardiometabolic traits 108
FIGURES 109
Figure 2.1. Study scheme 109
Figure 3.1. Flowchart of participants in the Taiwan Puberty Longitudinal Study included in the project 1 110
Figure 3.2. Flowchart of participants in Chin-Shan Community Cardiovascular Cohort and Taiwan Biobank surveys included in the project 2 111
Figure 3.3. Flowchart of participants in Taiwan Biobank surveys included in the project 3 112
Figure 3.4. Quality control procedures for genome-wide association studies 113
Figure 3.5. Test Mediation using Baron and Kenny's Approach 114
Figure 3.6. Directed acyclic graph (DAG) illustrating direct and indirect effects of variable X on Y with mediator M. 115
Figure 3.7. Counterfactual graphical models for mediation analysis. 116
Figure 3.8. Flowchart of the pleiotropy study (subproject 3) procedure 117
Figure 4.1. Proportion of the mediated effects of earlier age at menarche on the risk of coronary artery disease 118
Figure 4.2. Pleiotropic enrichment of cardiometabolic traits conditioned on association with p values of age at menarche. 119
Figure 4.3. Conjunctional false discovery rate Manhattan plot of −log10 values for the associated cardiometabolic traits. 120
Figure 4.4. Functional gene network for novel pleiotropic loci from the present analysis and previously confirmed cardiometabolic traits 121
Figure 4.5. Shared biological pathways between significant genetic loci 122
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dc.language.isozh_TW-
dc.title早發育年齡與心血管疾病風險之因果中介及全基因體多效性分析zh_TW
dc.titleEarly Pubertal Timing and the Risk of Cardiovascular Diseases: Causal Mediation and Genome-wide Pleiotropy Analysesen
dc.typeThesis-
dc.date.schoolyear111-2-
dc.description.degree博士-
dc.contributor.oralexamcommittee陳揚卿;黃彥棕;杜裕康;盧子彬;張慶國;曾翎威zh_TW
dc.contributor.oralexamcommitteeYang-Ching Chen;Yen-Tsung Huang;Yu-Kang Tu;Tzu-Pin Lu;Chin-Kuo Chang;Ling-Wei Chenen
dc.subject.keyword早發育年齡,心血管疾病,中介因子,基因多效性,分子機轉,zh_TW
dc.subject.keywordearly puberty,cardiovascular diseases,mediators,genetic pleiotropy,en
dc.relation.page122-
dc.identifier.doi10.6342/NTU202300833-
dc.rights.note未授權-
dc.date.accepted2023-05-31-
dc.contributor.author-college公共衛生學院-
dc.contributor.author-dept流行病學與預防醫學研究所-
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