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研究生:黃麗卿
研究生(外文):Lee-Ching Hwang
論文名稱:台灣地區代謝症候群的盛行率及發生率與代謝症候群的進展:男女性別之差異
論文名稱(外文):Prevalence and Incidence of the Metabolic Syndrome and its Development in Taiwan: Focus on Gender Differences
指導教授:陳建仁陳建仁引用關係陳秀熙陳秀熙引用關係
指導教授(外文):Chien-Jen ChenTony Hsiu-Hsi Chen
學位類別:博士
校院名稱:國立臺灣大學
系所名稱:預防醫學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2006
畢業學年度:95
語文別:英文
論文頁數:153
中文關鍵詞:代謝症候群盛行率發生率性別差異Markov 模式
外文關鍵詞:metabolic syndromeprevalenceincidencegender differenceMarkov model.
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心血管疾病(包含冠狀動脈心臟病與腦血管疾病)及糖尿病是台灣地區十大死因中重要致死疾病,總括來說25.9%死亡是由此導致的,醫療費用佔中央健康保險局每年醫療支出的14.5%。代謝症候群患者聚集數種心血管疾病危險因子於一身,如血脂異常、血壓偏高、血糖偏高與腹部肥胖,增加了糖尿病與冠狀動脈心臟病的發生率,也增加心血管疾病的死亡率。目前,代謝症候群的盛行率研究在各個族群中相繼報導,但是在台灣尚未有全國性的資料呈現,此論文目的之ㄧ即以台灣具代表性的資料估計代謝症候群的盛行率,並以社區篩檢資料呈現代謝症候群的發生率,分析其危險因子,討論性別差異現象,以提供心血管疾病及糖尿病高危險群早期篩檢與處理計畫的參考。
女性的心血管疾病發生年齡約晚男性10年,而心血管疾病發生之前,其心血管疾病危險因子進行已久。女性在50 歲之前與男性比較,有較低的血壓、較低的三酸甘油酯,較高的高密度脂蛋白膽固醇與較少的腹部脂肪推積,但是年齡增加後這些保護現象即消失,有兩種理論解釋心血管疾病男女性別差異的原因,一是雌性素保護作用,再者是鐵質減少作用。既然各種心血管疾病危險因子存在男女性別差異,聚集數個危險因子的代謝症候群男女性別差異狀況也值得探討,此論文第二個目的即是探討代謝症候群演進的男女性別差異狀況。
台灣三高研究計畫族群中,代謝症候群盛行率不亞於其他亞洲國家,使用四種不同的代謝症候群定義,盛行率約為男性16.1至20.4%,女性13.3至15.3%。如果使用MetS-IDF(C)標準可能低估代謝症候群對CVD的危險性,使用MetS-AHA(C)標準納入最多個案,盛行率的估計較MetS-TW多出1.2%。基隆社區整合性篩檢研究計畫族群追蹤年數為3.8年,使用MetS-AHA(C)定義,在沒有心血管疾病的族群,代謝症候群發生率每一千人年男性93.8,女性81.7,有代謝症候群者其回轉率為每一千人年男性148.7,女性143.9。在盛行率與發生率的年齡層曲線圖可見男性在50歲以前高於女性,是因為男性有較高的三酸甘油酯與血壓,而50歲以後則呈現女性高於男性的現象,是女性腰圍增加快速的緣故。有關代謝症候群的進展方面,三高計劃的資料分析顯示,在代謝症候群五項組成中,男女性別在組成項目進展順序上相似,血脂異常是最早出現的,其次是腹部肥胖,血壓偏高與血糖偏高皆出現較晚。女性出現第一個組成的年齡較男性年輕,但是進展至代謝症候群較男性晚,男女在代謝症候群進展上相差5年;如果體重沒有過重而且有運動習慣者,代謝症候群的進展較慢,尤其是男性延緩進展的年數較女性明顯。分析基隆社區整合性篩檢研究計畫資料,以Markov模式預測35歲與56.5歲經過十年的累積發生率,35歲男性經過十年有42.1%發生代謝症候群,女性則有36.7%,56.5歲男性經過十年有45.9%發生代謝症候群,女性則有55.1%;如果將大腰圍的人皆減少一英吋的腰圍而重新計算轉移機率,且重新建立Markov模式,十年的累積發生率可以減少11%。有關代謝症候群的危險因子,包含年齡增加、BMI數值增加與無運動習慣是男女性共同的因子,男性抽菸習慣與女性有糖尿病家族史也是危險因子;在男性體重正常組代謝症候群發生率為每一千人年38.4,體重過重組為72.1而肥胖組為161.3,女性也有相似的趨勢,Cox 模式控制相關變項後,體重過重的相對危險性為1.9-2.3倍,肥胖的相對危險性為4.3-4.7倍,且在追蹤期中,每年體重增加1公斤可以增加發生代謝症候群危險約50%;若是體重減輕可以增加代謝症候群者回轉的機會。
結論是腰圍過大的標準並非最早出現的項目,不能等待腰圍過大之後才開始進行代謝症候群診斷與治療,男性在中年以前應特別注意三酸甘油酯過高與血壓過高的問題,而女性應注意高密度脂蛋白過低的威脅,且在停經前後應格外重視腰圍的增加。推行健康積極的生活型態,例如健康飲食、活動量的增加、戒菸活動,改善體重過重或減少增加體重等預防與治療代謝症候群。
Cardiovascular diseases (CVD), including coronary heart disease and cerebral vascular disease, and diabetes mellitus (DM) are the principal causes of death in Taiwan, currently contributing 25.9% of national mortality and 14.5% of medical expenditure in the 2004 National Health Insurance budget. The metabolic syndrome (MetS) is a clustering of cardiovascular disease risk factors including dyslipidemia, hypertension, hyperglycemia and abdominal obesity. Individuals with the MetS have increased incidence of DM and coronary heart disease, and mortality from CVD. The prevalence of the MS has been observed in many ethnic groups but not yet by a nationwide survey in Taiwan. This thesis attempts to describe the prevalence and incidence of the MetS in Taiwanese adults, and this should provide valuable data for early identification and appropriate management of high risk people of CVD and DM.
Onset of CVD such as coronary heart disease begins approximately 10 years later in women than men. Cardiovascular gender differences are apparent long before CVD appears in men and women. Until the age of 50 years, women have lower systolic and diastolic BPs, lower TG, higher HDL and less visceral fat than men, but this protection disappears rapidly with increasing age. Two hypotheses, the estrogen protective effects and iron depletion effects, were raised to explain the phenomenon of gender differences. Therefore, this thesis also attempts to describe the development of the MetS, focusing on gender differences.
There were a high prevalence of the MetS and its components in TwSHHH study population (aged 20-79.9 years). The four MetS criteria sets were met by the following percentages of subjects: modified ATP III definition by 18.3% of men and 13.6% of women; MetS-IDF(C) by 16.1% of men and 13.3% of women, MetS-TW by 19.5% of men and 13.8% of women, and MetS-AHA(C) by 20.4% of men and 15.3% of women. Using the MetS-IDF(C) criteria in Taiwan might lead to underestimation of the risk of CVD. In KCIS study population those who did not have CVD, age-adjusted incidence rates of the MetS were 93.8 and 81.7 per 1000 person-years in men and in women, respectively. The resolution rates of the MetS were 148.7 and 143.9 per 1000 person-years in men and in women, respectively, during 3.8-year follow up, according to the MetS-AHA(C) definition. Men had significantly higher prevalence and incidence before the age group of 50 years because men had more high TG and high BP components than women did. The prevalence and incidence of the MetS in women increased rapidly beyond the age group of 50 years and became higher than in men, due to increasing WC. Data from TwSHHH study revealed that lipid components of the MetS appeared the earliest. Women had the first isolated component earlier, but the full feature of the MetS showed up later than men. We found that a BMI <23kg/m2 and exercise behavior could delay the development of the MetS in both genders, but more significantly in men than in women.
The Markov model was established for the prediction of the MetS development The model initiated with no component state would expect to have the MetS in 42.1% men and in 34.7% women after passing 10 cycles in young age group; contrarily, in 45.9% men and in 55.1% women in old age group. The model initiated with no component state and reducing WC for 1 inch in large WC group retarded the development of the MetS about 11%.
Older age, higher baseline BMI and physical inactivity were associated with increased hazard ratios of the MetS in both genders However, current smoking habit for men and family histories of diabetes for women, respectively, were significant different risk factors. Increased weight gain had a significant positive association with the risk of developing the MetS Increased weight loss had a significant positive association with the resolution of the MetS.
In conclusion, we could not wait the individuals attain their large WC to take action, because large WC was always not the first component. We need to attach importance to high TG (≥150 mg/dL) and high BP (≥130/85 mmHg) in men and low HDL (<50 mg/dL) in women before their middle age. Women of perimenopasual or postmenopausal age should pay much attention to their WC increasing problems. Detecting these individuals with the MetS and implementing preventive lifestyle interventions—diet education, physical activity, weight control, smoking cessation, and related behavior modification—is a high priority of preventive medicine of controlling for chronic metabolic diseases.
ABBREVIATIONS 4
LEGENDS OF TABLES AND FIGURES 5
中文摘要 7
ABSTRACT 10
CHAPTER 1 INTRODUCTION 14
CHAPTER 2 LITERATURE REVIEW 17
2.1 GENDER DIFFERENCES IN DEFINITIONS OF THE METS 17
2.2 GENDER DIFFERENCES IN DYSLIPIDEMIA 20
2.3 GENDER DIFFERENCES IN HIGH BLOOD PRESSURE 21
2.4 GENDER DIFFERENCES IN FAT CELL EXCESS 23
2.5 GENDER DIFFERENCES IN INSULIN RESISTANCE 24
2.6 PATHOPHYSIOLOGY OF THE METS: FOCUS ON GENDER DIFFERENCES 26
2.6.1 Insulin resistance 27
2.6.2 Excess fat cells 28
2.6.3 Genes and fetal malnutrition 29
2.6.4 The estrogen hypothesis 30
2.6.5 The iron hypothesis 31
2.7 PREVALENCE OF THE METS 33
2.7.1 Prevalence in worldwide populations 33
2.7.2 Gender difference in prevalence of the MetS 35
2.8 ARGUMENT ABOUT THE METS 36
CHAPTER 3 UNANSWERED QUESTIONS, HYPOTHESIS AND AIMS 43
3.1 UNANSWERED QUESTIONS 43
3.2 HYPOTHESIS AND AIMS 44
3.2.1 RESEARCH QUESTIONS 44
3.2.2 AIMS OF THESIS 45
CHAPTER 4 SUBJECTS AND METHODS 48
4.1 THE TAIWANESE SURVEY ON THE PREVALENCE OF HYPERGLYCEMIA, HYPERLIPIDEMIA, AND HYPERTENSION (TWSHHH) 48
4.2 THE KEELUNG COMMUNITY-BASED INTEGRATED SCREENING PROGRAM (KCIS) 53
CHAPTER 5 RESULTS AND DISCUSSIONS 58
5.1 PREVALENCE OF THE METS IN TAIWAN 58
5.2 INCIDENCE OF THE METS IN TAIWAN 74
5.3 GENDER DIFFERENCE ON THE DEVELOPMENT OF THE METS 84
5.4 DESCRIPTION AND PREDICTION OF THE DEVELOPMENT OF THE METS: A LONGITUDINAL ANALYSIS USING A MARKOV MODEL APPROACH 97
5.5 INFLUENCE OF CHANGES IN BODY WEIGHT ON THE INCIDENCE AND RESOLUTION OF THE METS 117
CHAPTER 6 CONCLUSIONS AND IMPLICATIONS 132
6.1 CONCLUSIONS 132
6.2 CLINICAL IMPLICATIONS 133
6.3 FUTURE RESEARCH DIRECTIONS 134
CHAPTER 7 REFERENCES 135
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