飲食營養成分組成與肝硬化、肝癌有關


  July 10, 2009 — 一項發表於7月號肝臟學期刊的大型世代研究結果顯示,飲食組成可能影響進展為肝硬化與肝癌。
  
  來自西雅圖華盛頓大學與退休事務Puget Sound健康照護系統、醫學部門與研究優化獎助計劃的George N. loannou醫師與其同事們寫到,飲食成分因素是造成肥胖、胰島素抗性與糖尿病重要且可能的原因。飲食中脂肪的量與組成會促進或是保護發生或是進展成脂肪肝。
  
  作者們寫到,如果飲食成分影響脂肪肝的形成或是進展,這可能在美國三個最重要的肝臟疾病自然史上扮演部分角色:分別是非酒精性脂肪肝疾病、C型肝炎(HCV)、與酒精性肝疾病。
  
  過去的研究已經證實,高脂肪飲食會誘發兔與鼠類動物發生嚴重的肝臟脂肪變性、發炎與肝臟小葉中心纖維化,然而,低動物蛋白的飲食,對B型肝炎病毒轉殖老鼠與降低肝臟損傷及肝細胞惡性腫瘤發生率下降有關。
  
  在這項研究中,研究者們想要確認飲食攝取是否與美國群眾之後發生肝硬化相關或是肝癌相關死亡、或是住院有關。
  
  他們檢視第一國家健康與營養檢驗普查(HNANES I)的數據,這是一項收納14,407位受試者,在1971年到1975年間由國家癌症中心為了健康統計所進行的斷面研究。該項研究使用一種24小時飲食回憶問卷,接著以營養組成數據資料庫的資料來計算蛋白質、碳水化合物、與脂肪克數,以這些資料來確定試驗前的飲食攝取。NHANES I流行病學追蹤研究接著收集在介入期間特定健康狀況的資料,透過個人面談、住院記錄、以及健康證明收集資料。
  
  為了這項研究,loannou醫師與其團隊評估了9,221位來自NHANES I流行病學後續追蹤研究的成人(年齡25-74歲,其中82.9%是白人),這些受試者在加入原本那項研究時並沒有肝硬化的證據。
  
  這項研究潛在的影響因子,包括蛋白質、碳水化合物、脂肪、茶、咖啡或酒精的每日攝取量;性別;種族;年齡;教育學識;居住地理區域;糖尿病;身體質量指數;以及肩胛骨下與三頭肌皮膚皺摺比值。除此之外,當收納NHANES I受試者時,還沒有B型肝炎病毒與HCV RNA檢測,研究者們利用來自NHANES III研究,一項自1988年到1994年之間進行的斷面型研究,該項研究包括病毒肝炎血清學檢驗。
  
  在平均追蹤13.3年之間,研究團隊發現9,221位受試者中有118位有肝硬化的新診斷,而5位有肝癌的新診斷。
  
  在校正潛在的影響因子後,研究團隊發現飲食中高蛋白的病患,因為肝硬化、肝癌住院或是死亡的風險較高(P=0.0001),然而,那些報告飲食中富含碳水化合物的受試者們風險顯著較低(P=0.003)。
  
  除此之外,攝取膽固醇與肝硬化或肝癌風險較高有關(P=0.007),而攝取的熱量總量、脂肪總量、以及血中膽固醇濃度則與其無關。作者們寫到,因為膽固醇濃度從未被證實與人類肝臟疾病有關,這可能是我們這項研究最重要的發現。
  
  以NHANES III的數據,研究團隊發現HCV感染並未與任何飲食成分有關。他們寫到,缺乏這樣的關係代表原本的肝臟疾病並不會改變飲食攝取型態,反之可能使飲食中蛋白質、碳水化合物、膽固醇、以及或許其他脂肪組成之間與形成肝硬化或是肝癌是有差異是合理的。
  
  試驗限制包括使用24小時飲食回憶記錄,這可能無法真實反應長期飲食攝取型態,以及缺乏HCV感染數據,這是美國造成肝硬化與肝癌的主要原因之一。然而,作者們解釋,因為NHANES III研究的數據,HCV感染不太可能是一個未經控制影響因子的重要來源。
  
  他們的結論是,我們的研究引起了飲食因素可能是重要、可控制、且目前為止造成肝臟疾病進展一個未確認的可能性。
  
  這項研究由美國肝臟基金會與美國肝臟疾病研究協會Jan Albrecht獎項贊助。作者們表示沒有相關資金上的往來。
  

Dietary Nutrient Composition Associated With Cirrhosis, Liver Cancer

By Deborah Brauser
Medscape Medical News

July 10, 2009 — Dietary composition may affect the progression of cirrhosis and liver cancer, according to results of a large cohort study reported in the July issue of Hepatology.

"Dietary factors are important and probably causative risk factors for obesity, insulin resistance, and diabetes, which are the most important, known risk factors for hepatic steatosis," write George N. Ioannou, MD, MS, from the Division of Gastroenterology, Department of Medicine and Research Enhancement Award Program, Veterans Affairs Puget Sound Health Care System and University of Washington in Seattle, and colleagues. In addition, "It is possible that the quantity and composition of dietary lipid can either promote or protect against the development or progression of hepatic steatosis."

The authors write that if dietary composition affects the development or progression of hepatic steatosis, it is likely to play a part in the natural history of the 3 most important liver conditions in the United States: nonalcoholic fatty liver disease, hepatitis C virus (HCV) infection, and alcoholic liver disease.

Previous research has shown that a high-cholesterol diet in rabbits and mice induced profound steatosis, inflammation, and cetrilobular fibrosis, whereas a diet low in animal protein for hepatitis B virus transgenic mice was associated with decreased liver injury and decreased incidence of hepatocellular carcinoma.

In this study, the investigators sought to determine whether dietary intake was associated with the subsequent development of cirrhosis-related or liver cancer–related death or hospitalization in the US population.

They examined data from the first National Health and Nutrition Examination Survey (NHANES I), a cross-sectional study of 14,407 participants conducted between 1971 and 1975 by the National Center for Health Statistics. It ascertained dietary intake at baseline using a 24-hour dietary recall questionnaire and then used a Nutrient Composition Data Bank to calculate grams of protein, carbohydrate, and fat consumed. The NHANES I Epidemiologic Follow-up Study then collected data on specific health conditions that developed in the intervening years, through personal interviews, hospitalization records, and death certificates.

For this study, Dr. Ioannou and his team evaluated a cohort of 9221 adults (aged 25 – 74 years, 82.9% white) from the NHANES I Epidemiologic Follow-up Study who were without evidence of cirrhosis at entry into the original study.

Potential confounders identified included daily consumption of protein, carbohydrate, fat, tea or coffee, and alcohol; sex; race; age; educational attainment; geographical region; diabetes; body mass index; and subscapular-to-triceps skin fold ratio. In addition, as hepatitis B and HCV RNA testing was not available when the NHANES I participants were recruited, the investigators used data from NHANES III, a cross-sectional study from 1988 to 1994 that included measurements of viral hepatitis serologies.

During an average follow-up of 13.3 years, the investigative team found that 118 of the 9221 participants had a new diagnosis of cirrhosis and 5 had a new diagnosis of liver cancer.

After adjusting for the potential confounders, the investigators found that patients who reported a diet high in protein were at higher risk for hospitalization or death because of cirrhosis or liver cancer (P = .0001), whereas those reporting a diet high in carbohydrates were at a significantly lower risk (P = .003).

In addition, cholesterol consumption was associated with a higher risk for cirrhosis or liver cancer (P = .007), whereas total number of calories, total quantity of fat consumed, and serum cholesterol level were not. The authors write that because cholesterol has never before been linked to human liver disease, this strong association "is potentially our study's most important finding."

Using the NHANES III data, the investigators found no association between any dietary composition and HCV infection. They write that this lack of association "strongly suggests that the presence of underlying liver disease does not cause a change in dietary intake and instead makes it more plausible that differences in dietary intake of proteins, carbohydrates, cholesterol, and perhaps other lipid components contribute to the development of cirrhosis or liver cancer."

Study limitations include the 24-hour dietary recall, which may not accurately reflect long-term dietary intake, and the absence of data on HCV infection, a major cause of cirrhosis and liver cancer in the United States. However, the authors explain that because of the NHANES III study data, "HCV infection is unlikely to be an important source of uncontrolled confounding."

They conclude, "Our study raises the possibility that dietary factors may be important, modifiable, and hitherto unrecognized determinants of liver disease progression."

This study was supported by the American Liver Foundation and American Association for the Study of Liver Diseases Jan Albrecht Award. The authors have disclosed no relevant financial relationships.

Hepatology. 2009;50:175–184.

    
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