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作者：Deborah Brauser
出处：WebMD医学新闻
July 10, 2009 — 一项发表于7月号肝脏学杂志的大型研究结果显示，饮食组成可能影响疾病进展为肝硬化与肝癌。
来自西雅图华盛顿大学与退休事务Puget Sound健康照护系统、医学部门与研究优化奖助计划的George N. loannou医师与其同事们写到，饮食成分因素是造成肥胖、胰岛素抗性与糖尿病重要且可能的原因。饮食中脂肪的量与组成会促进或是保护发生或是进展成脂肪肝。
作者们写到，如果饮食成分影响脂肪肝的形成或是进展，这可能在美国三个最重要的肝脏疾病自然史上扮演部分角色：分别是非酒精性脂肪肝疾病、丙型肝炎（HCV）、与酒精性肝疾病。
过去的研究已经证实，高脂肪饮食会诱发兔与鼠类动物发生严重的肝脏脂肪变性、炎症与肝脏小叶中心纤维化，然而，低动物蛋白的饮食，对乙型肝炎病毒克隆老鼠与降低肝脏损伤及肝细胞恶性肿瘤发生率下降有关。
在这项研究中，研究者们想要确认饮食摄取是否与美国人群发生肝硬化相关或是肝癌相关死亡、或是住院有关。
他们检查了第一国家健康与营养检验普查（HNANES I）的数据，这是一项收纳14,407位受试者，在1971年到1975年间由国家癌症中心为了健康统计所进行的横断面研究。该项研究使用一种24小时饮食回忆问卷，接着以营养组成数据数据库的资料来计算蛋白质、碳水化合物、与脂肪克数，以这些资料来确定试验前的饮食摄取。NHANES I流行病学追踪研究接着收集在介入期间特定健康状况的资料，透过个人面谈、住院记录、以及健康证明收集资料。
为了这项研究，loannou医师与其团队评估了9,221位来自NHANES I流行病学后续追踪研究的成人（年龄25-74岁，其中82.9%是白人），这些受试者在加入原本那项研究时并没有肝硬化的证据。
这项研究潜在的影响因子，包括蛋白质、碳水化合物、脂肪、茶、咖啡或酒精的每日摄取量；性别；种族；年龄；教育学识；居住地理区域；糖尿病；身体质量指数；以及肩胛骨下与三头肌皮肤皱折比值。除此之外，当收纳NHANES I受试者时，还没有乙型肝炎病毒与HCV RNA检测，研究者们利用来自NHANES III研究，一项自1988年到1994年之间进行的断面型研究，该项研究包括病毒肝炎血清学检验。
在平均追踪13.3年之间，研究团队发现9,221位受试者中有118位有肝硬化的新诊断，而5位有肝癌的新诊断。
在校正潜在的影响因子后，研究团队发现饮食中高蛋白的病患，因为肝硬化、肝癌住院或是死亡的风险较高（P=0.0001），然而，那些报告饮食中富含碳水化合物的受试者们风险显著较低（P=0.003）。
除此之外，摄取胆固醇与肝硬化或肝癌风险较高有关（P=0.007），而摄取的热量总量、脂肪总量、以及血中胆固醇浓度则与其无关。作者们写到，因为胆固醇浓度从未被证实与人类肝脏疾病有关，这可能是我们这项研究最重要的发现。
以NHANES III的数据，研究团队发现HCV感染并未与任何饮食成分有关。他们写到，缺乏这样的关系代表原本的肝脏疾病并不会改变饮食摄取型态，反之可能使饮食中蛋白质、碳水化合物、胆固醇、以及或许其他脂肪组成之间与形成肝硬化或是肝癌是有差异是合理的。
试验限制包括使用24小时饮食回忆记录，这可能无法真实反应长期饮食摄取型态，以及缺乏HCV感染数据，这是美国造成肝硬化与肝癌的主要原因之一。然而，作者们解释，因为NHANES III研究的数据，HCV感染不太可能是一个未经控制影响因子的重要来源。
他们的结论是，本研究引出了饮食因素可能是重要、可控制、且目前为止造成肝脏疾病进展一个未确认的可能性。
这项研究由美国肝脏基金会与美国肝脏疾病研究协会Jan Albrecht奖项赞助。作者们表示没有相关资金上的往来。
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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发表于 2009-7-21 11:25:43
