McNamara D J
Egg Nutrition Center, 1050 17th St. NW, Suite 560, Washington, DC 20036, USA.
Biochim Biophys Acta. 2000 Dec 15;1529(1-3):310-20. doi: 10.1016/s1388-1981(00)00156-6.
The perceived relationship between dietary cholesterol, plasma cholesterol and atherosclerosis is based on three lines of evidence: animal feeding studies, epidemiological surveys, and clinical trials. Over the past quarter century studies investigating the relationship between dietary cholesterol and atherosclerosis have raised questions regarding the contribution of dietary cholesterol to heart disease risk and the validity of dietary cholesterol restrictions based on these lines of evidence. Animal feeding studies have shown that for most species large doses of cholesterol are necessary to induce hypercholesterolemia and atherosclerosis, while for other species even small cholesterol intakes induce hypercholesterolemia. The species-to-species variability in the plasma cholesterol response to dietary cholesterol, and the distinctly different plasma lipoprotein profiles of most animal models make extrapolation of the data from animal feeding studies to human health extremely complicated and difficult to interpret. Epidemiological surveys often report positive relationships between cholesterol intakes and cardiovascular disease based on simple regression analyses; however, when multiple regression analyses account for the colinearity of dietary cholesterol and saturated fat calories, there is a null relationship between dietary cholesterol and coronary heart disease morbidity and mortality. An additional complication of epidemiological survey data is that dietary patterns high in animal products are often low in grains, fruits and vegetables which can contribute to increased risk of atherosclerosis. Clinical feeding studies show that a 100 mg/day change in dietary cholesterol will on average change the plasma total cholesterol level by 2.2-2.5 mg/dl, with a 1.9 mg/dl change in low density lipoprotein (LDL) cholesterol and a 0.4 mg/dl change in high density lipoprotein (HDL) cholesterol. Data indicate that dietary cholesterol has little effect on the plasma LDL:HDL ratio. Analysis of the available epidemiological and clinical data indicates that for the general population, dietary cholesterol makes no significant contribution to atherosclerosis and risk of cardiovascular disease.
膳食胆固醇、血浆胆固醇与动脉粥样硬化之间的假定关系基于三条证据:动物喂养研究、流行病学调查和临床试验。在过去的四分之一世纪里,研究膳食胆固醇与动脉粥样硬化之间关系的研究对膳食胆固醇对心脏病风险的贡献以及基于这些证据进行膳食胆固醇限制的有效性提出了质疑。动物喂养研究表明,对于大多数物种而言,需要大剂量的胆固醇才能诱发高胆固醇血症和动脉粥样硬化,而对于其他物种,即使是少量的胆固醇摄入也会诱发高胆固醇血症。不同物种对膳食胆固醇的血浆胆固醇反应存在差异,而且大多数动物模型的血浆脂蛋白谱明显不同,这使得将动物喂养研究的数据外推至人类健康极其复杂且难以解释。流行病学调查通常基于简单回归分析报告胆固醇摄入量与心血管疾病之间的正相关关系;然而,当多元回归分析考虑到膳食胆固醇和饱和脂肪热量的共线性时,膳食胆固醇与冠心病发病率和死亡率之间不存在关联。流行病学调查数据的另一个复杂之处在于,富含动物产品的饮食模式通常谷物、水果和蔬菜含量较低,而这些食物会增加动脉粥样硬化的风险。临床喂养研究表明,膳食胆固醇每天变化100毫克,平均会使血浆总胆固醇水平变化2.2 - 2.5毫克/分升,低密度脂蛋白(LDL)胆固醇变化1.9毫克/分升,高密度脂蛋白(HDL)胆固醇变化0.4毫克/分升。数据表明,膳食胆固醇对血浆LDL:HDL比值影响很小。对现有流行病学和临床数据的分析表明,对于一般人群来说,膳食胆固醇对动脉粥样硬化和心血管疾病风险没有显著影响。