Khosla P, Sundram K
Foster Biomedical Research Laboratory, Brandeis University, Waltham, MA, USA.
Prog Lipid Res. 1996;35(2):93-132. doi: 10.1016/0163-7827(95)00014-3.
It should be clear from the preceding sections that the effects of dietary fatty acids on plasma lipids get more complicated the more we try to simplify them! We have presented one argument as to how different fatty acids may interact to impact human plasma lipids. This is by no means an endorsement that ours is the only argument. Nevertheless, a strong case can be made for 14:0 and 18:2 as being the key players in this scenario. The role of palmitic acid seems to be the most controversial. While clearly certain studies do indeed reveal 16:0 to be hypercholesterolemic relative to 18:1, the data from studies suggesting that it behaves similarly to 18:1 are equally compelling. What is certain is that it is erroneous to assume that 16:0 is the major cholesterol-raising SFA simply because it is the most abundant SFA in the diet. Clearly, 18:0 cannot be considered cholesterol-elevating. One is therefore left with the 12-16C SFA. However, 12:0 and 14:0 are only of concern if diets contain palm-kernel, coconut oil or dairy products as major dietary constituents. Accordingly one is left with 16:0 and its response is highly dependent on the metabolic status as well as the age of the subjects being used. While "elderly" hypercholesterolemic humans clearly benefit from decreased 16:0 (and all SFA) consumption, "younger" normocholesterolemic subjects fail to show such clear-cut effects. Additionally, the concomitant levels of dietary cholesterol and 18:2 also have a major bearing on the cholesterolemic response of 16:0 As far as guidelines for the general public are concerned, clearly for people with TC > 225 and LDL-C > 130 mg/dl and/or those who are overweight (i.e. those percieved to be at high risk), the primary emphasis should clearly be on reducing total fat consumption. Decreasing saturated fat consumption will invariably also lower dietary cholesterol consumption. The latter manouver will generally lower TC and LDL-C. Whether the reduction occurs because of the removal of 14:0, or 16:0 and/or dietary cholesterol is a mute point, since most dietary guidelines advocate curtailing intake of animal and dairy products, which will result in reductions of all the SFA. It remains to be established whether life-long adherence to the above dietary guidelines in those subjects with normal cholesterol levels and an absence of the other conventional risk factors for CHD, will result in a subsequent decrease in CHD risk. In the latest NCEP report 39 million Americans were targeted as those who would benefit from reductions in LDL-C, principally by dietary means. This is indeed a very high number. But that leaves almost 220 million Americans! For them the age old recommendation to consume a moderate fat load, maintain ideal body weight and eat a varied and balanced diet would still appear to be the most powerful advice.
从前面的章节应该可以清楚地看出，我们越是试图简化膳食脂肪酸对血浆脂质的影响，情况就变得越复杂！我们已经提出了一种关于不同脂肪酸如何相互作用以影响人体血浆脂质的观点。这绝不是认可我们的观点是唯一的观点。然而，有充分的理由认为14:0和18:2是这种情况下的关键因素。棕榈酸的作用似乎最具争议性。虽然某些研究确实清楚地表明16:0相对于18:1具有高胆固醇血症作用，但表明它与18:1表现相似的研究数据同样令人信服。可以确定的是，仅仅因为16:0是饮食中最丰富的饱和脂肪酸就认为它是主要的升高胆固醇的饱和脂肪酸，这种假设是错误的。显然，18:0不能被认为会升高胆固醇。因此就剩下12 - 16碳的饱和脂肪酸。然而，只有当饮食中以棕榈仁油、椰子油或乳制品作为主要成分时，12:0和14:0才值得关注。因此就剩下16:0，其反应高度依赖于所研究对象的代谢状态以及年龄。虽然“老年”高胆固醇血症患者显然受益于减少16:0（以及所有饱和脂肪酸）的摄入，但“年轻”的正常胆固醇水平受试者并未表现出如此明显的效果。此外，膳食胆固醇和18:2的伴随水平也对16:0的胆固醇血症反应有重大影响。就针对普通公众的指导方针而言，显然对于总胆固醇（TC）> 225且低密度脂蛋白胆固醇（LDL - C）> 130mg/dl的人以及/或者超重者（即那些被认为处于高风险的人），首要重点显然应该是减少总脂肪的摄入。减少饱和脂肪的摄入必然也会降低膳食胆固醇的摄入。后一种做法通常会降低总胆固醇和低密度脂蛋白胆固醇。这种降低是因为去除了14:0、16:0和/或膳食胆固醇，这是一个无关紧要的问题，因为大多数膳食指南都提倡减少动物和乳制品的摄入，这将导致所有饱和脂肪酸的减少。对于那些胆固醇水平正常且没有其他冠心病传统风险因素的受试者，终身坚持上述膳食指南是否会导致冠心病风险随后降低，仍有待确定。在最新的美国国家胆固醇教育计划（NCEP）报告中，3900万美国人被确定为将从降低低密度脂蛋白胆固醇中受益的人群，主要通过饮食方式。这确实是一个非常高的数字。但这仍留下了近2.2亿美国人！对于他们来说，长期以来建议摄入适量脂肪、保持理想体重并食用多样化和均衡饮食的建议似乎仍然是最有力的建议。
