Effects of dietary fatty acid composition on plasma cholesterol.

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.