Saturated fatty acids clinical studies

This finding has been replicated several times in clinical studies. Let me cite one example. In a careful metabolic study carried out in 1990, Mensink and Katan determined the plasma LDL/HDL ratio when 10% of the energy from oleic acid was replaced in the diet by either the corresponding trans fat or the corresponding saturated fatty acid, stearic acid. The resulting LDL/HDL ratios were 2.02 on the oleic acid diet, 2.34 on the stearic acid diet, and 2.58 on the trans fatty acid diet. This is one more example of the impact of small structural changes in molecules on their biological properties. 

As indicated above, there are many possible oxidation products of the different polyenoic acids. It is probably naive to ascribe the effects of dietary intervention reported thus far to such metabolites. Carefully controlled clinical studies will be needed before these questions can be satisfactorily answered. However, subjects on diets containing highly saturated fatty acids clearly show increased platelet aggregation when compared with other study groups. Such diets (eg, in Finland and the USA) are associated with higher rates of myocardial infarction than are more polyunsaturated diets (eg, in Italy). 

Dietary supplementation studies with n-3 fatty acids alone have generally not been promising in atopic dermatitis. An initial double-blind study reported a subjective improvement on fish oil compared with the control OA, but no objective improvement on physician assessment.179 A further double-blind study using EPA with saturated fatty acids as the control, showed equal improvement with both supplements and the benefit was attributed to increased clinician guidance,180 while a multicenter study showed a similar improvement in clinical score in subjects taking fish oil or corn oil.181 The latter results might possibly reflect a beneficial effect of both EFA-containing oils, but more likely imply a placebo effect, and illustrate the problems posed both in selection of a suitable control and the interpretation of such studies. 

Clinical studies show that dietary cholesterol is a less potent regulator of plasma cholesterol than are saturated fatty acids. Results from meta-analyses predict that plasma cholesterol response to a 100 mg/day change in dietary cholesterol will be from 0.06 to 0.07 mmol/L. The data show that although dietary cholesterol elevates plasma total cholesterol and LDL-cholesterol level, it also increases the level of HDL-cholesterol such that there is little overall effect on the LDL HDL ratio (McNamara, 2000). 

Evidence from well-conducted prospective epidemiological studies does not suggest that consumption of saturated fat and cholesterol is associated with an increased risk of CHD. Randomized clinical trials that reduced the intake of saturated fatty acids and cholesterol and increased the intake of polyunsaturated fatty acids to lower plasma cholesterol levels did not significantly improve CHD or total mortality. The minor improvement in CHD events for trials of the potent cholesterol-lowering statin drugs may result, to an unknown extent, from their pleiotropic effects and cannot be used to justify the lipid hypothesis. 

In the early 1990s, a series of well-designed clinical studies convincingly demonstrated that TFAs increased plasma total and LDL-cholesterol to levels similar to those produced by saturated fatty acids. More than this, TFAs reduced plasma HDL-cholesterol level. The overall effect was that the ratio of LDL-cholesterol to HDL-cholesterol was approximately double that for an equivalent intake of saturated fatty acids (Ascherio et al., 1999). In addition, TFAs adversely affect other CHD risk factors. Plasma triglycerides and Lp[a] levels are increased (Ascherio et al., 1999) and it was shown recently that consumption of TFAs was associated with a deleterious increase in small, dense LDL particles (Mauger et al., 2003). 

The relationship of dietary saturated fat to plasma cholesterol levels and to CHD was graphically demonstrated by the Seven Countries Study involving 16 cohorts, in which saturated fat intake explained up to 73% of the total variance in CHD across these cohorts. In the Nurses Health Study, the effect of saturated fatty acids was much more modest, especially if saturates were replaced by carbohydrates. The most effective replacement for saturated fatty acids in terms of CHD prevention is by polyunsaturated fatty acids (PUFAs). This agrees with the outcome of large randomized clinical trials, in which replacement of saturated and trans fats by polyunsaturated vegetable oils effectively lowered CHD risk. 

Functional foods and materials that improve fat metabolism have been extensively studied. Diets for weight loss generally recommend restricting intakes of energy, total fats, and saturated fats. In contrast, we have focused on the nature of the glycerol esters rather than on the fatty acid composition of oils, and have found that DAG, particularly in the 1,3-isoform, have metabolic characteristics distinct from those of TAG and are less likely to become stored body fat. A cooking oil product containing at least 80% (w/w) DAG has been on the market in Japan as a food for specified health use (FOSHU) since 1999. In this chapter, the nutritional characteristics and beneficial health effects of DAG observed in several clinical studies are outlined and possible mechanisms for these effects are discussed. 

---