Effects of dietary palmitic and oleic acids on lipoprotein cholesterol.

Recently, Temme et al (1) reported the effects of feeding diets enriched in lauric, palmitic, or olcic acid on plasma lipids in 32 normocholcstcrolemic men and women. The results showed that lauric acid was more hypercholesterolemic than palmitic acid and both were hypercholesterotemic compared with olcic acid. The subjects consumed solid food diets and the authors managed an 8% of energy exchange between lauric and palmitic acid whereas other fatty acids were held relatively constant. The observed differences between the lauric and palmitic acid-enriched diets could not be explained on the basis of the somewhat higher myristic acid content of the former diet, and accordingly, the observed plasma lipid changes would appear to suggest that tauric acid per se was more hypcrchotcstcrolcmic than palmitic acid. However, we believe that another important aspect of the study by Temme et al (I), relating to the effects of palmitic and olcic acids, deserves comment. Among the two test diets rich in palmitic acid or otcic acid, the authors also managed an ‘ 8% of energy exchange between these fatty acids. The other fatty acids were either unchanged (lauric and myristic) or differed by “ ‘0.8% of energy (linotcic). It is difficult to assign any significance to such a small difference between the linoleic acid content of the two diets, especially because the dietary fatty acid content was calculated on the basis of food records and used published nutrient databases. Thus, the diets were effectively looking at a bona fide exchange between palmitic and olcic acids. However, this fatty acid exchange resulted in no significant differences in any of the measured variables (namely plasma total cholesterol, low-density-lipoprotcin cholesterol, high-density-lipoprotcin cholesterol, plasma triacylglycerols or apolipoprotcins A-I and B) in their male subjects. This result agrees with recent data from normocholesterolemic men (2-4) and women (2, 4). To our knowledge, this is the first data to report on the “equivalence” of these two fatty acids when subjects consumed diets with a Western-type fat load (‘ 40% of energy) but not a Western-type cholesterol load (“25 mgI MJ). The other studies that reported that palmitic and olcic acids exerted equivalent effects on plasma lipids (2-4) used similar cholesterol loads (‘ 25-30 mgIMJ) but tower dietary fat loads (‘ ‘30% of energy). Palmitic acid, the most abundant saturated fatty acid (SFA) in the diet has generally been regarded as the major contributor to dietary SFA-induccd hypercholesterolemia (5). However, beginning with the nonhuman primate studies of Hayes et al (reviewed in reference 6), it was proposed (7) that in situations of “normal” lipoprotcin metabolism (ic, the use of normocholesterolemic subjects) with tow dietary cholesterol intake (< 300 mg/d) and adequate intakes of linolcic acid (‘ ‘4-5% of energy), the dietary fatty acid-induced response to plasma cholesterol is dependent primarily on the intakes of myristic and linolcic acids. In such situations, if myristic and linolcic acids arc equalized across diets, the exchange of other fatty acids would not affect plasma lipids. This may partly explain the results of Temme et at. Although the palmitate-olcate exchange did not produce identical lipid responses in their female subjects, a diet-sex effect may have been responsible. It should be pointed out that the regression data on which the palmitate-olcate equivalence scenario was proposed (7), was derived solely from male subjects (cebus monkeys and humans), and its extrapolation to females has yet to be resolved. We recently reviewed 36 human studies encompassing 148 different diets (8). In 27 of the studies (83 diets), which used normocholesterolemic subjects consuming whole-food diets with < 300 mg dietary cholesterol per day, the observed plasma cholesterol response correlated highly significantly with that predicted on the basis of the dietary myristic and linoleic acid content. Applying this analysis to the male subjects from the Temme et at study, we calculated that the palmitic acid-rich diet would have resulted in a 0. l4-mmol/L (5 mg/dL) higher total plasma cholesterol concentration than the olcic acid-rich diet. The observed difference was a nonsignificant 0.19 mmol/L (7 mgldL). Had the dietary tinolcic acid content of both diets been identical, the difference would have been somewhat less. The fact that our analysis closely “predicted” such a response is not important because any regression prediction can match an observed response merely by chance. What is more important is that the data from Temme et at ( 1 ), as well as the above-mentioned human studies (2-4), add credence to the underlying metabolic factors (for the palmitate-olcate equivalence), which form the basis for the regression analysis. Thus, the study by Temme et al (1), in conjunction with recent human studies (2-4), adds further support to the notion that under certain situations (eg, moderate fat load and/or moderate cholesterol load?), palmitic and olcic acids can be “interchanged” without compromising plasma lipids. We would agree with Temme et at (1) that total dietary fat intake may moderate the cholesterolemic effect of palmitic acid. This is an important issue that needs to be addressed in future studies.