Effect of Dietary Fatty Acids on Serum Lipids and Lipoproteins.

January 1, 1992 Human Health and Nutrition Data 0 Comments

Effect of Dietary Fatty Acids on Serum Lipids and Lipoproteins.

Year: 1992
Authors: R Mensink, M Katan.
Publication Name: Arteroisclerosis and Thrombosis.
Publication Details: Volume 12; Page 911.


Early research demonstrated that replacing dietary carbohydrates with certain saturated fatty acids (SFA) resulted in an increase in serum cholesterol levels. In contrast, the opposite effect has been observed when carbohydrates are replaced with polyunsaturated fatty acids. In the early 1960’s, statistical formulas were developed that correlated the effects of individual fatty acids on serum cholesterol levels and subsequent risk of coronary heart disease (CHD). Policies for the dietary prevention of ischemic heart disease were based upon these formulae. In the late 1980’s, it was determined that these statistical formulas may not be appropriate as they do not differentiate between the effects of diet on LDL and HDL cholesterol. The objective of review was to identify well-controlled trials that assessed the effect of dietary fatty acids on serum lipoproteins in humans, and using these, to derive equations that relate changes in dietary fatty acid intake to serum HDL, LDL, total, and triglyceride (TG) concentrations. A total of 27 controlled trials published between 1970 and 1991 met specific inclusion criteria as follows: 1) a thorough control of food intake, with dietary fatty acids being the sole variable; 2) a design that eliminated the effect of nonspecific drifts of the outcome variables with time; 3) feeding periods that were sufficiently long enough to attain equilibrium (14 d or more); and 4) subject who did not suffer from gross disturbances of lipid metabolism. Diets were excluded if they were specifically enriched with very long chain n3 fatty acids (i.e. fish oil), trans isomers of unsaturated fatty acids, or stearic acid due to its differential effect on cholesterol values compared to other SFAs. The trials that met inclusion criteria yielded 65 data points and included 682 volunteers; 474 men and 208 women. The youngest volunteers were just under 20 years of age, while the oldest were greater than 70 years. Sixteen trials included men only, with the remaining trials including both men and women. An assessment of the data demonstrated that under isocaloric, metabolic-ward conditions, all three classes of fatty acids (SFA, MUFA and PUFA) would elevate HDL-C when replacing carbohydrates in the diet. The effect diminished with increasing unsaturation of the fatty acid. SFAs were found to strongly elevate LDL cholesterol levels, while PUFAs had a modest but significant LDL-C lowering effect relative to carbohydrates. The effect of MUFAs on LDL-C was found to be neutral, although not statistically significant. The data demonstrated that a 10% replacement of dietary energy from SFA by carbohydrates, would yield an LDL-C lowering of 0.33 mmol/l. On average, this translates to a replacement of 27g SFA with 60g starch. Similarly, if this same amount of carbohydrate is replaced by PUFA, LDL-C levels are predicted to drop an additional 0.14 mmol/L. The predicted effect on total serum cholesterol was found to be similar to that of LDL-C. Replacement of carbohydrates by fat was found to decrease the level of TGs, independent of the nature of the fat. In this regard, although PUFA had the greatest TG lowering effect, regression coefficients did not differ significantly between the three classes of fatty acids. Replacement of SFA by unsaturated fatty acids raised the HDL to LDL-C ratio, whereas replacement by carbohydrates had no effect. Overall, the regression equation predicted very little improvement in risk of CHD risk if carbohydrates replaced SFAs. This is in obvious disagreement with a large body of epidemiological evidence which has demonstrated that low-fat, high carbohydrate diets are associated with low risk for CHD. These data also raise the question as to whether replacement of fat by carbohydrate, versus replacement of SFA by unsaturated fat, is the optimal strategy for reducing CHD risk. This publication generated a number of subsequent clinical trials that focused upon answering the debate. The overall consensus for CHD risk reduction appears to be that replacing SFA by unsaturated fatty acids is more effective than replacement by carbohydrates.

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