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Back to Symposium 2007

Diet and LDL Subclasses

Ronald Krauss, MD

Director, Atherosclerosis Research, Children’s Hospital Oakland Research Institute; Guest Senior Scientist, Department of Genome Sciences, Lawrence Berkeley National Laboratory; Adjunct Professor, Department of Nutritional Sciences, University of California at Berkeley

The atherogenic dyslipidemia seen in patients with obesity, diabetes, and the metabolic syndrome includes elevated plasma levels of triglyceride along with reduced high-density lipoprotein (HDL) cholesterol (C). Low-density lipoprotein (LDL) cholesterol levels are not characteristically elevated, but there is a change in LDL metabolism resulting in an increase in a subclass of small, dense (sd) cholesterol-depleted LDL particles.

There is evidence that increases in sdLDL contribute to cardiovascular risk and that the risk is reduced by treatments that lower sdLDL levels. Approximately one-third of men and one-fifth of postmenopausal women have a lipoprotein profile characterized by a predominance of sdLDL particles (LDL phenotype B).

We have shown that low-fat/high-carbohydrate diets can induce expression of phenotype B in a large proportion of otherwise healthy individuals. Recently, we tested the effects on this lipoprotein profile of moderate dietary carbohydrate reduction (54% vs. 39% vs. 26% of energy) both before and after weight loss (~7%) in 178 overweight or obese but otherwise healthy men. In addition, effects of lower (9%) vs. higher (15%) saturated fat intake were tested in conjunction with the 26% carbohydrate diet. The 26% carbohydrate low-saturated fat diet reduced atherogenic lipid measurements, including triglyceride, sdLDL mass and total/HDL-C ratio and increased LDL particle size compared with 54% carbohydrate. Following diet-induced weight loss and stabilization, all these variables showed significantly greater changes, and LDL-C showed significantly greater reductions, in the group that remained on the 54% carbohydrate vs. the group on the 26% carbohydrate diet. Lipoprotein changes with higher vs. lower saturated fat on the 26% carbohydrate diet were similar except that LDL-C was reduced to a greater extent with low saturated fat. There were no differences, however, in reductions of sdLDL; the lesser reduction in total LDL-C with high saturated fat was due to greater offsetting increases in larger, more cholesterol-enriched LDL particles.

Thus, similar improvements in atherogenic dyslipidemia can be achieved by both reduced carbohydrate intake in the absence of weight loss and by weight loss on a higher carbohydrate diet. Hence, for overweight or obese individuals unable to maintain weight loss, moderate carbohydrate restriction offers a means of improving lipid-related cardiovascular disease risk. Moreover, on such diets, reductions in small, dense LDL are independent of saturated fat intake.

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