British Journal of Nutrition

Research Article

Flow-mediated vasodilation is not impaired when HDL-cholesterol is lowered by substituting carbohydrates for monounsaturated fat

Nicole M. de Rosea1 c1, Michiel L. Botsa2, Els Siebelinka1, Evert Schoutena1 and Martijin B. Katana1a3

a1 Division of Human Nutrition and Epidemiology, Wageningen University, Wageningen, the Netherlands

a2 Julius Center for Patient Oriented Research, University Medical Center, Utrecht, the Netherlands

a3 The Wageningen Center for Food Sciences, Wageningen, the Netherlands


Low-fat diets, in which carbohydrates replace some of the fat, decrease serum cholesterol. This decrease is due to decreases in LDL-cholesterol but in part to possibly harmful decreases in HDL-cholesterol. High-oil diets, in which oils rich in monounsaturated fat replace some of the saturated fat, decrease serum cholesterol mainly through LDL-cholesterol. We used these two diets to investigate whether a change in HDL-cholesterol would change flow-mediated vasodilation, a marker of endothelial function. We fed thirty-two healthy volunteers two controlled diets in a 2×3·5 weeks' randomised cross-over design to eliminate variation in changes due to differences between subjects. The low-fat diet contained 59·7 % energy (en%) as carbohydrates and 25·7 en% as fat (7·8 en% as monounsaturates); the oil-rich diet contained 37·8 en% as carbohydrates and 44·4 en% as fat (19·3 en% as monounsaturates). Average (SD) SERUM HDL-CHOLESTEROL AFTER THE LOW-FAT DIET WAS 0·21 (sd 0·12) mmol/l (8·1 mg/dl) lower than after the oil-rich diet. Serum triacylglycerols were 0·22 (sd 0·28) mmol/l (19·5 mg/dl) higher after the low-fat diet than after the oil-rich diet. Serum LDL and homocysteine concentrations remained stable. Flow-mediated vasodilation was 4·8 (SD 2·9) after the low-fat diet and 4·1 (SD 2·7) after the oil-rich diet (difference 0·7 %; 95 % CI -0·6, 1·9). Thus, although the low-fat diet produced a lower HDL-cholesterol than the high-oil diet, flow-mediated vasodilation, an early marker of cardiovascular disease, was not impaired.

(Received September 29 2000)

(Revised January 08 2001)

(Accepted January 30 2001)


c1 * Corresponding author: Ms N. M. de Roos, fax +31 317 483342, email