Extract

The editorial refers to ‘Differential effects on inhibition of cholesterol absorption by plant stanol and plant sterol esters in apoE−/− mice’ by O. Weingärtner et al., pp. 484–492, this issue.

What are the pertinent questions with regard to dietary supplementation of phytosterols and -stanols? For many years now it has generally been accepted that mechanisms leading to a decrease in serum cholesterol lead to a decrease in atherogenesis. Hence, for many years, the use of phytosterols and -stanols, molecules from plant cell membranes resembling cholesterol, has been advocated as a safe and efficient dietary adduct lowering serum LDL cholesterol.1 Just like zoosterols, phytosterols are taken up via the Niemann Pick C1-like 1 protein, thus competing for intestinal uptake. The standard western-type diet contains around 200–400 mg plant sterols, around 50 mg plant stanols, and about 300 mg cholesterol. Dietary addition of either phytosterols or phytostanols, the saturated form of plant sterols, leads to a comparable serum cholesterol decrease; stanols, however, are taken up 10 to 50 times less efficiently. Two grams of sterols decrease serum LDL cholesterol by about 10% while simultaneously doubling serum plant sterol concentrations.2

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