Cardiovascular Health: The Role of Plant Sterols and Stanols.

Article by Arnie Gitomer

The purpose of this article is to present information, based on the current status of scientific support, regarding the use of plant sterols and stanols as dietary supplements and as components of functional foods. This information is based, in part, on the scientific back grounder published by the National Nutritional Foods Association.

INTRODUCTION: Plant sterols and stanols are plant-derived lipids. The sterols are defined chemically by their sidechains and by the presence of a hydroxyl group and a double bond. Cholesterol is a sterol found in animals; the plant-derived sterols are often called phytosterols. In stanols the double bond has been saturated (hydrogenated). The phytosterols can combine with sugars to form glycosides, commonly referred to as sterolins. Both sterols and stanols can be esterified with fatty acids to form esters; the esters are more soluble in oil than the free sterols and stanols.

In the American diet about 80mg of phytosterols are consumed daily; vegetarian and Japanese diets contain about 345 and 400mg/d, respectively. The best dietary sources are unrefined plant oils, seeds, nuts, and legumes (1A). Commonly found sterols include beta-sitosterol, campesterol, and stigmasterol. Western diets contain about 20-50mg/d of plant stanols, largely from cereal grains (2A).

In humans only about 5% of phytosterols are absorbed, with the actual rate varying for individual sterols. Unabsorbed sterols may undergo metabolism by intestinal bacteria (3A).

Many studies in humans and laboratory animals have demonstrated that phytosterol ingestion can reduce blood levels of total and LDL-cholesterol (4A). A recent review of 16 published human studies found significant reductions reported in 15; in 590 total subjects the mean reductions were 10% in total cholesterol and 13% in LDL-cholesterol (3A). In clinical trials, phytosterol esters or non-esterified stanols (2.4g/d) in margarine, butter or low-fat foods over 4-week periods reduced LDL-cholesterol by 14% and 8%, respectively, in hypercholesterolemic subjects. The LDL-cholesterol increase produced by ingestion of butter fat was prevented by addition of phytosterols (5A). Similar results were reported in normocholesterolemic subjects receiving 1g/d of plant stanol esters in low-fat yogurt (6A) and in hypercholesterolemics ingesting 2g/d of sterol-ester or stanol-ester in margarines in a low fat diet over a 4-week period (7A). Daily ingestion of 1.6g of phytosterol-esters in margarine lowered total and LDL-cholesterol levels in children with familial hypercholesterolemia who were maintained on a diet recommended for that condition (8A).

The mechanism of the cholesterol lowering effect is not fully understood. The phytosterols and stanols are known to interfere with intestinal absorption of cholesterol by mechanisms involving their close molecular similarity. The reduction in dietary cholesterol absorption actually increases liver synthesis of cholesterol (3A, 5A, 7A). Phytosterols and stanols may increase the number of cellular LDL receptors, thus increasing disposal of LDL-cholesterol (9A).

The U.S. Food and Drug Administration (FDA) has issued an interim final rule allowing health claims for the reduction of coronary heart disease risk by ingestion of 1.3g/d of plant sterol esters or 3.4g/d plant stanol esters, to be consumed in two servings at different times of the day (2A). Numerous additional comments have been submitted to FDA asking them to broaden the applicability of the health claim to other phyto-sterol products.

A number of studies have demonstrated an anticancer effect of phytosterols. Beta-sitosterol inhibits the growth of human prostate cancer and colon cancer cells in vitro