Throughout much of human evolution, it is likely that large amounts of plant foods were consumed (1). In addition to being rich in fiber and plant protein, the diets of our ancestors were also rich in phytosterols—plant-derived sterols that are similar in structure and function to cholesterol. There is increasing evidence that the reintroduction of plant foods providing phytosterols into the modern diet can improve serum lipid (cholesterol) profiles and reduce the risk of cardiovascular disease (2).
Although cholesterol is the predominant sterol in animals, including humans, a variety of sterols are found in plants (3). Nutritionists recognize two classes of phytosterols: (1) sterols, which have a double bond in the sterol ring (Figure 1); and (2) stanols, which lack a double bond in the sterol ring (Figure 2). The most abundant sterols in plants and the human diet are sitosterol and campesterol. Stanols are also present in plants, but they comprise only about 10% of total dietary phytosterols. Cholesterol in human blood and tissues is derived from the diet as well as endogenous cholesterol synthesis. In contrast, all phytosterols in human blood and tissues are derived from the diet because humans cannot synthesize phytosterols (4).
Numerous clinical trials have found that daily consumption of foods enriched with free or esterified forms of plant sterols or stanols lowers concentrations of serum total and LDL cholesterol (10, 32-35). A meta-analysis that combined the results of 18 controlled clinical trials found that the consumption of spreads providing an average of 2 g/d of plant sterols or stanols lowered serum LDL cholesterol concentrations by 9-14% (36). More recently, a meta-analysis that combined the results of 23 controlled clinical trials found that the consumption of plant foods providing an average of 3.4 g/d of plant sterols or stanols decreased LDL cholesterol concentrations by about 11% (37). Another meta-analysis examined the results of 23 clinical trials of plant sterol-enriched foods and 27 clinical trials of plant stanol-enriched foods, separately (11). At doses of at least 2 g/d, both plant sterols and stanols decreased LDL cholesterol concentrations by about 10%. Doses higher than 2 g/d did not substantially improve the cholesterol-lowering effects of plant sterols or stanols. Most recently, a meta-analysis that analyzed the results of 59 randomized controlled trials found that reductions in LDL cholesterol are greater in those with higher baseline levels of LDL cholesterol(38). The results of studies providing lower doses of plant sterols or stanols suggest that 0.8-1.0 g/d is the lowest dose that results in clinically significant LDL cholesterol reductions of at least 5% (39-43). In general, trials that have compared the cholesterol-lowering efficacy of plant sterols with that of stanols have found them to be equivalent (44-46). Few of these studies lasted longer than four weeks, but at least two studies have found that the cholesterol-lowering effects of plant sterols and stanols last for up to one year (26, 47). In addition to data from controlled clinical trials, a 5-year study that examined the customary use of phytosterol/-stanol enriched margarines under free-living conditions found beneficial effects on cholesterol levels (48). Recently, concerns have been raised that plant sterols are not as effective as stanols in maintaining long-term LDL-cholesterol reductions (49-51). Long-term trials that directly compare the efficacy of plant sterols and plant stanols are needed to address these concerns (11).
(Coronary Heart Disease Risk)
The effect of long-term use of foods enriched with plant sterols or stanols on coronary heart disease (CHD) risk is not known. The results of numerous intervention trials suggest that a 10% reduction in LDL cholesterol induced by medication or diet modification could decrease the risk of CHD by as much as 20% (52). The National Cholesterol Education Program (NCEP) Adult Treatment Panel III has included the use of plant sterol or stanol esters (2 g/d) as a component of maximal dietary therapy for elevated LDL cholesterol (53). The addition of plant sterol- or stanol-enriched foods to a heart healthy diet that is low in saturated fat and rich in fruits and vegetables, whole grains, and fiber offers the potential for additive effects in CHD risk reduction. For example, following a diet that substituted monounsaturated and polyunsaturated fats for saturated fat resulted in a 9% reduction in serum LDL cholesterol after 30 days, but the addition of 1.7 g/d of plant sterols to the same diet resulted in a 24% reduction (54). More recently, 1-month adherence to a diet providing a portfolio of cholesterol-lowering foods, including plant sterols (1 g/1,000 kcal), soy protein, almonds, and viscous fibers lowered serum LDL cholesterol concentrations by an average of 30%—a decrease that was not significantly different from that induced by statin (drugs that inhibit the enzyme, HMG-CoA reductase) therapy (55). However, analysis of individuals on such a cholesterol-lowering diet for one year found that the average LDL cholesterol reduction was only 13%, but almost a third of the participants experienced LDL cholesterol reductions >20% (56). Plant sterols are the major component in this diet responsible for the observed reductions in cholesterol concentrations (57). The U.S. Food and Drug Administration (FDA) has authorized the use of health claims on food labels indicating that regular consumption of foods enriched with plant sterol or stanol esters may reduce the risk of heart disease (58).
Click here to read the article from Linus Pauling Institute in its entirety.