• Phytosterols are plant-derived compounds that are similar in structure and function to cholesterol. (More information)
  • Early human diets were rich in phytosterols, providing as much as 1 g/day; however, the typical Western diet today is relatively low in phytosterols. (More information)
  • Phytosterols inhibit the intestinal absorption of cholesterol. (More information)
  • Numerous clinical trials have demonstrated that daily consumption of foods enriched with at least 0.8 g of plant sterols or stanols lowers serum LDL cholesterol. (More information)
  • Although some epidemiological studies have found that higher intakes of plant foods containing phytosterols are associated with decreased cancer risk, it is not clear whether phytosterols or other compounds in plant foods are the protective factors. (More information)
  • The results of a few clinical trials suggest that phytosterol supplementation at relatively low doses can improve urinary tract symptoms related to benign prostatic hyperplasia, but further research is needed to confirm these findings. (More information)
  • Foods rich in phytosterols include unrefined vegetable oils, whole grains, nuts, and legumes. (More information)
  • Foods and beverages with added plant sterols or stanols are now available in many countries throughout the world, and many countries now allow health claims for such commercial products.
    (More information)


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).

Figure 1. Chemical Structures of Cholesterol, Sitosterol, and Campesterol.

Figure 2. Chemical Structures of Sitostanol and Campestanol.


Phytosterols: a collective term for plant-derived sterols and stanols.

Plant sterols or stanols: terms generally applied to plant-derived sterols or stanols; these phytochemicals are added to foods or supplements.

Plant sterol or stanol esters: plant sterols or stanols that have been esterified by creating an ester bond between a fatty acid and the sterol or stanol. Esterification occurs in intestinal cells and is also an industrial process. Esterification makes plant sterols and stanols more fat-soluble so they are easily incorporated into fat-containing foods, including margarines and salad dressings. In this article, the weights of plant sterol and stanol esters are expressed as the equivalent weights of free (unesterified) sterols and stanols.

Metabolism and Bioavailability

Absorption and metabolism of dietary cholesterol

Dietary cholesterol must be incorporated into mixed micelles in order to be absorbed by the cells that line the intestine (enterocytes) (5). Mixed micelles are mixtures of bile salts, lipids (fats), and sterols formed in the small intestine after a fat-containing meal is consumed. Inside the enterocyte, cholesterol is esterified and incorporated into triglyceride-rich lipoproteins known as chylomicrons, which enter the circulation (6). As circulating chylomicrons become depleted of triglycerides, they become chylomicron remnants, which are taken up by the liver. In the liver, cholesterol from chylomicron remnants may be repackaged into other lipoproteins for transport throughout the circulation or, alternatively, secreted into bile, which is released into the small intestine.

Absorption and metabolism of dietary phytosterols

Although varied diets typically contain similar amounts of phytosterols and cholesterol, serum phytosterol concentrations are usually several hundred times lower than serum cholesterol concentrations in humans (7). Less than 10% of dietary phytosterols are systemically absorbed, in contrast to about 50-60% of dietary cholesterol (8). Like cholesterol, phytosterols must be incorporated into mixed micelles before they are taken up by enterocytes. Once inside the enterocyte, systemic absorption of phytosterols is inhibited by the activity of efflux transporters, consisting of a pair of ATP-binding cassette (ABC) proteins known as ABCG5 and ABCG8 (4). ABCG5 and ABCG8 each form one half of a transporter that secretes phytosterols and unesterified cholesterol from the enterocyte into the intestinal lumen. Phytosterols are secreted back into the intestine by ABCG5/G8 transporters at a much greater rate than cholesterol, resulting in much lower intestinal absorption of dietary phytosterols than cholesterol. Within the enterocyte, phytosterols are not as readily esterified as cholesterol, so they are incorporated into chylomicrons at much lower concentrations. Those phytosterols that are incorporated into chylomicrons enter the circulation and are taken up by the liver. Once inside the liver, phytosterols are rapidly secreted into bile by hepatic ABCG5/G8 transporters. Although cholesterol may also be secreted into bile, the rate of phytosterol secretion into bile is much greater than cholesterol secretion (9). Thus, the low serum concentrations of phytosterols relative to cholesterol can be explained by decreased intestinal absorption and increased excretion of phytosterols into bile.

Biological Activities

Effects on cholesterol absorption and lipoprotein metabolism

It is well-established that high intakes of plant sterols or stanols can lower serum total and LDL cholesterol concentrations in humans (see Cardiovascular disease) (10, 11). In the intestinal lumen, phytosterols displace cholesterol from mixed micelles and inhibit cholesterol absorption (12). In humans, the consumption of 1.5-1.8 g/day of plant sterols or stanols reduced cholesterol absorption by 30-40% (13, 14). At higher doses (2.2 g/day of plant sterols), cholesterol absorption was reduced by 60% (15). In response to decreased cholesterol absorption, tissue LDL-receptor expression was increased, resulting in increased clearance of circulating LDL (16). Decreased cholesterol absorption is also associated with increased cholesterol synthesis, and increasing phytosterol intake has been found to increase endogenous cholesterol synthesis in humans (13). Despite the increase in cholesterol synthesis induced by increasing phytosterol intake, the net result is a reduction in serum LDL cholesterol concentration.

Other biological activities

Experiments in cell culture and animal models suggest that phytosterols may have biological activities unrelated to cholesterol lowering. However, their significance in humans is not yet known.

Alterations in cell membrane properties

Cholesterol is an important structural component of mammalian cell membranes (17). Displacement of cholesterol with phytosterols has been found to alter the physical properties of cell membranes in vitro (18), which could potentially affect signal transduction or membrane-bound enzyme activity (19, 20). Limited evidence from an animal model of hemorrhagic stroke suggested that very high intakes of plant sterols or stanols displaced cholesterol in red blood cell membranes, resulting in decreased deformability and potentially increased fragility (21, 22). However, daily phytosterol supplementation (1 g/1,000 kcal) for four weeks did not alter red blood cell fragility in humans (23).

Alterations in testosterone metabolism

Limited evidence from animal studies suggests that very high phytosterol intakes can alter testosterone metabolism by inhibiting 5α-reductase, a membrane-bound enzyme that converts testosterone to dihydrotestosterone, a more potent metabolite (24, 25). It is not known whether phytosterol consumption alters testosterone metabolism in humans. No significant changes in free or total serum testosterone concentrations were observed in men who consumed 1.6 g/day of plant sterol esters for one year (26).

Induction of apoptosis in cancer cells

Unlike normal cells, cancerous cells lose their ability to respond to death signals that initiate apoptosis (programmed cell death). Sitosterol has been found to induce apoptosis when added to cultured human prostate (27), breast (28), and colon cancer cells (29).

Anti-inflammatory effects

Limited data from cell culture and animal studies suggest that phytosterols may attenuate the inflammatory activity of immune cells, including macrophages and neutrophils (30, 31).

Disease Prevention

Cardiovascular disease

Foods enriched with plant sterols or stanols

LDL cholesterol: 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/day 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/day 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/day, both plant sterols and stanols decreased LDL cholesterol concentrations by about 10%. Doses higher than 2 g/day 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/day 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/day) 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 fruit 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/day of plant sterols to the same diet resulted in a 24% reduction (54). More recently, one-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 US 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).

Dietary phytosterols

Clinical trials finding daily consumption of foods enriched with plant sterols or stanols can significantly lower LDL cholesterol concentrations do not account for naturally occurring phytosterols in the diet (59). Relatively few studies have considered the effects of dietary phytosterol intakes on serum LDL cholesterol concentrations. Dietary phytosterol intakes have been estimated to range from about 150-450 mg/day in various populations (60). Limited evidence suggests that dietary phytosterols may play an important role in decreasing cholesterol absorption. A cross-sectional study in the UK found that dietary phytosterol intakes were inversely related to serum total and LDL cholesterol concentrations even after adjusting for saturated fat and fiber intake (61). Similarly, an analysis in a Swedish population found that dietary intake of phytosterols was inversely associated with total cholesterol in both men and women and with LDL cholesterol in women (62). In single meal tests, removal of 150 mg of phytosterols from corn oil increased cholesterol absorption by 38% (63), and removal of 328 mg of phytosterols from wheat germ increased cholesterol absorption by 43% (64). Although more research is needed, these findings suggest that dietary intakes of phytosterols from plant foods could have an important impact on cardiovascular health.


Limited data from animal studies suggest that very high intakes of phytosterols, particularly sitosterol, may inhibit the growth of breast and prostate cancer (65-67). Only a few epidemiological studies have examined associations between dietary phytosterol intakes and cancer risk in humans because databases providing information on the phytosterol content of commonly consumed foods have only recently been developed. A series of case-control studies in Uruguay found that dietary phytosterol intakes were lower in people diagnosed with stomach, lung, or breast cancer than in cancer-free control groups (68-70). Case-control studies in the US found that women diagnosed with breast or endometrial (uterine) cancer had lower dietary phytosterol intakes than women who did not have cancer (71, 72). In contrast, another case-control study in the US found that men diagnosed with prostate cancer had higher dietary campesterol intakes than men who did not have cancer, but total phytosterol consumption was not associated with prostate cancer risk (73). Although some epidemiological studies have found that higher intakes of plant foods containing phytosterols are associated with decreased cancer risk, it is not clear whether the protective factors are phytosterols or other compounds in plant foods.

Disease Treatment

Benign Prostatic Hyperplasia (BPH)

Benign prostatic hyperplasia (BPH) is the term used to describe a noncancerous enlargement of the prostate. The enlarged prostate may exert pressure on the urethra, resulting in difficulty urinating. Plant extracts that provide a mixture of phytosterols (marketed as β-sitosterol) are often included in herbal therapies for urinary symptoms related to BPH. However, relatively few controlled studies have examined the efficacy of phytosterol supplements in men with symptomatic BPH. In a six-month study of 200 men with symptomatic BPH, 60 mg/day of a β-sitosterol preparation improved symptom scores, increased peak urinary flow, and decreased post-void residual urine volume compared to placebo (74). A follow-up study reported that these improvements were maintained for up to 18 months in the 38 participants who continued β-sitosterol treatment (75). Similarly, in a six-month study of 177 men with symptomatic BPH, 130 mg/day of a different β-sitosterol preparation improved urinary symptom scores, increased peak urinary flow, and decreased post-void residual urine volume compared to placebo (76). A systematic review that combined the results of these and two other controlled clinical trials found that β-sitosterol extracts increased peak urinary flow by an average of 3.9 ml/second and decreased post-void residual volume by an average of 29 ml (77). Although the results of a few clinical trials suggest that relatively low doses of phytosterols can improve lower urinary tract symptoms related to BPH, further research is needed to confirm these findings (78).



Unlike the typical diet in most developed countries today, the diets of our ancestors were rich in phytosterols, likely providing as much as 1,000 mg/day (1). Present-day dietary phytosterol intakes have been estimated to vary from 150-450 mg/day in different populations (3). Vegetarians, particularly vegans, generally have the highest intakes of dietary phytosterols (79). Phytosterols are found in all plant foods, but the highest concentrations are found in unrefined plant oils, including vegetable, nut, and olive oils (3). Nuts, seeds, whole grains, and legumes are also good dietary sources of phytosterols (5). The phytosterol contents of selected foods are presented in Table 1. For information on the nutrient content of specific foods, search the USDA food composition database.

Table 1. Total Phytosterol Content of Selected Foods (80-83)
Food Serving Phytosterols (mg)
Wheat germ ½ cup (57 g)
Rice bran oil 1 tablespoon (14 g)
Sesame oil 1 tablespoon (14 g)
Corn oil 1 tablespoon (14 g)
Canola oil 1 tablespoon (14 g)
Peanuts 1 ounce (28 g)
Wheat bran ½ cup (29 g)
Almonds 1 ounce (28 g)
Brussels sprouts ½ cup (78 g)
Rye bread 2 slices (64 g)
Macadamia nuts 1 ounce (28 g)
Olive oil 1 tablespoon (14 g)
Take Control® spread 1 tablespoon (14 g)
1,650 mg plant sterol esters
(1,000 mg free sterols)
Benecol® spread 1 tablespoon (14 g)
850 mg plant stanol esters
(500 mg free stanols) 

Food enriched with plant sterols and plant stanols

The majority of clinical trials that demonstrated a cholesterol-lowering effect used plant sterol or stanol esters solubilized in fat-containing foods, such as margarine or mayonnaise (11). More recent studies indicate that low-fat or even nonfat foods can effectively deliver plant sterols or stanols if they are adequately solubilized (10, 59). Plant sterols or stanols added to low-fat yogurt (43, 84-86), low-fat milk (87-89), low-fat cheese (90), dark chocolate (91), and orange juice (92, 93) have been reported to lower LDL cholesterol in controlled clinical trials. A variety of foods containing added plant sterols or stanols, including margarines, mayonnaises, vegetable oils, salad dressings, yogurt, milk, soy milk, orange juice, snack bars, and meats, are available in the US, Europe, Asia, Australia, and New Zealand (10). A recent meta-analysis found that plant sterols/stanols added to fat spreads, mayonnaise, salad dressings, milk, or yogurt were more effective in reducing LDL cholesterol levels compared to when plant sterols/stanols were incorporated into other products, such as chocolate, orange juice, cheese, meats, and cereal bars (38). Available research indicates that the maximum effective dose for lowering LDL cholesterol is about 2 g/day (11) and the minimum effective dose is 0.8-1.0 g/day (10). In the majority of clinical trials that demonstrated a cholesterol-lowering effect, the daily dose of plant sterols or stanols was divided among two or three meals, which may be more effective in lowering LDL cholesterol (38). However, consumption of the daily dose of plant sterols or stanols with a single meal has been found to lower LDL cholesterol in a few clinical trials (43, 85, 86, 94, 95).


Phytosterol supplements marketed as β-sitosterol are available without a prescription in the US. Doses of 60-130 mg/day of β-sitosterol have been found to alleviate the symptoms of benign prostatic hyperplasia (BPH) in a few clinical trials (see Benign prostatic hyperplasia). Soft gel chews providing 0.5 g of plant stanols are being marketed for cholesterol-lowering at a recommended dose of 2 g/day. Phytosterol supplements should be taken with meals that contain fat.


In the United States, plant sterols and stanols added to a variety of food products are generally recognized as safe (GRAS) by the FDA (96). Additionally, the Scientific Committee on Foods of the EU concluded that plant sterols and stanols added to various food products are safe for human use (97). However, the Committee recommended that intakes of plant sterols and stanols from food products should not exceed 3 g/day because there is no evidence of health benefits at higher intakes and there might be undesirable effects at high intakes.

Adverse effects

Few adverse effects have been associated with regular consumption of plant sterols or stanols for up to one year. People who consumed a plant sterol-enriched spread providing 1.6 g/day did not report any more adverse effects than those consuming a control spread for up to one year (26), and people consuming a plant stanol-enriched spread providing 1.8-2.6 g/day for one year did not report any adverse effects (47). Consumption of up to 8.6 g/day of phytosterols in margarine for three to four weeks was well-tolerated by healthy men and women and did not adversely affect intestinal bacteria or female hormone levels (98). Although phytosterols are usually well-tolerated, nausea, indigestion, diarrhea, and constipation have occasionally been reported (74, 76).

Sitosterolemia (Phytosterolemia)

Sitosterolemia, also known as phytosterolemia, is a very rare hereditary disease that results from inheriting a mutation in both copies of the ABCG5 or ABCG8 gene (99). Individuals who are homozygous for a mutation in either transporter protein have dramatically elevated serum phytosterol concentrations due to increased intestinal absorption and decreased biliary excretion of phytosterols. Although serum cholesterol concentrations may be normal or only mildly elevated, individuals with sitosterolemia are at high risk for premature atherosclerosis. People with sitosterolemia should avoid foods or supplements with added plant sterols (10). Two studies have examined the effect of plant sterol consumption in heterozygous carriers of sitosterolemia, a more common condition. Consumption of 3 g/day of plant sterols for four weeks by two heterozygous carriers (100) and consumption of 2.2 g/day of plant sterols for 6-12 weeks by 12 heterozygous carriers did not result in abnormally elevated serum phytosterols (101).

Pregnancy and lactation

Plant sterols or stanols added to foods or supplements are not recommended for pregnant or breast-feeding women because their safety has not been studied (10). At present, there is no evidence that high dietary intakes of naturally occurring phytosterols, such as those consumed by vegetarian women, adversely affects pregnancy or lactation.

Drug interactions

The LDL cholesterol-lowering effects of plant sterols or stanols may be additive to those of HMG-CoA reductase inhibitors (statins) (102, 103). The results of controlled clinical trials suggest that consumption of 2-3 g/day of plant sterols or stanols by individuals on statin therapy may result in an additional 7-11% reduction in LDL cholesterol, an effect comparable to doubling the statin dose (50, 104-106). Consumption of 4.5 g/day of stanol esters for eight weeks did not affect prothrombin times (INR) in patients on warfarin (Coumadin) for anticoagulation (107).

Nutrient interactions

Fat-soluble vitamins (vitamins A, D, E, and K)

Because plant sterols and stanols decrease cholesterol absorption and serum LDL cholesterol concentrations, their effects on fat-soluble vitamin status have also been studied in clinical trials. Plasma vitamin A (retinol) concentrations were not affected by plant stanol or sterol ester consumption for up to one year (11, 26). Although the majority of studies found no changes in plasma vitamin D (25-hydroxyvitamin D3) concentrations, one placebo-controlled study in individuals consuming 1.6 g/day of sterol esters for one year observed a small (7%) but statistically significant decrease in plasma 25-hydroxyvitamin D3 concentrations (26). There is little evidence that plant sterol or stanol consumption adversely affects vitamin K status. Consumption of 1.6 g/day of sterol esters for six months was associated with a nonsignificant 14% decrease in plasma vitamin K1 concentrations, but carboxylated osteocalcin, a functional indicator of vitamin K status, was unaffected (26). In other studies of shorter duration, consumption of plant sterol and stanol esters did not significantly change plasma concentrations of vitamin K1 (108, 109) or vitamin K-dependent clotting factors (110). Consumption of plant sterol or stanol-enriched foods has been found to decrease plasma vitamin E (α-tocopherol) concentrations in a number of studies (11, 109). However, those decreases generally do not persist when plasma α-tocopherol concentrations are standardized to LDL cholesterol concentrations. This suggests that observed reductions in plasma α-tocopherol are due in part to reductions in its carrier lipoprotein, LDL. In general, consumption of plant sterol- and stanol-enriched foods at doses of 1.5 g/day or more have not been found to have adverse effects on fat-soluble vitamin status in well-nourished populations.


Dietary carotenoids are fat-soluble phytochemicals that circulate in lipoproteins. A number of studies have observed 10-20% reductions in plasma carotenoids after short-term and long-term consumption of plant sterol- or stanol-enriched foods (11). Even when standardized to serum total or LDL cholesterol concentrations, decreases in α-carotene, β-carotene, and lycopene may persist, suggesting that phytosterols can inhibit the absorption of these carotenoids (111). It is not clear whether reductions in plasma carotenoid concentrations confer any health risks, but several studies have found that increasing intakes of carotenoid-rich fruit and vegetables can prevent phytosterol-induced decreases in plasma carotenoids (112). In one case, advice to consume five daily servings of fruit and vegetables, including one serving of carotenoid-rich vegetables, was enough to maintain plasma carotenoid levels in people consuming 2.5 g/day of plant sterol or stanol esters (113).

Authors and Reviewers

Originally written in 2005 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University

Updated in September 2008 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University

Reviewed in September 2008 by:
Peter J.H. Jones, Ph.D.
Professor of Nutrition
Director, Mary Emily Clinical Nutrition Research Center
School of Dietetics and Human Nutrition
McGill University

Copyright 2005-2016  Linus Pauling Institute 


1.  Jenkins DJ, Kendall CW, Marchie A, et al. The Garden of Eden–plant based diets, the genetic drive to conserve cholesterol and its implications for heart disease in the 21st century. Comp Biochem Physiol A Mol Integr Physiol. 2003;136(1):141-151.  (PubMed)

2.  Kendall CW, Jenkins DJ. A dietary portfolio: maximal reduction of low-density lipoprotein cholesterol with diet. Curr Atheroscler Rep. 2004;6(6):492-498.  (PubMed)

3.  Ostlund RE, Jr. Phytosterols in human nutrition. Annu Rev Nutr. 2002;22:533-549.  (PubMed)

4.  Sudhop T, Lutjohann D, von Bergmann K. Sterol transporters: targets of natural sterols and new lipid lowering drugs. Pharmacol Ther. 2005;105(3):333-341.  (PubMed)

5.  de Jong A, Plat J, Mensink RP. Metabolic effects of plant sterols and stanols (Review). J Nutr Biochem. 2003;14(7):362-369.  (PubMed)

6.  Plat J, Mensink RP. Plant stanol and sterol esters in the control of blood cholesterol levels: mechanism and safety aspects. Am J Cardiol. 2005;96(1 Suppl):15-22.  (PubMed)

7.  von Bergmann K, Sudhop T, Lutjohann D. Cholesterol and Plant Sterol Absorption: Recent Insights. Am J Cardiol. 2005;96(1S):10-14.  (PubMed)

8.  Ostlund RE, Jr., McGill JB, Zeng CM, et al. Gastrointestinal absorption and plasma kinetics of soy Delta(5)-phytosterols and phytostanols in humans. Am J Physiol Endocrinol Metab. 2002;282(4):E911-916.  (PubMed)

9.  Sudhop T, Sahin Y, Lindenthal B, et al. Comparison of the hepatic clearances of campesterol, sitosterol, and cholesterol in healthy subjects suggests that efflux transporters controlling intestinal sterol absorption also regulate biliary secretion. Gut. 2002;51(6):860-863.  (PubMed)

10.  Berger A, Jones PJ, Abumweis SS. Plant sterols: factors affecting their efficacy and safety as functional food ingredients. Lipids Health Dis. 2004;3(1):5.  (PubMed)

11.  Katan MB, Grundy SM, Jones P, Law M, Miettinen T, Paoletti R. Efficacy and safety of plant stanols and sterols in the management of blood cholesterol levels. Mayo Clin Proc. 2003;78(8):965-978.  (PubMed)

12.  Nissinen M, Gylling H, Vuoristo M, Miettinen TA. Micellar distribution of cholesterol and phytosterols after duodenal plant stanol ester infusion. Am J Physiol Gastrointest Liver Physiol. 2002;282(6):G1009-1015.  (PubMed)

13.  Jones PJ, Raeini-Sarjaz M, Ntanios FY, Vanstone CA, Feng JY, Parsons WE. Modulation of plasma lipid levels and cholesterol kinetics by phytosterol versus phytostanol esters. J Lipid Res. 2000;41(5):697-705.  (PubMed)

14.  Normen L, Dutta P, Lia A, Andersson H. Soy sterol esters and beta-sitostanol ester as inhibitors of cholesterol absorption in human small bowel. Am J Clin Nutr. 2000;71(4):908-913.  (PubMed)

15.  Richelle M, Enslen M, Hager C, et al. Both free and esterified plant sterols reduce cholesterol absorption and the bioavailability of beta-carotene and alpha-tocopherol in normocholesterolemic humans. Am J Clin Nutr. 2004;80(1):171-177.  (PubMed)

16.  Plat J, Mensink RP. Effects of plant stanol esters on LDL receptor protein expression and on LDL receptor and HMG-CoA reductase mRNA expression in mononuclear blood cells of healthy men and women. FASEB J. 2002;16(2):258-260.  (PubMed)

17.  Mouritsen OG, Zuckermann MJ. What’s so special about cholesterol? Lipids. 2004;39(11):1101-1113.  (PubMed)

18.  Halling KK, Slotte JP. Membrane properties of plant sterols in phospholipid bilayers as determined by differential scanning calorimetry, resonance energy transfer and detergent-induced solubilization. Biochim Biophys Acta. 2004;1664(2):161-171.  (PubMed)

19.  Awad AB, Chen YC, Fink CS, Hennessey T. beta-Sitosterol inhibits HT-29 human colon cancer cell growth and alters membrane lipids. Anticancer Res. 1996;16(5A):2797-2804.  (PubMed)

20.  Leikin AI, Brenner RR. Fatty acid desaturase activities are modulated by phytosterol incorporation in microsomes. Biochim Biophys Acta. 1989;1005(2):187-191.  (PubMed)

21.  Ratnayake WM, L’Abbe MR, Mueller R, et al. Vegetable oils high in phytosterols make erythrocytes less deformable and shorten the life span of stroke-prone spontaneously hypertensive rats. J Nutr. 2000;130(5):1166-1178.  (PubMed)

22.  Ratnayake WM, Plouffe L, L’Abbe MR, Trick K, Mueller R, Hayward S. Comparative health effects of margarines fortified with plant sterols and stanols on a rat model for hemorrhagic stroke. Lipids. 2003;38(12):1237-1247.  (PubMed)

23.  Jones PJ, Raeini-Sarjaz M, Jenkins DJ, et al. Effects of a diet high in plant sterols, vegetable proteins, and viscous fibers (dietary portfolio) on circulating sterol levels and red cell fragility in hypercholesterolemic subjects. Lipids. 2005;40(2):169-174.  (PubMed)

24.  Awad AB, Hartati MS, Fink CS. Phytosterol feeding induces alteration in testosterone metabolism in rat tissues. J Nutr Biochem. 1998;9(12):712-717.

25.  Cabeza M, Bratoeff E, Heuze I, Ramirez E, Sanchez M, Flores E. Effect of beta-sitosterol as inhibitor of 5 alpha-reductase in hamster prostate. Proc West Pharmacol Soc. 2003;46:153-155.  (PubMed)

26.  Hendriks HF, Brink EJ, Meijer GW, Princen HM, Ntanios FY. Safety of long-term consumption of plant sterol esters-enriched spread. Eur J Clin Nutr. 2003;57(5):681-692.  (PubMed)

27.  von Holtz RL, Fink CS, Awad AB. beta-Sitosterol activates the sphingomyelin cycle and induces apoptosis in LNCaP human prostate cancer cells. Nutr Cancer. 1998;32(1):8-12.  (PubMed)

28.  Awad AB, Roy R, Fink CS. Beta-sitosterol, a plant sterol, induces apoptosis and activates key caspases in MDA-MB-231 human breast cancer cells. Oncol Rep. 2003;10(2):497-500.  (PubMed)

29.  Choi YH, Kong KR, Kim YA, et al. Induction of Bax and activation of caspases during beta-sitosterol-mediated apoptosis in human colon cancer cells. Int J Oncol. 2003;23(6):1657-1662.  (PubMed)

30.  Awad AB, Toczek J, Fink CS. Phytosterols decrease prostaglandin release in cultured P388D1/MAB macrophages. Prostaglandins Leukot Essent Fatty Acids. 2004;70(6):511-520.  (PubMed)

31.  Navarro A, De las Heras B, Villar A. Anti-inflammatory and immunomodulating properties of a sterol fraction from Sideritis foetens Clem. Biol Pharm Bull. 2001;24(5):470-473.  (PubMed)

32.  St-Onge MP, Jones PJ. Phytosterols and human lipid metabolism: efficacy, safety, and novel foods. Lipids. 2003;38(4):367-375.  (PubMed)

33.  Moruisi KG, Oosthuizen W, Opperman AM. Phytosterols/stanols lower cholesterol concentrations in familial hypercholesterolemic subjects: a systematic review with meta-analysis. J Am Coll Nutr. 2006;25(1):41-48.  (PubMed)

34.  Ellegard LH, Andersson SW, Normen AL, Andersson HA. Dietary plant sterols and cholesterol metabolism. Nutr Rev. 2007;65(1):39-45.  (PubMed)

35.  Van Horn L, McCoin M, Kris-Etherton PM, et al. The evidence for dietary prevention and treatment of cardiovascular disease. J Am Diet Assoc. 2008;108(2):287-331.  (PubMed)

36.  Law M. Plant sterol and stanol margarines and health. BMJ. 2000;320(7238):861-864.  (PubMed)

37.  Chen JT, Wesley R, Shamburek RD, Pucino F, Csako G. Meta-analysis of natural therapies for hyperlipidemia: plant sterols and stanols versus policosanol. Pharmacotherapy. 2005;25(2):171-183.  (PubMed)

38.  AbuMweis SS, Barake R, Jones P. Plant sterols/stanols as cholesterol lowering agents: A meta-analysis of randomized controlled trials. Food & Nutrition Research. 2008; DOI: 10.3402/fnr.v52i0.1811.  (PubMed)

39.  Hendriks HF, Weststrate JA, van Vliet T, Meijer GW. Spreads enriched with three different levels of vegetable oil sterols and the degree of cholesterol lowering in normocholesterolaemic and mildly hypercholesterolaemic subjects. Eur J Clin Nutr. 1999;53(4):319-327.  (PubMed)

40.  Miettinen TA, Vanhanen H. Dietary sitostanol related to absorption, synthesis and serum level of cholesterol in different apolipoprotein E phenotypes. Atherosclerosis. 1994;105(2):217-226.  (PubMed)

41.  Pelletier X, Belbraouet S, Mirabel D, et al. A diet moderately enriched in phytosterols lowers plasma cholesterol concentrations in normocholesterolemic humans. Ann Nutr Metab. 1995;39(5):291-295.  (PubMed)

42.  Sierksma A, Weststrate JA, Meijer GW. Spreads enriched with plant sterols, either esterified 4,4-dimethylsterols or free 4-desmethylsterols, and plasma total- and LDL-cholesterol concentrations. Br J Nutr. 1999;82(4):273-282.  (PubMed)

43.  Volpe R, Niittynen L, Korpela R, et al. Effects of yoghurt enriched with plant sterols on serum lipids in patients with moderate hypercholesterolaemia. Br J Nutr. 2001;86(2):233-239.  (PubMed)

44.  Hallikainen MA, Sarkkinen ES, Gylling H, Erkkila AT, Uusitupa MI. Comparison of the effects of plant sterol ester and plant stanol ester-enriched margarines in lowering serum cholesterol concentrations in hypercholesterolaemic subjects on a low-fat diet. Eur J Clin Nutr. 2000;54(9):715-725.  (PubMed)

45.  Vanstone CA, Raeini-Sarjaz M, Parsons WE, Jones PJ. Unesterified plant sterols and stanols lower LDL-cholesterol concentrations equivalently in hypercholesterolemic persons. Am J Clin Nutr. 2002;76(6):1272-1278.  (PubMed)

46.  Weststrate JA, Meijer GW. Plant sterol-enriched margarines and reduction of plasma total- and LDL-cholesterol concentrations in normocholesterolaemic and mildly hypercholesterolaemic subjects. Eur J Clin Nutr. 1998;52(5):334-343.  (PubMed)

47.  Miettinen TA, Puska P, Gylling H, Vanhanen H, Vartiainen E. Reduction of serum cholesterol with sitostanol-ester margarine in a mildly hypercholesterolemic population. N Engl J Med. 1995;333(20):1308-1312.  (PubMed)

48.  Wolfs M, de Jong N, Ocke MC, Verhagen H, Monique Verschuren WM. Effectiveness of customary use of phytosterol/-stanol enriched margarines on blood cholesterol lowering. Food Chem Toxicol. 2006;44(10):1682-1688.  (PubMed)

49.  Miettinen TA, Gylling H. Plant stanol and sterol esters in prevention of cardiovascular diseases. Ann Med. 2004;36(2):126-134.  (PubMed)

50.  O’Neill FH, Brynes A, Mandeno R, et al. Comparison of the effects of dietary plant sterol and stanol esters on lipid metabolism. Nutr Metab Cardiovasc Dis. 2004;14(3):133-142.  (PubMed)

51.  O’Neill FH, Sanders TA, Thompson GR. Comparison of efficacy of plant stanol ester and sterol ester: short-term and longer-term studies. Am J Cardiol. 2005;96(1A):29D-36D.  (PubMed)

52.  National Cholesterol Education Program. Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). National Heart Lung and Blood Institute, National Institutes of Health. 2002.

53.  Grundy SM. Stanol Esters as a Component of Maximal Dietary Therapy in the National Cholesterol Education Program Adult Treatment Panel III Report. Am J Cardiol. 2005;96(1 Suppl):47-50.  (PubMed)

54.  Jones PJ, Ntanios FY, Raeini-Sarjaz M, Vanstone CA. Cholesterol-lowering efficacy of a sitostanol-containing phytosterol mixture with a prudent diet in hyperlipidemic men. Am J Clin Nutr. 1999;69(6):1144-1150.  (PubMed)

55.  Jenkins DJ, Kendall CW, Marchie A, et al. Direct comparison of a dietary portfolio of cholesterol-lowering foods with a statin in hypercholesterolemic participants. Am J Clin Nutr. 2005;81(2):380-387.  (PubMed)

56.  Jenkins DJ, Kendall CW, Faulkner DA, et al. Assessment of the longer-term effects of a dietary portfolio of cholesterol-lowering foods in hypercholesterolemia. Am J Clin Nutr. 2006;83(3):582-591.  (PubMed)

57.  Jenkins DJ, Kendall CW, Nguyen TH, et al. Effect of plant sterols in combination with other cholesterol-lowering foods. Metabolism. 2008;57(1):130-139.  (PubMed)

58.  Food and Drug Administration. Health claims: plant sterol/stanol esters and risk of coronary heart disease (CHD). US Government Printing Office. 2002. Available at: Accessed 3/3/15.

59.  Ostlund RE, Jr. Phytosterols and cholesterol metabolism. Curr Opin Lipidol. 2004;15(1):37-41.  (PubMed)

60.  Ostlund RE, Jr., Racette SB, Stenson WF. Effects of trace components of dietary fat on cholesterol metabolism: phytosterols, oxysterols, and squalene. Nutr Rev. 2002;60(11):349-359.  (PubMed)

61.  Andersson SW, Skinner J, Ellegard L, et al. Intake of dietary plant sterols is inversely related to serum cholesterol concentration in men and women in the EPIC Norfolk population: a cross-sectional study. Eur J Clin Nutr. 2004;58(10):1378-1385.  (PubMed)

62.  Klingberg S, Ellegard L, Johansson I, et al. Inverse relation between dietary intake of naturally occurring plant sterols and serum cholesterol in northern Sweden. Am J Clin Nutr. 2008;87(4):993-1001.  (PubMed)

63.  Ostlund RE, Jr., Racette SB, Okeke A, Stenson WF. Phytosterols that are naturally present in commercial corn oil significantly reduce cholesterol absorption in humans. Am J Clin Nutr. 2002;75(6):1000-1004.  (PubMed)

64.  Ostlund RE, Jr., Racette SB, Stenson WF. Inhibition of cholesterol absorption by phytosterol-replete wheat germ compared with phytosterol-depleted wheat germ. Am J Clin Nutr. 2003;77(6):1385-1389.  (PubMed)

65.  Ju YH, Clausen LM, Allred KF, Almada AL, Helferich WG. beta-Sitosterol, beta-Sitosterol Glucoside, and a Mixture of beta-Sitosterol and beta-Sitosterol Glucoside Modulate the Growth of Estrogen-Responsive Breast Cancer Cells In Vitro and in Ovariectomized Athymic Mice. J Nutr. 2004;134(5):1145-1151.  (PubMed)

66.  Awad AB, Fink CS, Williams H, Kim U. In vitro and in vivo (SCID mice) effects of phytosterols on the growth and dissemination of human prostate cancer PC-3 cells. Eur J Cancer Prev. 2001;10(6):507-513.  (PubMed)

67.  Awad AB, Downie A, Fink CS, Kim U. Dietary phytosterol inhibits the growth and metastasis of MDA-MB-231 human breast cancer cells grown in SCID mice. Anticancer Res. 2000;20(2A):821-824.  (PubMed)

68.  De Stefani E, Boffetta P, Ronco AL, et al. Plant sterols and risk of stomach cancer: a case-control study in Uruguay. Nutr Cancer. 2000;37(2):140-144.  (PubMed)

69.  Mendilaharsu M, De Stefani E, Deneo-Pellegrini H, Carzoglio J, Ronco A. Phytosterols and risk of lung cancer: a case-control study in Uruguay. Lung Cancer. 1998;21(1):37-45.  (PubMed)

70.  Ronco A, De Stefani E, Boffetta P, Deneo-Pellegrini H, Mendilaharsu M, Leborgne F. Vegetables, fruits, and related nutrients and risk of breast cancer: a case-control study in Uruguay. Nutr Cancer. 1999;35(2):111-119.  (PubMed)

71.  McCann SE, Freudenheim JL, Marshall JR, Brasure JR, Swanson MK, Graham S. Diet in the epidemiology of endometrial cancer in western New York (United States). Cancer Causes Control. 2000;11(10):965-974.  (PubMed)

72.  McCann SE, Freudenheim JL, Marshall JR, Graham S. Risk of human ovarian cancer is related to dietary intake of selected nutrients, phytochemicals and food groups. J Nutr. 2003;133(6):1937-1942.  (PubMed)

73.  Strom SS, Yamamura Y, Duphorne CM, et al. Phytoestrogen intake and prostate cancer: a case-control study using a new database. Nutr Cancer. 1999;33(1):20-25.  (PubMed)

74.  Berges RR, Windeler J, Trampisch HJ, Senge T. Randomised, placebo-controlled, double-blind clinical trial of beta-sitosterol in patients with benign prostatic hyperplasia. Beta-sitosterol Study Group. Lancet. 1995;345(8964):1529-1532.  (PubMed)

75.  Berges RR, Kassen A, Senge T. Treatment of symptomatic benign prostatic hyperplasia with beta-sitosterol: an 18-month follow-up. BJU Int. 2000;85(7):842-846.  (PubMed)

76.  Klippel KF, Hiltl DM, Schipp B. A multicentric, placebo-controlled, double-blind clinical trial of beta-sitosterol (phytosterol) for the treatment of benign prostatic hyperplasia. German BPH-Phyto Study group. Br J Urol. 1997;80(3):427-432.  (PubMed)

77.  Wilt TJ, MacDonald R, Ishani A. beta-sitosterol for the treatment of benign prostatic hyperplasia: a systematic review. BJU Int. 1999;83(9):976-983.  (PubMed)

78.  Dreikorn K. The role of phytotherapy in treating lower urinary tract symptoms and benign prostatic hyperplasia. World J Urol. 2002;19(6):426-435.  (PubMed)

79.  Nair PP, Turjman N, Kessie G, et al. Diet, nutrition intake, and metabolism in populations at high and low risk for colon cancer. Dietary cholesterol, beta-sitosterol, and stigmasterol. Am J Clin Nutr. 1984;40(4 Suppl):927-930.  (PubMed)

80.  US Department of Agriculture, Agricultural Research Service. USDA Nutrient Database for Standard Reference, Release 20. 2007. Available at: Accessed 7/24/08.

81.  Normen L, Bryngelsson S, Johnsson M, et al. The phytosterol content of some cereal foods commonly consumed in Sweden and in the Netherlands. J Food Compos Anal. 2002;15(6):693-704.

82.  Normen L, Johnsson M, Andersson H, van Gameren Y, Dutta P. Plant sterols in vegetables and fruits commonly consumed in Sweden. Eur J Nutr. 1999;38(2):84-89.  (PubMed)

83.  Phillips KM, Ruggio DM, Toivo JI, Swank MA, Simpkins AH. Free and esterified sterol composition of edible oils and fats. J Food Compos Anal. 2002;15(2):123-142.

84.  Mensink RP, Ebbing S, Lindhout M, Plat J, van Heugten MM. Effects of plant stanol esters supplied in low-fat yoghurt on serum lipids and lipoproteins, non-cholesterol sterols and fat soluble antioxidant concentrations. Atherosclerosis. 2002;160(1):205-213.  (PubMed)

85.  Plana N, Nicolle C, Ferre R, et al. Plant sterol-enriched fermented milk enhances the attainment of LDL-cholesterol goal in hypercholesterolemic subjects. Eur J Nutr. 2008;47(1):32-39.  (PubMed)

86.  Doornbos AM, Meynen EM, Duchateau GS, van der Knaap HC, Trautwein EA. Intake occasion affects the serum cholesterol lowering of a plant sterol-enriched single-dose yoghurt drink in mildly hypercholesterolaemic subjects. Eur J Clin Nutr. 2006;60(3):325-333.  (PubMed)

87.  Noakes M, Clifton PM, Doornbos AME, Trautwein EA. Plant sterol ester-enriched milk and yoghurt effectively reduce serum cholesterol in modestly hypercholesterolemic subjects. Eur J Clin Nutr. 2005;44(4):214-222.  (PubMed)

88.  Thomsen AB, Hansen HB, Christiansen C, Green H, Berger A. Effect of free plant sterols in low-fat milk on serum lipid profile in hypercholesterolemic subjects. Eur J Clin Nutr. 2004;58(6):860-870.  (PubMed)

89.  Seppo L, Jauhiainen T, Nevala R, Poussa T, Korpela R. Plant stanol esters in low-fat milk products lower serum total and LDL cholesterol. Eur J Nutr. 2007;46(2):111-117.  (PubMed)

90.  Jauhiainen T, Salo P, Niittynen L, Poussa T, Korpela R. Effects of low-fat hard cheese enriched with plant stanol esters on serum lipids and apolipoprotein B in mildly hypercholesterolaemic subjects. Eur J Clin Nutr. 2006;60(11):1253-1257.  (PubMed)

91.  Allen RR, Carson L, Kwik-Uribe C, Evans EM, Erdman JW, Jr. Daily consumption of a dark chocolate containing flavanols and added sterol esters affects cardiovascular risk factors in a normotensive population with elevated cholesterol. J Nutr. 2008;138(4):725-731.  (PubMed)

92.  Devaraj S, Jialal I, Vega-Lopez S. Plant sterol-fortified orange juice effectively lowers cholesterol levels in mildly hypercholesterolemic healthy individuals. Arterioscler Thromb Vasc Biol. 2004;24(3):e25-28.  (PubMed)

93.  Devaraj S, Autret BC, Jialal I. Reduced-calorie orange juice beverage with plant sterols lowers C-reactive protein concentrations and improves the lipid profile in human volunteers. Am J Clin Nutr. 2006;84(4):756-761.  (PubMed)

94.  Matvienko OA, Lewis DS, Swanson M, et al. A single daily dose of soybean phytosterols in ground beef decreases serum total cholesterol and LDL cholesterol in young, mildly hypercholesterolemic men. Am J Clin Nutr. 2002;76(1):57-64.  (PubMed)

95.  Plat J, van Onselen EN, van Heugten MM, Mensink RP. Effects on serum lipids, lipoproteins and fat soluble antioxidant concentrations of consumption frequency of margarines and shortenings enriched with plant stanol esters. Eur J Clin Nutr. 2000;54(9):671-677.  (PubMed)

96.  Food and Drug Administration. GRAS Notice No. GRN 000112. 2003. Available at: Accessed 3/3/15.

97.  Scientific Committee on Food. Opinion on Applications for Approval of a Variety of Plant Sterol-Enriched Foods. 2003. Available at:

98.  Ayesh R, Weststrate JA, Drewitt PN, Hepburn PA. Safety evaluation of phytosterol esters. Part 5. Faecal short-chain fatty acid and microflora content, faecal bacterial enzyme activity and serum female sex hormones in healthy normolipidaemic volunteers consuming a controlled diet either with or without a phytosterol ester-enriched margarine. Food Chem Toxicol. 1999;37(12):1127-1138.  (PubMed)

99.  Berge KE. Sitosterolemia: a gateway to new knowledge about cholesterol metabolism. Ann Med. 2003;35(7):502-511.  (PubMed)

100.  Stalenhoef AF, Hectors M, Demacker PN. Effect of plant sterol-enriched margarine on plasma lipids and sterols in subjects heterozygous for phytosterolaemia. J Intern Med. 2001;249(2):163-166.  (PubMed)

101.  Kwiterovich PO, Jr., Chen SC, Virgil DG, Schweitzer A, Arnold DR, Kratz LE. Response of obligate heterozygotes for phytosterolemia to a low-fat diet and to a plant sterol ester dietary challenge. J Lipid Res. 2003;44(6):1143-1155.  (PubMed)

102.  Normen L, Holmes D, Frohlich J. Plant sterols and their role in combined use with statins for lipid lowering. Curr Opin Investig Drugs. 2005;6(3):307-316.  (PubMed)

103.  Thompson GR. Additive effects of plant sterol and stanol esters to statin therapy. Am J Cardiol. 2005;96(1 Suppl):37-39.  (PubMed)

104.  Blair SN, Capuzzi DM, Gottlieb SO, Nguyen T, Morgan JM, Cater NB. Incremental reduction of serum total cholesterol and low-density lipoprotein cholesterol with the addition of plant stanol ester-containing spread to statin therapy. Am J Cardiol. 2000;86(1):46-52.  (PubMed)

105.  Neil HA, Meijer GW, Roe LS. Randomised controlled trial of use by hypercholesterolaemic patients of a vegetable oil sterol-enriched fat spread. Atherosclerosis. 2001;156(2):329-337.  (PubMed)

106.  Simons LA. Additive effect of plant sterol-ester margarine and cerivastatin in lowering low-density lipoprotein cholesterol in primary hypercholesterolemia. Am J Cardiol. 2002;90(7):737-740.  (PubMed)

107.  Nguyen TT, Dale LC. Plant stanol esters and vitamin K. Mayo Clin Proc. 1999;74(6):642-643.  (PubMed)

108.  Raeini-Sarjaz M, Ntanios FY, Vanstone CA, Jones PJ. No changes in serum fat-soluble vitamin and carotenoid concentrations with the intake of plant sterol/stanol esters in the context of a controlled diet. Metabolism. 2002;51(5):652-656.  (PubMed)

109.  Korpela R, Tuomilehto J, Hogstrom P, et al. Safety aspects and cholesterol-lowering efficacy of low fat dairy products containing plant sterols. Eur J Clin Nutr. 2006;60(5):633-642.  (PubMed)

110.  Plat J, Mensink RP. Vegetable oil based versus wood based stanol ester mixtures: effects on serum lipids and hemostatic factors in non-hypercholesterolemic subjects. Atherosclerosis. 2000;148(1):101-112.   (PubMed)

111.  Plat J, Mensink RP. Effects of diets enriched with two different plant stanol ester mixtures on plasma ubiquinol-10 and fat-soluble antioxidant concentrations. Metabolism. 2001;50(5):520-529.  (PubMed)

112.  Ntanios FY, Duchateau GS. A healthy diet rich in carotenoids is effective in maintaining normal blood carotenoid levels during the daily use of plant sterol-enriched spreads. Int J Vitam Nutr Res. 2002;72(1):32-39.  (PubMed)

113.  Noakes M, Clifton P, Ntanios F, Shrapnel W, Record I, McInerney J. An increase in dietary carotenoids when consuming plant sterols or stanols is effective in maintaining plasma carotenoid concentrations. Am J Clin Nutr. 2002;75(1):79-86.  (PubMed) 


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