Stanol esters is a heterogeneous group ofchemical compounds known to reduce the level oflow-density lipoprotein (LDL)cholesterol inblood when ingested,[1] though to a much lesser degree than prescription drugs such asstatins.[2] The starting material isphytosterols from plants. These are firsthydrogenated to give a plant stanol (phytostanol) which is thenesterified with a mixture offatty acids also derived from plants. Plant stanol esters are found naturally, occurring in small quantities in fruits, vegetables, nuts, seeds, cereals, legumes, and vegetable oils.
Stanol ester is often added torapeseed oil-basedmargarine or other foods for its health benefits. Studies have indicated that consumption of about 2-3 grams per day provides a reduction in LDL cholesterol of about 10-15%.[3]
The compound itself passes through thegut, with very little entering theblood stream orlymph. Its presence in the gut, however, reduces both the amount ofcholesterol the body absorbs from food and the reabsorption of the cholesterol component ofbile. Despite a well documented cholesterol lowering effect, there are no data available indicating thatfunctional foods supplemented with plant sterol esters reduce cardiovascular events.[4] They are used in food products such asBenecol.
Sterol esters can also be used for the same purpose. These compounds have the same effect to LDL, but they are partially absorbed by the body. The effects of higher serum plant sterol levels are so far not completely understood.
Plant sterols arecholesterol-like molecules found in all plant foods, with the highest concentrations occurring invegetable oils. Plant sterols are plant equivalents ofcholesterol and have a very similar molecular structure. According to their structure, they can be divided into sterols and stanols, stanols being a saturated subgroup of sterols.[citation needed]
Plant stanols are present in small amounts in human diet. Their main sources arewhole-grain foods, mostlywheat andrye. The daily intake of stanols in the averagewestern diet is about 60 mg/d, whereas the intake of plant sterols is about 150–300 mg/d and that of cholesterol is 500–800 mg/d. The relatively low natural levels of stanols in the diet are too low to have a significant effect onserum cholesterol levels.[citation needed]
Following evidence from toxicological studies and numerousclinical trials, stanols are characterised as safe by authorities in several European Union countries and by the USFood and Drug Administration (FDA).[citation needed]
Stanol esters are a saturated subgroup of sterol esters. Plant stanol esters in Benecol products arefatty acid esters of plant sterols. The sterol part of the molecule is sitostanol or campestanol while the fatty acid residue originates from different vegetable oils.
Plant stanol esters have the following physical properties:
These physical properties can be tailored by changing the fatty acid composition. In different technological applications of Benecol products, thefatty acid part is selected so that the melting properties, texture and other characteristics of the plant stanol ester closely resemble the properties of the fat it replaces.
Under normal storage and food preparation conditions, plant stanol esters are very stable because they are more resistant tooxidation than the commonestvegetable oils.
Using plant stanol esters in food applications instead of conventional fats does not decrease the shelf life of the end product. As is the case for all fats and oils, stanol esters should be protected from heat, air and light to prevent oxidation. If long-term storage is required, plant stanol esters are typically refrigerated in solid form. Furthermore, the usualantioxidants can be added to plant stanol ester products as they are to other oils or fats to minimise oxidation.
Esterified plant stanols have been proven to reducecholesterol in a number of randomised, placebo-controlled double-blindclinical trials. However absolutely no effect on clinical endpoints such as CVD or mortality was demonstrated.
Plant stanols reduce both cholesterol and plant sterol levels in serum. This may be of importance since elevated plant sterol concentrations have been identified as an independentrisk factor forcoronary heart disease (CHD). TwoABC transporters (ABCG5 and ABCG8) play an important role in the regulating the intestinal absorption of plant sterols by resecreting previously absorbed plant sterols from theenterocytes back into theintestinal lumen.
Mutations in these transporter proteins lead to a rare congenital disease called sitosterolaemia, which is characterised by:
It was recently shown that polymorphisms in the ABCG5 and ABCG8 genes contribute to modifying serum plant sterol levels in healthy, non-sitosterolaemic individuals. Furthermore, severalepidemiological studies have shown that the risk of developing heart disease seems to be increased even at more "normal" plant sterol levels.[1][4][5][6][7] Since statins were shown to increase serum plant sterol concentrations,[8][9] patients should probably not be treated with statins alone but with a combination therapy focusing simultaneously on improving the serum lipoprotein profile and lowering serum plant sterol concentrations.
The molecular mode of actions of stanols has been described in several preclinical andclinical trials and can be divided into two steps:
As a consequence of the reduced absorption of cholesterol, the absorption of fat-soluble components other than cholesterol, such asvitamins andantioxidants, may also be reduced. Like cholesterol,carotenoids andtocopherols are transported bylipoproteins. Since the number ofLDL particles in circulation decreases after consumption of plant sterols or stanols, plasma concentrations of carotenoids and tocopherols also decrease. This is why these antioxidants are often standardized to plasma lipid concentrations.
The results of randomised,placebo-controlled trials on the effects of plant sterols or stanols on fat-soluble vitamins and antioxidants were summarised in 2003.[10] Significant reductions were only seen in clinical trials for hydrocarboncarotenoids. These reductions are probably caused by reduced absorption and lower plasma concentrations of the carrier, LDL.
After correcting for cholesterol levels, only the reduction in theβ-carotene level remained. It is important, however, that carotenoid and tocopherol levels remained within the normal ranges. Clinical trials also showed that when following the recommended diet, including consumption of vegetables and fruit, carotenoid levels did not decrease.[11][12] Plasma concentrations ofretinol (vitamin A),25-hydroxyvitamin D andvitamin K are unaffected by dietary plant sterols and stanols.