Sterols are plant lipids that have similar structures to the animal lipid cholesterol. Examples of sterols common to the human diet include β-sitosterol, campesterol and stigmasterol present in foods such as cereals, nuts and legumes. Because of their similar structure, plant sterols may interact with the same proteins as cholesterol and this may therefore have implications for cholesterol absorption and metabolism. For example, some evidence suggests that plant sterols might decrease the absorption of cholesterol through interaction with transporters along the enterocytes of the gut, thus reducing cholesterol absorption. Supplementation of hypercholesterolaemic individuals with products containing plant sterols lowers low density lipoprotein (LDL) cholesterol and this has lead some researchers to suggest that plant sterols may be beneficial to health. However, the long-term effects of high intakes of plant sterols on mortality are not known, and uncertainty still exists between the relationship between dietary sterols and cholesterol metabolism.
Because sterols may have useful health properties, researchers have investigated the effects of sterol fortified spreads on cholesterol absorption and cholesterol plasma levels. These spreads tend to be enriched margarine, with levels of sterols above those normally found in the diet. In one such study1, 82 hyperlipidaemic subjects randomly consumed either a placebo or low-fat margarine containing 2 g/d of sterols that comprised of 58.7 % β-sitosterol, 22.0 % campesterol, 9.6 % stigmasterol, with 2.4 % other sterols. After a 4 week washout period, subjects then crossed-over to the other treatment. The results showed that absorption of campesterol was greater than that for β-sitosterol with an absorption ratio of campesterol to β-sitosterol of around 4.5. Subjects with the highest basal plasma levels of sterols were more efficient at absorbing both cholesterol and plant sterols and had the lowest endogenous rates of synthesis.
Consumption of sterols in the margarine reduced the absorption efficiency of cholesterol by 34.3 %, but also reduced the absorption efficiency of campesterol and β-sitosterol by 36.5 and 39.3 %, respectively. However, the decrease in the absorption of cholesterol was associated with a 33 % increase in endogenous synthesis compared to the control. Therefore these data show that consumption of plant sterols decrease cholesterol (and sterol) absorption and this is compensated for by an increase in the synthesis of cholesterol. This is not surprising because it is known that decreasing dietary cholesterol intake through restriction also increases endogenous synthesis. This is the reason that low cholesterol diets do not reduce plasma levels of cholesterol. The fact that baseline levels of cholesterol synthesis were greatest in those with the lowest ability to absorb dietary cholesterol also supports the contention that the liver compensates for cholesterol restriction with up-regulated production.
While the data from this study are interesting, they do not suggest benefits from the consumption of plant sterols. Sterols are currently being researched with regard their cholesterol lowering effects, but in higher intakes than are normally present in the diet. This current trend to use plant sterols in a pharmacological manner is worrying because no clinical trials have been performed to assess their effects on total mortality. In fact, there is data to show that pharmacologically high concentrations of sterols may be detrimental to the health. High levels of sterols occur in a condition called phytosterolaemia (sitosterolaemia) and this results in atherogenic lesions and an increased risk of cardiovascular disease. The assumption that the reduction in LDL seen with high concentrations of plant sterols will translate into a health benefit is not therefore established, because it fails to take into account the possible increased risk from the plant sterols.
Sterol absorption is tightly controlled by the enterocytes of the gut. Sterols absorption is around 0.4 to 3.5 % in humans. Absorption of the closely related stanol compounds are even lower at 0.02 to 0.3 % in humans. This absorption difference is reflected in the plasma levels of sterols that can be 30 times higher than for stanols. Sterols are poorly absorbed because once absorbed across the apical surface of the enterocyte, they are effluxed back to the lumen of the gut, presumably to be excreted. In comparison to the low absorption of sterols and stanols, cholesterol absorption is between 35 and 70 % in humans. Worryingly, animals fed pharmacological levels of sterols accumulate them in tissues such as the liver, skin, aorta, adipose and adrenal glands, but the implications for human nutrition are not known, and even more worryingly have not been investigated.
Sterols are known to lower LDL, total and the ratio of LDL to high density lipoprotein (HDL) cholesterol, when used pharmacologically. From this a reduction in cardiovascular disease is inferred. However, this is the same logic that gave us the cholesterol theory of cardiovascular disease, which has subsequently been shown to be erroneous. Much of the supposition regarding the possible benefits of high intakes of sterols has come from animals experiment. Similar models were used to show that high intakes of cholesterol were able to cause atherosclerosis. However, the relevance of models using genetically deficient animals to infer possible effects to humans is questionable. In addition, administration of high levels of plant sterols and stanols has been shown to lower plasma levels of carotenoids and vitamin E in humans, both of which may be protective of cardiovascular disease. The health benefits of sterol therapy are therefore far from settled.
RdB
