we hear in the news and in commercials that plant sterols are good for us and lower cholesterol levels. we are even fortifying certain foods and some baby aspirin with these phytosterols. yet these phytosterols may be more atherogenic (have the ability to initiate or accelerate atherogenesis — formation of fat deposits on the inner lining of blood vessels) than cholesterol in certain groups of people. stanols on the other hand are good for everyone and do lower cholesterol levels. let’s start with some definitions: * cholesterol is a sterol. a sterol is a steroid with an alcohol group attached to it. * stanols are saturated or reduced sterols that are similar to cholesterol but have a methyl or an ethyl group attached to them. this difference minimizes stanol absorption in the intestines. * cholestanol is a stanol. cholesterol can be broken down by the liver into cholestanol and thus is a by-product of cholesterol metabolism. if sterols or stanols are esterified (combined with fatty acids) then they can be incorporated into margarine. we consume many sterols from plant sources (sitosterol campesterol and stigmasterol) shellfish (desmosterol and fucosterol) and animal sources (cholesterol). all of these sterols with the exception of cholesterol are collectively referred to as noncholesterol sterols. collectively these sterols can be called phytosterols. sitosterol represents about 80% of all noncholesterol sterols in the diet and is the most well known noncholesterol sterol in the diet. when fats (triglycerides) enter the intestine in our food they are broken down into their basic building blocks. the main breakdown products are called fatty acids. these fatty acids and sterols from dietary sources are packaged into what is called a micelle. these micelles “ferry” these fatty acids and sterols to the intestinal lining (epithelium). they are then absorbed by passive diffusion into the intestinal cells. passive diffusion is a biological principle that substances flow through a semi-permeable tissue from an area of higher concentration to an area of lesser concentration. there is no pump required to get them out of the intestine and ultimately into the bloodstream. most humans absorb about 50% of sterols in the intestines. however there are some people who are what is termed” hyperabsorbers” (they absorb 60-80%) and some are “hypoabsorbers” (they absorb less than 50%). noncholesterol sterols are not esterified as humans do not have the enzymes necessary for that. when these unesterified sterols get into an arterial wall they are more atherogenic than cholesterol (an esterified sterol). this means they have a greater artery clogging potential than does cholesterol. if one lacks these transporters (homozygote) all sterols are absorbed and none are pumped back out: this is a very rare homozygous condition leading to the disease called sitosterolemia or phytosterolemia. it is associated with severe atherosclerosis as noncholesterol sterols (which cannot be esterified) are more atherogenic than cholesterol. heterozygotes people who have some transporter function eliminate some but not all of these phytosterols. stanols do not require these transporters to get back into these intestines. this is the reason that they are safe and effective to reduce cholesterol. stanols are commercially available in the supermarket in a product called benecol. in summary noncholesterol sterols serve no physiologic function in man. all sterols are atherogenic if they accumulate in the arterial wall. stanols are saturated sterols. they are not absorbed and can be used therapeutically to reduce cholesterol absorption from the intestine.
what is the critical difference between a sterol and a stanol?