cholesterol
American Heritage Dictionary:
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cho·les·ter·ol
n.
A white crystalline substance, C27H45OH, found in animal tissues and various foods, that is normally synthesized by the liver and is important as a constituent of cell membranes and a precursor to steroid hormones. Its level in the bloodstream can influence the pathogenesis of certain conditions, such as the development of atherosclerotic plaque and coronary artery disease.
[cholester(in), former name for cholesterol (CHOLE- + Greek stereos, solid + -IN) + -OL1 (so called because it was first found in gallstones).]
Britannica Concise Encyclopedia:
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cholesterol
Waxy organic compound found in blood and all animal tissues. It is a steroid, with molecular formula C27H46O, containing four rings in its structure. Cholesterol is essential to life; it is a primary component of cell membranes and a starting or intermediate material from which the body makes bile acids, other steroid hormones, and vitamin D. It is made in the liver and some other organs, in greater or lesser amounts depending on the amount recently consumed in the diet. It circulates in the blood in compounds called lipoproteins, since it is not water-soluble alone. Excess cholesterol in the blood forms deposits in arteries ( arteriosclerosis), which can lead to coronary heart disease. Michael Brown (born 1941) and Joseph Goldstein (born 1940) won a Nobel Prize in 1985 for their work in discovering this process. Since the body makes cholesterol from fats, blood cholesterol cannot be reduced by limiting only the amount of cholesterol in the diet; the amount of fat, especially saturated fat ( saturation, fatty acid) must also be reduced. triglyceride.
For more information on cholesterol, visit Britannica.com.
McGraw-Hill Science & Technology Encyclopedia:
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Cholesterol
A cyclic hydrocarbon alcohol commonly classified as a lipid because it is insoluble in water but soluble in a number of organic solvents. It is the major sterol in all vertebrate cells and the most common sterol of eukaryotes. In vertebrates, the highest concentration of cholesterol is in the myelin sheath that surrounds nerves and in the plasma membrane that surrounds all cells.
Cholesterol can exist either in the free (unesterified) form (see structure below) or in the esterified form, in which a fatty acid is
Cholesterol, together with phospholipids and proteins, is important in the maintenance of normal cellular membrane fluidity. At physiological temperatures, the cholesterol molecule interacts with the fatty acids of the membrane phospholipids and causes increased packing of the lipid molecules and hence a reduction of membrane fluidity. Thus, all vertebrate cells require cholesterol in their membranes in order for the cell to function normally. Cholesterol is also important as a precursor for a number of other essential compounds, including steroid hormones, bile acids, and vitamin D. See also Steroid.
Cellular cholesterol is obtained both from the diet, following its absorption in the intestine, and from synthesis within all cells of the body. Foods that are particularly high in cholesterol include eggs, red meat, and organs such as liver and brain. About 40–50% of the dietary cholesterol is absorbed from the intestine per day. In contrast, plant sterols are very poorly absorbed. Cholesterol synthesis occurs in all vertebrate cells but is highest in the liver, intestine, and skin, and in the brain at the time of myelination.
Cholesterol and cholesteryl esters are essentially insoluble in water. In order to transport these compounds around the body in the blood, the liver and intestine produce various lipid-protein complexes, called lipoproteins, which serve to solubilize them. Lipoproteins are large, complex mixtures of cholesterol, cholesteryl esters, phospholipids, triglycerides (fats), and various proteins. The major lipoproteins include chylomicrons, very low density lipoprotein (VLDL), low-density lipoprotein, and high-density lipoprotein (HDL).
Total plasma cholesterol levels of less than 200 mg/100 ml are considered desirable. Values of 200–239 or greater than 239 mg per 100 ml are considered, respectively, borderline high or high risk values, indicating the potential for a heart attack. High levels of low-density lipoprotein in the plasma are associated with increased risk of atherosclerosis, (“hardening of the arteries”), which involves deposition of cholesterol and other lipids in the artery wall. Diets low in cholesterol and saturated fats often result in a reduction in total plasma and LDL cholesterol levels. Such changes in blood cholesterol levels are thought to be beneficial and to reduce the incidence of heart attacks.
Oxford Food & Nutrition Dictionary:
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cholesterol
The principal sterol in animal tissues, an essential component of cell membranes and the precursor for the formation of the steroid hormones. It is transported in the plasma lipoproteins. Not a dietary essential, since it is synthesized in the body. Eggs contain about 450 mg, milk 14 mg, cheese 70-120 mg, brain 2.2 mg, liver and kidney 300-600 mg, poultry 70-100 mg, and fish 50-60 mg/100 g.
An elevated plasma concentration of cholesterol is a risk factor for atherosclerosis. The synthesis of cholesterol in the body is increased by a high intake of saturated fats, but apart from people with a rare genetic defect in the regulation of cholesterol synthesis, dietary intake of cholesterol does not affect the plasma concentration very much, since there is normally strict control over the rate of synthesis. See also hypercholesterolaemia; hyperlipidaemia; HMG CoA reductase inhibitors;
Oxford Food & Fitness Dictionary:
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cholesterol
A white, waxy substance, related to fats. It occurs naturally in most animal tissue. Foods particularly rich in cholesterol include eggs and offal.
Many people are surprised to learn that cholesterol has a number of essential functions in the human body: it is used in tissue repair; for strengthening cell membranes; and for the manufacture of bile salts, steroid hormones (including the sex hormones, oestrogen and testosterone), and vitamin D. There is little danger of cholesterol deficiency because it can be manufactured in the liver from fats, carbohydrates, and proteins.
The problems associated with cholesterol arise because modern diets in northern Europe and North America often result in over-production. A lot of cholesterol is not used but is deposited in the walls of blood vessels where it increases the risk of coronary heart disease and atherosclerosis. The most influential factor in raising blood cholesterol levels is eating foods high in saturated fat. Nicotine increases deposition of cholesterol in the walls of blood vessels. Hereditary factors are also important determinants of blood cholesterol levels.
A good diet can decrease blood cholesterol levels. Soluble fibre, polyunsaturated fat (especially fish fats which contain omega-3 fatty acids), and monounsaturated fat (such as olive oil) may all lower cholesterol levels. Regular aerobic exercise helps to reduce deposition of cholesterol in blood vessels.
Blood cholesterol levels vary considerably and there is no universally accepted safe level, but the following are guidelines used by most doctors:
| CHOLESTEROL LEVELS | |
|---|---|
| desirable levels | <5.2 mmol/l (<200 mg/dl) |
| slightly raised | 5.2-6.4 mmol/l (200-250 mg/dl) |
| high | 6.5-7.8 mmol/l (251-300 mg/dl) |
| very high | >7.8 mmol/l (>300 mg/dl) |
Several cholesterol test-kits can be bought over the counter. If used properly, these can give quite accurate readings, but interpreting the results is not easy, and the results may make a person unnecessarily anxious. A number of factors can affect blood cholesterol levels temporarily. Exercising or eating before the test can raise levels by more than 15 per cent. It is normal for cholesterol levels to fluctuate, so at least two tests, separated by one or two months, are needed to give a reliable average. People who are worried about their cholesterol level should have it checked properly by a doctor.
Although many people with high cholesterol levels have an increased risk of coronary heart disease, the effects of treatment are not straightforward. Treatment has been linked to increases in deaths from other causes (notably violent deaths). Cholesterol testing may be advisable for those at greatest risk (such as those with a family history of high cholesterol levels or coronary heart disease) and who are prepared to change their lifestyle. But many doctors believe that automatic screening and self-testing may turn healthy people into patients chronically anxious about their cholesterol levels. As one medical textbook states ‘It may be healthier not to know’.
Oxford Companion to the Body:
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cholesterol
Many people are now aware of their own blood cholesterol level, have it measured regularly and eat diets high in polyunsaturates. This is because they know that high cholesterol levels in the blood, and fat-rich diets, are likely to lead to heart attacks and strokes, particularly in later life. Some also know that the narrowing of arteries, particularly the coronary arteries, is due to the deposition of atherosclerotic plaques, made largely of cholesterol, on the walls of the vessels. Narrowing of the arteries reduces the flow rate, especially as flow depends on the fourth power of the radius. Thus, at a given pressure, reducing the radius to one half of normal would reduce the flow rate to one sixteenth of the original value. Adequate flow can then only be maintained by a rise in blood pressure.
The importance of cholesterol in the body can be gauged from the words of Brown and Goldstein in their Nobel Prize Lecture in 1985. They described cholesterol as the ‘most decorated’ molecule in biology, as no less than 13 Nobel awards had been made to those who spent their lives studying the substance, adding that ‘the property that makes it useful in cell membranes, namely its absolute insolubility in water, also makes it lethal’.
Cholesterol was first isolated from gallstones in 1784. It is a neutral lipid, a sterol, and an important constituent of cell membranes. Cholesterol is obtained through the diet and synthesized in the body, in the liver and the intestine. When the intake is high, synthesis is suppressed. The cholesterol molecule has 27 carbon atoms, yet the synthesis of this complex molecule is from 2-carbon fragments (acetyl CoA) in a very complex biosynthetic process. Cholesterol is the necessary precursor of several sterol (steroid) hormones, such as the sex hormones testosterone and oestrogens, and the adrenal steroid hormones, including cortisol. Not surprisingly — remembering that cholesterol was found first in gall stones — cholesterol is used to make bile salts, the constituents of bile which take an essential part in fat absorption from the gut.
To understand how atherosclerotic plaques become deposited in arteries it is necessary to understand how the highly insoluble cholesterol is moved about the body. The agents which transport cholesterol are the lipoproteins — consisting, as their name implies, of a lipid and a protein component. Fats and cholesterol absorbed from the diet are transported as ‘chylomicrons’ from the intestine to the liver, where the fats are rapidly metabolized, and cholesterol is incorporated into low density lipoprotein (LDL) along with phospholipid molecules and one molecule of a huge protein called B-100. LDL is the main cholesterol transporter, transferring it from the liver to all other parts of the body. Since cholesterol is an essential component of all cell membranes it will be needed anywhere new cells are being formed.
The B-100 protein is a key component of LDL, as it is the molecule that is recognized by LDL receptors in the membrane of all cells. After this recognition, the LDL complex is internalized and broken down in the cell, which thus has its vital supply of cholesterol delivered to it. The LDL receptor is recycled back to the membrane to wait for another LDL. When the supply of cholesterol is plentiful the LDL receptors are ‘down regulated’ (their numbers are reduced), leaving low density lipoprotein circulating in the blood with its potentially lethal cargo of cholesterol. Eventually the cholesterol is deposited in a variety of sites, including the skin, but it is the deposition in blood vessels that leads to the start of atherosclerotic disease.
These processes were worked out in the researches of Brown and Goldstein in the 1970s from studies on patients with familial hypercholesterolamia — excessively high blood cholesterol. In this genetic disease, LDL membrane receptors are absent, so the uptake of LDL into cells is prevented. Heterozygotes (who have inherited one normal gene and one gene for this disease from their parents) have only half the normal number of LDL receptors. Normal persons have about 175 mg cholesterol per 100 ml of blood plasma, while those with the disease have over 600 mg/100 ml and heterozygotes about 300 mg/100 ml. Homozygotes with the disease usually die in infancy of coronary artery occlusion.
— Alan W. Cuthbert
See also bile; fats; gall bladder.
Oxford A-Z of Medicinal Drugs:
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cholesterol
A complex molecule that has a core structure similar to that of a steroid molecule; it is attached to a fatty acid to form cholesterol ester. Cholesterol is vital to life, being an essential component of all animal cell membranes (plants do not contain cholesterol), and is required to make bile acids (needed for fat absorption), adrenal hormones corticosteroids, sex hormones (androgens, oestrogens), and vitamin D. Cholesterol forms part of the diet and is also synthesized in the body, mainly in the liver. It is carried in the blood by lipoproteins. Too much cholesterol in the bloodstream (hypercholesterolaemia: see hyperlipidaemia) can lead to deposits (plaques) on the inner wall of the arteries, giving rise to atherosclerosis. In the advanced stage, usually when a vessel is more than 50% blocked, atherosclerosis can result in thrombosis, causing a stroke or heart attack. A high circulating concentration of low-density lipoprotein (low-density lipoproteins) cholesterol is one of the most important risk factors for developing coronary heart disease. It enhances the adverse effects of other risk factors, such as smoking, obesity, hypertension, and diabetes. Reducing circulating cholesterol lowers the incidence of heart attacks and other events related to coronary artery disease. Cholesterol reduction is achieved by dietary modification (reducing the intake of saturated fats and increasing consumption of fibre, oats, and pulses), which is the usual first-line treatment, or by lipid-lowering drugs. It is important that other cardiovascular risk factors are also addressed.
| chlortetracycline, chlortalidone, chlorpromazine hydrochloride | |
| choline salicylate, cholinergic drugs, chromones |
Oxford Dictionary of Sports Science & Medicine:
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cholesterol
A lipid-related compound found in tissues and manufactured in the liver. Cholesterol has a number of essential functions: it is important for body tissue repair; it is a constituent of cell membranes which it helps strengthen; it forms the starting point of steroid manufacture and is involved in the formation of several hormones; it forms bile salts; and it is the raw material for vitamin D. Dietary sources of cholesterol include animal products such as eggs, meat, and cheese. A high-fat diet can increase blood cholesterol levels. Nicotine (from tobacco smoking) increases deposition of cholesterol in arterial walls, but hereditary factors are also important determinants of blood cholesterol levels. High blood cholesterol levels are associated with cardiovascular diseases. Blood cholesterol levels can be decreased by taking regular aerobic exercise and eating a low-fat diet. A deficiency of cholesterol is rare. See also high-density lipoproteins, low-density lipoproteins.
Columbia Encyclopedia:
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cholesterol
cholesterol (kəlĕs'tərōl'), fatty lipid found in the body tissues and blood plasma of vertebrates; it is only sparingly soluble in water, but much more soluble in some organic solvents. A steroid, cholesterol can be found in large concentrations in the brain, spinal cord, and liver. The liver is the most important site of cholesterol biosynthesis, although other sites include the adrenal glands and reproductive organs. By means of several enzymatic reactions, cholesterol is synthesized from acetic acid; it then serves as the major precursor for the synthesis of vitamin D3, of the various steroid hormones, including cortisol, cortisone, and aldosterone in the adrenal glands, and of the sex hormones progesterone, estrogen, and testosterone. Cholesterol is excreted from the liver in the form of a secretion known as bile; it sometimes crystallizes in the gall bladder to form gallstones. The insolubility of cholesterol in water is also a factor in the development of atherosclerosis (see arteriosclerosis), the pathological deposition of plaques of cholesterol and other lipids on the insides of major blood vessels, a condition associated with coronary artery disease. This buildup of cholesterol in the blood vessels may constrict the passages considerably and inhibit the flow of blood to and from the heart. Recent research has shown that the relative abundance of certain protein complexes, called lipoproteins, to which cholesterol becomes attached may be the real cause of cholesterol buildup in the blood vessels. High-density lipoprotein (HDL) carries cholesterol out of the bloodstream for excretion, while low-density lipoprotein (LDL) carries it back into the system for use by various body cells. Researchers believe that HDL and LDL levels in the bloodstream may be at least as important as cholesterol levels, and now measure both to determine risk for heart disease. Reducing consumption of foods containing cholesterol and saturated fat has been found to lower blood cholesterol levels. Cholesterol levels can also be reduced with drugs, most especially with HMG-CoA reductase inhibitors (commonly called "statins"), such as lovastatin (Mevacor) and atorvastatin (Lipitor), and by regular exercise.
Gale Encyclopedia of Food & Culture:
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Cholesterol
Cholesterol is one of the most widely disseminated organic compounds in the animal kingdom. Almost three hundred years ago, Antonio Vallisnieri observed that gallstones were soluble in turpentine or alcohol. Poulletier de la Salle, some thirty years later, demonstrated that the main constituent of gallstones could be crystallized from alcohol. This substance was thought to be a wax until 1815, when Michel Eugène Chevreul showed that it was not saponifiable and gave it the name "cholesterine" derived from the Greek chole, bile, and steros, solid. Soon thereafter, it was isolated from blood, brain, tumors, and egg yolk. The isolated compounds were shown to be identical. In 1843 Vogel found it in atherosclerotic arteries.
The chemical structure of cholesterol was elucidated over the years beginning in 1859. The compound was shown to contain a secondary hydroxyl group and a double bond. The exact empirical formula (C27H46O) was established in 1888 by Friedrich Reinitzer. Proof of structure was obtained chiefly through the brilliant work of Adolf Windaus and Heinrich Wieland. The structure of cholesterol suggested by Windaus and Wieland in the 1920s was incorrect, but that does not detract in any way from their contribution. The true structure was established in the 1930s based on X-ray diffraction data.
There were many suggestions regarding the biological synthesis of cholesterol. The biosynthetic pathway became accessible with the introduction of radioactive carbon in the 1940s. The biosynthetic scheme was generally elucidated by the work of Konrad Bloch, George Popjak, and John Cornforth. It was first shown that cholesterol could be synthesized in mammals and ergosterol in yeast from small organic molecules. Eventually it was shown that all twenty-seven carbon atoms of cholesterol were derived from the two carbon atoms of acetate. The methyl group of acetate contributed fifteen of the twenty-seven carbons of cholesterol and the carboxyl group contributed twelve. The pathway began with the condensation of two acetate residues to give acetoacetate and addition of one more two-carbon moiety to yield hydroxymethylglutaric acid (HMG). HMG lost a carbon atom and the resulting compound rearranged to provide an isoprene unit. Two five-carbon units combined to give a geranyl derivative that added another isoprene to give a farnesyl unit. Two farnesyl units united to provide squalene (C30H50), a hydrocarbon found in the livers of some species of shark that cyclyzed to yield lanosterol, a thirty-carbon atom sterol also found in sheep wool. In a series of rearrangements and demethylations, lanosterol yielded cholesterol. The key step in this complex synthetic pathway involves the reduction of HMG-CoA. Inhibition of HMG-CoA reductase is the basis of a number of potent new serum cholesterol-lowering drugs.
Cholesterol represents about 0.2 percent of the weight of the human body. As Table 1 shows, the bulk of the body's cholesterol is present in two tissues; one is the brain and nerve tissue, the other is muscle. In the brain, cholesterol is thought to act as an insulator, but there have been relatively few studies of the metabolism of brain cholesterol. The next large reservoir of cholesterol is muscle. Between them, nervous tissue and muscle carry 44 percent of the body's cholesterol. The cholesterol in these reservoirs turns over slowly.
Cholesterol is ubiquitous in the human body, where it plays structural and metabolic roles. Together with phospholipid, cholesterol is present in every cell membrane. In the adrenals, cholesterol is converted to adrenocortical hormones such as cortisone. In the gonads, cholesterol is converted to the appropriate sex hormone—estradiol in women, testosterone in men. The cholesterol in skin is the precursor of 7-dehydrocholesterol, which is ultimately converted to vitamin D. The major catabolic products of cholesterol are the bile acids—cholic and chenodeoxycholic. These are designated as the primary bile acids; they are metabolized in the liver to deoxycholic and lithocholic acids. It has been estimated that over 90 percent of biologically synthesized cholesterol is metabolized to bile acids. In general, the body synthesizes more cholesterol than it ingests.
Table 1
| Distribution of cholesterol in a 70-kg man | ||
| Tissue | Cholesterol content (g) | % of Total |
| Brain, nervous system | 32.0 | 23 |
| Connective tissue, body fluids | 31.3 | 22 |
| Muscle | 30.0 | 21 |
| Skin | 12.6 | 9 |
| Blood | 10.8 | 8 |
| Bone marrow | 7.5 | 5 |
| Liver | 5.1 | 4 |
| Heart, lungs, kidneys, spleen | 5.0 | 4 |
| Alimentary tract | 3.8 | 3 |
| Adrenals | 1.2 | 1 |
| Skeleton | 0.7 | — |
| Other glands | 0.2 | — |
In 1912 Nicolai Anitschkow showed that cholesterolfed rabbits developed aortic deposits similar to early human atherosclerosis. His experiments presented a possible explanation of human atherosclerosis and that particular debate has not yet abated. Simultaneously with Anitschkow's studies, A. I. Ignatowski demonstrated the atherogenic potential of animal protein, but compared to work on cholesterol and fat there has only been a desultory interest in protein effects.
Since Anitschkow's results were obtained by dietary manipulation, the view that dietary cholesterol was implicated in atherogenesis was accepted generally. With development of simple, rapid methods of cholesterol analysis, it became possible to screen populations for blood cholesterol content. Large epidemiological studies were launched and their results helped to develop the concept of risk factors for heart disease. Currently, the major risk factors are hypercholesterolemia, hypertension, smoking, obesity, and maleness. However, emerging data suggest that homocysteinemia and inflammation (due to infection with cytomegalovirus or chlamydia pneumoniae) are also important factors.
When cholesterol is ingested, it is emulsified with phospholipid and absorbed. The absorbed lipid circulates in the blood as a water soluble lipid-protein complex called lipoprotein. Initially, absorbed cholesterol is part of a large, triglyceride-rich particle called the chylomicron. In the course of circulation, the triglyceride is removed by activity of cellular lipases and the particles become smaller and their cholesterol content increases. The cholesterol-containing, lipid-protein complex consists of several fractions that are separable by virtue of their hydrated densities. In general terms, the four major fractions are the triglyceride-rich chylomicrons and very low density (VLDL), the cholesterol-rich low density (LDL), and the protein-rich high density (HDL).
Due to development by John Gofman of methods for ultracentrifugal separation of lipoproteins, researchers have been able to isolate and study lipoproteins. The cholesterol-rich low density lipoproteins (LDL) are thought to be major risk factors for coronary disease. It was demonstrated that oxidized LDL is the real villain in coronary disease. It also was shown that LDL can be subfractionated into small, dense and large "fluffy" particles. The small particles appear to infiltrate the artery preferentially. Researchers also know that the process of atherogenesis is not simple and is mediated by an array of small proteins. The high-density lipoproteins are about 50 percent protein. In the simplest terms, LDL facilitates entry of cholesterol into cells and HDL facilitates its removal. LDL receptors on the cell surface facilitate LDL uptake. The proteins of lipoproteins are very important because they provide recognition by cells, and it is now becoming evident that genetic differences in apolipoproteins may dictate susceptibility to disease as well as chances for the efficacy of medication.
The effects of dietary cholesterol became a concern shortly after Anitschkow's observation and warnings regarding excess levels of cholesterol intake, which constitute one of the foundations of dietary therapy. Since cholesterol occurs only in food of animal origin, it was a simple extension to seek an explanation of the role of cholesterol by examining the lipids of food from animal sources. Although no dietary fat is totally saturated or unsaturated, attention also turned to effects of fat saturation.
The amount of cholesterol in the average American diet is in the range of 300–350 mg/day. It used to be much higher. The levels of cholesterol in a number of common animal foods are given in Table 2. It is evident that most muscle contains about the same amount of cholesterol, 81 ± 7 mg/100g. Cholesterol content of butter (per 100 g) is high, but we rarely eat more than 5–10 g of butter per meal. Shrimp is high in cholesterol but very low in fat. Eggs are also high in cholesterol. Continuing research nevertheless indicates that the cholesterol level of a food per se has little effect on serum cholesterol levels. The cholesterolemic effect is a function of dietary fat saturation. It has been shown that the absorption of cholesterol is more a function of the accompanying dietary fat than of cholesterol itself. Saturated dietary fat leads to higher cholesterol levels than does unsaturated fat. This observation is true for most people who are called "non-responders" (to dietary cholesterol). A small number of people are "responders," meaning they absorb more cholesterol, regardless of accompanying fat. In the late 1960s, Keys and Hegsted developed formulas for estimating changes in serum cholesterol based upon changes in dietary fat. There have been a number of more complex formulas developed, but the originals are referred to most often today. Essentially, they found saturated fatty acids to be hypercholesterolemic and unsaturated fatty acids to lower cholesterol. Stearic acid was considered neutral. The polyunsaturated fats lower cholesterol across the board so that HDL cholesterol (the "good" cholesterol) falls as does LDL cholesterol. Oleic acid seems to affect only LDL cholesterol. The reduction in total cholesterol may not be as profound, but the LDL/HDL cholesterol ratio is improved. Recent findings show that the structure of individual triglycerides may also influence their atherogenicity.
In summary, cholesterol is a substance that appears in all cells and also has a number of metabolic functions.
Table 2
| Cholesterol content (mg/100g) of selected foods | |
| Food source | Cholesterol (mg/100g) |
| Egg | 504 |
| Butter | 250 |
| Shrimp | 150 |
| Mackerel | 95 |
| Herring | 85 |
| Chicken | 81 |
| Turkey | 74 |
| Lamb | 71 |
| Veal | 71 |
| Beef | 68 |
| Pork | 62 |
| Flounder | 50 |
| Milk | 15 |
It is synthesized in the body and is part of every cell membrane. Cholesterol is metabolized to adrenocortical or sex hormones, bile acids, and vitamin D. Levels of serum cholesterol are related to risk of coronary disease, but it should be borne in mind that cardiovascular disease is a metabolic disease, not one of cholesterol deposition. Dietary cholesterol is absorbed, but its effects on serum cholesterol are slight. Generally, there is an increase of about 2 mg of serum cholesterol for every 100 mg ingested. Cholesterol should be viewed as a chemical necessary for life and not as a toxic substance. As with so many other aspects of life, moderation is the key.
Bibliography
Gibbons, G. F., K. A. Mitropoulos, and Nick B. Myant. Biochemistry of Cholesterol. Amsterdam: Elsevier Biomedical Press, 1982.
Howell, Wanda H., et al. "Plasma Lipid and Lipoprotein Responses to Dietary Fat and Cholesterol: A Meta Analysis." American Journal of Clinical Nutrition 65 (1997): 1747–1764.
Keys, Ancel, Joseph T. Anderson, and Francisco Grande. "Serum Cholesterol Response to Changes in Diet, IV: Particular Fatty Acids in the Diet." Metabolism 14 (1965): 776–787.
Kritchevsky, David. Cholesterol. New York: Wiley, 1958.
Kritchevsky, David. "Food Lipids and Atherosclerosis." In Food Lipids and Health, edited by Richard E. McDonald and David B. Min. New York: M. Dekker, 1996.
Leinoneu, M. "Chlamydia pneumoniae and Other Risk Factors for Atherosclerosis." Journal of Infectious Diseases 181, Suppl. 3 (2000): S414–S416.
Myant, Nick B. The Biology of Cholesterol and Related Steroids. London: Heinemann Medical Books, 1981.
Myant, Nick B. Cholesterol Metabolism, LDL, and the LDL Receptor. San Diego, Calif.: Academic Press, Inc., 1990.
—David Kritchevsky
Dictionary of Cultural Literacy: Health:
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cholesterol
(kuh-les-tuh-rawl, kuh-les-tuh-rohl)
A white soapy substance found in the tissues of the body and in certain foods, such as animal fats, oils, and egg yolks. Cholesterol has been linked to heart disease and atherosclerosis. (It collects on the walls of arteries and interferes with the flow of blood.) High levels of cholesterol in the blood are considered to be unhealthy. (See saturated fats, HDL, and LDL.)
Word Tutor:
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cholesterol
IN BRIEF: A waxy substance found in the body and in certain foods.
Having high cholesterol is unhealthy for many people.
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Wiley Dictionary of Flavors:
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Cholesterol
A fat-soluble waxy substance that is found in animal-derived foods. Humans can generate cholesterol or it can be derived from ingesting foods containing it. Serum cholesterol, the amount of cholesterol in the blood, has been linked to deposits in the vascular linings and can cause circulatory blockage and subsequent coronary thrombosis (heart attack). Stanols and sterols have been seen to lower cholesterol. See Fat, HDL, LDL.
Oxford Dictionary of Biochemistry:
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cholesterol
cholest-5-en-3β-ol; the principal sterol of vertebrates and the precursor of many steroids, including bile acids and steroid hormones. It is found in all animal tissues, especially brain and spinal cord, in the bile, and in gallstones, being a component of the plasma membrane lipid bilayer. Both cholesterol and cholesterol esters are present in plasma lipoproteins and excessive levels in the plasma are implicated in atherogenesis. It is synthesized from acetyl-CoA via hydroxymethylglutaryl-CoA and squalene, by enzymes in the cytosol (acetyl-CoA → mevalonate), peroxisomes (mevalonate → farnesyl pyrophosphate), and endoplasmic reticulum (farnesyl pyrophosphate → cholesterol). Deficiency of cholesterol occurs in Smith-Lemli-Opitz syndrome. Cholesterol accumulates in hypercholesterolemia, cholesterol ester storage disease, Wolman disease, and some forms of Niemann-Pick disease.
| cholesteric, cholestasis, cholestanol | |
| cholesterol 7α-monooxygenase, cholesterol ester storage disease, cholesterol monooxygenase |
Saunders Veterinary Dictionary:
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cholesterol
A steroid alcohol found in animal fats and oils, bile, blood, brain tissue, milk, egg yolk, myelin sheaths of nerve fibers, liver, kidneys and adrenal glands. It is a necessary component of all cell surface and intracellular membranes and a constituent of myelin in nervous tissue; it is a precursor of bile acids and steroid hormones, and it occurs in the most common type of gallstone, in atheroma of the arteries, in various cysts, and in carcinomatous tissue. Most of the body's cholesterol is synthesized, but some is obtained in the diet.
The preoccupation in human medicine with the relationship between cholesterol and the development of atheromatous plaques in the coronary arteries is not reflected in veterinary medicine. The importance of cholesterol to the veterinarian is limited to the measurement of blood cholesterol levels as an indicator of liver disease or thyroid activity.
- c. pneumonia — see endogenous-lipid pneumonia.
Mosby's Dental Dictionary:
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cholesterol
(kəles′tərôl)
n
n
A lipid common to all animal, but not plant, cells. As a sterol, it contains the cyclopentanophenanthrene nucleus. High levels are found in nerve tissue, atheromas, gallstones, and cysts. Normally 140 to 220 mg are present in 100 ml of blood.
Random House Word Menu:
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categories related to 'cholesterol'
- Nutrition For Fitness - cholesterol: fatty substance found in foodstuffs, or formed by body itself, that coats and constricts arteries
- Physiology - cholesterol: steroid molecule that is precursor of steroid hormones and bile salts, component of plasma membranes, and present in fat and blood
Bradford's Crossword Solver's Dictionary:
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cholesterol
See crossword solutions for the clue Cholesterol.
Wikipedia on Answers.com:
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Cholesterol
| Cholesterol | |
|---|---|
 |
|
 |
|
|
(3β)-cholest-5-en-3-ol |
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|
Other names
(10R,13R)-10,13-dimethyl-17-(6-methylheptan-2-yl)-2,3,4,7,8,9,11,12,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-ol |
|
| Identifiers | |
| CAS number | 57-88-5  |
| PubChem | 5997 |
| ChemSpider | 5775 |
| UNII | 97C5T2UQ7J |
| KEGG | D00040 |
| ChEBI | CHEBI:16113 |
| ChEMBL | CHEMBL112570 |
| Jmol-3D images | Image 1 |
|
|
|
|
| Properties | |
| Molecular formula | C27H46O |
| Molar mass | 386.65 g/mol |
| Appearance | white crystalline powder[1] |
| Density | 1.052 g/cm3 |
| Melting point |
148–150 °C[1] |
| Boiling point |
360 °C (decomposes) |
| Solubility in water | 0.095 mg/L (30 °C) |
| Solubility | soluble in acetone, benzene, chloroform, ethanol, ether, hexane, isopropyl myristate, methanol |
 (verify) (what is:  / ?)Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) |
|
| Infobox references | |
Cholesterol, from the Greek chole- (bile) and stereos (solid) followed by the chemical suffix -ol for an alcohol, is an organic chemical substance classified as a waxy steroid of fat. It is an essential structural component of mammalian cell membranes and is required to establish proper membrane permeability and fluidity.
In addition to its importance within cells, cholesterol is an important component in the hormonal systems of the body for the manufacture of bile acids, steroid hormones, and vitamin D. Cholesterol is the principal sterol synthesized by animals; in vertebrates it is formed predominantly in the liver. Small quantities are synthesized in other cellular organisms (eukaryotes) such as plants and fungi. It is almost completely absent among prokaryotes, i.e. bacteria.
Although cholesterol is important and necessary for human health, high levels of cholesterol in the blood have been linked to damage to arteries and cardiovascular disease.[2]
François Poulletier de la Salle first identified cholesterol in solid form in gallstones, in 1769. However, it was only in 1815 that chemist Eugène Chevreul named the compound "cholesterine".[3]
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Physiology
Since cholesterol is essential for all animal life, it is primarily synthesized from simpler molecules within each cell, a complex 37 step process which starts with the intracellular protein enzyme HMG-CoA reductase. However, normal and especially high levels of fats (including cholesterol) within the blood circulation, depending on how it is transported within lipoproteins, are strongly associated with progression of atherosclerosis.
For a person of about 68 kg (150 pounds), typical total body cholesterol synthesis is about 1 g (1,000 mg) per day, and total body content is about 35 g, primarily located within all the membranes of all the cells of the body. Typical daily dietary intake of additional cholesterol, in the United States, is 200–300 mg.[4]
However, most ingested cholesterol is esterified and esterified cholesterol is poorly absorbed. The body also compensates for any absorption of additional cholesterol by reducing cholesterol synthesis.[5]. For these reasons, cholesterol intake in food has little, if any, effect on total body cholesterol content or concentrations of cholesterol in the blood.
Cholesterol is recycled. It is excreted by the liver via the bile into the digestive tract, in a non-esterified form. Typically about 50% of the excreted cholesterol is reabsorbed by the small bowel back into the bloodstream.
Some plants make cholesterol in very small amounts.[6] Plants manufacture phytosterols (substances chemically similar to cholesterol produced within plants), which can compete with cholesterol for reabsorption in the intestinal tract, thus potentially reducing cholesterol reabsorption.[7] However, phytosterols are foreign to animal cells and, if absorbed, accelerate the progression of atherosclerosis. When intestinal lining cells absorb phytosterols, in place of cholesterol, they usually excrete the phytosterol molecules back into the GI tract, an important protective mechanism.
Function
Cholesterol is required to build and maintain membranes; it modulates membrane fluidity over the range of physiological temperatures. The hydroxyl group on cholesterol interacts with the polar head groups of the membrane phospholipids and sphingolipids, while the bulky steroid and the hydrocarbon chain are embedded in the membrane, alongside the nonpolar fatty acid chain of the other lipids. Through the interaction with the phospholipid fatty acid chains, cholesterol increases membrane packing, which reduces membrane fluidity.[8] In this structural role, cholesterol reduces the permeability of the plasma membrane to neutral solutes,[9] protons, (positive hydrogen ions) and sodium ions.[10]
Within the cell membrane, cholesterol also functions in intracellular transport, cell signaling and nerve conduction. Cholesterol is essential for the structure and function of invaginated caveolae and clathrin-coated pits, including caveola-dependent and clathrin-dependent endocytosis. The role of cholesterol in such endocytosis can be investigated by using methyl beta cyclodextrin (MβCD) to remove cholesterol from the plasma membrane. Recently, cholesterol has also been implicated in cell signaling processes, assisting in the formation of lipid rafts in the plasma membrane. Lipid raft formation brings receptor proteins in close proximity with high concentrations of second messenger molecules.[11] In many neurons, a myelin sheath, rich in cholesterol, since it is derived from compacted layers of Schwann cell membrane, provides insulation for more efficient conduction of impulses.[12]
Within cells, cholesterol is the precursor molecule in several biochemical pathways. In the liver, cholesterol is converted to bile, which is then stored in the gallbladder. Bile contains bile salts, which solubilize fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat-soluble vitamins, A, D, E, and K. Cholesterol is an important precursor molecule for the synthesis of vitamin D and the steroid hormones, including the adrenal gland hormones cortisol and aldosterone, as well as the sex hormones progesterone, estrogens, and testosterone, and their derivatives.
Some research indicates cholesterol may act as an antioxidant.[13]
Dietary sources
Animal fats are complex mixtures of triglycerides, with lesser amounts of phospholipids and cholesterol. As a consequence, all foods containing animal fat contain cholesterol to varying extents.[14] Major dietary sources of cholesterol include cheese, egg yolks, beef, pork, poultry, fish, and shrimp.[15] Human breast milk also contains significant quantities of cholesterol.[16]
From a dietary perspective, cholesterol is not found in significant amounts in plant sources.[15][17] In addition, plant products such as flax seeds and peanuts contain cholesterol-like compounds called phytosterols, which are believed to compete with cholesterol for absorption in the intestines.[18] Phytosterols can be supplemented through the use of phytosterol-containing functional foods or nutraceuticals that are widely recognized as having a proven LDL cholesterol-lowering efficacy.[19] Current supplemental guidelines recommend doses of phytosterols in the 1.6-3.0 grams per day range (Health Canada, EFSA, ATP III,FDA) with a recent meta-analysis demonstrating an 8.8% reduction in LDL-cholesterol at a mean dose of 2.15 gram per day.[20] However, the benefits of a diet supplemented with phytosterol has been questioned.[21][22]
Total fat intake also plays a role in blood cholesterol levels. This effect is thought to come about by changes in the quantity of cholesterol and lipoproteins that are synthesized by the body. In particular, saturated, monounsaturated and polyunsaturated fats have been shown to increase HDL-based cholesterol levels, with saturated fats also increasing LDL-based cholesterol levels.[23] Trans fats have been shown to reduce levels of HDL whilst increasing levels of LDL.[24] Based on such evidence and evidence implicating low HDL and high LDL levels in cardiovascular disease (see Hypercholesterolemia), many health authorities advocate reducing LDL cholesterol through changes in diet in addition to other lifestyle modifications.[2] The USDA for example recommends that those wishing to reduce their cholesterol through a change in diet should aim to consume less than 7% of their daily energy needs from saturated fat and fewer than 200 mg of cholesterol per day.[25] An alternative view is that any reduction to dietary cholesterol intake could be counteracted by the organs compensating to try to keep blood cholesterol levels constant.[26]
However, the The China Study uses epidemiological evidence to claim that casein raises blood cholesterol even more than the ingested saturated fat or cholesterol.[27]
Biosynthesis
All animal cells manufacture cholesterol with relative production rates varying by cell type and organ function. About 20–25% of total daily cholesterol production occurs in the liver; other sites of higher synthesis rates include the intestines, adrenal glands, and reproductive organs. Synthesis within the body starts with one molecule of acetyl CoA and one molecule of acetoacetyl-CoA, which are hydrated to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA). This molecule is then reduced to mevalonate by the enzyme HMG-CoA reductase. This step is the regulated, rate-limiting and irreversible step in cholesterol synthesis and is the site of action for the statin drugs (HMG-CoA reductase competitive inhibitors).
Mevalonate is then converted to 3-isopentenyl pyrophosphate in three reactions that require ATP. Mevalonate is decarboxylated to isopentenyl pyrophosphate, which is a key metabolite for various biological reactions. Three molecules of isopentenyl pyrophosphate condense to form farnesyl pyrophosphate through the action of geranyl transferase. Two molecules of farnesyl pyrophosphate then condense to form squalene by the action of squalene synthase in the endoplasmic reticulum. Oxidosqualene cyclase then cyclizes squalene to form lanosterol. Finally, lanosterol is then converted to cholesterol.[28]
Konrad Bloch and Feodor Lynen shared the Nobel Prize in Physiology or Medicine in 1964 for their discoveries concerning the mechanism and regulation of cholesterol and fatty acid metabolism.
Regulation of cholesterol synthesis
Biosynthesis of cholesterol is directly regulated by the cholesterol levels present, though the homeostatic mechanisms involved are only partly understood. A higher intake from food leads to a net decrease in endogenous production, whereas lower intake from food has the opposite effect. The main regulatory mechanism is the sensing of intracellular cholesterol in the endoplasmic reticulum by the protein SREBP (sterol regulatory element-binding protein 1 and 2).[29] In the presence of cholesterol, SREBP is bound to two other proteins: SCAP (SREBP-cleavage-activating protein) and Insig1. When cholesterol levels fall, Insig-1 dissociates from the SREBP-SCAP complex, allowing the complex to migrate to the Golgi apparatus, where SREBP is cleaved by S1P and S2P (site-1 and -2 protease), two enzymes that are activated by SCAP when cholesterol levels are low. The cleaved SREBP then migrates to the nucleus and acts as a transcription factor to bind to the sterol regulatory element (SRE), which stimulates the transcription of many genes. Among these are the low-density lipoprotein (LDL) receptor and HMG-CoA reductase. The former scavenges circulating LDL from the bloodstream, whereas HMG-CoA reductase leads to an increase of endogenous production of cholesterol.[30] A large part of this signaling pathway was clarified by Dr. Michael S. Brown and Dr. Joseph L. Goldstein in the 1970s. In 1985, they received the Nobel Prize in Physiology or Medicine for their work. Their subsequent work shows how the SREBP pathway regulates expression of many genes that control lipid formation and metabolism and body fuel allocation.
Cholesterol synthesis can be turned off when cholesterol levels are high, as well. HMG CoA reductase contains both a cytosolic domain (responsible for its catalytic function) and a membrane domain. The membrane domain functions to sense signals for its degradation. Increasing concentrations of cholesterol (and other sterols) cause a change in this domain's oligomerization state, which makes it more susceptible to destruction by the proteosome. This enzyme's activity can also be reduced by phosphorylation by an AMP-activated protein kinase. Because this kinase is activated by AMP, which is produced when ATP is hydrolyzed, it follows that cholesterol synthesis is halted when ATP levels are low.[31]
Plasma transport and regulation of absorption
See also: Blood lipids
Cholesterol is only slightly soluble in water; it can dissolve and travel in the water-based bloodstream at exceedingly small concentrations. Since cholesterol is insoluble in blood, it is transported in the circulatory system within lipoproteins, complex discoidal particles that have an exterior composed of amphiphilic proteins and lipids whose outward-facing surfaces are water-soluble and inward-facing surfaces are lipid-soluble; triglycerides and cholesterol esters are carried internally. Phospholipids and cholesterol, being amphipathic, are transported in the surface monolayer of the lipoprotein particle.
In addition to providing a soluble means for transporting cholesterol through the blood, lipoproteins have cell-targeting signals that direct the lipids they carry to certain tissues. For this reason, there are several types of lipoproteins within blood called, in order of increasing density, chylomicrons, very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). The more lipid and less protein a lipoprotein has the less dense it is. The cholesterol within all the various lipoproteins is identical, although some cholesterol is carried as the "free" alcohol and some is carried as fatty acyl esters referred to as cholesterol esters. However, the different lipoproteins contain apolipoproteins, which serve as ligands for specific receptors on cell membranes. In this way, the lipoprotein particles are molecular addresses that determine the start- and endpoints for cholesterol transport.
Chylomicrons, the least dense type of cholesterol transport molecules, contain apolipoprotein B-48, apolipoprotein C, and apolipoprotein E in their shells. Chylomicrons are the transporters that carry fats from the intestine to muscle and other tissues that need fatty acids for energy or fat production. Cholesterol that is not used by muscles remains in more cholesterol-rich chylomicron remnants, which are taken up from here to the bloodstream by the liver.
VLDL molecules are produced by the liver and contain excess triacylglycerol and cholesterol that is not required by the liver for synthesis of bile acids. These molecules contain apolipoprotein B100 and apolipoprotein E in their shells. During transport in the bloodstream, the blood vessels cleave and absorb more triacylglycerol from IDL molecules, which contain an even higher percentage of cholesterol. The IDL molecules have two possible fates: Half are into metabolism by HTGL, taken up by the LDL receptor on the liver cell surfaces, and the other half continue to lose triacylglycerols in the bloodstream until they form LDL molecules, which have the highest percentage of cholesterol within them.
LDL molecules, therefore, are the major carriers of cholesterol in the blood, and each one contains approximately 1,500 molecules of cholesterol ester. The shell of the LDL molecule contains just one molecule of apolipoprotein B100, which is recognized by the LDL receptor in peripheral tissues. Upon binding of apolipoprotein B100, many LDL receptors become localized in clathrin-coated pits. Both the LDL and its receptor are internalized by endocytosis to form a vesicle within the cell. The vesicle then fuses with a lysosome, which has an enzyme called lysosomal acid lipase that hydrolyzes the cholesterol esters. Now within the cell, the cholesterol can be used for membrane biosynthesis or esterified and stored within the cell, so as to not interfere with cell membranes.
Synthesis of the LDL receptor is regulated by SREBP, the same regulatory protein as was used to control synthesis of cholesterol de novo in response to cholesterol presence in the cell. When the cell has abundant cholesterol, LDL receptor synthesis is blocked so new cholesterol in the form of LDL molecules cannot be taken up. On the converse, more LDL receptors are made when the cell is deficient in cholesterol. When this system is deregulated, many LDL molecules appear in the blood without receptors on the peripheral tissues. These LDL molecules are oxidized and taken up by macrophages, which become engorged and form foam cells. These cells often become trapped in the walls of blood vessels and contribute to artherosclerotic plaque formation. Differences in cholesterol homeostasis affect the development of early atherosclerosis (carotid intima-media thickness).[32] These plaques are the main causes of heart attacks, strokes, and other serious medical problems, leading to the association of so-called LDL cholesterol (actually a lipoprotein) with "bad" cholesterol.[31]
Also, HDL particles are thought to transport cholesterol back to the liver for excretion or to other tissues that use cholesterol to synthesize hormones in a process known as reverse cholesterol transport (RCT).[33] Having large numbers of large HDL particles correlates with better health outcomes.[34] In contrast, having small numbers of large HDL particles is independently associated with atheromatous disease progression within the arteries.
Metabolism, recycling and excretion
Cholesterol is susceptible to oxidation and easily forms oxygenated derivatives known as oxysterols. Three different mechanisms can form these; autoxidation, secondary oxidation to lipid peroxidation, and cholesterol-metabolizing enzyme oxidation. A great interest in oxysterols arose when they were shown to exert inhibitory actions on cholesterol biosynthesis.[35] This finding became known as the “oxysterol hypothesis”. Additional roles for oxysterols in human physiology include their: participation in bile acid biosynthesis, function as transport forms of cholesterol, and regulation of gene transcription.[36]
Cholesterol is oxidized by the liver into a variety of bile acids.[37] These, in turn, are conjugated with glycine, taurine, glucuronic acid, or sulfate. A mixture of conjugated and nonconjugated bile acids, along with cholesterol itself, is excreted from the liver into the bile. Approximately 95% of the bile acids are reabsorbed from the intestines, and the remainder are lost in the feces.[38] The excretion and reabsorption of bile acids forms the basis of the enterohepatic circulation, which is essential for the digestion and absorption of dietary fats. Under certain circumstances, when more concentrated, as in the gallbladder, cholesterol crystallises and is the major constituent of most gallstones. Although, lecithin and bilirubin gallstones also occur, but less frequently.[39] Every day, up to 1 g of cholesterol enters the colon. This cholesterol originates from the diet, bile, and desquamated intestinal cells, and can be metabolized by the colonic bacteria. Cholesterol is converted mainly into coprostanol, a nonabsorbable sterol that is excreted in the feces. A cholesterol-reducing bacterium origin has been isolated from human feces.[40][non-primary source needed]
Significance
Hypercholesterolemia
Main articles: hypercholesterolemia and lipid hypothesis
According to the lipid hypothesis, abnormal cholesterol levels (hypercholesterolemia) — that is, higher concentrations of LDL and lower concentrations of functional HDL — are strongly associated with cardiovascular disease because these promote atheroma development in arteries (atherosclerosis). This disease process leads to myocardial infarction (heart attack), stroke, and peripheral vascular disease. Since higher blood LDL, especially higher LDL particle concentrations and smaller LDL particle size, contribute to this process more than the cholesterol content of the HDL particles,[41] LDL particles are often termed "bad cholesterol" because they have been linked to atheroma formation. On the other hand, high concentrations of functional HDL, which can remove cholesterol from cells and atheroma, offer protection and are sometimes referred to as "good cholesterol". These balances are mostly genetically determined, but can be changed by body build, medications, food choices, and other factors.[42]
Conditions with elevated concentrations of oxidized LDL particles, especially "small dense LDL" (sdLDL) particles, are associated with atheroma formation in the walls of arteries, a condition known as atherosclerosis, which is the principal cause of coronary heart disease and other forms of cardiovascular disease. In contrast, HDL particles (especially large HDL) have been identified as a mechanism by which cholesterol and inflammatory mediators can be removed from atheroma. Increased concentrations of HDL correlate with lower rates of atheroma progressions and even regression. A 2007 study pooling data on almost 900,000 subjects in 61 cohorts demonstrated that blood total cholesterol levels have an exponential effect on cardiovascular and total mortality, with the association more pronounced in younger subjects. Still, because cardiovascular disease is relatively rare in the younger population, the impact of high cholesterol on health is still larger in older people.[43]
Elevated levels of the lipoprotein fractions, LDL, IDL and VLDL are regarded as atherogenic (prone to cause atherosclerosis).[44] Levels of these fractions, rather than the total cholesterol level, correlate with the extent and progress of atherosclerosis. Conversely, the total cholesterol can be within normal limits, yet be made up primarily of small LDL and small HDL particles, under which conditions atheroma growth rates would still be high. In contrast, however, if LDL particle number is low (mostly large particles) and a large percentage of the HDL particles are large, then atheroma growth rates are usually low, even negative, for any given total cholesterol concentration.[citation needed] Recently, a post hoc analysis of the IDEAL and the EPIC prospective studies found an association between high levels of HDL cholesterol (adjusted for apolipoprotein A-I and apolipoprotein B) and increased risk of cardiovascular disease, casting doubt on the cardioprotective role of "good cholesterol".[45]
Elevated cholesterol levels are treated with a strict diet consisting of low saturated fat, trans fat-free, low cholesterol foods,[46][47] often followed by one of various hypolipidemic agents, such as statins, fibrates, cholesterol absorption inhibitors, nicotinic acid derivatives or bile acid sequestrants.[48] Extreme cases have previously been treated with partial ileal bypass surgery, which has now been superseded by medication. Apheresis-based treatments are still used for very severe hyperlipidemias that are either unresponsive to treatment or require rapid lowering of blood lipids.[citation needed]
Multiple human trials using HMG-CoA reductase inhibitors, known as statins, have repeatedly confirmed that changing lipoprotein transport patterns from unhealthy to healthier patterns significantly lowers cardiovascular disease event rates, even for people with cholesterol values currently considered low for adults.[citation needed] Studies have also found that statins reduce atheroma progression.[49] As a result, people with a history of cardiovascular disease may derive benefit from statins irrespective of their cholesterol levels,[50] and in men without cardiovascular disease, there is benefit from lowering abnormally high cholesterol levels ("primary prevention").[51] Primary prevention in women is practiced only by extension of the findings in studies on men,[52] since in women, none of the large statin trials has shown a reduction in overall mortality or in cardiovascular endpoints.[53]
| Level mg/dL | Level mmol/L | Interpretation |
| < 200 | < 5.2 | Desirable level corresponding to lower risk for heart disease |
| 200–240 | 5.2–6.2 | Borderline high risk |
| > 240 | > 6.2 | High risk |
The 1987 report of National Cholesterol Education Program, Adult Treatment Panels suggests the total blood cholesterol level should be: < 200 mg/dL normal blood cholesterol, 200–239 mg/dL borderline-high, > 240 mg/dL high cholesterol.[54] The American Heart Association provides a similar set of guidelines for total (fasting) blood cholesterol levels and risk for heart disease:[55]
However, as today's testing methods determine LDL ("bad") and HDL ("good") cholesterol separately, this simplistic view has become somewhat outdated. The desirable LDL level is considered to be less than 100 mg/dL (2.6 mmol/L),[56] although a newer upper limit of 70 mg/dL (1.8 mmol/L) can be considered in higher-risk individuals based on some of the above-mentioned trials. A ratio of total cholesterol to HDL—another useful measure—of far less than 5:1 is thought to be healthier. Of note, typical LDL values for children before fatty streaks begin to develop is 35 mg/dL.[citation needed]
Total cholesterol is defined as the sum of HDL, LDL, and VLDL. Usually, only the total, HDL, and triglycerides are measured. For cost reasons, the VLDL is usually estimated as one-fifth of the triglycerides and the LDL is estimated using the Friedewald formula (or a variant): estimated LDL = [total cholesterol] − [total HDL] − [estimated VLDL]. VLDL can be calculated by dividing total triglycerides by five. Direct LDL measures are used when triglycerides exceed 400 mg/dL. The estimated VLDL and LDL have more error when triglycerides are above 400 mg/dL.[57]
Given the well-recognized role of cholesterol in cardiovascular disease, some studies have shown an inverse correlation between cholesterol levels and mortality. A 2009 study of patients with acute coronary syndromes found an association of hypercholesterolemia with better mortality outcomes.[58] In the Framingham Heart Study, in subjects over 50 years of age, they found an 11% increase overall and 14% increase in cardiovascular disease mortality per 1 mg/dL per year drop in total cholesterol levels. The researchers attributed this phenomenon to the fact that people with severe chronic diseases or cancer tend to have below-normal cholesterol levels.[59] This explanation is not supported by the Vorarlberg Health Monitoring and Promotion Programme, in which men of all ages and women over 50 with very low cholesterol were likely to die of cancer, liver diseases, and mental diseases. This result indicates the low-cholesterol effect occurs even among younger respondents, contradicting the previous assessment among cohorts of older people that this is a proxy or marker for frailty occurring with age.[60]
The vast majority of doctors and medical scientists consider that there is a link between cholesterol and atherosclerosis as discussed above;[61] a small group of scientists, united in The International Network of Cholesterol Skeptics, questions the link.[62]
Hypocholesterolemia
Abnormally low levels of cholesterol are termed hypocholesterolemia. Research into the causes of this state is relatively limited, but some studies suggest a link with depression, cancer, and cerebral hemorrhage. In general, the low cholesterol levels seem to be a consequence, rather than a cause, of an underlying illness.[43]
Cholesterol testing
 |
The examples and perspective in this section report US measures, whereas the measure in many places is mmol/L, into which they need to be converted, therefore the section may not represent a worldwide view of the subject. Please improve this article and discuss the issue on the talk page. (October 2009) |
The American Heart Association recommends testing cholesterol every five years for people aged 20 years or older.[63]
A blood sample after 12-hour fasting is taken by a doctor, or a home cholesterol-monitoring device is used to determine a lipoprotein profile. This measures total cholesterol, LDL (bad) cholesterol, HDL (good) cholesterol, and triglycerides. It is recommended to test cholesterol at least every five years if a person has total cholesterol of 200 mg/dL or more, or if a man over age 45 or a woman over age 50 has HDL (good) cholesterol less than 40 mg/dL, or there are other risk factors for heart disease and stroke. (In different countries measurements are given in mg/dL or mmol/L; 1 mmol/L is 38.665 mg/dL.)
Interactive pathway map
Click on genes, proteins and metabolites below to link to respective articles. [64]
Cholesteric liquid crystals
Some cholesterol derivatives (among other simple cholesteric lipids) are known to generate the liquid crystalline "cholesteric phase". The cholesteric phase is, in fact, a chiral nematic phase, and it changes colour when its temperature changes. This makes cholesterol derivatives useful for indicating temperature in liquid crystal display thermometers and in temperature-sensitive paints.
See also
- Arcus senilis "Cholesterol ring" in the eyes
- Bile salts
- Cholesterol embolism
- Cholesterol total synthesis
- Diet and heart disease
- Lipid profile
- Niemann–Pick disease Type C
- Oxycholesterol
- Triglycerides
- Vertical Auto Profile
Additional images
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Steroidogenesis, using cholesterol as building material
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Space-filling model of the Cholesterol molecule
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Numbering of the steroid nuclei
References
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External links
- Cholesterol bound to proteins in the PDB
- Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults US National Institutes of Health Adult Treatment Panel III
- Aspects of fat digestion and metabolism – UN/WHO Report 1994
- American Heart Association – "About Cholesterol"
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This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
Translations:
Top
Cholesterol
Dansk (Danish)
n. - kolesterol
Nederlands (Dutch)
cholesterol
Français (French)
n. - cholestérol
Deutsch (German)
n. - Cholesterin, Gallenfett
Ελληνική (Greek)
n. - (βιολ.) χοληστερόλη
Italiano (Italian)
colesterolo
Português (Portuguese)
n. - colesterol (m) (Quím.)
Español (Spanish)
n. - colesterol
Svenska (Swedish)
n. - kolesterol
中文（简体）(Chinese (Simplified))
胆固醇
中文（繁體）(Chinese (Traditional))
n. - 膽固醇
العربيه (Arabic)
(الاسم) كولسترول, دهن الصفراء, شحم المرارة
עברית (Hebrew)
n. - כוהל מוצק שריכוז גבוה שלו בדם עלול לגרום הסתיידות עורקים, כולסטרול
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