Kolesterol

Struktura molekule kolesterola

Kolesterol je alkohol koji se nalazi u staničnim membranama svih tkiva, a potreban je za
normalan rad organizma. Kolesterol se svrstava i u sterole jer je u njegovom sastavu
kombinacija steroida i alkohola. Male količine kolesterola se nalaze i u
membranama biljaka i gljiva.
Organizam koristi kolesterol u stvaranju hormona, vitamina A, D i E te žučnih kiselina. Manji dio
kolesterola se nalazi u krvi. Ako se taj kolesterol nakuplja na stijenkamakrvnih žila, može doći do
začepljenja ili smanjenog krvnog protoka. Posljedice na zdravlje mogu biti velike, pa se u takvim
slučajevima količina kolesterola u krvi regulira medicinskim preparatima.
Kemijska formula kolesterola je C27H46O.

Cholesterol
From Wikipedia, the free encyclopedia

Cholesterol

IUPAC name
(3β)-cholest-5-en-3-ol

Systematic name
2,15-dimethyl-14-(1,5-dimethylhexyl)tetracyclo[8.7.0.02,7.011,15]heptadec-7-en-5-ol

Other names

095 mg/L (30 °C) ater Solubility soluble in acetone. from the Ancient Greek chole.9.8.052 g/cm3 Melting point 148–150 °C[2] Boiling point 360 °C (decomposes) Solubility inw 0.4. It is a sterol (or modifiedsteroid).65 g/mol Appearance white crystalline powder[2] Density 1. . methanol Except where noted otherwise. 100 kPa) Cholesterol.15.13-dimethyl-17-(6-methylheptan-2-yl)-2.17dodecahydro-1H-cyclopenta[a]phenanthren-3-ol. ether.(bile) and stereos (solid) followed by the chemical suffix -ol for an alcohol. Cholesterin. Cholesteryl alcohol [1] Properties Molecular C27H46O formula Molar mass 386. benzene. [3] a lipid molecule and is biosynthesized by many animal cells because it is an essential structural component of animal cell membranes that is required to maintain both membrane structural integrity and fluidity.14.7.chloroform.11.isopropyl myristate.12. ethanol.3. hexa ne. data are given for materials in their standard state (at 25 °C (77 °F).13R)-10.(10R.16. is an organic molecule.

primarily located within the membranes of all the cells of the body. bile acids. a complex 37-step process that starts with the intracellular protein enzyme HMG-CoA reductase. In vertebrates the hepatic cells typically produce greater amounts than other cells. which require cholesterol for growth. However.[4] Cholesterol is the principal sterol synthesized by animals. For a man of about 68 kg (150 lb). seven to ten hours after ingestion. the levels significantly increase. [12] When intestinal lining cells absorb phytosterols. However. effect on total body cholesterol content or concentrations of cholesterol in the blood. during the first seven hours after ingestion of cholesterol. [10] Cholesterol is recycled. [9] For these reasons.[11] Plants manufacture phytosterols (substances chemically similar to cholesterol produced within plants). they usually excrete the phytosterol molecules back into the GI tract.000 mg) per day. All kinds of cells in animals can produce it. depending on how they are transported within lipoproteins. and total body content is approximately 35 g. although there are some exceptions such as Mycoplasma. and vitamin D.[8] Most ingested cholesterol is esterified. is 200–300 mg. In addition to its importance within cells. in place of cholesterol. which can compete with cholesterol for reabsorption in the intestinal tract.[6][7] Physiology Since cholesterol is essential for all animal life. it was not until 1815 that chemist Michel Eugène Chevreul named the compound "cholesterine". Typical daily dietary intake of additional cholesterol. Typically about 50% of the excreted cholesterol is reabsorbed by the small bowel back into the bloodstream. are strongly associated with the progression of atherosclerosis. an important protective mechanism. cholesterol also serves as a precursor for the biosynthesis of steroid hormones. . typical total body-cholesterol synthesis is approximately 1 g (1.Cholesterol enables animal cells to (a) not need a cell wall (like plants & bacteria) to protect membrane integrity/cell-viability and thus be able to (b) change shape and (c) move about (unlike bacteria and plant cells which are restricted by their cell walls). The body also compensates for any absorption of additional cholesterol by reducing cholesterol synthesis. Plants make cholesterol in very small amounts. each cell synthesizes it from simpler molecules. The liver excretes it in a non-esterified form (via bile) into the digestive tract. if any. It is almost completely absent among prokaryotes (bacteria and archaea). normal and particularly high levels of fats (including cholesterol) in the blood circulation. thus potentially reducing cholesterol reabsorption. and esterified cholesterol is poorly absorbed. cholesterol will show little. in the United States. However.[5] François Poulletier de la Salle first identified cholesterol in solid form in gallstones in 1769.

In the liver.[4] Some research indicates cholesterol may act as an antioxidant.[24] Phytosterols can be supplemented through the use of phytosterolcontaining functional foods or nutraceuticals that are widely recognized as having a proven LDL cholesterol-lowering efficacy. Cholesterol is an important precursor molecule for the synthesis of vitamin D and the steroid hormones. cholesterol is not found in significant amounts in plant sources. As a consequence.Function[edit] Cholesterol is required to build and maintain membranes. with lesser amounts of phospholipids and cholesterol.8% reduction in LDL-cholesterol at a mean dose of . Recently. poultry. D. The hydroxyl group on cholesterol interacts with the polar head groups of the membrane phospholipids and sphingolipids.[21] Human breast milk also contains significant quantities of cholesterol. including the adrenal gland hormones cortisol and aldosterone. E.[15] hydrogen ions. [22] From a dietary perspective. which solubilize fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat-soluble vitamins. [13] The structure of the tetracyclic ring of cholesterol contributes to the decreased fluidity of the cell membrane as the molecule is in a trans conformation making all but the side chain of cholesterol rigid and planar. A. fish. since it is derived from compacted layers of Schwann cell membrane. plant products such as flax seeds and peanuts contain cholesterol-like compounds called phytosterols. provides insulation for more efficient conduction of impulses. which reduces membrane fluidity. Bile contains bile salts.[14] In this structural role. and K.[20] Major dietary sources of cholesterol include cheese. egg yolks. estrogens.[25] Current supplemental guidelines recommend doses of phytosterols in the 1.[17]In many neurons. cholesterol is the precursor molecule in several biochemical pathways. a myelin sheath. The role of cholesterol in such endocytosis can be investigated by using methyl beta cyclodextrin (MβCD) to remove cholesterol from the plasma membrane. ATP III. cholesterol is converted to bile.0 grams per day range (Health Canada. rich in cholesterol. while the bulky steroid and the hydrocarbon chain are embedded in the membrane. as well as the sex hormones progesterone.[19] Dietary sources[edit] Animal fats are complex mixtures of triglycerides.[16] Within the cell membrane. beef. and testosterone. cell signaling and nerve conduction. Lipid raft formation brings receptor proteins in close proximity with high concentrations of second messenger molecules. Through the interaction with the phospholipid fatty-acid chains. including caveola-dependent and clathrindependent endocytosis. cholesterol reduces the permeability of the plasma membrane to neutral solutes. alongside the nonpolar fatty-acid chain of the other lipids.[18] Within cells. and their derivatives. Cholesterol is essential for the structure and function of invaginated caveolae and clathrin-coated pits. assisting in the formation of lipid rafts in the plasma membrane. [21][23] In addition. which are believed to compete with cholesterol for absorption in the intestines. cholesterol also functions in intracellular transport. cholesterol increases membrane packing.FDA) with a recent meta-analysis demonstrating an 8. and shrimp. and sodium ions. it modulates membrane fluidity over the range of physiological temperatures. all foods containing animal fat contain cholesterol to varying extents. cholesterol has also been implicated in cell signaling processes. pork.6-3. which is then stored in the gallbladder. EFSA.

[38] In the presence of cholesterol. many health authorities advocate reducing LDL cholesterol through changes in diet in addition to other lifestyle modifications. [35] This molecule is then reduced to mevalonate by the enzyme HMG-CoA reductase.[26] However. SREBP is bound to two other proteins: SCAP (SREBP cleavage activating protein) and Insig1. which is a key metabolite for various biological reactions. Mevalonate is then converted to 3-isopentenyl pyrophosphate in three reactions that require ATP. 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. LDL. [31] The USDA. 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). Insig-1 dissociates from the . adrenal glands. A higher intake from food leads to a net decrease in endogenous production. About 20–25% of total daily cholesterol production occurs in the liver.[27][28] Fat intake also plays a role in blood-cholesterol levels.[36][37] 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.[34] Biosynthesis[edit] All animal cells manufacture cholesterol for their use. [30] Based on such evidence and evidence implicating low HDL and high LDL levels in cardiovascular disease (see Hypercholesterolemia). Regulation of cholesterol synthesis[edit] Biosynthesis of cholesterol is directly regulated by the cholesterol levels present.2. other sites of higher synthesis rates include the intestines.15 gram per day. Synthesis within the body starts with one molecule of acetyl CoA and one molecule of acetoacetyl-CoA. This is the regulated. When cholesterol levels fall. Finally.[29] Trans fats have been shown to reduce levels of HDL while increasing levels of LDL. lanosterol is converted to cholesterol through a 19-step process.[35] Oxidosqualene cyclase then cyclizes squalene to form lanosterol. with relative production rates varying by cell type and organ function. rate-limiting and irreversible step in cholesterol synthesis and is the site of action for the statin drugs (HMG-CoA reductase competitive inhibitors). whereas lower intake from food has the opposite effect. and total cholesterol levels. while replacing carbohydrates with saturated fat was shown to increase HDL. which are hydrated to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA). though the homeostatic mechanisms involved are only partly understood. Three molecules of isopentenyl pyrophosphate condense to form farnesyl pyrophosphate through the action of geranyl transferase.[33] Other research has found that an increase in the consumption of saturated fats and cholesterol decreases overall serum cholesterol. Isocalorically replacing dietary carbohydrates with monounsaturated and polyunsaturated fats has been shown to lower serum LDL and total cholesterol levels and increase serum HDL levels. Mevalonate is decarboxylated to isopentenyl pyrophosphate. the benefits of a diet supplemented with phytosterol has been questioned. and reproductive organs.[32] 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. for example. Two molecules of farnesyl pyrophosphate then condense to formsqualene by the action of squalene synthase in the endoplasmic reticulum.

Cholesterol within different lipoproteins is identical. Chylomicrons carry fats from the intestine to muscle and other tissues in need of fatty acids for energy or fat production. Michael S. In 1985. cholesterol is transported inside lipoproteins. Triglycerides and cholesterol esters are carried internally. Instead. andhigh-density lipoprotein (HDL). which allows the complex to migrate to the Golgi apparatus. The membrane domain senses signals for its degradation. they received the Nobel Prize in Physiology or Medicine for their work.[40] Plasma transport and regulation of absorption[edit] See also: Blood lipids Cholesterol is only slightly soluble in water. directing their lipid payload to specific tissues. In order of increasing density. apolipoprotein C. complex discoidal particles with exterior amphiphilic proteins and lipids. HMG-CoA reductase contains both a cytosolic domain (responsible for its catalytic function) and a membrane domain. whose outward-facing surfaces are water-soluble and inward-facing surfaces are lipid-soluble. Brown and Dr. Lipoproteins contain apolipoproteins. Cholesterol synthesis can also be turned off when cholesterol levels are high. known also as cholesterol esters. being amphipathic. Among these are the low-density lipoprotein (LDL) receptor and HMG-CoA reductase. while others as fatty acyl esters.SREBP-SCAP complex. Lower protein/lipid ratios make for less dense lipoproteins. . whereas HMG-CoA reductase leads to an increase of endogenous production of cholesterol. are transported in the monolayer surface of the lipoprotein particle. Unused cholesterol remains in more cholesterol-rich chylomicron remnants.and end points of cholesterol transport. and taken up from here to the bloodstream by the liver. which determine the start. Because this kinase is activated by AMP. Phospholipids and cholesterol. and acts as a transcription factor to bind to the sterol regulatory element (SRE). which makes it more susceptible to destruction by theproteosome. Increasing concentrations of cholesterol (and other sterols) cause a change in this domain's oligomerization state. Goldstein in the 1970s. Chylomicrons. which stimulates the transcription of many genes. Lipoprotein particles thus include these molecular addresses. which is produced when ATP is hydrolyzed. although some is carried as "free" alcohol. two enzymes that are activated by SCAP when cholesterol levels are low. contain apolipoprotein B48. intermediate-density lipoprotein (IDL). Joseph L. Here SREBP is cleaved by S1P and S2P (site-1 and -2 protease). very-low-density lipoprotein (VLDL). they are chylomicrons. the least dense cholesterol transport molecules. it follows that cholesterol synthesis is halted when ATP levels are low. This enzyme's activity can also be reduced by phosphorylation by an AMP-activated protein kinase. [39] A large part of this signaling pathway was clarified by Dr. which bind to specific receptors on cell membranes. The LDL receptor former scavenges circulating LDL from the bloodstream. it dissolves into the (water-based) bloodstream only at exceedingly small concentrations. low-density lipoprotein (LDL). and apolipoprotein E in their shells. The cleaved SREBP then migrates to the nucleus. Their subsequent work shows how the SREBP pathway regulates expression of many genes that control lipid formation and metabolism and body fuel allocation. There are several types of lipoproteins in the blood.

[45] . secondary oxidation to lipid peroxidation. IDL molecules are then consumed in two processes: half is metabolized by HTGL and taken up by the LDL receptor on the liver cell surfaces. Both LDL and its receptor form vesicles within a cell via endocytosis. leading to the association of so-called LDL cholesterol (actually a lipoprotein) with "bad" cholesterol. LDL molecule shells contain just one molecule of apolipoprotein B100. and regulation of gene transcription. Each one contains approximately 1. in a process known as reverse cholesterol transport (RCT). recycling and excretion[edit] Cholesterol is susceptible to oxidation and easily forms oxygenated derivatives known as oxysterols. autoxidation. Upon binding of apolipoprotein B100. These foam cells often become trapped in the walls of blood vessels and contribute to atherosclerotic plaque formation. to prevent new cholesterol in LDL molecules from being taken up. These vesicles then fuse with a lysosome. Blood vessels cleave and absorb triacylglycerol from IDL molecules. LDL particles are the major blood cholesterol carriers. These molecules contain apolipoprotein B100 and apolipoprotein E in their shells. LDL receptor synthesis proceeds when a cell is deficient in cholesterol. and its synthesis is regulated by SREBP. Three different mechanisms can form these. and other serious medical problems. The cholesterol can then be used for membrane biosynthesis or esterified and stored within the cell. [41] These plaques are the main causes of heart attacks.[40] HDL particles are thought to transport cholesterol back to the liver.[43] whereas low numbers of HDL particles is associated with atheromatous disease progression in the arteries. according to its presence inside the cell. [42] Large numbers of HDL particles correlates with better health outcomes. while the other half continues to lose triacylglycerols in the bloodstream until they become LDL molecules. Differences in cholesterol homeostasis affect the development of early atherosclerosis (carotid intima-media thickness). These LDL molecules are oxidized and taken up by macrophages.500 molecules of cholesterol ester. strokes. the same protein that controls the synthesis of cholesterol de novo. Conversely. A great interest in oxysterols arose when they were shown to exert inhibitory actions on cholesterol biosynthesis. and cholesterol-metabolizing enzyme oxidation. [44] This finding became known as the “oxysterol hypothesis”. with the highest concentration of cholesterol within them. A cell with abundant cholesterol will have its LDL receptor synthesis blocked.VLDL molecules are produced by the liver from triacylglycerol and cholesterol which was not used in the synthesis of bile acids. recognized byLDL receptors in peripheral tissues. so as to not interfere with the cell membranes. where the lysosomal acid lipase enzyme hydrolyzes the cholesterol esters. either for excretion or for other tissues that synthesize hormones. Metabolism. LDL receptors are used up during cholesterol absorption. LDL molecules without receptors begin to appear in the blood. Additional roles for oxysterols in human physiology include their: participation in bile acid biosynthesis.. function as transport forms of cholesterol. When this process becomes unregulated. which become engorged and form foam cells. increasing the concentration of cholesterol. many LDL receptors concentrate in clathrin-coated pits.

medications. high concentrations of functional HDL.[48] 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. up to 1 g of cholesterol enters the colon. [46] Cholesterol is oxidized by the liver into a variety of bile acids. cholesterol crystallises and is the major constituent of most gallstones. which is the principal cause of coronary heart disease and other forms .In biochemical experiments radiolabelled forms of cholesterol. Under certain circumstances. Since higher blood LDL. These balances are mostly genetically determined. is excreted from the liver into the bile. taurine.[47] These. are associated with atheroma formation in the walls of arteries. As a result. a condition known as atherosclerosis. A mixture of conjugated and nonconjugated bile acids. This disease process leads to myocardial infarction (heart attack). These derivatives undergo degradation upon storage and it is essential to purify cholesterol prior to use. are conjugated with glycine. [54] LDL particles are often termed "bad cholesterol" because they have been linked to atheroma formation.[56] Conditions with elevated concentrations of oxidized LDL particles. especially "small dense LDL" (sdLDL) particles. Resistin also adversely impacts the effects of statins.[52][53] Clinical significance[edit] Hypercholesterolemia[edit] Main articles: hypercholesterolemia and lipid hypothesis According to the lipid hypothesis. and peripheral vascular disease. but can be changed by body build. lecithin and bilirubin gallstones also occur. a protein secreted by fat tissue. This cholesterol originates from the diet.[49] Every day. and other factors. contribute to this process more than the cholesterol content of the HDL particles. stroke. Although. along with cholesterol itself. in turn.[50][non-primary source needed] Although cholesterol is a steroid generally associated with mammals. which can remove cholesterol from cells and atheroma. a nonabsorbable sterol that is excreted in the feces. On the other hand. the liver is less able to clear cholesterol from the bloodstream. and desquamated intestinal cells. offer protection and are sometimes referred to as "good cholesterol". such as tritiated-cholesterol are used. but less frequently. and the remainder are lost in the feces. abnormal cholesterol levels (hypercholesterolemia) — actually higher concentrations of LDL particles and lower concentrations of functional HDL particles — are strongly associated with cardiovascular disease because these promote atheroma development in arteries (atherosclerosis). when more concentrated.[51] Many of these cholesterol-regulated genes are homologues of fatty acid β-oxidation genes. increasing the risk of heart disease. Cholesterol is converted mainly into coprostanol. bile. Resistinaccelerates the accumulation of LDL in arteries. food choices. the human pathogen Mycobacterium tuberculosis is able to completely degrade this molecule and contains a large number of genes that are regulated by its presence. and can be metabolized by the colonic bacteria. especially higher LDL particle concentrations and smaller LDL particle size. Approximately 95% of the bile acids are reabsorbed from the intestines. or sulfate. as in the gallbladder. but have evolved in such a way as to bind large steroid substrates like cholesterol. glucuronic acid.[55] Resistin. A cholesterol-reducing bacterium origin has been isolated from human feces. the main cholesterol-reducing drug used in the treatment and prevention of cardiovascular disease. Cholesterol can be purified using small Sephadex LH-20 columns. has been shown to increase the production of LDL in human liver cells and also degrades LDL receptors in the liver.

Still.[60][61] often followed by one of various hypolipidemic agents. 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. rather than the total cholesterol level. even for people with cholesterol values currently considered low for adults. low cholesterol foods. Conversely. correlate with the extent and progress of atherosclerosis.[65] and in men without cardiovascular disease.0 mmol/L [193 mg/dL]). known as statins. A 2007 study pooling data on almost 900. the effect was statistically significant for both genders. LDL.[63] Studies have also found that statins reduce atheroma progression.[68] In 2008. none of the large statin trials conducted prior to 2007 demonstrated a statistically significant reduction in overall mortality or in cardiovascular endpoints. without significant heterogeneity by gender. 20 mg/day of rosuvastatin for 1. [67] since.[57] Elevated levels of the lipoprotein fractions. because cardiovascular disease is relatively rare in the younger population.000 subjects in 61 cohorts demonstrated that blood total cholesterol levels have an exponential effect on cardiovascular and total mortality. IDL and VLDL are regarded as atherogenic (prone to cause atherosclerosis). 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.[66] Primary prevention in women was originally practiced only by extension of the findings in studies on men.of cardiovascular disease. in apparently healthy adults with increased levels of the inflammatory biomarker high-sensitivity Creactive protein but with low initial LDL. people with a history of cardiovascular disease may derive benefit from statins irrespective of their cholesterol levels (total cholesterol below 5. casting doubt on the cardioprotective role of "good cholesterol". have repeatedly confirmed that changing lipoprotein transport patterns from unhealthy to healthier patterns significantly lowers cardiovascular disease event rates. a large clinical trial reported that. such as statins.[69] Though this result was met with some skepticism. yet be made up primarily of small LDL and small HDL particles. with the association more pronounced in younger subjects. cholesterol absorption inhibitors. nicotinic acid derivatives or bile acid sequestrants.[citation needed] Multiple human trials using HMG-CoA reductase inhibitors.9 years resulted in a 44% reduction in the incidence of cardiovascular events and a 20% reduction in all-cause mortality. [59] Elevated cholesterol levels are treated with a strict diet consisting of low saturated fat. the total cholesterol can be within normal limits.[64] As a result. the impact of high cholesterol on health is still larger in older people. later studies and meta-analyses likewise demonstrated statistically significant (but smaller) reductions in all-cause and cardiovascular mortality.[58] Levels of these fractions. In contrast. HDL particles (especially large HDL) have been identified as a mechanism by which cholesterol and inflammatory mediators can be removed from atheroma. trans fatfree.[62] Extreme cases have previously been treated with partial ileal bypass surgery. there is benefit from lowering abnormally high cholesterol levels ("primary prevention"). Increased concentrations of HDL correlate with lower rates of atheroma progressions and even regression. Recently. fibrates.[70] Level mg/d Level mmol/ Interpretation L L . in women. under which conditions atheroma growth rates would still be high.

LDL.2 High risk The 1987 report of National Cholesterol Education Program. HDL. levels of HDL. A 2009 study of patients with acute coronary syndromes found an association of hypercholesterolemia with better mortality outcomes. in which men of all ages and women over 50 with very low cholesterol were likely to die of cancer. The researchers attributed this phenomenon to the fact that people with severe chronic diseases or cancer tend to have below-normal cholesterol levels. > 240 mg/dL high cholesterol. liver diseases. only the total. as today's testing methods determine LDL ("bad") and HDL ("good") cholesterol separately. LDL and total cholesterol in mass and molar concentrations. VLDL can be calculated by dividing total triglycerides by five. Adult Treatment Panels suggests the total blood cholesterol level should be: < 200 mg/dL normal blood cholesterol. This result indicates the low-cholesterol effect occurs even . some studies have shown an inverse correlation between cholesterol levels and mortality.[75] In the Framingham Heart Study. Reference ranges for blood tests.2 Borderline high risk > 240 > 6.[73] although a newer upper limit of 70 mg/dL (1. Direct LDL measures are used when triglycerides exceed 400 mg/dL.2 Desirable level corresponding to lower risk for heart disease 200–240 5.6 mmol/L). showing usual. they found an 11% increase overall and 14% increase in cardiovascular disease mortality per 1 mg/dL per year drop in total cholesterol levels.[74] Given the well-recognized role of cholesterol in cardiovascular disease. The desirable LDL level is considered to be less than 100 mg/dL (2. in subjects over 50 years of age. among the blood constituents with the highest concentration.[71]The American Heart Association provides a similar set of guidelines for total (fasting) blood cholesterol levels and risk for heart disease: [72] However. is found in orange color at right. Usually. The estimated VLDL and LDL have more error when triglycerides are above 400 mg/dL. and mental diseases. as well as optimal.8 mmol/L) can be considered in higher-risk individuals based on some of the above-mentioned trials. that is. this simplistic view has become somewhat outdated. For cost reasons.2–6. [76] This explanation is not supported by the Vorarlberg Health Monitoring and Promotion Programme. A ratio of total cholesterol to HDL—another useful measure—of far less than 5:1 is thought to be healthier. and VLDL. and triglycerides are measured. Total cholesterol is defined as the sum of HDL. 200–239 mg/dL borderline-high.< 200 < 5. 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].

united in The International Network of Cholesterol Skeptics. Hypertension (or use of anti-hypertensive medications).among younger respondents. or if a man over age 45 or a woman over age 50 has HDL (good) cholesterol less than 1 mmol/L (40 mg/dL). which is often associated with low plasma cholesterol levels. and cigarette smoking. and cerebral hemorrhage. LDL (bad) cholesterol.[79] A 2014 meta analysis which followed over 500. low HDL.[80] Hypocholesterolemia[edit] Abnormally low levels of cholesterol are termed hypocholesterolemia. Cholesterol testing[edit] The American Heart Association recommends testing cholesterol every five years for people aged 20 years or older. This measures total cholesterol.[81] A separate set of American Heart Association guidelines issued in 2013 indicates that patients taking statin medications should have their cholesterol tested 4–12 weeks after their first dose and then every 3–12 months thereafter. proteins and metabolites below to link to respective articles.000 patients. [77] The vast majority of doctors and medical scientists consider that there is a link between cholesterol and atherosclerosis as discussed above. rather than a cause. or there are other risk factors for heart disease and stroke.2 mmol/L or more (200+ mg/dL). cancer. but some studies suggest a link with depression. and triglycerides.[57] A genetic defect in cholesterol synthesis causes Smith-Lemli-Opitz syndrome. family history of CAD and hypercholesterolemia. Research into the causes of this state is relatively limited. or a home cholesterol-monitoring device is used to determine a lipoprotein profile. It is recommended to test cholesterol at least every five years if a person has total cholesterol of 5. Other risk factors for heart disease include Diabetes. of an underlying illness. [[File: [§ 1] . the low cholesterol levels seem to be a consequence. In general. contradicting the previous assessment among cohorts of older people that this is a proxy or marker for frailty occurring with age. HDL (good) cholesterol.[78] a small group of scientists.[82] A blood sample after 12-hour fasting is taken by a doctor. concluded there is insufficient evidence to support the recommendation of high consumption of polyunsaturated fatty acids and low consumption of total saturated fats for cardiovascular health. [83] Interactive pathway map[edit] Click on genes. questions the link.

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. in fact. and it changes colour when its temperature changes. The cholesteric phase is.Cholesteric liquid crystals[edit] Some cholesterol derivatives (among other simple cholesteric lipids) are known to generate the liquid crystalline "cholesteric phase". although only two of them are of biochemical significance (nat-cholesterol and ent-cholesterol. a chiral nematic phase. This makes cholesterol derivatives useful for indicating temperature in liquid crystal display thermometers and in temperature-sensitive paints. Stereoisomers[edit] Cholesterol has 256 stereoisomers.[84][85]) and only one of them occurs naturally (nat-cholesterol).