Clopidogrel

Clopidogrel is an oral antiplatelet agent (thienopyridine class) to inhibit blood clots in coronary artery disease, peripheral vascular disease, and cerebrovascular disease. It is marketed by Bristol-Myers Squibb and Sanofi-Aventis under the trade name Plavix, by Sun Pharmaceuticals under the trade name Clopilet, by Ranbaxy Laboratories under the trade name Ceruvin. It works by irreversibly inhibiting a receptor called P2Y12. Adverse effects include hemorrhage.

Clinical use

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Indications

Clopidogrel is indicated for:[2]
Prevention of vascular ischaemic events in patients with symptomatic atherosclerosis
Acute coronary syndrome without ST-segment elevation (NSTEMI),
ST elevation MI (STEMI)

It is also used, along with aspirin, for the prevention of thrombosis after placement of intracoronary stent. [2]

International guidelines granted the highest grade of recommendation for NSTE-ACS, PCI and stent,[clarification needed] for Clopidogrel in addition to Aspirin. Consensus-based therapeutic guidelines recommend also the use of clopidogrel, instead of aspirin, in patients requiring antiplatelet therapy but with a history of gastric ulceration, as inhibition of the synthesis of prostaglandins by aspirin (acetylsalicylic acid) can exacerbate this condition. A study has shown that in patients with healed aspirin-induced ulcers, however, patients receiving aspirin plus the proton pump inhibitor esomeprazole had a lower incidence of recurrent ulcer bleeding than patients receiving clopidogrel. [3] However, a more recent study suggested that prophylaxis with proton pump inhibitors along with clopidogrel following acute coronary syndrome may increase adverse outcomes, possibly due to inhibition of CYP2C19 which is required for activation of clopidogrel, itself a pro-drug.[4]

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Dosage forms

Clopidogrel is marketed as clopidogrel bisulfate (clopidogrel hydrogen sulfate), most commonly under the trade names Plavix, as 75 mg oral tablets.

Atorvastatin

Atorvastatin (INN) (pronounced /əˌtɔrvəˈstætən/) (Lipitor, Pfizer), is a member of the drug class known as statins, used for lowering blood cholesterol. It also stabilizes plaque and prevents strokes through anti-inflammatory and other mechanisms.

Atorvastatin inhibits HMG-CoA reductase, the rate-determining enzyme located in hepatic tissue that produces mevalonate, a small molecule used in the synthesis of cholesterol and other mevalonate derivatives. This lowers the amount of cholesterol produced which in turn lowers the total amount of LDL cholesterol. Atorvastatin was first synthesized in 1985 by Bruce Roth while working at Parke-Davis Warner-Lambert Company (now Pfizer). With 2008 sales of US$12.4 billion, Lipitor is likely the top-selling drug in the world.[1] US patent protection is scheduled to expire in June 2011.[2] However, Pfizer made an agreement with Ranbaxy Laboratories to delay the generic launch in the US until November 2011.[1]

Lipitor is not the only statin; there are several other statins on the market.[3][4]

Contraindications
Active liver disease: cholestasis, hepatic encephalopathy, hepatitis, and jaundice.
Unexplained elevations in AST or ALT levels
Pregnancy.
Breast-feeding.

Fluvastatin

Fluvastatin (Lescol, Canef, Vastin) is a member of the drug class of statins, used to treat hypercholesterolemia and to prevent cardiovascular disease. It has also been shown to exhibit antiviral activity against Hepatitis C.[1]

Pravastatin

Pravastatin (marketed as Pravachol or Selektine) is a member of the drug class of statins, used for lowering cholesterol and preventing cardiovascular disease. Initially known as CS-514, it was originally identified in a bacterium called Nocardia autotrophica by researchers of the Sankyo Pharma Inc..[1] It is presently being marketed outside Japan by the pharmaceutical company Bristol-Myers Squibb.

The U.S. Food and Drug Administration approved generic pravastatin for sale in the United States for the first time on April 24, 2006. Generic pravastatin sodium tablets (10 mg, 20 mg and 40 mg) are manufactured by TEVA Pharmaceuticals in Kfar Sava, Israel.[2]

Simvastatin

Simvastatin (INN) (pronounced /ˈsɪmvəstætɨn/), (marketed under the trade names Zocor, Simlup, Simcard, Simvacor, and others) is a hypolipidemic drug belonging to the class of pharmaceuticals called "statins". It is used to control hypercholesterolemia (elevated cholesterol levels) and to prevent cardiovascular disease. Simvastatin is a synthetic derivate of a fermentation product of Aspergillus terreus.

Simvastatin is a powerful lipid-lowering drug that can decrease low density lipoprotein (LDL) levels by up to 50%. It is used in doses of 5 mg up to 80 mg. Higher doses (160 mg) have been found to be too toxic, while giving only minimal benefit in terms of lipid lowering. There is no real effect on HDL and triglyceride levels.

From recent research it has become apparent that simvastatin and other statins inhibit the progression of atherosclerosis beyond their effects on LDL. Many explanations have been proposed, for example its inhibitory effect on macrophages in the atherosclerotic plaque lesions.

In one non-randomized study, simvastatin halved the risk of developing dementia or Parkinson's disease.[3]

Lovastatin

Lovastatin is a member of the drug class of statins, used for lowering cholesterol (hypolipidemic agent) in those with hypercholesterolemia and so preventing cardiovascular disease. Lovastatin is a naturally occurring drug found in food such as oyster mushrooms[1] and red yeast rice[2].

Lovastatin is an inhibitor of 3-hydroxy-3methylglutaryl-coenzyme A reductase (HMG-CoA reductase), an enzyme which catalyzes the conversion of HMG-CoA to mevalonate.[20] Mevalonate is a required building block for cholesterol biosynthesis and lovastatin interferes with its production by acting as a reversible competitive inhibitor for HMG-CoA which binds to the HMG-CoA reductase. Lovastatin, being inactive in the native form, the form in which it is administered,is hydrolysed to the β-hydroxy acid form in the body and it is this form which is active.

Some commmen madicien for Cholesterol

madicien for Cholesterol

Is lowering LDL cholesterol enough?

Unfortunately, the prevention and treatment of atherosclerosis are more complicated than just lowering LDL cholesterol levels. LDL cholesterol reduction is only half of the battle against atherosclerosis. Individuals who have normal or only mildly elevated LDL cholesterol levels can still develop atherosclerosis and heart attacks even in the absence of other risk factors such as cigarette smoking, high blood pressure, and diabetes mellitus. Additionally, successfully lowering elevated LDL cholesterol levels cannot always prevent atherosclerosis and heart attacks. In many clinical trials to lower LDL cholesterol, there were patients who adhered to their assigned diets, faithfully took their cholesterol-lowering medications, and successfully lowered their LDL cholesterol to target levels, yet still suffered progressive atherosclerosis and heart attacks. It is clear that while lowering LDL cholesterol below NCEP target levels is an important step, there are other factors involved.

What is ezetimibe (Zetia)?

Ezetimibe lowers blood cholesterol by blocking the absorption of cholesterol, including dietary cholesterol, from the intestines. It does not affect, however, the absorption of triglycerides or fat-soluble vitamins. Ezetimibe was approved by the FDA in October, 2002.

Ezetimibe can be used alone or together with a statin drug. Ezetimibe used alone is modestly effective in lowering LDL cholesterol. At a dose of 10 mg/day it can reduce LDL cholesterol by approximately 17%. When used with a statin, it can reduce LDL cholesterol level further than a statin alone. However, there is insufficient scientific data to determine whether a statin-ezetimibe combination actually further reduces heart attack or stroke risks. A new combination drug, Vytorin, is available and combines 10 mg of Zetia with 20, 40, or 80 mg of Zocor.

Ezetimibe is probably most useful in avoiding having to use high doses of a statin to achieve the 2004 NCEP LDL cholesterol targets in certain patients. Using lower doses of a statin probably reduces the risk of muscle injury. A statin-ezetimibe combination may also be helpful in treating patients with very high LDL cholesterol who cannot attain LDL cholesterol targets even with maximal doses of statins. Ezetimibe can be taken with or without food and at the same time as statin drugs.

Ezetimibe is well-tolerated. The overall rate of side effects with ezetimibe in clinical studies was similar to that reported with a placebo (an inactive sugar pill). Diarrhea, abdominal pain, back pain, joint pain, and sinusitis were the most commonly reported side effects, occurring in 1 in every 25 to 30 patients.

What are bile acid sequestrants?

Bile acid sequestrants such as Cholestyramine (Questran), colestipol (Colestid), and colesevelam (Welchol) are medications for lowering LDL cholesterol. Bile acid sequestrants bind bile acids in the intestine and cause more of the bile acids to be excreted in the stool. This reduces the amount of bile acids returning to the liver and forces the liver to produce more bile acids to replace the bile acids lost in the stool. In order to produce more bile acids, the liver converts more cholesterol into bile acids, which lowers the level of cholesterol in the blood.

Bile acid sequestrants have modest LDL cholesterol-lowering effects. Low doses (for example 8 gram/day of Cholestyramine) can lower LDL cholesterol by 10%-15 %. But even high doses (24 gram/day of cholestyramine) can only lower LDL cholesterol by approximately 25%. Therefore, bile acid sequestrants used alone are not as effective as statins in lowering LDL cholesterol.

However, bile acid sequestrants are most useful in combining with a statin or niacin to aggressively lower LDL cholesterol levels. The statin-bile acid sequestrant combination can lower LDL cholesterol levels by approximately 50%, lower than a statin alone. A statin-niacin combination can substantially reduce LDL cholesterol and elevate HDL cholesterol. For more, please read our article on Bile Acid Sequestrants.

What are fibric acid derivatives (fibrates)?

Fibric acid derivatives (fibrates) are effective medications in lowering blood triglyceride levels. Fibrates lower blood triglyceride levels by inhibiting the liver production of VLDL (the triglyceride-rich lip-protein fraction), and by speeding up the removal of triglycerides from the blood. Fibrates are also modestly effective in increasing blood HDL cholesterol levels. However, fibrates are not effective in lowering LDL cholesterol. Examples of fibrates available in the United Sates include Gemfibrozil (Lopid) and fenofibrate (Tricor).

Very high triglyceride levels (usually > 1000 mg/dl) can cause pancreatitis (inflammation of the pancreas that can result in a serious an illness with severe abdominal pain). By lowering the blood triglycerides, fibrates are used to prevent pancreatitis.

Fibrates are not effective in lowering LDL cholesterol and cannot be used alone in lowering LDL cholesterol levels. However, when a high risk patient (see NCEP recommendations above) also has high blood triglyceride or low HDL cholesterol levels, doctors may consider combining a fibrate, such as fenofibrate (Tricor), with a statin. Such a combination will not only lower the LDL cholesterol, but will also lower blood triglycerides and increase HDL cholesterol levels.

Fibrates have also been used alone to prevent heart attacks especially in patients with elevated blood triglycerides and low HDL cholesterol levels. In one large study, gemfibrozil decreased the risk of heart attacks but did not affect the overall survival of persons with high cholesterol levels. For more, please read our article on Fibrates.

What is nicotinic acid (niacin)?

Nicotinic acid (niacin) is a B vitamin. An average American diet contains 15-30 mg of niacin per day. However, in treating blood cholesterol and triglyceride disorders, high doses (1-3 grams a day) of nicotinic acid are necessary. Nicotinic acid is available in several preparations that include immediate release niacin, sustained release prescription brand Niaspan, and over- the- counter (OTC) sustained release niacin. OTC preparations are not federally regulated, and some OTC preparations may have no active ingredient. Thus, they would be ineffective in either lowering LDL or raising HDL cholesterol. Some formulations of OTC sustained release niacin have been associated with liver toxicity and rare cases of fulminant (usually fatal without liver transplantation) hepatitis have been reported. The prescription brand sustained release Niaspan has been found in clinical trials to cause only minor elevations in blood liver enzymes without causing significant liver disease.

Nicotinic acid is most effective in increasing HDL cholesterol and it is also modestly effective in lowering LDL cholesterol, Lp(a) cholesterol, and triglyceride levels (see below). Nicotinic acid is most suited for individuals whose only problem is low HDL cholesterol. Nicotinic acid used alone can raise HDL cholesterol levels by 30% or more. Nicotinic acid is not as effective as a statin in lowering LDL cholesterol levels. Therefore, when low HDL cholesterol is accompanied by high LDL cholesterol, most doctors use a statin to decrease the LDL cholesterol first. If necessary, nicotinic acid can be added to a statin to further raise HDL cholesterol levels.

Advicor is a combination product approved for use in the United States. It is a combination of sustained release niacin with lovastatin. Advicor is useful in patients who need to both significantly lower their LDL cholesterol and increase HDL cholesterol. For more, please read our article on Nicotinic acid.

What is nicotinic acid (niacin)?

Nicotinic acid (niacin) is a B vitamin. An average American diet contains 15-30 mg of niacin per day. However, in treating blood cholesterol and triglyceride disorders, high doses (1-3 grams a day) of nicotinic acid are necessary. Nicotinic acid is available in several preparations that include immediate release niacin, sustained release prescription brand Niaspan, and over- the- counter (OTC) sustained release niacin. OTC preparations are not federally regulated, and some OTC preparations may have no active ingredient. Thus, they would be ineffective in either lowering LDL or raising HDL cholesterol. Some formulations of OTC sustained release niacin have been associated with liver toxicity and rare cases of fulminant (usually fatal without liver transplantation) hepatitis have been reported. The prescription brand sustained release Niaspan has been found in clinical trials to cause only minor elevations in blood liver enzymes without causing significant liver disease.

Nicotinic acid is most effective in increasing HDL cholesterol and it is also modestly effective in lowering LDL cholesterol, Lp(a) cholesterol, and triglyceride levels (see below). Nicotinic acid is most suited for individuals whose only problem is low HDL cholesterol. Nicotinic acid used alone can raise HDL cholesterol levels by 30% or more. Nicotinic acid is not as effective as a statin in lowering LDL cholesterol levels. Therefore, when low HDL cholesterol is accompanied by high LDL cholesterol, most doctors use a statin to decrease the LDL cholesterol first. If necessary, nicotinic acid can be added to a statin to further raise HDL cholesterol levels.

Advicor is a combination product approved for use in the United States. It is a combination of sustained release niacin with lovastatin. Advicor is useful in patients who need to both significantly lower their LDL cholesterol and increase HDL cholesterol. For more, please read our article on Nicotinic acid.

What are the statin drugs?

The statins are the most widely used, and also the most powerful medications for lowering LDL cholesterol. Numerous large, randomized, double-blind, placebo-controlled, , clinical trials (controlled trials) have shown that statins reduce heart attacks (and strokes) and improve survival. Statins are well tolerated with low side effect rates when used long term. Statins not only lower blood LDL cholesterol levels, they also modestly increase HDL cholesterol levels and modestly decrease triglyceride levels. The statins that are now on pharmacy shelves in the U.S. (putting the generic name first followed by the brand name in parentheses) are:
rosuvastatin ( Crestor) 
fluvastatin sodium (Lescol) made by Novartis 
atorvastatin calcium (Lipitor) made by Parke-Davis and Pfizer 
lovastatin (Mevacor) made by Merck 
pravastatin sodium (Pravachol) made by Bristol-Myers Squibb 
simvastatin (Zocor) made by Merck
pitavastatin (Livalo) made by Kowa Company Ltd.

Studies have consistently shown that lowering LDL cholesterol with diet and statins reduces the risk of a second heart attack. The prevention of recurrent heart attacks in patients who have already suffered a heart attack is called secondary prevention.

Studies have also demonstrated that reducing LDL cholesterol with lifestyle changes and statins reduces the risk of having the first heart attack. Prevention of heart attacks in those who have never had a heart attack is called primary prevention.

Studies have also confirmed that reducing LDL cholesterol benefits both men and women, and the elderly. For more, please read our article on Statins

Lipid altering medications commonly used in the United States

Medication class Medication examples Effects on blood lipids 
statins Pravachol, Mevacor, Lipitor, Lescol, Crestor, Zocor Most effective in lowering LDL, mildly effective in increasing HDL, mildly effective in lowering triglycerides 
Nicotinic acid (Niacin) Niacin, Niaspan, Slo-Niacin Most effective in increasing HDL, effective in lowering triglycerides, mildly to modestly effective in lowering LDL 
Fibric acid Lopid, Tricor Most effective in lowering triglycerides, effective in increasing HDL, minimally effective in lowering LDL 
Bile acid sequestrants Questran, Welchol, Colestid Mildly to modestly effective in lowering LDL, no effect on HDL and triglycerides 
Cholesterol absorption inhibitors Zetia Mildly to modestly effective in lowering LDL, no effect on HDL and triglycerides 
Combining nicotinic acid with statin Advicor (lovastatin+niaspan) Effective in lowering LDL and triglycerides and increasing HDL
Combining a statin with an absorption inhibitor Vytorin (Zocor + Zetia) Synergistic in lowering LDL and effective in lowering LDL with low doses of each ingredient

What are lipid-altering medications?

Lipid altering medications are used in lowering blood levels of undesirable lipids such as LDL cholesterol and triglycerides and increasing blood levels of desirable lipids such as HDL cholesterol. Several classes of medications are available in the United States, including HMG CoA reductase inhibitors (statins), nicotinic acid, fibric acid derivatives, and medications that decrease intestinal cholesterol absorption (bile acid sequestrants and cholesterol absorption inhibitors). Some of these medications are primarily useful in lowering LDL cholesterol, others in lowering triglycerides, and some in elevating HDL cholesterol. Medications also can be combined to more aggressively lower LDL, as well as in lowering LDL and increasing HDL at the same time.

What are triglycerides, chylomicrons, and VLDL?

Triglyceride is a fatty substance that is composed of three fatty acids. Like cholesterol, triglyceride in the blood either comes from the diet or the liver. Also, like cholesterol, triglyceride cannot dissolve and circulate in the blood without combining with a lipoprotein. Thus, after a meal, the triglyceride and cholesterol that are absorbed into the intestines are packaged into round particles called chylomicrons before they are released into the blood circulation.

A chylomicron is a collection of cholesterol and triglyceride that is surrounded by a lipoprotein outer coat. (Chylomicrons contain 90% triglyceride and 10% cholesterol.) 

The liver removes triglyceride and chylomicrons from the blood, and it synthesizes and packages triglyceride into VLDL (very low-density lipoprotein) particles and releases them back into the blood circulation.

What are triglycerides, chylomicrons, and VLDL?

Triglyceride is a fatty substance that is composed of three fatty acids. Like cholesterol, triglyceride in the blood either comes from the diet or the liver. Also, like cholesterol, triglyceride cannot dissolve and circulate in the blood without combining with a lipoprotein. Thus, after a meal, the triglyceride and cholesterol that are absorbed into the intestines are packaged into round particles called chylomicrons before they are released into the blood circulation.

A chylomicron is a collection of cholesterol and triglyceride that is surrounded by a lipoprotein outer coat. (Chylomicrons contain 90% triglyceride and 10% cholesterol.) 

The liver removes triglyceride and chylomicrons from the blood, and it synthesizes and packages triglyceride into VLDL (very low-density lipoprotein) particles and releases them back into the blood circulation.

Why is HDL the good cholesterol?

HDL is the good cholesterol because it protects the arteries from the atherosclerosis process. HDL cholesterol extracts cholesterol particles from the artery walls and transports them to the liver to be disposed through the bile. It also interferes with the accumulation of LDL cholesterol particles in the artery walls.

The risk of atherosclerosis and heart attacks in both men and is strongly related to HDL cholesterol levels. Low levels of HDL cholesterol are linked to a higher risk, whereas high HDL cholesterol levels are associated with a lower risk.

Very low and very high HDL cholesterol levels can run in families. Families with low HDL cholesterol levels have a higher incidence of heart attacks than the general population, while families with high HDL cholesterol levels tend to live longer with a lower frequency of heart attacks.

Like LDL cholesterol, life style factors and other conditions influence HDL cholesterol levels. HDL cholesterol levels are lower in persons who smoke cigarettes, eat a lot of sweets, are overweight and inactive, and in patients with type II diabetes mellitus.

HDL cholesterol is higher in people who are lean, exercise regularly, and do not smoke cigarettes. Estrogen increases a person's HDL cholesterol, which explains why women generally have higher HDL levels than men do.

For individuals with low HDL cholesterol levels, a high total or LDL cholesterol blood level further increases the incidence of atherosclerosis and heart attacks. Therefore, the combination of high levels of total and LDL cholesterol with low levels of HDL cholesterol is undesirable whereas the combination of low levels of total and LDL cholesterol and high levels of HDL cholesterol is favorable.

The 2004 NCEP treatment goals according to risk categories

High risk patients are those who already have coronary heart disease (such as a prior heart attack), diabetes mellitus, abdominal aortic aneurysm, or those who already have atherosclerosis of the arteries to the brain and extremities (such as patients with strokes, TIA's (mini-strokes), and peripheral vascular diseases). High risk patients also include those with 2 or more risk factors (e.g., smoking, hypertension, or a family history of early heart attacks) that places them at a greater than 20 percent chance of having a heart attack within 10 years. (A person's chance of having a heart attack can be calculated by using the Framingham Heart Study Score Sheets, at http://nhlbi.nih.gov/about/framingham/riskabs.htm). 
Very high -risk patients are those who have coronary heart disease in addition to having either multiple risk factors (especially diabetes), or severe and poorly controlled risk factors (such as continued smoking), or metabolic syndrome (a constellation of risk factors associated with obesity, including high triglycerides and low HDL). Patients hospitalized for acute coronary syndromes are also at very high risk. 
Moderately high risk patients are those who have neither coronary heart disease nor diabetes mellitus, but have multiple (2 or more) risk factors for coronary heart disease that put them at a 10 to 20 percent risk of heart attack within 10 years. (Use the Framingham Heart Study Score Sheets, at http://nhlbi.nih.gov/about/framingham/riskabs,htm to calculate the 10 year risk.) 
Moderate risk patients are those who have neither CHD nor diabetes mellitus, but have 2 or more risk factors for coronary heart disease that put them at a <10% risk of heart attack within 10 years. 
Lower risk patients are those with 0 to 1 risk factor for coronary heart disease.

What are the 2004 NCEP cholesterol treatment guidelines?

After reviewing these large randomized cholesterol-lowering trials, The National Cholesterol Education Program (NCEP) expert panel published their new recommendations. The new NCEP recommendations, presented in the June, 2004 issue of Circulation, are:
The report advised physicians to consider more intensive LDL cholesterol-lowering for people at very high, high, and moderately high risk for a heart attack. These options include setting lower treatment goals for LDL cholesterol and initiating cholesterol-lowering drug therapy at lower LDL thresholds, as compared to ATP III guidelines published in 2001. For example, for patients with a very high risk of heart attacks, the LDL cholesterol treatment goal remains at <100mg/dl, but the report advised doctors to consider the option of lowering the LDL cholesterol (usually using a statin plus lifestyle changes) to < 70 mg/dl. 
The report emphasized the importance of initiating therapeutic lifestyle changes (TLC) to modify lifestyle-related risk factors (obesity, physical inactivity, metabolic syndrome, high blood triglyceride levels and low HDL cholesterol levels). TLC Lifestyle changes have the potential to reduce heart attack and stroke risks through several mechanisms beyond the lowering of LDL cholesterol. 
When LDL-lowering medication is used for very high, high or moderately high risk patients, the report advises that the intensity of LDL-lowering drug therapy be sufficient to achieve at least a 30 to 40 percent reduction in LDL cholesterol levels. 
When a very high or high risk patient also has high blood triglyceride or low HDL cholesterol levels, doctors may consider combining nicotinic acid or a fibrate with a statin. Nicotinic acid and fibrates are more effective than statins in lowering triglycerides and increasing HDL. 
Age should not be a consideration since older persons also benefit from lowering LDL cholesterol. Thus, it is never too late or the patient too old to begin lifestyle changes and medications to lower LDL cholesterol. A word of caution is in order. Elderly patients are more likely to have liver and kidney dysfunction, and are also more likely to be on multiple medications some of which may interfere with the breakdown of cholesterol-lowering drugs such as statins. Thus lower dosing may be necessary to avoid adverse side effects

What determines the level of LDL cholesterol in the blood?

The liver not only manufactures and secretes LDL cholesterol into the blood; it also removes LDL cholesterol from the blood. A high number of active LDL receptors on the liver surfaces is associated with the rapid removal of LDL cholesterol from the blood and low blood LDL cholesterol levels. A deficiency of LDL receptors is associated with high LDL cholesterol blood levels.

Both heredity and diet have a significant influence on a person's LDL, HDL and total cholesterol levels. For example, familial hypercholesterolemia (FH) is a common inherited disorder whose victims have a diminished number or nonexistent LDL receptors on the surface of liver cells. People with this disorder also tend to develop atherosclerosis and heart attacks during early adulthood.

Diets that are high in saturated fats and cholesterol raise the levels of LDL cholesterol in the blood. Fats are classified as saturated or unsaturated (according to their chemical structure). Saturated fats are derived primarily from meat and dairy products and can raise blood cholesterol levels. Some vegetable oils made from coconut, palm, and cocoa are also high in saturated fats.

What are LDL and HDL cholesterol?

LDL cholesterol is called "bad" cholesterol, because elevated levels of LDL cholesterol are associated with an increased risk of coronary heart disease. LDL lipoprotein deposits cholesterol on the artery walls, causing the formation of a hard, thick substance called cholesterol plaque. Over time, cholesterol plaque causes thickening of the artery walls and narrowing of the arteries, a process called atherosclerosis.

HDL cholesterol is called the "good cholesterol" because HDL cholesterol particles prevent atherosclerosis by extracting cholesterol from the artery walls and disposing of them through the liver. Thus, high levels of LDL cholesterol and low levels of HDL cholesterol (high LDL/HDL ratios) are risk factors for atherosclerosis, while low levels of LDL cholesterol and high level of HDL cholesterol (low LDL/HDL ratios) are desirable.

Total cholesterol is the sum of LDL (low density) cholesterol, HDL (high density) cholesterol, VLDL (very low density) cholesterol, and IDL (intermediate density) cholesterol.

What is cholesterol?

Cholesterol is a fatty substance (a lipid) that is an important part of the outer lining (membrane) of cells in the body of animals. Cholesterol is also found in the blood circulation of humans. The cholesterol in a person's blood originates from two major sources; dietary intake and liver production. Dietary cholesterol comes mainly from meat, poultry, fish, and dairy products. Organ meats, such as liver, are especially high in cholesterol content, while foods of plant origin contain no cholesterol. After a meal, cholesterol is absorbed by the intestines into the blood circulation and is then packaged inside a protein coat. This cholesterol-protein coat complex is called a chylomicron.

The liver is capable of removing cholesterol from the blood circulation as well as manufacturing cholesterol and secreting cholesterol into the blood circulation. After a meal, the liver removes chylomicrons from the blood circulation. In between meals, the liver manufactures and secretes cholesterol back into the blood circulation.