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All The Info On The New Cholesterol Findings

Thursday, October 9th, 2008

Cholesterol, although a fat, is an essential nutrient for the body. It is made in the liver. The liver produces cholesterol in the necessary quantities for health.

Food that helps to lower cholesterol levels

Other foods that can lower the cholesterol levels are fruits and vegetables. This type of food doesn’t contain that much cholesterol so whatever you eat, you won’t be adding to its levels.

Another great thing about fruit and vegetables is the fact that they are great sources of fibres that the body also needs to combat LDL cholesterol. Berries as well as fruit that is citrus and carrots are just some of the fruit you can count on for combating LDL.

Soya is another food that can dramatically reduce the levels of cholesterol in the body. Fibre rich food, soya as well as almonds and plant sterols also reduce cholesterol levels by as much as 20 percent, according to a recent study. Eating oats, olive oil and barley are also great ways to lower LDL.

To lower LDL, it’s important to consciously avoid foods that are deep-fried. If you have to eat fried foods, make sure that the oil that you use is vegetable oil.

Never use butter as this is rich in saturated fats. Instead, use margarine as a substitute. Steam, braise, boil or bake your food these are both tastier and healthier.

It’s not just the food

There are many factors that contribute to the rise in the levels of cholesterol. In addition to one’s eating lifestyle, there is the age, gender, genes, family history and of course the amount of physical activity that’s done. Exercise is certainly very important in keeping LDL cholesterol at bay. Not only that, it strengthens the body’s resistance as well as improves blood circulation.

One reason for the high levels of cholesterol, could be due to the wide variety of fast food being offered these days at the grocery store and in restaurants. But is there one food product that can be called the best to lower cholesterol? Probably not as a well balanced diet comes from all of the food groups.

Lowering cholesterol quick tips

* Instead of drinking full cream milk on cornflakes or whole grain, try using non or low fat milk instead. The taste is almost the same, but is much healthier.
* Instead of ordering a steak change your menu to lean meat instead, but be careful as even lean meat has fat, although not as much and tastes just as good as the big steak.
* The healthiest thing to have either for lunch and/or dinner is food that comes from the ocean. Fish or shellfish is known to contain concentrates of Omega 3, which is very effective in lowering cholesterol.
* Eating a candy bar or a slice of cake is tempting, but they are rich in fat – although there are low fat and cholesterol free chocolate cake recipe. Try nuts or fruits instead, which are rich in fibre as well as contain vitamins and minerals that are lots healthier than the candy or cake.
* In each meal, don’t forget to add fruit where possible. A salad works well or grated carrots as a side dish. There should be a balance whenever eating meat or fish.
* Chicken is not so good if it’s fried, steamed is far better and a healthier way of cooking it – but remember to remove the skin.

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Cholesterol Diet Good Lowering

Tuesday, June 24th, 2008

How to Lower Your Cholesterol?

Cholesterol Lowering Drugs and Cholesterol Lowering Diet

Whatever the reasons may be for your high blood cholesterol level – diet, heredity, or both – the treatment your doctor will prescribe first is a diet. If your blood cholesterol level has not decreased sufficiently after carefully following the diet for 6 months, your doctor may consider adding cholesterol-lowering medication to your dietary treatment. Remember, diet is a very essential step in the treatment of high blood cholesterol.

Cholesterol-lowering medications are more effective when combined with diet. Thus they are meant to supplement, not replace, a low-saturated fat, low-cholesterol diet.

Summary of Diet Guidelines for Lowering High Blood Cholesterol Levels

* Eat less high-fat food (especially those high in saturated fat)
* Replace part of the saturated fat in your diet with unsaturated fat
* Eat less high-cholesterol food
* Choose foods high in complex carbohydrates (starch and fiber)
* Reduce your weight, if you are overweight

Eat Less High-fat Food

Dietary Fat

There are two major types of dietary fat – saturated and unsaturated. Unsaturated fats are further classified as either polyunsaturated or monounsaturated fats. Together, saturated and unsaturated fats equal total fat. All foods containing fat contain a mixture of these fats.

Reduce Total Fat Intake

One of the goals in your blood cholesterol-lowering diet is to eat less total fat, because this is an effective way to eat less saturated fat. Because fat is the richest source of calories, this will also help reduce the number of calories you eat every day. If you are overweight, weight loss is another important step in lowering blood cholesterol levels (as discussed later in this brochure). If you are not overweight, be sure to replace the fat calories by eating more food high in complex carbohydrates.

Remember: When you decrease the amount of total fat you eat, you are likely to reduce the saturated fat and calories in your diet.

Saturated Fat

Saturated fat raises your blood cholesterol level more than anything else in your diet. The best way to reduce your blood cholesterol level is to reduce the amount of saturated fat you eat.

Animal Fats

Animal products as a group are a major source of saturated fat in the average American diet. Butter, cheese, whole milk, ice cream, and cream all contain high amounts of saturated fat. Saturated fat is also concentrated in the fat that surrounds meat and in the white streaks of fat in the muscle of meat (marbling). Poultry, fish, and shellfish also contain saturated fat, although generally less than meat.

Hydrogenated Fat – Known As Trans Fatty Acids or Trans-Fats

Trans fats are created during the food manufacturing process when cheap vegetable oils undergo a process called “hydrogenation” – they have hydrogen added to them to make them solid and less likely to become rancid. Unfortunately, trans fats are even worse for our heart than saturated fat, as they encourage atherosclerosis (narrowing of the arteries).

Vegetable Fats

A few vegetable fats – coconut oil, cocoa butter (found in chocolate), palm kernel oil, and palm oil – are high in saturated fat. These vegetable fats are found in many commercially baked goods, such as cookies and crackers, and in nondairy substitutes, such as whipped toppings, coffee creamers, cake mixes, and even frozen dinners. They also can be found in some snack foods like chips, candy bars, and buttered popcorn. Because these vegetable fats are not visible in these foods (unlike the fat in meats) it is important for you to read food labels. The label may tell you how much saturated fat a food contains, which will help you choose foods lowest in saturated fats.

Remember: Saturated fats are found primarily in animal products. But a few vegetable fats and many commercially processed foods also contain saturated fat. Read labels carefully. Choose foods wisely.

Substitute Unsaturated Fat for Saturated Fat

Unsaturated fat actually helps to lower cholesterol levels when it is substituted for saturated fat. Therefore, health professionals recommend that, when you do eat fats, unsaturated fats (polyunsaturated and monounsaturated fats) be substituted for part of the saturated fat whenever possible.

Polyunsaturated fats are found primarily in safflower, corn, soybean, cottonseed, sesame, and sunflower oils, which are common cooking oils. Polyunsaturated fats are also contained in most salad dressings. But be cautious. Commercially prepared salad dressings also may be high in saturated fats, and therefore careful inspection of labels is important. The word “hydrogenated” on a label means that some of the polyunsaturated fat has been converted to saturated fat.

Another type of polyunsaturated fat is found in the oils of fish and shellfish (often referred to as fish oils, or omega-3 fatty acids). This type of polyunsaturated fat is found in greatest amounts in such fatty fish as herring, salmon, and mackerel. There is little evidence that omega-3 fatty acids are useful for reducing LDL-cholesterol levels. However, fish is a good food choice for this diet play anyway because it is low in saturated fat. The use of fish oil supplements are not recommended for the treatment of high blood cholesterol because it is not known whether long-term ingestion of omega-3 fatty acids will lead to undesirable side effects.

Olive and canola oil (rapeseed oil) are examples of oils that are high in monounsaturated fats. Like other vegetable oils, these oils are used in cooking as well as in salads. Recently, research has shown that substituting monounsaturated fat, like substituting polyunsaturated fat, for saturated fat reduces blood cholesterol levels.

Remember: Unsaturated fats when substituted for saturated fats help lower blood cholesterol levels.

Eat Less High-Cholesterol Food

Dietary cholesterol is a waxy, fat-like substance found in foods that come from animals. Although it is not the same as saturated fat, dietary cholesterol also can raise your blood cholesterol level. Therefore, it is important to eat less food that is high in cholesterol. While cholesterol is needed for normal body function, your liver makes enough for your body’s needs so that you don’t need to eat any cholesterol at all.

Dietary Cholesterol in Food

Cholesterol is found in eggs, dairy products, meat, poultry, fish, and shellfish. Egg yolks and organ meats (liver, kidney, sweetbread, brain) are particularly rich sources of cholesterol. High-fat dairy products, meat, and poultry all have similar amounts of cholesterol. Fish generally has less cholesterol, but shellfish varies in cholesterol content. Foods of plant origin, like fruits, vegetables, grains, cereals, nuts, and seeds, contain no cholesterol.

Since cholesterol is not a fat, you can find it in both high-fat and low-fat animal foods. In other words, even if a food is low in fat, it may be high in cholesterol. For instance, organ meats, like liver, are low in fat, but are high in cholesterol.

Because many foods such as dairy products and some meats are high in both saturated fat and cholesterol, it is important to limit the amount of these high-fat foods that you eat, choosing lean meats and low-fat dairy products whenever possible.

Remember: Organ meats and egg yolks are high in cholesterol. High-fat dairy products, meat, and poultry have similar amounts of cholesterol. Some fish has less. Foods of plant origin like fruits, vegetables, vegetable oils, grains, cereals, nuts, and seeds contain no cholesterol.

Substitute Low GI Carbohydrates for Saturated Fat

Breads, pasta, rice, cereals, dried peas and beans, fruits, and vegetables are good sources of complex carbohydrates (starch and fiber). Low-GI varieties are excellent substitutes for foods that are high in saturated fat and cholesterol. The type of fiber found in foods such as oat and barley bran, some fruits like apples and oranges, and in some dried beans may even help reduce blood cholesterol levels.

Contrary to popular belief, high-carbohydrate foods (like pasta, rice, potatoes) are lower in calories than foods high in fat. In addition, they are good sources of vitamins and minerals. What adds calories to these foods is the addition of butter, rich sauces, whole milk, or cream, which are high in fat, especially saturated fat. It is important not to add these to the high-carbohydrate foods you are substituting for foods high in fat.

Remember: Foods that are high in complex carbohydrates, if eaten plain, are low in saturated fat and cholesterol as well as being good sources of vitamins, minerals, and fiber.

Maintain a Desirable Weight

People who are overweight frequently have higher blood cholesterol levels than people of desirable weight.

You can reduce your weight by eating fewer calories and by increasing your physical activity on a regular basis. By reducing the amount of fat in your diet, you will be cutting down on the richest source of calories. Substituting foods that are high in complex carbohydrates for high-fat foods will also help you lose weight, because many high-carbohydrate foods contain little fat and thus fewer calories.

Fat Contains Twice the Calories of Carbs and Protein

Fat has more than twice the calories as the same amount of protein or carbohydrate. Protein and carbohydrate both have about 4 calories in each gram, but all fat-saturated, polyunsaturated or monounsaturated fat – has 9 calories in each gram. Thus, foods that are high in fat are high in calories. And all calories count. So, to maintain a desirable weight, it is important to eat no more calories than your body needs.

Remember: To achieve or maintain a desirable weight, your caloric intake must not exceed the number of calories your body burns.

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Cholesterol Diet High Cholesterol

Saturday, June 21st, 2008

High cholesterol affects about 17% of Americans ages 20 and older, contributing to atherosclerotic heart disease, which is the single leading cause of death and disability in the developed world. This medical dictionary covers the terms used in the report, What to do about High Cholesterol, and includes details on how to lower and watch your cholesterol through tests and diets.

* antioxidant: A substance that inhibits oxidation.

* apolipoproteins: Proteins that combine with cholesterol and triglyceride to form lipoproteins.

* atherosclerosis: Development of cholesterol-rich plaque on the inner walls of arteries, which can eventually obstruct blood flow.

* atherosclerotic plaque: A cholesterol-rich deposit on an artery wall.

* biological variability: Fluctuations that occur naturally over time in the levels of a substance such as cholesterol in a person’s body.

* cholesterol: A fatlike substance that is produced by the liver and found in all food from animal sources; an essential component of body cells and a precursor of bile acids and certain hormones.

* chylomicron: A large, extremely low-density lipoprotein that transports triglyceride from the intestine to fat tissue in the body.

* combined hyperlipidemia: A condition in which LDL and triglyceride levels are very high.

* familial combined hyperlipidemia: An inherited disorder in which the liver overproduces VLDL, causing high levels of cholesterol or triglycerides, or both.

* familial hypercholesterolemia: An inherited disorder in which the liver cannot properly remove LDL particles from the blood, causing a very high cholesterol level.

* fasting lipid profile: A laboratory test to determine the relative levels of HDL, LDL, and total cholesterol in the blood. Also referred to as a lipoprotein analysis, full lipid profile, or cholesterol profile.

* fatty acids: The primary building blocks of lipids.

* foam cells: Lipid-laden cells, named for their foamy appearance under the microscope, which contribute to the formation of atherosclerotic plaque.

* high-density lipoprotein (HDL): A lipoprotein that protects the arteries by transporting cholesterol from body cells to the liver for elimination.

* hydrogenation: The addition of hydrogen to a compound, particularly to solidify unsaturated oils.

* lipids: Fats, oils, and waxes that serve as building blocks for cells or as energy sources for the body.

* lipoproteins: Protein-covered fat particles that enable cholesterol to move easily through the blood.

* low-density lipoprotein (LDL): A lipoprotein that transports cholesterol from the liver to the rest of the body, which can cause the buildup of plaque in the arteries.

* monounsaturated fats: Fatty acids; abundant in olive, peanut, sesame, and canola oils.

* oxidation: A process in which oxygen combines with a substance, altering its structure and changing or destroying its normal function.

* platelets: Minute, colorless disks in the blood that are instrumental in clotting.

* polyunsaturated fats: Fatty acids that are abundant in soybean, corn, cottonseed, safflower, and sunflower oils.

* saturated fats: Fatty acids that are abundant in red meat, lard, butter, cheese, and some vegetable oils, in which each molecule carries the maximum number of hydrogen atoms.

* trans fats: Fatty acids (such as those found in solid margarine) that have been reshaped by hydrogenation; also called trans fatty acids.

* triglyceride: The primary type of fat in the body and in the diet, formed from three fatty-acid molecules and one glycerol molecule.

* unsaturated fats: Fatty acids in which some of the hydrogen atoms in each molecule have been replaced by double bonds; includes monounsaturated and polyunsaturated fats.

* very-low-density lipoprotein (VLDL): A lipoprotein that transports triglyceride manufactured in the liver to fat tissue in the body; eventually becomes low-density lipoprotein (LDL) after the triglyceride has been removed.

In foods, cholesterol is found in eggs, dairy products, meat, and poultry. Egg yolks and organ meats (liver, kidney, sweetbread, and brain) are high in cholesterol. Fish generally contains less cholesterol than other meats, but some shellfish are high in cholesterol.

Foods of plant origin (vegetables, fruits, grains, cereals, nuts, and seeds) contain no cholesterol.

Fat content is not a good measure of cholesterol content. For example, liver and other organ meats are low in fat, but very high in cholesterol.

Therapeutic Lifestyle Changes (TLC) is a set of things you can do to help lower your LDL cholesterol. The main parts of TLC are:

* The TLC Diet. This is a low-saturated-fat, low-cholesterol eating plan that calls for less than 7% of calories from saturated fat and less than 200 mg of dietary cholesterol per day. The TLC diet recommends only enough calories to maintain a desirable weight and avoid weight gain. If your LDL is not lowered enough by reducing your saturated fat and cholesterol intakes, the amount of soluble fiber in your diet can be increased. Certain food products that contain plant stanols or plant sterols (for example, cholesterol-lowering margarines) can also be added to the TLC diet to boost its LDL-lowering power.
* Weight Management. Losing weight if you are overweight can help lower LDL and is especially important for those with a cluster of risk factors that includes high triglyceride and/or low HDL levels and being overweight with a large waist measurement (more than 40 inches for men and more than 35 inches for women).
* Physical Activity. Regular physical activity (30 minutes on most, if not all, days) is recommended for everyone. It can help raise HDL and lower LDL and is especially important for those with high triglyceride and/or low HDL levels who are overweight with a large waist measurement.

Foods low in saturated fat include fat-free or 1percent dairy products, lean meats, fish, skinless poultry, whole grain foods, and fruits and vegetables. Look for soft margarines (liquid or tub varieties) that are low in saturated fat and contain little or no trans fat (another type of dietary fat that can raise your cholesterol level). Limit foods high in cholesterol such as liver and other organ meats, egg yolks, and full-fat dairy products.

Good sources of soluble fiber include oats, certain fruits (such as oranges and pears) and vegetables (such as brussels sprouts and carrots), and dried peas and beans.

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Cholesterol Diet Free Plan

Saturday, June 7th, 2008

Getting a free low fat diet plan from me is just the first step. You have to put in the work! Personally, I prefer the term ‘low saturated-fat diet plan’ since the plan I am about to give you is low in saturated fats, and rich in the ‘good fats’.

How can fat be good for you?

That’s exactly what I thought when I started out as a personal trainer. The answer lies in a series of hormones called eicosanoids. These hormones control every major function in the body. They are influenced by the type and amount of fat you eat, and your lifesyle.

A well designed, free, low fat diet plan combined with a healthy lifestyle (exercise, sound sleep, low stress) is the secret to weight loss. The food list below is an extension of the low cholesterol diet food list.

Important components of a low fat diet plan.

Fruits and vegetables – Fiber.

Eat at least 3 to 5 servings of fruits and vegetables each day. Fruits and vegetables are very low in saturated fat and total fat, and have no cholesterol. When shopping, remember to buy fruits and vegetables to eat as snacks, desserts, salads, side dishes, and main dishes.

Add a variety of vegetables to meat stews or casseroles or make a vegetarian (meatless) main dish. Raw vegetables are crucial to the success of my free low fat diet plan. Try carrots, broccoli, cauliflower, lettuce and store in the refrigerator for quick and easy use in cooking or snacking.

Serve fresh fruit for dessert or freeze (banana, berries, melon, grapes) for a delicious frozen treat. Display fresh fruit in a bowl in the kitchen to make fruit easier to grab as a snack.

To keep naturally lowfat vegetables low in fat and saturated fat, season with herbs, spices, lemon juice, vinegar, fat free or lowfat mayonnaise or salad dressing.

Breads, Cereals, Rice, Pasta, and Other Grains.

Breads, cereals, rice, pasta, and other grains, and dry beans and peas are generally high in starch and fiber and low in saturated fat and calories.

They also have no dietary cholesterol, except for some bakery breads and sweet bread products made with high fat, high cholesterol milk, butter and eggs.

Like fruits and vegetables, naturally low fat, low cholesterol breads and other foods in this group are also good choices. You should be eating 6 to 11 servings of foods from this group each day.

Choose whole grain breads and rolls often. They have more fiber than white breads and are an important component of the free low fat diet plan. Buy dry cereals, most are low in fat.

Limit the high fat granola, muesli, and oat bran types that are made with coconut or coconut oil and nuts, which increases the saturated fat content.

Add fat free milk or 1% milk instead of whole or low fat (2% milk) to save saturated fat and cholesterol.

Buy pasta and rice to use as entrees. Hold the high fat sauces (butter, cheese, cream, white). Limit sweet baked goods that are made with lots of saturated fat, mostly from butter, eggs, and whole milk such as croissants, pastries, muffins, biscuits, butter rolls, and doughnuts. These are also high in cholesterol.

Sweets and Snacks.

Some sweets and snacks, like baked goods (cakes and cookies) cheese crackers, and some chips are high in saturated fat and cholesterol.

The following foods are allowed in the free low fat diet plan, but please do not go overboard. fat free or low fat brownies, cakes, cheesecake, cupcakes, and pastries. Frozen lowfat or nonfat yogurt, fruit ices, ice milk, sherbet, and sorbet.

Caution – these treats may be low in fat, most are not low in calories. So indulge occasionally, especially if you are trying to control your weight with a low fat diet.

Low fat snack foods.

Every free low fat diet plan should include foods as snacks.

Soy chips.
Ready-to-eat cereals without added sugar.
Frozen grapes or banana slices; or other fresh fruit.
Low fat or fat free crackers.
No-oil baked tortilla chips.
Popcorn (air popped or “light”).
Pretzels.
Raw vegetables with nonfat or low fat dip.

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Eating Your Way to Lower Cholesterol

Wednesday, February 6th, 2008

Although cholesterol drugs are in the news lately, what is getting lost in the discussion is the fact that it’s possible to lower your cholesterol without drugs. It’s just not as easy.

In fact, many doctors think dietary changes are too difficult for most of their patients. While they typically encourage better eating and a diet low in saturated fat, they also prescribe cholesterol-lowering drugs called statins as a faster way to lower bad cholesterol.

But many people can’t tolerate statins and their side effects. Others simply don’t want to take a pill every day or shoulder the cost of a prescription. For those patients, dietary changes may be a better option.

In 2006, The American Journal of Clinical Nutrition reported on a study of 55 patients with high cholesterol who, over the course of a year, started eating a diet rich in soy proteins, fiber and almonds. All those foods may have cholesterol-lowering properties. Twenty-one patients managed to lower their cholesterol by 20 percent or more by the end of the year. The researchers noted that whether the patient was motivated and actually stuck with the diet most of the time was key.

Journalist Tom Burton, a former colleague, wrote about his own efforts to lower cholesterol without drugs for The Wall Street Journal. He found that many doctors don’t really know how to advise patients about dietary changes to lower cholesterol. He found one who did and used him as a nutrition “coach” to help him figure out which changes would be most effective for him.

The problem for Mr. Burton was that he already had a pretty healthful diet. He ran four miles most days and had given up red meat and most cheese. But his bad cholesterol was 169 mg/dL — far above the 100 mg/dL most doctors recommend. Doctors were telling him statin drugs were in his future.

After documenting his eating habits, Mr. Burton was advised by his doctor to cut out a favorite dish — roast chicken with the skin on. He was told that more of his protein should come from fish, beans and nuts. He phased out the chicken as well as shrimp and squid, which are high in dietary cholesterol. He began including steel-cut oatmeal, eggplant, roasted soybeans, whole-wheat pasta and Brussels sprouts in his diet. He also increased his exercise. His cholesterol numbers were slow to move, but eventually they did, dropping 33 percent.

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Lipitor Complete Information

Thursday, January 24th, 2008

DESCRIPTION

Lipitor (atorvastatin calcium) is a synthetic lipid-lowering agent. Atorvastatin is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis.

Atorvastatin calcium is [R-(R*, R*)]-2-(4-fluorophenyl)-β, δ-dihydroxy-5-(1-methylethyl)-3-phenyl-4-[(phenylamino) carbonyl]-1H-pyrrole-1-heptanoic acid, calcium salt (2:1) trihydrate. The empirical formula of atorvastatin calcium is (C33H34FN2O5)2Ca•3H2O and its molecular weight is 1209.42.

Atorvastatin calcium is a white to off-white crystalline powder that is insoluble in aqueous solutions of pH 4 and below. Atorvastatin calcium is very slightly soluble in distilled water, pH 7.4 phosphate buffer, and acetonitrile, slightly soluble in ethanol, and freely soluble in methanol.

Lipitor tablets for oral administration contain 10, 20, 40 or 80 mg atorvastatin and the following inactive ingredients: calcium carbonate, USP; candelilla wax, FCC; croscarmellose sodium, NF; hydroxypropyl cellulose, NF; lactose monohydrate, NF; magnesium stearate, NF; microcrystalline cellulose, NF; Opadry White YS-1-7040 (hypromellose, polyethylene glycol, talc, titanium dioxide); polysorbate 80, NF; simethicone emulsion.

CLINICAL PHARMACOLOGY

Mechanism of Action

Atorvastatin is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. Cholesterol and triglycerides circulate in the bloodstream as part of lipoprotein complexes. With ultracentrifugation, these complexes separate into HDL (high-density lipoprotein), IDL (intermediate-density lipoprotein), LDL (low-density lipoprotein), and VLDL (very-low-density lipoprotein) fractions. Triglycerides (TG) and cholesterol in the liver are incorporated into VLDL and released into the plasma for delivery to peripheral tissues. LDL is formed from VLDL and is catabolized primarily through the high-affinity LDL receptor. Clinical and pathologic studies show that elevated plasma levels of total cholesterol (total-C), LDL-cholesterol (LDL-C), and apolipoprotein B (apo B) promote human atherosclerosis and are risk factors for developing cardiovascular disease, while increased levels of HDL-C are associated with a decreased cardiovascular risk.

In animal models, Lipitor lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell-surface to enhance uptake and catabolism of LDL; Lipitor also reduces LDL production and the number of LDL particles. Lipitor reduces LDL-C in some patients with homozygous familial hypercholesterolemia (FH), a population that rarely responds to other lipid-lowering medication(s).

A variety of clinical studies have demonstrated that elevated levels of total-C, LDL-C, and apo B (a membrane complex for LDL-C) promote human atherosclerosis. Similarly, decreased levels of HDL-C (and its transport complex, apo A) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of total-C and LDL-C, and inversely with the level of HDL-C.

Lipitor reduces total-C, LDL-C, and apo B in patients with homozygous and heterozygous FH, nonfamilial forms of hypercholesterolemia, and mixed dyslipidemia. Lipitor also reduces VLDL-C and TG and produces variable increases in HDL-C and apolipoprotein A-1. Lipitor reduces total-C, LDL-C, VLDL-C, apo B, TG, and non-HDL-C, and increases HDL-C in patients with isolated hypertriglyceridemia. Lipitor reduces intermediate density lipoprotein cholesterol (IDL-C) in patients with dysbetalipoproteinemia.

Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including VLDL, intermediate density lipoprotein (IDL), and remnants, can also promote atherosclerosis. Elevated plasma triglycerides are frequently found in a triad with low HDL-C levels and small LDL particles, as well as in association with non-lipid metabolic risk factors for coronary heart disease. As such, total plasma TG has not consistently been shown to be an independent risk factor for CHD. Furthermore, the independent effect of raising HDL or lowering TG on the risk of coronary and cardiovascular morbidity and mortality has not been determined.

Pharmacodynamics

Atorvastatin as well as some of its metabolites are pharmacologically active in humans. The liver is the primary site of action and the principal site of cholesterol synthesis and LDL clearance. Drug dosage rather than systemic drug concentration correlates better with LDL-C reduction. Individualization of drug dosage should be based on therapeutic response (see DOSAGE AND ADMINISTRATION).

Pharmacokinetics and Drug Metabolism

Absorption

Atorvastatin is rapidly absorbed after oral administration; maximum plasma concentrations occur within 1 to 2 hours. Extent of absorption increases in proportion to atorvastatin dose. The absolute bioavailability of atorvastatin (parent drug) is approximately 14% and the systemic availability of HMG-CoA reductase inhibitory activity is approximately 30%. The low systemic availability is attributed to presystemic clearance in gastrointestinal mucosa and/or hepatic first-pass metabolism. Although food decreases the rate and extent of drug absorption by approximately 25% and 9%, respectively, as assessed by Cmax and AUC, LDL-C reduction is similar whether atorvastatin is given with or without food. Plasma atorvastatin concentrations are lower (approximately 30% for Cmax and AUC) following evening drug administration compared with morning. However, LDL-C reduction is the same regardless of the time of day of drug administration (see DOSAGE AND ADMINISTRATION).

Distribution

Mean volume of distribution of atorvastatin is approximately 381 liters. Atorvastatin is ≥98% bound to plasma proteins. A blood/plasma ratio of approximately 0.25 indicates poor drug penetration into red blood cells. Based on observations in rats, atorvastatin is likely to be secreted in human milk (see CONTRAINDICATIONS, Pregnancy and Lactation, and PRECAUTIONS, Nursing Mothers).

Metabolism

Atorvastatin is extensively metabolized to ortho- and parahydroxylated derivatives and various beta-oxidation products. In vitro inhibition of HMG-CoA reductase by ortho- and parahydroxylated metabolites is equivalent to that of atorvastatin. Approximately 70% of circulating inhibitory activity for HMG-CoA reductase is attributed to active metabolites. In vitro studies suggest the importance of atorvastatin metabolism by cytochrome P450 3A4, consistent with increased plasma concentrations of atorvastatin in humans following coadministration with erythromycin, a known inhibitor of this isozyme (see PRECAUTIONS, Drug Interactions). In animals, the ortho-hydroxy metabolite undergoes further glucuronidation.

Excretion

Atorvastatin and its metabolites are eliminated primarily in bile following hepatic and/or extra-hepatic metabolism; however, the drug does not appear to undergo enterohepatic recirculation. Mean plasma elimination half-life of atorvastatin in humans is approximately 14 hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20 to 30 hours due to the contribution of active metabolites. Less than 2% of a dose of atorvastatin is recovered in urine following oral administration.

Special Populations

Geriatric

Plasma concentrations of atorvastatin are higher (approximately 40% for Cmax and 30% for AUC) in healthy elderly subjects (age ≥65 years) than in young adults. Clinical data suggest a greater degree of LDL-lowering at any dose of drug in the elderly patient population compared to younger adults (see PRECAUTIONS section; Geriatric Use subsection).

Gender

Plasma concentrations of atorvastatin in women differ from those in men (approximately 20% higher for Cmax and 10% lower for AUC); however, there is no clinically significant difference in LDL-C reduction with LIPITOR between men and women.

Renal Insufficiency

Renal disease has no influence on the plasma concentrations or LDL-C reduction of atorvastatin; thus, dose adjustment in patients with renal dysfunction is not necessary (see DOSAGE AND ADMINISTRATION).

Hemodialysis

While studies have not been conducted in patients with end-stage renal disease, hemodialysis is not expected to significantly enhance clearance of atorvastatin since the drug is extensively bound to plasma proteins.

Hepatic Insufficiency

In patients with chronic alcoholic liver disease, plasma concentrations of atorvastatin are markedly increased. Cmax and AUC are each 4-fold greater in patients with Childs-Pugh A disease. Cmax and AUC are approximately 16-fold and 11-fold increased, respectively, in patients with Childs-Pugh B disease (see CONTRAINDICATIONS).

Clinical Studies
Prevention of Cardiovascular Disease

In the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT), the effect of Lipitor (atorvastatin calcium) on fatal and non-fatal coronary heart disease was assessed in 10,305 hypertensive patients 40–80 years of age (mean of 63 years), without a previous myocardial infarction and with TC levels ≤251 mg/dl (6.5 mmol/l). Additionally all patients had at least 3 of the following cardiovascular risk factors: male gender (81.1%), age >55 years (84.5%), smoking (33.2%), diabetes (24.3%), history of CHD in a first-degree relative (26%), TC:HDL >6 (14.3%), peripheral vascular disease (5.1%), left ventricular hypertrophy (14.4%), prior cerebrovascular event (9.8%), specific ECG abnormality (14.3%), proteinuria/albuminuria (62.4%). In this double-blind, placebo-controlled study patients were treated with anti-hypertensive therapy (Goal BP <140/90 mm Hg for non-diabetic patients, <130/80 mm Hg for diabetic patients) and allocated to either Lipitor 10 mg daily (n=5168) or placebo (n=5137), using a covariate adaptive method which took into account the distribution of nine baseline characteristics of patients already enrolled and minimized the imbalance of those characteristics across the groups. Patients were followed for a median duration of 3.3 years.

The effect of 10 mg/day of Lipitor on lipid levels was similar to that seen in previous clinical trials.

Lipitor significantly reduced the rate of coronary events [either fatal coronary heart disease (46 events in the placebo group vs. 40 events in the Lipitor group) or nonfatal MI (108 events in the placebo group vs. 60 events in the Lipitor group)] with a relative risk reduction of 36% [(based on incidences of 1.9% for Lipitorvs. 3.0% for placebo), p=0.0005. The risk reduction was consistent regardless of age, smoking status, obesity or presence of renal dysfunction. The effect of Lipitor was seen regardless of baseline LDL levels. Due to the small number of events, results for women were inconclusive.

Lipitor also significantly decreased the relative risk for revascularization procedures by 42%. Although the reduction of fatal and non-fatal strokes did not reach a pre-defined significance level (p=0.01), a favorable trend was observed with a 26% relative risk reduction (incidences of 1.7% for Lipitor and 2.3% for placebo). There was no significant difference between the treatment groups for death due to cardiovascular causes (p=0.51) or noncardiovascular causes (p=0.17).

In the Collaborative Atorvastatin Diabetes Study (CARDS), the effect of Lipitor (atorvastatin calcium) on cardiovascular disease (CVD) endpoints was assessed in 2838 subjects (94% White, 68% male), ages 40–75 with type 2 diabetes based on WHO criteria, without prior history of cardiovascular disease and with LDL≤ 160 mg/dL and TG ≤600 mg/dL. In addition to diabetes, subjects had 1 or more of the following risk factors: current smoking (23%), hypertension (80%), retinopathy (30%), or microalbuminuria (9%) or macroalbuminuria (3%). No subjects on hemodialysis were enrolled in the study. In this multicenter, placebo-controlled, double-blind clinical trial, subjects were randomly allocated to either Lipitor 10 mg daily (1429) or placebo (1411) in a 1:1 ratio and were followed for a median duration of 3.9 years. The primary endpoint was the occurrence of any of the major cardiovascular events: myocardial infarction, acute CHD death, unstable angina, coronary revascularization, or stroke. The primary analysis was the time to first occurrence of the primary endpoint.

Baseline characteristics of subjects were: mean age of 62 years, mean HbA1c 7.7%; median LDL-C 120 mg/dL; median TC 207 mg/dL; median TG 151 mg/dL; median HDL-C 52mg/dL.

The effect of Lipitor 10 mg/ day on lipid levels was similar to that seen in previous clinical trials.

Lipitor significantly reduced the rate of major cardiovascular events (primary endpoint events) (83 events in the LIPITOR group vs. 127 events in the placebo group) with a relative risk reduction of 37%, HR 0.63, 95% CI (0.48,0.83) (p=0.001). An effect of Lipitor was seen regardless of age, sex, or baseline lipid levels.

Effect of Lipitor 10 mg/day on Time to Occurrence of Major Cardiovascular Event (myocardial infarction, acute CHD death, unstable angina, coronary revascularization, or stroke) in CARDS.

Lipitor significantly reduced the risk of stroke by 48% (21 events in the Lipitor group vs 39 events in the placebo group), HR 0.52, 95% CI (0.31,0.89) (p=0.016) and reduced the risk of MI by 42% (38 events in the Lipitor group vs 64 events in the placebo group), HR 0.58, 95.1% CI (0.39, 0.86) (p=0.007). There was no significant difference between the treatment groups for angina, revascularization procedures, and acute CHD death.

There were 61 deaths in the Lipitor group vs 82 deaths in the placebo group, (HR 0.73, p=0.059).

In the Treating to New Targets Study (TNT), the effect of Lipitor 80 mg/day vs. Lipitor 10 mg/day on the reduction in cardiovascular events was assessed in 10,001 subjects (94% white, 81% male, 38% ≥65 years) with clinically evident coronary heart disease who had achieved a target LDL-C level <130 mg/dL after completing an 8-week, open-label, run-in period with Lipitor 10 mg/day. Subjects were randomly assigned to either 10 mg/day or 80 mg/day of LIPITOR and followed for a median duration of 4.9 years. The primary endpoint was the time-to-first occurrence of any of the following major cardiovascular events (MCVE): death due to CHD, non-fatal myocardial infarction, resuscitated cardiac arrest, and fatal and non-fatal stroke. The mean LDL-C, TC, TG, non-HDL and HDL cholesterol levels at 12 weeks were 73, 145, 128, 98 and 47 mg/dL during treatment with 80 mg of LIPITOR and 99, 177, 152, 129 and 48 mg/dL during treatment with 10 mg of Lipitor.

Treatment with Lipitor 80 mg/day significantly reduced the rate of MCVE (434 events in the 80mg/day group vs 548 events in the 10 mg/day group) with a relative risk reduction of 22%, HR 0.78, 95% CI (0.69,0.89), p=0.0002 (see Figure 3 and Table 1). The overall risk reduction was consistent regardless of age (<65, ≥65) or gender.

Of the events that comprised the primary efficacy endpoint, treatment with LIPITOR 80 mg/day significantly reduced the rate of nonfatal, non-procedure related MI and fatal and non-fatal stroke, but not CHD death or resuscitated cardiac arrest (Table 1). Of the predefined secondary endpoints, treatment with Lipitor 80 mg/day significantly reduced the rate of coronary revascularization, angina and hospitalization for heart failure, but not peripheral vascular disease. The reduction in the rate of CHF with hospitalization was only observed in the 8% of patients with a prior history of CHF.

There was no significant difference between the treatment groups for all-cause mortality (Table 1). The proportions of subjects who experienced cardiovascular death, including the components of CHD death and fatal stroke were numerically smaller in the Lipitor 80 mg group than in the Lipitor 10 mg treatment group. The proportions of subjects who experienced noncardiovascular death were numerically larger in the Lipitor 80 mg group than in the Lipitor10 mg treatment group.

In the Incremental Decrease in Endpoints Through Aggressive Lipid Lowering Study (IDEAL), treatment with Lipitor 80 mg/day was compared to treatment with simvastatin 20–40 mg/day in 8,888 subjects up to 80 years of age with a history of CHD to assess whether reduction in CV risk could be achieved. Patients were mainly male (81%), white (99%) with an average age of 61.7 years, and an average LDL-C of 121.5 mg/dL at randomization; 76% were on statin therapy. In this prospective, randomized, open-label, blinded endpoint (PROBE) trial with no run-in period, subjects were followed for a median duration of 4.8 years. The mean LDL-C, TC, TG, HDL and non-HDL cholesterol levels at Week 12 were 78, 145, 115, 45 and 100 mg/dL during treatment with 80 mg of Lipitor and 105, 179, 142, 47 and 132 mg/dL during treatment with 20–40 mg of simvastatin.

There was no significant difference between the treatment groups for the primary endpoint, the rate of first major coronary event (fatal CHD, nonfatal MI and resuscitated cardiac arrest): 411 (9.3%) in the Lipitor 80 mg/day group vs. 463 (10.4%) in the simvastatin 20–40 mg/day group, HR 0.89, 95% CI ( 0.78,1.01), p=0.07.

There were no significant differences between the treatment groups for all-cause mortality: 366 (8.2%) in the Lipitor 80 mg/day group vs. 374 (8.4%) in the simvastatin 20–40 mg/day group. The proportions of subjects who experienced CV or non-CV death were similar for the Lipitor 80 mg group and the simvastatin 20–40 mg group.

Hypercholesterolemia (Heterozygous Familial and Nonfamilial) and Mixed Dyslipidemia (Fredrickson Types IIa and IIb)

Lipitor reduces total-C, LDL-C, VLDL-C, apo B, and TG, and increases HDL-C in patients with hypercholesterolemia and mixed dyslipidemia. Therapeutic response is seen within 2 weeks, and maximum response is usually achieved within 4 weeks and maintained during chronic therapy.

Lipitor is effective in a wide variety of patient populations with hypercholesterolemia, with and without hypertriglyceridemia, in men and women, and in the elderly. Experience in pediatric patients has been limited to patients with homozygous FH. In two multicenter, placebo-controlled, dose-response studies in patients with hypercholesterolemia, Lipitor given as a single dose over 6 weeks significantly reduced total-C, LDL-C, apo B, and TG.

In patients with Fredrickson Types IIa and IIb hyperlipoproteinemia pooled from 24 controlled trials, the median (25th and 75th percentile) percent changes from baseline in HDL-C for atorvastatin 10, 20, 40, and 80 mg were 6.4 (-1.4, 14), 8.7(0, 17), 7.8(0, 16), and 5.1 (-2.7, 15), respectively. Additionally, analysis of the pooled data demonstrated consistent and significant decreases in total-C, LDL-C, TG, total-C/HDL-C, and LDL-C/HDL-C.

In three multicenter, double-blind studies in patients with hypercholesterolemia, Lipitor was compared to other HMG-CoA reductase inhibitors. After randomization, patients were treated for 16 weeks with either Lipitor 10 mg per day or a fixed dose of the comparative agent.

The impact on clinical outcomes of the differences in lipid-altering effects between treatments shown in Table 3 is not known. Table 3 does not contain data comparing the effects of atorvastatin 10 mg and higher doses of lovastatin, pravastatin, and simvastatin. The drugs compared in the studies summarized in the table are not necessarily interchangeable.

Hypertriglyceridemia (Fredrickson Type IV)

The response to Lipitor in 64 patients with isolated hypertriglyceridemia treated across several clinical trials is shown in the table below. For the atorvastatin-treated patients, median (min, max) baseline TG level was 565 (267–1502).

Dysbetalipoproteinemia (Fredrickson Type III)

The results of an open-label crossover study of 16 patients (genotypes: 14 apo E2/E2 and 2 apo E3/E2) with dysbetalipoproteinemia (Fredrickson Type III)

Homozygous Familial Hypercholesterolemia

In a study without a concurrent control group, 29 patients ages 6 to 37 years with homozygous FH received maximum daily doses of 20 to 80 mg of Lipitor. The mean LDL-C reduction in this study was 18%. Twenty-five patients with a reduction in LDL-C had a mean response of 20% (range of 7% to 53%, median of 24%); the remaining 4 patients had 7% to 24% increases in LDL-C. Five of the 29 patients had absent LDL-receptor function. Of these, 2 patients also had a portacaval shunt and had no significant reduction in LDL-C. The remaining 3 receptor-negative patients had a mean LDL-C reduction of 22%.

Heterozygous Familial Hypercholesterolemia in Pediatric Patients

In a double-blind, placebo-controlled study followed by an open-label phase, 187 boys and postmenarchal girls 10–17 years of age (mean age 14.1 years) with heterozygous familial hypercholesterolemia (FH) or severe hypercholesterolemia were randomized to Lipitor (n=140) or placebo (n=47) for 26 weeks and then all received Lipitor for 26 weeks. Inclusion in the study required 1) a baseline LDL-C level ≥ 190 mg/dL or 2) a baseline LDL-C ≥ 160 mg/dL and positive family history of FH or documented premature cardiovascular disease in a first- or second-degree relative. The mean baseline LDL-C value was 218.6 mg/dL (range: 138.5–385.0 mg/dL) in the Lipitor group compared to 230.0 mg/dL (range: 160.0–324.5 mg/dL) in the placebo group. The dosage of Lipitor (once daily) was 10 mg for the first 4 weeks and up-titrated to 20 mg if the LDL-C level was > 130 mg/dL. The number of Lipitor-treated patients who required up-titration to 20 mg after Week 4 during the double-blind phase was 80 (57.1%).

Lipitor significantly decreased plasma levels of total-C, LDL-C, triglycerides, and apolipoprotein B during the 26 week double-blind phase.

The mean achieved LDL-C value was 130.7 mg/dL (range: 70.0–242.0 mg/dL) in the Lipitor group compared to 228.5 mg/dL (range: 152.0–385.0 mg/dL) in the placebo group during the 26 week double-blind phase.

The safety and efficacy of doses above 20 mg have not been studied in controlled trials in children. The long-term efficacy of Lipitor therapy in childhood to reduce morbidity and mortality in adulthood has not been established.

INDICATIONS AND USAGE

Prevention of Cardiovascular Disease

In adult patients without clinically evident coronary heart disease, but with multiple risk factors for coronary heart disease such as age, smoking, hypertension, low HDL-C, or a family history of early coronary heart disease, Lipitor is indicated to:

* Reduce the risk of myocardial infarction
* Reduce the risk of stroke
* Reduce the risk for revascularization procedures and angina

In patients with type 2 diabetes, and without clinically evident coronary heart disease, but with multiple risk factors for coronary heart disease such as retinopathy, albuminuria, smoking, or hypertension, Lipitor is indicated to:

* Reduce the risk of myocardial infarction
* Reduce the risk of stroke

In patients with clinically evident coronary heart disease, Lipitor is indicated to:

* Reduce the risk of non-fatal myocardial infarction
* Reduce the risk of fatal and non-fatal stroke
* Reduce the risk for revascularization procedures
* Reduce the risk of hospitalization for CHF
* Reduce the risk of angina

Hypercholesterolemia

Lipitor is indicated:

1. as an adjunct to diet to reduce elevated total-C, LDL-C, apo B, and TG levels and to increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Fredrickson Types IIa and IIb);
2. as an adjunct to diet for the treatment of patients with elevated serum TG levels(Fredrickson Type IV);
3. for the treatment of patients with primary dysbetalipoproteinemia (Fredrickson Type III) who do not respond adequately to diet;
4. to reduce total-C and LDL-C in patients with homozygous familial hypercholesterolemia as an adjunct to other lipid-lowering treatments (eg, LDL apheresis) or if such treatments are unavailable;
5. as an adjunct to diet to reduce total-C, LDL-C, and apo B levels in boys and postmenarchal girls, 10 to 17 years of age, with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present:

a.
LDL-C remains ≥ 190 mg/dL or
b.
LDL-C remains ≥ 160 mg/dL and:
* there is a positive family history of premature cardiovascular disease or
* two or more other CVD risk factors are present in the pediatric patient

Therapy with lipid-altering agents should be a component of multiple-risk-factor intervention in individuals at increased risk for atherosclerotic vascular disease due to hypercholesterolemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol only when the response to diet and other nonpharmacological measures has been inadequate (see National Cholesterol Education Program (NCEP) Guidelines.

After the LDL-C goal has been achieved, if the TG is still ≥200 mg/dL, non-HDL-C (total-C minus HDL-C) becomes a secondary target of therapy. Non-HDL-C goals are set 30 mg/dL higher than LDL-C goals for each risk category.

Prior to initiating therapy with LIPITOR, secondary causes for hypercholesterolemia (e.g., poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinemias, obstructive liver disease, other drug therapy, and alcoholism) should be excluded, and a lipid profile performed to measure total-C, LDL-C, HDL-C, and TG. For patients with TG <400 mg/dL (<4.5 mmol/L), LDL-C can be estimated using the following equation: LDL-C = total-C - (0.20 × [TG] + HDL-C). For TG levels >400 mg/dL (>4.5 mmol/L), this equation is less accurate and LDL-C concentrations should be determined by ultracentrifugation.

LIPITOR has not been studied in conditions where the major lipoprotein abnormality is elevation of chylomicrons (Fredrickson Types I and V).

CONTRAINDICATIONS

Active liver disease or unexplained persistent elevations of serum transaminases.

Hypersensitivity to any component of this medication.

Pregnancy and Lactation

Atherosclerosis is a chronic process and discontinuation of lipid-lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolemia. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Since HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, they may cause fetal harm when administered to pregnant women. Therefore, HMG-CoA reductase inhibitors are contraindicated during pregnancy and in nursing mothers. ATORVASTATIN SHOULD BE ADMINISTERED TO WOMEN OF CHILDBEARING AGE ONLY WHEN SUCH PATIENTS ARE HIGHLY UNLIKELY TO CONCEIVE AND HAVE BEEN INFORMED OF THE POTENTIAL HAZARDS. If the patient becomes pregnant while taking this drug, therapy should be discontinued and the patient apprised of the potential hazard to the fetus.

WARNINGS

Liver Dysfunction

HMG-CoA reductase inhibitors, like some other lipid-lowering therapies, have been associated with biochemical abnormalities of liver function. Persistent elevations (>3 times the upper limit of normal [ULN] occurring on 2 or more occasions) in serum transaminases occurred in 0.7% of patients who received atorvastatin in clinical trials. The incidence of these abnormalities was 0.2%, 0.2%, 0.6%, and 2.3% for 10, 20, 40, and 80 mg, respectively.

One patient in clinical trials developed jaundice. Increases in liver function tests (LFT) in other patients were not associated with jaundice or other clinical signs or symptoms. Upon dose reduction, drug interruption, or discontinuation, transaminase levels returned to or near pretreatment levels without sequelae. Eighteen of 30 patients with persistent LFT elevations continued treatment with a reduced dose of atorvastatin.

It is recommended that liver function tests be performed prior to and at 12 weeks following both the initiation of therapy and any elevation of dose, and periodically (e.g., semiannually) thereafter. Liver enzyme changes generally occur in the first 3 months of treatment with atorvastatin. Patients who develop increased transaminase levels should be monitored until the abnormalities resolve. Should an increase in ALT or AST of >3 times ULN persist, reduction of dose or withdrawal of atorvastatin is recommended.

Atorvastatin should be used with caution in patients who consume substantial quantities of alcohol and/or have a history of liver disease. Active liver disease or unexplained persistent transaminase elevations are contraindications to the use of atorvastatin (see CONTRAINDICATIONS).

Skeletal Muscle

Rare cases of rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with atorvastatin and with other drugs in this class.

Uncomplicated myalgia has been reported in atorvastatin-treated patients (see ADVERSE REACTIONS). Myopathy, defined as muscle aches or muscle weakness in conjunction with increases in creatine phosphokinase (CPK) values >10 times ULN, should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevation of CPK. Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Atorvastatin therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed or suspected.

The risk of myopathy during treatment with drugs in this class is increased with concurrent administration of cyclosporine, fibric acid derivatives, erythromycin, clarithromycin, combination of ritonavir plus saquinavir or lopinavir plus ritonavir, niacin, or azole antifungals. Physicians considering combined therapy with atorvastatin and fibric acid derivatives, erythromycin, clarithromycin, a combination of ritonavir plus saquinavir or lopinavir plus ritonavir, immunosuppressive drugs, azole antifungals, or lipid-modifying doses of niacin should carefully weigh the potential benefits and risks and should carefully monitor patients for any signs or symptoms of muscle pain, tenderness, or weakness, particularly during the initial months of therapy and during any periods of upward dosage titration of either drug. Lower starting and maintenance doses of atorvastatin should be considered when taken concomitantly with the aforementioned drugs (See DRUG INTERACTIONS). Periodic creatine phosphokinase (CPK) determinations may be considered in such situations, but there is no assurance that such monitoring will prevent the occurrence of severe myopathy.

Atorvastatin therapy should be temporarily withheld or discontinued in any patient with an acute, serious condition suggestive of a myopathy or having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (e.g., severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders, and uncontrolled seizures).

PRECAUTIONS
General

Before instituting therapy with atorvastatin, an attempt should be made to control hypercholesterolemia with appropriate diet, exercise, and weight reduction in obese patients, and to treat other underlying medical problems (see INDICATIONS AND USAGE).

Information for Patients

Patients should be advised to report promptly unexplained muscle pain, tenderness, or weakness, particularly if accompanied by malaise or fever.

Drug Interactions

The risk of myopathy during treatment with HMG-CoA reductase inhibitors is increased with concurrent administration of fibric acid derivatives, lipid-modifying doses of niacin or cytochrome P450 3A4 inhibitors (e.g. cyclosporine, erythromycin, clarithromycin, and azole antifungals) (see WARNINGS, Skeletal Muscle).

Inhibitors of cytochrome P450 3A4

Atorvastatin is metabolized by cytochrome P450 3A4. Concomitant administration of atorvastatin with inhibitors of cytochrome P450 3A4 can lead to increases in plasma concentrations of atorvastatin. The extent of interaction and potentiation of effects depends on the variability of effect on cytochrome P450 3A4.

Clarithromycin

Concomitant administration of atorvastatin 80 mg with clarithromycin (500 mg twice daily) resulted in a 4.4-fold increase in atorvastatin AUC (see WARNINGS, Skeletal Muscle, and DOSAGE AND ADMINISTRATION).

Erythromycin

In healthy individuals, plasma concentrations of atorvastatin increased approximately 40% with co-administration of atorvastatin and erythromycin, a known inhibitor of cytochrome P450 3A4 (see WARNINGS, Skeletal Muscle).

Combination of Protease Inhibitors

Concomitant administration of atorvastatin 40 mg with ritonavir plus saquinavir (400 mg twice daily) resulted in a 3-fold increase in atorvastatin AUC. Concomitant administration of atorvastatin 20 mg with lopinavir plus ritonavir (400 mg+100 mg twice daily) resulted in a 5.9-fold increase in atorvastatin AUC (see WARNINGS, Skeletal Muscle, and DOSAGE AND ADMINISTRATION).

Itraconazole

Concomitant administration of atorvastatin (20 to 40 mg) and itraconazole (200 mg) was associated with a 2.5–3.3-fold increase in atorvastatin AUC.

Diltiazem hydrochloride

Co-administration of atorvastatin (40 mg) with diltiazem (240 mg) was associated with higher plasma concentrations of atorvastatin.

Cimetidine

Atorvastatin plasma concentrations and LDL-C reduction were not altered by co-administration of cimetidine.

Grapefruit juice

Contains one or more components that inhibit CYP 3A4 and can increase plasma concentrations of atorvastatin, especially with excessive grapefruit juice consumption (>1.2 liters per day).

Cyclosporine

Atorvastatin and atorvastatin-metabolites are substrates of the OATP1B1 transporter. Inhibitors of the OATP1B1 (e.g. cyclosporine) can increase the bioavailability of atorvastatin. Concomitant administration of atorvastatin 10 mg and cyclosporine 5.2 mg/kg/day resulted in an 8.7-fold increase in atorvastatin AUC. In cases where co-administration of atorvastatin with cyclosporine is necessary, the dose of atorvastatin should not exceed 10 mg (see WARNINGS, Skeletal Muscle).

Inducers of cytochrome P450 3A4

Concomitant administration of atorvastatin with inducers of cytochrome P450 3A4 (eg efavirenz, rifampin) can lead to variable reductions in plasma concentrations of atorvastatin. Due to the dual interaction mechanism of rifampin, simultaneous co-administration of atorvastatin with rifampin is recommended, as delayed administration of atorvastatin after administration of rifampin has been associated with a significant reduction in atorvastatin plasma concentrations.

Antacid

When atorvastatin and Maalox® TC suspension were coadministered, plasma concentrations of atorvastatin decreased approximately 35%. However, LDL-C reduction was not altered.

Antipyrine

Because atorvastatin does not affect the pharmacokinetics of antipyrine, interactions with other drugs metabolized via the same cytochrome isozymes are not expected.

Colestipol

Plasma concentrations of atorvastatin decreased approximately 25% when colestipol and atorvastatin were coadministered. However, LDL-C reduction was greater when atorvastatin and colestipol were coadministered than when either drug was given alone.

Digoxin

When multiple doses of atorvastatin and digoxin were coadministered, steady-state plasma digoxin concentrations increased by approximately 20%. Patients taking digoxin should be monitored appropriately.

Oral Contraceptives

Coadministration of atorvastatin and an oral contraceptive increased AUC values for norethindrone and ethinyl estradiol by approximately 30% and 20%. These increases should be considered when selecting an oral contraceptive for a woman taking atorvastatin.

Warfarin

Atorvastatin had no clinically significant effect on prothrombin time when administered to patients receiving chronic warfarin treatment.

Amlodipine

In a drug-drug interaction study in healthy subjects, co-administration of atorvastatin 80 mg and amlodipine 10 mg resulted in an 18% increase in exposure to atorvastatin which was not clinically meaningful.

Endocrine Function

HMG-CoA reductase inhibitors interfere with cholesterol synthesis and theoretically might blunt adrenal and/or gonadal steroid production. Clinical studies have shown that atorvastatin does not reduce basal plasma cortisol concentration or impair adrenal reserve. The effects of HMG-CoA reductase inhibitors on male fertility have not been studied in adequate numbers of patients. The effects, if any, on the pituitary-gonadal axis in premenopausal women are unknown. Caution should be exercised if an HMG-CoA reductase inhibitor is administered concomitantly with drugs that may decrease the levels or activity of endogenous steroid hormones, such as ketoconazole, spironolactone, and cimetidine.

CNS Toxicity

Brain hemorrhage was seen in a female dog treated for 3 months at 120 mg/kg/day. Brain hemorrhage and optic nerve vacuolation were seen in another female dog that was sacrificed in moribund condition after 11 weeks of escalating doses up to 280 mg/kg/day. The 120 mg/kg dose resulted in a systemic exposure approximately 16 times the human plasma area-under-the-curve (AUC, 0–24 hours) based on the maximum human dose of 80 mg/day. A single tonic convulsion was seen in each of 2 male dogs (one treated at 10 mg/kg/day and one at 120 mg/kg/day) in a 2-year study. No CNS lesions have been observed in mice after chronic treatment for up to 2 years at doses up to 400 mg/kg/day or in rats at doses up to 100 mg/kg/day. These doses were 6 to 11 times (mouse) and 8 to 16 times (rat) the human AUC (0–24) based on the maximum recommended human dose of 80 mg/day.

CNS vascular lesions, characterized by perivascular hemorrhages, edema, and mononuclear cell infiltration of perivascular spaces, have been observed in dogs treated with other members of this class. A chemically similar drug in this class produced optic nerve degeneration (Wallerian degeneration of retinogeniculate fibers) in clinically normal dogs in a dose-dependent fashion at a dose that produced plasma drug levels about 30 times higher than the mean drug level in humans taking the highest recommended dose.

Carcinogenesis, Mutagenesis, Impairment of Fertility

In a 2-year carcinogenicity study in rats at dose levels of 10, 30, and 100 mg/kg/day, 2 rare tumors were found in muscle in high-dose females: in one, there was a rhabdomyosarcoma and, in another, there was a fibrosarcoma. This dose represents a plasma AUC (0–24) value of approximately 16 times the mean human plasma drug exposure after an 80 mg oral dose.

A 2-year carcinogenicity study in mice given 100, 200, or 400 mg/kg/day resulted in a significant increase in liver adenomas in high-dose males and liver carcinomas in high-dose females. These findings occurred at plasma AUC (0–24) values of approximately 6 times the mean human plasma drug exposure after an 80 mg oral dose.

In vitro, atorvastatin was not mutagenic or clastogenic in the following tests with and without metabolic activation: the Ames test with Salmonella typhimurium and Escherichia coli, the HGPRT forward mutation assay in Chinese hamster lung cells, and the chromosomal aberration assay in Chinese hamster lung cells. Atorvastatin was negative in the in vivo mouse micronucleus test.

Studies in rats performed at doses up to 175 mg/kg (15 times the human exposure) produced no changes in fertility. There was aplasia and aspermia in the epididymis of 2 of 10 rats treated with 100 mg/kg/day of atorvastatin for 3 months (16 times the human AUC at the 80 mg dose); testis weights were significantly lower at 30 and 100 mg/kg and epididymal weight was lower at 100 mg/kg. Male rats given 100 mg/kg/day for 11 weeks prior to mating had decreased sperm motility, spermatid head concentration, and increased abnormal sperm. Atorvastatin caused no adverse effects on semen parameters, or reproductive organ histopathology in dogs given doses of 10, 40, or 120 mg/kg for two years.

Pregnancy
Pregnancy Category X

See CONTRAINDICATIONS

Safety in pregnant women has not been established. Atorvastatin crosses the rat placenta and reaches a level in fetal liver equivalent to that of maternal plasma. Atorvastatin was not teratogenic in rats at doses up to 300 mg/kg/day or in rabbits at doses up to 100 mg/kg/day. These doses resulted in multiples of about 30 times (rat) or 20 times (rabbit) the human exposure based on surface area (mg/m2).

In a study in rats given 20, 100, or 225 mg/kg/day, from gestation day 7 through to lactation day 21 (weaning), there was decreased pup survival at birth, neonate, weaning, and maturity in pups of mothers dosed with 225 mg/kg/day. Body weight was decreased on days 4 and 21 in pups of mothers dosed at 100 mg/kg/day; pup body weight was decreased at birth and at days 4, 21, and 91 at 225 mg/kg/day. Pup development was delayed (rotorod performance at 100 mg/kg/day and acoustic startle at 225 mg/kg/day; pinnae detachment and eye opening at 225 mg/kg/day). These doses correspond to 6 times (100 mg/kg) and 22 times (225 mg/kg) the human AUC at 80 mg/day. Rare reports of congenital anomalies have been received following intrauterine exposure to HMG-CoA reductase inhibitors. There has been one report of severe congenital bony deformity, tracheo-esophageal fistula, and anal atresia (VATER association) in a baby born to a woman who took lovastatin with dextroamphetamine sulfate during the first trimester of pregnancy. Lipitor should be administered to women of child-bearing potential only when such patients are highly unlikely to conceive and have been informed of the potential hazards. If the woman becomes pregnant while taking Lipitor, it should be discontinued and the patient advised again as to the potential hazards to the fetus.

Nursing Mothers

Nursing rat pups had plasma and liver drug levels of 50% and 40%, respectively, of that in their mother’s milk. Because of the potential for adverse reactions in nursing infants, women taking Lipitor should not breast-feed (see CONTRAINDICATIONS).

Pediatric Use

Safety and effectiveness in patients 10–17 years of age with heterozygous familial hypercholesterolemia have been evaluated in a controlled clinical trial of 6 months duration in adolescent boys and postmenarchal girls. Patients treated with LIPITOR had an adverse experience profile generally similar to that of patients treated with placebo, the most common adverse experiences observed in both groups, regardless of causality assessment, were infections. Doses greater than 20 mg have not been studied in this patient population. In this limited controlled study, there was no detectable effect on growth or sexual maturation in boys or on menstrual cycle length in girls (see CLINICAL PHARMACOLOGY, Clinical Studies section; ADVERSE REACTIONS, Pediatric Patients (ages 10–17 years); and DOSAGE AND ADMINISTRATION, Heterozygous Familial Hypercholesterolemia in Pediatric Patients (10–17 years of age). Adolescent females should be counseled on appropriate contraceptive methods while on Lipitor therapy (see CONTRAINDICATIONS and PRECAUTIONS, Pregnancy). Lipitor has not been studied in controlled clinical trials involving pre-pubertal patients or patients younger than 10 years of age.

Clinical efficacy with doses up to 80 mg/day for 1 year have been evaluated in an uncontrolled study of patients with homozygous FH including 8 pediatric patients (see CLINICAL PHARMACOLOGY, Clinical Studies: Homozygous Familial Hypercholesterolemia).

Geriatric Use

The safety and efficacy of atorvastatin (10–80 mg) in the geriatric population (≥65 years of age) was evaluated in the ACCESS study. In this 54-week open-label trial 1,958 patients initiated therapy with atorvastatin 10 mg. Of these, 835 were elderly (≥65 years) and 1,123 were non-elderly. The mean change in LDL-C from baseline after 6 weeks of treatment with atorvastatin 10 mg was –38.2% in the elderly patients versus –34.6% in the non-elderly group.

The rates of discontinuation due to adverse events were similar between the two age groups. There were no differences in clinically relevant laboratory abnormalities between the age groups.

Use in Patients with Recent Stroke or TIA

In a post-hoc analysis of the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) study where Lipitor 80 mg vs placebo was administered in 4,731 subjects without CHD who had a stroke or TIA within the preceding 6 months, a higher incidence of hemorrhagic stroke was seen in the Lipitor 80 mg group compared to placebo. Subjects with hemorrhagic stroke on study entry appeared to be at increased risk for hemorrhagic stroke.

ADVERSE REACTIONS

Lipitor is generally well-tolerated. Adverse reactions have usually been mild and transient. In controlled clinical studies of 2502 patients, <2% of patients were discontinued due to adverse experiences attributable to atorvastatin. The most frequent adverse events thought to be related to atorvastatin were constipation, flatulence, dyspepsia, and abdominal pain.

Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT)

In ASCOT (see CLINICAL PHARMACOLOGY, Clinical Studies) involving 10,305 participants treated with LIPITOR 10 mg daily (n=5,168) or placebo (n=5,137), the safety and tolerability profile of the group treated with Lipitor was comparable to that of the group treated with placebo during a median of 3.3 years of follow-up.

Collaborative Atorvastatin Diabetes Study (CARDS)

In CARDS (see CLINICAL PHARMACOLOGY, Clinical Studies) involving 2838 subjects with type 2 diabetes treated with LIPITOR 10 mg daily (n=1428) or placebo (n=1410), there was no difference in the overall frequency of adverse events or serious adverse events between the treatment groups during a median follow-up of 3.9 years. No cases of rhabdomyolysis were reported.

Treating to New Targets Study (TNT)

In TNT (see CLINICAL PHARMACOLOGY, Clinical Studies) involving 10,001 subjects with clinically evident CHD treated with Lipitor 10 mg daily (n=5006) or Lipitor 80 mg daily (n=4995), there were more serious adverse events and discontinuations due to adverse events in the high-dose atorvastatin group (92, 1.8%; 497, 9.9%, respectively) as compared to the low-dose group (69, 1.4%; 404, 8.1%, respectively) during a median follow-up of 4.9 years. Persistent transaminase elevations (≥3 × ULN twice within 4–10 days) occurred in 62 (1.3%) individuals with atorvastatin 80 mg and in nine (0.2%) individuals with atorvastatin 10 mg. Elevations of CK (≥ 10 × ULN) were low overall, but were higher in the high-dose atorvastatin treatment group (13, 0.3%) compared to the low-dose atorvastatin group (6, 0.1%).

Incremental Decrease in Endpoints Through Aggressive Lipid Lowering Study (IDEAL)

In IDEAL (see CLINICAL PHARMACOLOGY, Clinical Studies) involving 8,888 subjects treated with Lipitor 80 mg/day (n=4439) or simvastatin 20–40 mg daily (n=4449), there was no difference in the overall frequency of adverse events or serious adverse events between the treatment groups during a median follow-up of 4.8 years.

The following adverse events were reported, regardless of causality assessment in patients treated with atorvastatin in clinical trials. The events in italics occurred in ≥2% of patients and the events in plain type occurred in <2% of patients.

Body as a Whole: Chest pain, face edema, fever, neck rigidity, malaise, photosensitivity reaction, generalized edema.

Digestive System: Nausea, gastroenteritis, liver function tests abnormal, colitis, vomiting, gastritis, dry mouth, rectal hemorrhage, esophagitis, eructation, glossitis, mouth ulceration, anorexia, increased appetite, stomatitis, biliary pain, cheilitis, duodenal ulcer, dysphagia, enteritis, melena, gum hemorrhage, stomach ulcer, tenesmus, ulcerative stomatitis, hepatitis, pancreatitis, cholestatic jaundice.

Respiratory System: Bronchitis, rhinitis, pneumonia, dyspnea, asthma, epistaxis.

Nervous System: Insomnia, dizziness, paresthesia, somnolence, amnesia, abnormal dreams, libido decreased, emotional lability, incoordination, peripheral neuropathy, torticollis, facial paralysis, hyperkinesia, depression, hypesthesia, hypertonia.

Musculoskeletal System: Arthritis, leg cramps, bursitis, tenosynovitis, myasthenia, tendinous contracture, myositis.

Skin and Appendages: Pruritus, contact dermatitis, alopecia, dry skin, sweating, acne, urticaria, eczema, seborrhea, skin ulcer.

Urogenital System: Urinary tract infection, hematuria, albuminuria, urinary frequency, cystitis, impotence, dysuria, kidney calculus, nocturia, epididymitis, fibrocystic breast, vaginal hemorrhage, breast enlargement, metrorrhagia, nephritis, urinary incontinence, urinary retention, urinary urgency, abnormal ejaculation, uterine hemorrhage.

Special Senses: Amblyopia, tinnitus, dry eyes, refraction disorder, eye hemorrhage, deafness, glaucoma, parosmia, taste loss, taste perversion.

Cardiovascular System: Palpitation, vasodilatation, syncope, migraine, postural hypotension, phlebitis, arrhythmia, angina pectoris, hypertension.

Metabolic and Nutritional Disorders: Peripheral edema, hyperglycemia, creatine phosphokinase increased, gout, weight gain, hypoglycemia.

Hemic and Lymphatic System: Ecchymosis, anemia, lymphadenopathy, thrombocytopenia, petechia.

Postintroduction Reports

Adverse events associated with Lipitor therapy reported since market introduction, that are not listed above, regardless of causality assessment, include the following: anaphylaxis, angioneurotic edema, bullous rashes (including erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis), rhabdomyolysis, fatigue, and tendon rupture.

Pediatric Patients (ages 10–17 years)

In a 26-week controlled study in boys and postmenarchal girls (n=140), the safety and tolerability profile of Lipitor 10 to 20 mg daily was generally similar to that of placebo (see CLINICAL PHARMACOLOGY, Clinical Studies section and PRECAUTIONS, Pediatric Use).

OVERDOSAGE

There is no specific treatment for atorvastatin overdosage. In the event of an overdose, the patient should be treated symptomatically, and supportive measures instituted as required. Due to extensive drug binding to plasma proteins, hemodialysis is not expected to significantly enhance atorvastatin clearance.

DOSAGE AND ADMINISTRATION

The patient should be placed on a standard cholesterol-lowering diet before receiving Lipitor and should continue on this diet during treatment with Lipitor.

Hypercholesterolemia (Heterozygous Familial and Nonfamilial) and Mixed Dyslipidemia (Fredrickson Types IIa and IIb)

The recommended starting dose of Lipitor is 10 or 20 mg once daily. Patients who require a large reduction in LDL-C (more than 45%) may be started at 40 mg once daily. The dosage range of Lipitor is 10 to 80 mg once daily. Lipitor can be administered as a single dose at any time of the day, with or without food. The starting dose and maintenance doses of Lipitor should be individualized according to patient characteristics such as goal of therapy and response (see NCEP Guidelines, summarized in Table 7). After initiation and/or upon titration of Lipitor, lipid levels should be analyzed within 2 to 4 weeks and dosage adjusted accordingly.

Since the goal of treatment is to lower LDL-C, the NCEP recommends that LDL-C levels be used to initiate and assess treatment response. Only if LDL-C levels are not available, should total-C be used to monitor therapy.

Heterozygous Familial Hypercholesterolemia in Pediatric Patients (10–17 years of age)

The recommended starting dose of Lipitor is 10 mg/day; the maximum recommended dose is 20 mg/day (doses greater than 20 mg have not been studied in this patient population). Doses should be individualized according to the recommended goal of therapy (see NCEP Pediatric Panel Guidelines1, CLINICAL PHARMACOLOGY, and INDICATIONS AND USAGE). Adjustments should be made at intervals of 4 weeks or more.

Homozygous Familial Hypercholesterolemia

The dosage of Lipitor in patients with homozygous FH is 10 to 80 mg daily. LIPITOR should be used as an adjunct to other lipid-lowering treatments (e.g., LDL apheresis) in these patients or if such treatments are unavailable.

Concomitant Lipid Lowering Therapy

Lipitor may be used in combination with a bile acid binding resin for additive effect. The combination of HMG-CoA reductase inhibitors and fibrates should generally be avoided (see WARNINGS, Skeletal Muscle, and PRECAUTIONS, Drug Interactions for other drug-drug interactions).

Dosage in Patients With Renal Insufficiency

Renal disease does not affect the plasma concentrations nor LDL-C reduction of atorvastatin; thus, dosage adjustment in patients with renal dysfunction is not necessary (see CLINICAL PHARMACOLOGY, Pharmacokinetics).

Dosage in Patients Taking Cyclosporine, Clarithromycin or A Combination of Ritonavir plus Saquinavir or Lopinavir plus Ritonavir

In patients taking cyclosporine, therapy should be limited to Lipitor 10 mg once daily. In patients taking clarithromycin or in patients with HIV taking a combination of ritonavir plus saquinavir or lopinavir plus ritonavir, for doses of atorvastatin exceeding 20 mg appropriate clinical assessment is recommended to ensure that the lowest dose necessary of atorvastatin is employed (see WARNINGS, Skeletal Muscle, and PRECAUTIONS, Drug Interactions).

HOW SUPPLIED

Lipitor (atorvastatin calcium) is supplied as white, elliptical, film-coated tablets of atorvastatin calcium containing 10, 20, 40 and 80 mg atorvastatin.

10 mg tablets: coded “PD 155″ on one side and “10″ on the other.

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Foods That Prevent High Cholesterol

Monday, January 21st, 2008

Cholesterol is thought to become a problem for people over 40. Although this is not strictly true (as some children and young adults can also have high cholesterol), it is often the consequence of eating the wrong types of foods for many years. Certainly the metabolism has begun to slow down and the person is probably not as active as they used to be. They are probably well advanced in a career and have responsibilities, like a mortgage and children to raise, so it becomes easy to lose focus of their personal wellbeing at the expense of the family. Thus 40 seems to be a good age to start considering personal health issues. This article will cover what high cholesterol is and some foods that prevent high cholesterol.

According to the American Heart Association, normal cholesterol levels should be less than 200mg/dl (milligrams per deciliter of blood). Anything from 200 – 239mg/dl is considered borderline high. Anything over 239mg/dl is considered high. The only way you can determine this level is by having a blood test. Your doctor can administer the blood test and advise you on possible treatment if your numbers are high.

In most cases the treatment is simple. Modifying your diet and taking on more exercise will help to lower your high cholesterol. In some cases drugs may be used, but they are only prescribed in cases where the reading is extremely high or the diet/exercise has had no affect on reducing the cholesterol level.

In terms of food to eat it is also simple. You don’t need to go on any fad diet, just stick to a balanced diet that gives you the required vitamins and minerals. It should give you a good balance between carbohydrates, proteins and some fats.

Animals fats are the primary cause of excess cholesterol so you should avoid high fat dairy products. You should trim the fat off meat and look into eating leaner types and cuts of meat.

In terms of fats, you should restrict your fat intake to mono and polyunsaturated fats, like olive oil. You should avoid saturated fats and trans fats. These types of fats are often found in processed foods hence the reason to avoid packaged or processed foods. Fresh foods are best. This applies to meats but more so to vegetables and fruits. You should get as much fresh vegetables as you can. Steaming or boiling is best. This is the basic guideline for a balanced diet that will reduce or at least stabilize your cholesterol level. There are other foods that can actively reduce it.

Soluble fiber which can be found in oatmeal or porridge is thought to be good for reducing cholesterol. It works on two fronts. It prevents the absorption of cholesterol into the bloodstream. It cannot be completely metabolized by the body and is excreted, however, as it passes through the digestive system it attaches to LDL cholesterol thus helping to reduce the overall reading.

Another product that actively prevents high cholesterol is spreads that contain plant sterols. Plant sterols are the plant equivalent of animal sterols (or cholesterol) so they compete with animal sterols when they are being absorbed into the small intestine. Plant sterols are also added to things like fruit juices and yogurts.

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