International Data

What Say You?

How can we serve you better?

More content please... - 33.7%
A bit more pictures would be better - 19.4%
More up to date content - 12.3%
Nothing! your site is superb! - 34.6%



What should I know about Hyperlipidemia?

If your health professional says you have hyperlipidemia, this simply means the amount of fat in your blood is higher than it should be. ("Hyper" means high; "lipid" is another word for fat or fat-like substance; "emia" refers to the blood.) Although high cholesterol is the most famous form of hyperlipidemia, blood fats include more than just cholesterol. Triglycerides, phospholipids, and other fatty substances circulate continuously through the bloodstream on their way to and from organs and tissues.

High blood cholesterol gets the most attention because of the link between cholesterol and heart disease. Cholesterol has received a great deal of press, and medical experts agree that high blood cholesterol is a risk factor for heart disease. But cholesterol is not an enemy. The body needs cholesterol and manufactures its own supply. Essential for life, cholesterol plays many important roles. Cholesterol, along with other fats, is a key component of cells membranes. The body uses cholesterol as the building material for hormones such as estrogen and testosterone. Bile salts, which break the fat we eat into small particles that can be digested, are composed largely of cholesterol. Cholesterol is our friend, something the body requires, in the right places and amounts.

Abnormally high levels of cholesterol in the blood can lead to coronary heart disease and other serious conditions, due to build-up of cholesterol-filled plaque in the arteries. But cholesterol by itself is not the problem. Research has shown that abnormalities in the way cholesterol is transported in the blood are the culprits in setting the stage for arteries to become damaged and clogged with plaque. (This is the condition known as "atherosclerosis.")

Blood is a watery fluid. Since oil and water do not mix, fats do not travel in the blood in their free form. Instead, they are bundled together with other substances for transport through the blood vessels and delivery to destinations where they are needed in the body. Cholesterol and other fats are shipped in the form of fat-protein packages called "lipoproteins." Four groups of lipoproteins use the bloodstream as an aqueduct: LDL, VLDL, HDL, and chylomicrons. The protein portion of a lipoprotein forms a sort of shell around the fat and also directs the lipoprotein to its appointed delivery site in tissues and organs.

Chylomicrons, a major transport container for triglycerides, are large particles that carry digested fat from the intestines to the liver. (Fats are broken down into fatty acids in the digestive tract, and then packaged together in groups of three. A triglyceride contains three fatty acids attached to glycerol.) Rich in triglycerides, chylomicrons also ferry cholesterol absorbed from food to the liver. Fat-digesting enzymes break down chylomicrons fairly quickly, so most are gone from the blood after a 12 to 14 hour fast.

VLDL, or "very low-density lipoproteins" also transport triglycerides and cholesterol. Formed in the liver and intestines, VLDL carry about 10 to 15 percent of the cholesterol found in blood. VLDL delivers cholesterol and triglycerides to cells, which in turn put these lipid products to use.

Through the action of fat-digesting enzymes, VLDL becomes progressively smaller as it circulates through the bloodstream. Remnants of VLDL can contribute to plaque-formation in the arteries. VLDL also converts to LDL, which is the chief culprit in atherosclerosis.

LDL, or "low-density lipoprotein," is the blood lipid that cause the most concern. Compared to other lipoproteins, LDL has a much greater tendency to deposit cholesterol in the walls of blood vessels. Because LDL is the most plaque-forming form of cholesterol, the likelihood of developing atherosclerosis is directly related to the concentration of LDL in the blood. Lowering LDL is the primary goal in treating hyperlipidemia.

HDL, or "high-density lipoprotein", does not form plaque and is thus called the "good" cholesterol. HDL picks up cholesterol from the tissues and sends it back to the liver for removal from the body. When HDL levels are where they should be, your body is disposing of cholesterol properly. When treating high blood cholesterol, health professionals try to bring the HDL level up as LDL comes down.

The exact causes of high blood cholesterol are not known for certain, but diet and heredity are believed to be the major factors. Several types of hyperlipidemia have been identified. "Polygenic hypercholesterolemia," the most common one, can often be controlled with diet.

Two genetically-related forms of hyperlipidemia have been identified, but fortunately they are less common. "Familial hypercholesterolemia" which strikes only about 1 in 500 Americans, involves an inherited defect in the liver’s ability to pick up LDL returning from tissues. In others, genetic traits cause overproduction of particular lipoprotein components that favor atherosclerosis. People with these conditions often have a history of heart disease in the family.

Before recommending a treatment plan for high cholesterol and blood lipids, the health professional must first look for the cause. Tests can be performed to rule out other conditions that may elevate blood fat levels such as diabetes and thyroid disorders. Certain medications can raise blood lipids, so their use should be evaluated in people with hyperlipidemia.


World Health Organization, 2002.

  • Almost one fifth (18%) of global stroke events (mostly nonfatal events) and about 56% of global heart disease are attributable to total cholesterol levels above 3.2 mmol/l.
  • This amounts to about 4.4 million deaths (7.9% of the total) and 2.8% of the global disease burden.

U. S. Department of Health and Human Services Public Health Service, National Institutes of Health.

    Blood cholesterol levels in men and women begin to rise at about age 20. Women have lower blood cholesterol levels prior to menopause (45-60 yrs.) than men. Women’s levels rise after menopause becoming higher than men’s levels. Levels stabilize for men at around age 50. More than 1/2 of all adult Americans have blood cholesterol levels of 200 mg/dl or higher. 25% of adults 20 yrs. or older have "high" levels 240 mg/dl or above. People with 240 mg/dl or above are twice as likely to develop atherosclerosis.

Signs and Symptoms

The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.

With some forms of hyperlipidemia, there are definite signs and symptoms that alert the health professional to the problem. Other symptoms, more difficult to detect forms lack clear diagnostic signals, thus many people are not tested for blood lipid abnormalities until other complications appear.

The link between hyperlipemia and heart disease is strong. Experts agree that high blood cholesterol is a major cause of atherosclerosis. This condition, which clogs the arteries with plaque, begins when cholesterol attached to the arterial wall creates a "fatty streak." As the process continues, the artery can become completely plugged. When this occurs in a coronary artery, which feeds the heart, the stage for a heart attack is set.

Starting at age 20, adults should have both total cholesterol and HDL checked every five years. If hyperlipidemia is discovered, a complete work-up should be done to assess the situation. The health professional will take a complete physical look at family history and add up the risk factors for heart disease. Triglyceride levels will also be checked.

Other positive risk factors for the development of Coronary Heart Disease (CHD) include:
  • Age: men, 45 years of age or older and women over 55, or premature menopause without estrogen replacement therapy.
  • Family history of premature CHD (definite heart attack or sudden death before age 55 in father or other close male relative, or before 65 years of age in mother or other close female relative).
  • Current cigarette smoking.
  • High blood pressure (hypertension) (>140/90 mm Hg on blood pressure medications).
  • Low HDL cholesterol (<35mg/dl).
  • Diabetes mellitus.
  • High LDL cholesterol is a negative risk factor, one that reduces risk of CHD.

Treatment Options


The National Cholesterol Education Program (NCEP) recommends adults with hyperlipidemia have their total cholesterol measured and risk factors assessed. Ideally, the blood cholesterol level should be under 200 milligrams per deciliter (a tenth of a liter, or a little less than three and a half ounces). Levels between 200 and 239 are classified as borderline high. At this point, risk factors should be assessed to determine the degree of heart disease risk. Levels of 240 and above are classified as high blood cholesterol levels. If the total cholesterol is below 200 and the HDL is above 35mg/dl, no further follow up is necessary.

Cutting down the dietary intake of saturated fat and cholesterol and exercising regularly are the first steps in getting blood lipid levels under control. The Step 1 diet recommended by NCEP restricts total calories from fat to less than 30 percent of total daily calories. Saturated fat should not be more than 7 percent of daily calories, and daily cholesterol intake should not exceed 300mg/day.

In the Step II diet, saturated fat is restricted to less than 7 percent per day and daily cholesterol intake is reduced to 200mg/day. The Step 1 diet can reduce LDL levels by 5 to 7 percent. An additional 3 to 7 percent drop can be achieved with Step II. How conscientiously one follows the diet makes a difference in the results. Genetic factors may also influence the outcome.

A number of drugs are used to bring cholesterol levels down. The most common ones include: atorvastatin, cerivastatin, fluvastatin, pravastatin, simvastatin, and lovastatin. Collectively known as "statins," these drugs block an enzyme that increases cholesterol production in the liver. (They also deplete CoQ10, an important vitamin-like nutrient.)

Niacin (vitamin B3) has been known for over forty years as a cholesterol-lowering agent. Niacin can reduce total cholesterol and LDL, while raising HDL. Niacin, in its pure form, can cause side-effects such as temporary skin flushing, and thus has earned limited favor as a standard therapy for high cholesterol.

Other medications for lowering cholesterol include gemfibrozil, which promotes enzymes that break down cholesterol, and bile acid sequestrants (BASR) such as colestipol and cholestyramine, which aid the liver in removing cholesterol from the blood. Estrogen replacement therapy is generally recommended for postmenopausal women for lowering LDL cholesterol. Generally, LDL cholesterol is reduced by approximately 15-25 percent and HDL increases by 15-25 percent with a 0.625mg dose of synthetic estrogen.

Nutritional Suplementation


Chromium, an essential trace mineral, helps control blood cholesterol levels. In double-blind human trials, individuals taking 200mcg of chromium daily show significant decreases in both total cholesterol and LD, along with a slight elevation of the beneficial HDL-cholesterol. (1) Chromium has also been reported to improve blood levels in diabetics. (2) This in turn helps reduce cardiovascular risk. In general, American diets supply very little chromium. For much of the population, chromium deficiency may add to the risk of heart disease. People whose diets are high in refined sugar, athletes, pregnant women, and the elderly may be susceptible to chromium deficiency.

The body needs chromium to manufacture a key substance called "Glucose Tolerance Factor" (GTF). In addition to lowering elevated serum cholesterol levels, GTF may help lower triglycerides.

Vitamin C

Vitamin C is another nutrient that reportedly produces favorable changes in blood cholesterol levels. When vitamin C was given to 10 women in a double-blind study at a dose of 1,000mg daily for four weeks, LDL cholesterol dropped 16 percent, along with a slight improvement in HDL-cholesterol levels. A much larger study with 256 men and 221 women showed similar results. In both men and women, those individuals taking large doses of vitamin C experienced larger reductions in total cholesterol, LDL-cholesterol and triglycerides, and elevations of HDL-cholesterol. The ratio of total cholesterol to HDL, another key measurement, also improved. (3) , (4) Because vitamin C is an antioxidant, it also helps to prevent the oxidation of LDL by free radicals. LDL has an even greater tendency to deposit cholesterol in the arteries when it is oxidized. Blocking LDL oxidation may thus lower the risks for developing atherosclerosis. (5)

Vitamin B5

Pantethine is the active form of vitamin B5, also known as pantothenic acid. Pantethine has been reported to lower elevated triglycerides and LDL cholesterol while raising levels of the beneficial HDL cholesterol. (6) Pantethine apparently helps lower the amount of cholesterol made in the liver. In one study, a group of 24 women with cholesterol levels above 240ng/dl, took 900mg of pantethine daily for 16 weeks. Eighty percent of the women experienced significant lowering of total cholesterol and LDL-cholesterol levels and none reported any side effects. (7)

Omega-6 Fatty Acids

Omega-6 fatty acid, also known as linoleic acid, is a dietary fat that helps lower LDL-cholesterol levels. Under normal conditions, the body converts omega-6 into another important fatty acid known as gamma-linolenic acid (GLA). Studies show that GLA helps the body break down LDL-cholesterol and convert it to bile acids, which are eliminated through the colon. Researchers have reported that GLA is 170 times more effective at lowering LDL-cholesterol levels than omega-6 fatty acids. (8) It is important to note that partially hydrogenated oils may decrease the benefits of omega-6 fatty acids. Common in food products, hydrogenated oils contain a type of fat called "trans fatty acids" which block formation of GLA. It is important to carefully read labels and avoid consuming processed foods where partially hydrogenated fats and oils are contained in the list of ingredients.

Borage oil, black currant oil, and evening primrose oil all contain relatively high amounts of GLA, 26%, 18%, and 9% respectively. Therefore, consuming supplemental amounts of one of these oils on a daily basis is one of the most effective ways to lower LDL-cholesterol levels. These oils must be kept refrigerated. A commonly suggested dosage is one tablespoonful daily.

Vitamin E

Vitamin E is one of the most effective nutrients in preventing the oxidation of LDL-cholesterol by free radicals. (9) Vitamin E also helps keep platelets from clumping together and forming a blood clot inside an artery. In a large study, vitamin E supplementation of 400 to 800 IU daily resulted in a reduction in various heart disease indicators. Studies in the scientific literature report that doses of vitamin E ranging from 400 to 800 IU/day provide a substantial reduction in the amount of damaged LDL-cholesterol, the type of LDL that is a major player in atherosclerosis and heart disease. Some experts feel that using a combination of antioxidants including carotenoids, vitamin C, and selenium along with vitamin E is the best way to supplement.

Vitamin E comes in different forms including four tocopherols: alpha, beta, gamma, and delta. The natural form of vitamin E, d-alpha tocopherol, is reported to be better absorbed than synthetic forms of the vitamin. (10)

Coenzyme Q10 (CO-Q10)

CoQ10, a vitamin-like nutrient known to benefit heart health, is another antioxidant that, like vitamin E, can reportedly help to prevent the oxidation of LDL cholesterol as well as reduce risks associated with several other aspects of cardiovascular disease. CoQ10 circulates in the blood piggy-backed onto particles of LDL cholesterol. Adequate coenzyme Q10 is an important nutrient for protecting LDL-cholesterol from damage, which substantially reduces an individual’s risk for developing atherosclerosis. (11)

Many individuals with high cholesterol will be using a cholesterol-lowering drug, likely a member of the class of drugs known as the "statins." Though effective, these medications impair the body’s ability to manufacture coenzyme Q10. The drug known as gemfibrozil may also deplete coenzyme Q10. In addition to its protective role in preventing damage to LDL, CoQ10 powers the generation of energy at the cellular level. The heart is the most energy-demanding muscle in the body; a deficiency of coenzyme Q10 could adversely impact the heart.

Sterols (Sitosterol) and Sterolins (Sitosterolin)

There are many chemical constituents (termed phytochemicals) found in plant medicines that have beneficial pharmacological effects in humans. Some bioactive phytochemicals include tannins, resins, polysaccharides, saponins, glycosides, and volatile oils among others. Recent literature has reported that two of these phytochemicals, sterols and sterolins (plant "fats"), occur naturally in fruits, vegetables, seeds, and nuts and, have clinically beneficial effects in human subjects in many conditions.

Sterol is found in all plant-based foods, and sterolin is a glucoside moiety joined to the sterol chemical structure. Both sterols and sterolins were identified as early as 1922. In the natural state, these plant "fats" are bound to the fibers of the plant, making the sterols and sterolins difficult to be absorbed during the normal transit of digested food through our gut. Seeds are the richest source of the sterols and sterolins, but are usually removed during processing by the food industry.

Plant sterols and sterolins have been reported to be effective adjunctive agents in the management and treatment of disease states such as high cholesterol levels, benign prostatic hyperplasia, pulmonary tuberculosis, stress-induced immune suppression, and HIV among others. (12) , (13) , (14) , (15) , (16) Some of the most promising uses of these plant "fats" is in the management of autoimmune disorders such as lupus, multiple sclerosis, rheumatoid arthritis, and myasthenia gravis. Of note is that the sterols should be combined with sterolin in order to be an effective agent for the immune system. (17)

Sterols and sterolins have been reported to modulate the function of T-cells, significantly enhancing the proliferation of the CD-4 TH-1 cells and increasing the production of the interleukin 2 (IL2) and gamma-interferon (FN-g and IFN-y). (18) These results indicate that sterols and sterolins are adaptogenic in that they modulate the immune and stress response.

Care should be taken if an individual is taking immunosuppressive agents. Based on pharmacology, if an individual is taking hypocholesterolemic agents concurrently with plant sterols and sterolins, a dosage adjustment in the pharmaceutical medication may be necessary.

Soy Isoflavones

Soy protein has been reported to lower cholesterol in individuals with elevated cholesterol. (19) This fact that soy protein diets rather than animal protein diets can lower serum cholesterol levels tends to be well documented among animal studies, but has historically been inconclusive in humans. One evaluation comparing 38 controlled human clinical trials evaluated the relationship between serum cholesterol and soy protein intake. This evaluation concluded that an average soy protein intake of 47g per day led to significant decreases in lipid levels. The soy based diets led to a 9.3% decrease in total cholesterol, a 12.9% decrease in low-density lipoprotein (LDL) cholesterol, a 10.5% decrease in triglycerides, and a slight increase in high-density lipoprotein (HDL) cholesterol. (20)

Beta-1,3 Glucan

Beta-glucans appear to be the major cholesterol lowering agents in oat bran fiber. Studies reveal that soluble beta-1,3 glucans in oat bran can lower total cholesterol and LDL ("bad") cholesterol levels in patients with hyperlipidemia. (21) , (22) Similar cholesterol lowering effects are reported in studies where barley is used as the source of beta-1,3 glucans. (23)


Policosanol is a natural mixture from sugar cane wax that has cholesterol-lowering effects. (24) , (25) , (26) , (27) A new product has been developed that is made from beeswax, and is reported to be a more stable form than other products.

There have been several reports of policosanol lowering cholesterol levels in humans. One study has compared policosanol to HMG-CoA reductase inhibitors (cholesterol-lowering drugs known as "statins") in patients with high amounts of cholesterol in the blood. (28) A 24 percent decrease in LDL cholesterol (“bad cholesterol") was obtained with policosanol, compared with a 22% reduction with the drug lovastatin, and a 15 percent decrease with the drug simvastatin. HDL cholesterol (“good cholesterol") increased in patients on policosanol and did not change in the other drug treatment groups. Side effects of policosanol were mild and the liver was not affected. The authors concluded that policosanol is a safe and effective cholesterol-lowering agent.

Another large study was conducted to study the effects of policosanol in decreasing blood cholesterol levels. (29) Policosanol decreased LDL cholesterol and cholesterol, and it raised HDL cholesterol. Triglycerides did not change after the first 12 weeks, and were lower at the end of the study. Policosanol was reported safe and no drug interactions or side effects were seen.

Policosanol has also been reported to lower increased cholesterol and LDL cholesterol in people with non-insulin-dependent diabetes mellitus, possibly decreasing the development of coronary artery disease. Policosanol has protected against the development of atherosclerotic lesions in laboratory animal studies. (30)

Herbal Suplementation


A gummy resin tapped from a tree native to India, guggul has been used in the Indian (Ayurvedic) medical system for centuries as an anti-arthritic, carminative, antispasmodic, diaphoretic, and aphrodisiac herb. (31) In the early 1960's, researchers took notice of ancient Sanskrit texts that described the use of guggul for a condition called "coating and obstruction of channels." Intrigued by what seemed to be a very-old, yet accurate description of atherosclerosis, a group of scientists tested guggul on animals to see if the herb could lower blood lipids. Studies in humans demonstrated, convincingly, that guggul lowers total cholesterol, LDL, and trigycerides. After years of research, a standardized extract of guggul was approved for marketing in India in 1986 as a lipid-lowering drug. (32) Guggul has also been reported to inhibit platelet clumping, help break up blood clots in the blood, and protect the heart from being damaged by free radicals through an antioxidant effect. (33)


Garlic has been reported to lower total cholesterol, LDL cholesterol, and triglycerides, and increase HDL cholesterol. (34) , (35) , (36) Garlic may be of benefit in the prevention of heart disease and atherosclerosis. (37) , (38) Garlic may inhibit platelet aggragation and influence blood thickness through its ability to break down fibrin, a protein involved in blood clotting. (39) , (40) , (41) This leads to the use of garlic in the prevention of strokes, heart attacks, and dangerous blood clot formation. (42) , (43) , (44) Also, the antioxidant effect in aged garlic has been reported to be beneficial in preventing stroke and arteriosclerosis. (45)

One study reported no effect of garlic oil on blood lipids. (46) However, the product used was garlic oil, which is processed and heated garlic. The impact of processing is an important fact to keep in mind when choosing a garlic supplement. Changes can occur in garlic’s active ingredients when it is exposed to heat. Cooking or other processing that can render the garlic product virtually ineffective. Cooking is known to denature proteins, and therefore, may inactivate the enzyme (allinase) that is necessary in converting allinin into allicin, the major beneficial ingredient in garlic.

Also, research has reported that allinase may be irreversibly inhibited by stomach acid and, when in an acidic environment, may fail to form adequate amounts of allicin or other beneficial substances. (47) , (48) It is important to use a high quality garlic product. Garlic supplements often come as enteric-coated tablets, which are designed to dissolve in the small intestine rather than the stomach. A few studies have found that allicin may damage the liver in very large amounts. (49) , (50) However, there are positive studies showing no adverse effects with garlic preparations standardized for ability to release allicin.

Red Yeast Rice

In 1976, Japanese researchers reported the discovery of mevastatin, an ingredient isolated from the cultures of Penicillium citrinum and P. brevicompactin. (51) Mevastatin was found to be a potent inhibitor of the enzyme that promotes cholesterol production. Based on this, red rice yeast may be a helpful product in reducing high cholesterol and the risk of heart disease. (52)

In recent years, at least 34 separate clinical studies (17 controlled and 17 open-label) in China and the United States have tested M. purpureus red yeast rice as a cholesterol-lowering agent.

Psyllium Seed

Studies have shown that psyllium has the ability to lower cholesterol levels. (53) , (54) Fiber in the diet, especially soluble fiber, can reportedly reduce absorption of blood cholesterol and bile acids that can lower cholesterol levels. There have been several clinical trials reporting the effectiveness of psyllium in hyperlipidemia. (55) , (56) , (57) , (58) Researchers have further evaluated these trials together to determine their overall effect on cholesterol. They found that in 384 people taking 10.2 grams of psyllium per day, total cholesterol was lowered by 4 percent and LDL ("bad") cholesterol was lowered by 7 percent. (59)

Also of interest, is that adding psyllium to half the usual dose of medications known as bile acid sequestrants maintained the effectiveness and improved the tolerability of these medications. (60)

Diet & Lifestyle

Diet: The first and most important step for reducing cholesterol is to change the diet. Most low fat, low protein diets that are designed to improve cardiovascular risk are also a high-carbohydrate (no matter what the source) diet. This type of diet has proven to actually increase LDL cholesterol and triglycerides. Many foods labeled "cholesterol free" actually contain hydrogenated oils or trans-fatty acids, which have been associated with an increased risk of cardiovascular disease. (61) Partially hydrogenated oils may increase LDL, triglycerides, and lipoprotein levels, while decreasing HDL levels. (62) In addition, these foods are generally rich in refined sugars, which can raise insulin levels. Food selection is a key issue. Nutrition surveys indicate that only 9 percent of the American population eats five fruits and vegetables a day. People also do not include legumes or enough whole grains in their diet. These foods are essential for providing dietary fiber, which not only is known to reduce cholesterol levels, but also the water soluble fiber found in legumes helps to regulate blood sugar.

The second important dietary strategy for reducing heart disease is to cut down on the intake of essential fatty acids and, in particular, the omega-3 fatty acids. Low levels of omega-3 (alpha-linolenic acid), along with an excess of omega-6 (linoleic) fatty acids from refined polyunsaturated vegetable oils can contribute to increased triglycerides, raise blood pressure, and increase platelet stickiness.

Foods that may help to lower elevated cholesterol levels include soy products, oat bran, yogurt, carrots, walnuts, and onions. High fiber foods such as whole grains, vegetables, fruits, and legumes can also help to lower cholesterol levels. Although egg yolks contain high levels of cholesterol, studies report that eating eggs regularly does not elevate blood cholesterol levels in most people. (63) Although switching to a vegetarian (low-cholesterol) diet may help some individuals lower elevated cholesterol levels, many health professionals now believe that dietary cholesterol is not a major contributor to cholesterol levels.

In the late 1940's and early 1950's, food processors began dramatically increasing their use of inexpensive, polyunsaturated vegetable oils in the production of a wide variety of processed foods. During this time, food processors created a new industrial process called partial hydrogenation. This process involved bubbling hydrogen gas into the vegetable oils under extremely high temperatures and pressures with metal catalysts. This process changes the consistency of the vegetable oils from a liquid to the semi-solid hydrogenated fats and oils present in processed foods. The process of partial hydrogenation gave food processors another benefit. It increased the shelf life of processed food products by making the fats and oils in processed foods less likely to become rancid.

There are health-related problems associated with partially hydrogenated fats and oils. The high temperatures and pressures that are required during the process of partial hydrogenation causes many of the fats to change their shape, resulting in formation of the trans fatty acids mentioned above. One of the problems associated with trans fats is they block 6-delta desaturase, an enzyme that is required for the metabolism of cholesterol. By blocking this enzyme, trans fats inhibit the body’s ability to excrete cholesterol. Foods containing partially hydrogenated oils actually act to raise LDL-cholesterol levels and increase the risk of cardiovascular disease. (64)

Exercise: Regular exercise is another way to positively change cholesterol levels. Regular endurance exercise training has been associated with decreased levels of total cholesterol and increased HDL-cholesterol. (65) Various forms of aerobic exercise that can help improve HDL levels include regular walking, aerobics, dancing, jogging, swimming, and cycling.


  1. View Abstract: Press RI, et al. The effect of chromium picolinate on serum cholesterol and apolipoprotein fractions in human subjects. West J Med. 1990;152(1):41-45.
  2. View Abstract: Fox GN, et al. Chromium picolinate supplementation for diabetes mellitus. J Fam Prac. 1998;46(1):83-6.
  3. View Abstract: Jacques PF, et al. Ascorbic acid and plasma lipids. Epidemiology. 1994;5(1):19-26.
  4. View Abstract: Simon JA, et al. Relation of Serum Ascorbic Acid to Serum Lipids and Lipoproteins in US Adults. J Am Coll Nutr. 1998;17(3):250-5.
  5. View Abstract: Lynch SM, et al. Ascorbic acid and atherosclerotic cardiovascular disease. Subcell Biochem. 1996;25:331-67.
  6. View Abstract: Bertolini S, et al. Lipoprotein changes induced by pantethine in hyperlipoproteinemic patients: adults and children. Int J Clin Pharmacol Ther Toxicol. 1986;24(11):630-7.
  7. View Abstract: Binaghi P, et al. Evaluation of the cholesterol-lowering effectiveness of pantethine in women in perimenopausal age. Minerva Med. Jun1990;81(6):475-479.
  8. View Abstract: Horrobin D. How do polyunsaturated fatty acids lower plasma cholesterol levels? Lipids. Aug1983;18(8):558-562.
  9. View Abstract: Chan AC. Vitamin E and atherosclerosis. J Nutr. 1998;128(10):1593-6.
  10. View Abstract: Ferslew KE, et al. Pharmacokinetics and bioavailability of the RRR and all racemic stereoisomers of alpha-tocopherol in humans after single oral administration. J Clin Pharmacol. 1993;33(1):84-8.
  11. View Abstract: Langsjoen PH, et al. Overview of the use of CoQ10 in cardiovascular disease. Biofactors. 1999;9(2-4):273-84.
  12. Bouic PJD. Immunomodulation in HIV/AIDS: The Tygerberg/Stellenbosch university experience. AIDS Bulletin. Sept1997;6(3):18-20.
  13. Clerici M, Bevilacqua M, Vago T, et al. An Immunoendocrinological Hypothesis of HIV Infection. Lancet. Jun1994;343:1552-1553.
  14. View Abstract: Donald PR, Lamprecht JH, Freestone M, et al. A Randomized Placebo-controlled Trial of the Efficacy of Beta-sitosterol and Its Glucoside as Adjuvants in the Treatment of Pulmonary Tuberculosis. International Journal of Tuberculosis and Lung Disease. Jul1997;1(5):518-522.
  15. View Abstract: Berges RR, Windele J, Trampisch HJ, et al. Randomized, Placebo-controlled, Double-blind Clinical Trial of B-sitosterol in Patients with Benign Prostatic Hyperplasia. Lancet. Jun1995;345(8964):1529-32.
  16. View Abstract: Plat J, Kerckhoffs DA, Mensink RP. Therapeutic Potential of Plant Sterols and Stanols. Curr Opin Lipidol. Dec2000;11(6):571-6.
  17. View Abstract: Plat J, Kerckhoffs DA, Mensink RP. Therapeutic Potential of Plant Sterols and Stanols. Curr Opin Lipidol. Dec2000;11(6):571-6.
  18. View Abstract: Plat J, Kerckhoffs DA, Mensink RP. Therapeutic Potential of Plant Sterols and Stanols. Curr Opin Lipidol. Dec2000;11(6):571-6.
  19. Sirtori CR, et al. Role of Isoflavones in the Cholesterol Reduction by Soy Proteins in the Clinic. Am J Clin Nutr. Jan1997;65(1):166-67.
  20. View Abstract: Anderson JW, Cook-Newell ME, Johnstone BM. Meta-Analysis of the Effects of Soy Protein Intake on Serum Lipids. NEJM. Aug1995;333:5.
  21. View Abstract: Davidson MH, Dugan LD, Burns JH, et al. The hypocholesterolemic effects of beta-glucan in oatmeal and oat bran. A dose-controlled study. JAMA. Apr1991;265(14): 1833-9.
  22. View Abstract: Braaten JT, Wood PJ, Scott FW, et al. Oat beta-glucan reduces blood cholesterol concentration in hypercholesterolemic subjects. Eur J Clin Nutr. Jul1994;48(7):465-74.
  23. View Abstract: McIntosh GH, Whyte J, McArthur R, et al. Barley and wheat foods: influence on plasma cholesterol concentrations in hypercholesterolemic men. Am J Clin Nutr. May1991;53(5):1205-9.
  24. View Abstract: Menendez R, et al. Oral administration of policosanol inhibits in vitro copper ion-induced rat lipoprotein peroxidation. Physiol Behav. Aug1999;67(1):1-7.
  25. View Abstract: Alcocer L, et al. A comparative study of policosanol Versus acipimox in patients with type II hypercholesterolemia. Int J Tissue React. 1999;21(3):85-92.
  26. View Abstract: Batista J, et al. Effect of policosanol on hyperlipidemia and coronary heart disease in middle-aged patients. A 14-month pilot study. Int J Clin Pharmacol Ther. Mar1996;34(3):134-7.
  27. View Abstract: Canetti M, et al. A two-year study on the efficacy and tolerability of policosanol in patients with type II hyperlipoproteinaemia. Int J Clin Pharmacol Res. 1995;15(4):159-65.
  28. View Abstract: Prat H, et al. Comparative effects of policosanol and two HMG-CoA reductase inhibitors on type II hypercholesterolemia. Rev Med Chil. Mar1999;127(3):286-94.
  29. View Abstract: Mas R, et al. Effects of policosanol in patients with type II hypercholesterolemia and additional coronary risk factors. Clin Pharmacol Ther. Apr1999;65(4):439-47.
  30. View Abstract: Arruzazabala ML, et al. Protective effect of policosanol on atherosclerotic lesions in rabbits with exogenous hypercholesterolemia. Braz J Med Biol Res. Jul2000;33(7):835-840.
  31. Satyavati GV. Gum Guggul (Commiphora Mukul)--The Success Story of an Ancient Insight Leading to a Modern Discovery. Indian J Med Res. 1988;87:327-35.
  32. Satyavati GV, Dwarakanath C, Tripathi SN. Experimental Studies on Hypocholesterolemic Effect of Commiphora Mukul. Indian J Med Res. Oct1969;57(10):1950-62.
  33. Satyavati GV, et al. Guggulipid: A Promising Hypolipidemic Agent from Gum Guggul (Commiphora Wightii). Econ Med Plant Res. 1991;5:48-82.
  34. Ernst E. Cardioprotection and Garlic. Lancet. 1997;349(9045):131.
  35. View Abstract: Steiner M, et al. A Double-blind Crossover Study in Moderately Hypercholesterolemic Men that Compared the Effect of Aged Garlic Extract and Placebo Administration on Blood Lipids. Am J Clin Nutr. 1996;64(6):866-70.
  36. View Abstract: Agarwal KC. Therapeutic Actions of Garlic Constituents. Med Res Rev. 1996;16(1):111-24.
  37. Fogarty M. Garlic's Potential Role in Reducing Heart Disease. Br J Clin Pract. 1993;47(2):64-65.
  38. View Abstract: Orekhov AN, et al. Direct Anti-atherosclerosis-related Effects of Garlic. Ann Med. 1995;27(1):63-65.
  39. View Abstract: Kiesewetter H, et al. Effect of Garlic on Platelet Aggregation in Patients with Increased Risk of Juvenile Ischaemic Attack. Eur J Clin Pharmacol. 1993;45(4):333-36.
  40. View Abstract: Bordia A. Effect of Garlic on Blood Lipids in Patients with Coronary Heart Disease. Am J Clin Nutr. 1981;34(10):2100-03.
  41. Bordia A, et al. Protective Effect of Garlic Oil on the Changes Produced by 3 Weeks of Fatty Diet on Serum Cholesterol, Serum Triglycerides, Fibrinolytic Activity and Platelet Adhesiveness in Man. Indian Heart J. 1982;34(2): 86-88.
  42. View Abstract: Kendler BS. Garlic (Allium sativum) and Onion (Allium cepa): A Review of Their Relationship to Cardiovascular Disease. Prev Med. 1987;16(5):670-85.
  43. View Abstract: Arora RC, et al. The Long-term Use of Garlic in Ischemic Heart Disease--An Appraisal. Atherosclerosis. 1981;40(2): 175-79.
  44. View Abstract: Koscielny J, et al. The Antiatherosclerotic Effect of Allium sativum. Atherosclerosis. May1999;144(1):237-49.
  45. View Abstract: Ide N, et al. Aged Garlic Extract Attenuates Intracellular Oxidative Stress. Phytomedicine. May1999;6(2):125-31.
  46. Garlic Oil: No Impact on Lipids. Harv Heart Lett. Sep1998;9(1):6.
  47. View Abstract: Weber ND, et al. In Vitro Virucidal Effects of Allium sativum (garlic) Extract and Compounds. Planta Med. Oct1992;58(5):417-23.
  48. Freeman F, et al. Garlic Chemistry: Stability of s-2-propenyl)-2-propene-1-sulfinothioate (allicin) in Blood, Solvents, and Simulated Physiological Fluids. J Agric Food Chem. 1995;43:2332-2338.
  49. View Abstract: Egen-Schwind C, et al. Metabolism of Garlic Constituents in the Isolated Perfused Rat Liver. Planta Med. Aug1992;58(4):301-5.
  50. View Abstract: Egen-Schwind C, et al. Pharmacokinetics of Vinyldithiins, Transformation Products of Allicin. Planta Med. Feb1992;58(1):8-13.
  51. Endo A, Kuroda M, Tusija Y. ML-336, ML-236B and ML-236C, New Inhibitors of Cholesterogenesis Produced by Penicillium citrinum. J of Antibiotics. 1976;(29):1346-48.
  52. Grundy SM. HMG-CoA Reductase Inhibitors for Treatment of Hypercholesterolemia. New England J of Medicine. 1988;(319):24-33.
  53. View Abstract: Terpstra AH, Lapre JA, de Vries HT, et al. Hypocholesterolemic Effect of Dietary Psyllium in Female Rats. Ann Nutr Metab. Dec2000;44(5-6):223-228.
  54. View Abstract: Davidson MH, et al. Long-term effects of consuming foods containing psyllium seed husk on serum lipids in subjects with hypercholesterolemia. Am J Clin Nutr. Mar1998;67(3):367-76.
  55. View Abstract: Brown L, et al. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr. Jan1999;69(1):30-42.
  56. View Abstract: Anderson JW, et al. Long-term cholesterol-lowering effects of psyllium as an adjunct to diet therapy in the treatment of hypercholesterolemia. Am J Clin Nutr. Jun2000;71(6):1433-1438.
  57. View Abstract: Haskell WL, et al. Role of water-soluble dietary fiber in the management of elevated plasma cholesterol in healthy subjects. Am J Cardiol. Feb1992;69(5):433-9.
  58. View Abstract: Trautwein EA, et al. Psyllium, not pectin or guar gum, alters lipoprotein and biliary bile acid composition and fecal sterol excretion in the hamster. Lipids. Jun1998;33(6):573-82.
  59. View Abstract: Anderson JW, et al. Cholesterol-lowering effects of psyllium intake adjunctive to diet therapy in men and women with hypercholesterolemia: meta-analysis of 8 controlled trials. Am J Clin Nutr. Feb2000;71(2):472-9.
  60. View Abstract: Spence JD, et al. Combination therapy with colesipol and psyllium mucilloid in patients with hyperlipidemia. Ann Int Med. Oct1995;123(7):493-99.
  61. View Abstract: Lichtenstein A. Trans-fatty acids, blood lipids, and cardiovascular risk: where do we stand? Nutrition Reviews. 1993;51(1):340-3.
  62. View Abstract: Khosla P, Hayes KC. Dietary trans monounsaturated fatty acids negatively impact plasma lipids in humans: critical review of the evidence. J Am Coll Nutr. 1996;15(4):325-39.
  63. Morgan JM, et al. Effect of dietary (egg) cholesterol on serum cholesterol in free-living adults. J Appl Nutr. 1999;45(3,4):73-84.
  64. View Abstract: Booyens J, et al. The role of unnatural dietary trans and cis unsaturated fatty acids in the epidemiology of coronary artery disease. Med Hypotheses. 1988;25(3):175-82.
  65. View Abstract: Lennon DL, et al. Total cholesterol and HDL-cholesterol changes during acute, moderate-intensity exercise in men and women. Metabolism. 1983;32(3):244-49.