Vitamins, Fat-Soluble

Because they dissolve in fat , vitamins A, D, E, and K are called fat-soluble vitamins. They are absorbed from the small intestines , along with dietary fat, which is why fat malabsorption resulting from various diseases (e.g., cystic fibrosis, ulcerative colitis, Crohn's disease) is associated with poor absorption of these vitamins. Fat-soluble vitamins are primarily stored in the liver and adipose tissues . With the exception of vitamin K, fat-soluble vitamins are generally excreted more slowly than water-soluble vitamins, and vitamins A and D can accumulate and cause toxic effects in the body.

Vitamin A

Vitamin A was the first fat-soluble vitamin identified (in 1913). Vitamin A comprises the preformed retinoids, plus the precursor forms, the provitamin A carotenoids . Preformed retinoids is a collective term for retinol, retinal, and retinoic acid, all of which are biologically active. The provitamin A carotenoids include beta-carotene and others, which are converted to retinoids with varying degrees of efficiency. Retinoids are sensitive to heat, light, and oxidation by air. Beta-carotene is relatively more stable. Vitamin E helps protect vitamin A from oxidation. There is some loss of vitamin A with cooking, but only after boiling for a comparatively long period.

Retinoids are converted to retinol in the intestines and transported with dietary fat to the liver, where it is stored. A special transport protein , retinolbinding protein (RBP), transports vitamin A from the liver to other tissues. Carotenoids are absorbed intact at a much lower absorption rate than retinol. Of all the carotenoids, beta-carotene has the highest potential vitamin-A activity. The active forms of vitamin A have three basic functions: vision, growth and development of tissues, and immunity.

• Vision. Vitamin A combines with a protein called opsin to form rhodopsin in the rod cells of the retina. When vitamin A is inadequate, the lack of rhodopsin makes it difficult to see in dim light.
• Growth and development of tissues. Vitamin A is involved in normal cell differentiation—a process through which embryonic cells transform into mature tissue cells with highly specific functions. Vitamin A supports male and female reproductive processes and bone growth.
• Immunity. Vitamin A is essential for immune function and vitamin-A deficiency is associated with decreased resistance to infections. The severity of some infections, such as measles and diarrhea, is reduced by vitamin-A supplementation among those who suffer from vitamin-A deficiency.

It has been suggested that beta-carotene and other carotenoids (also called phytochemicals ) may function as antioxidants by neutralizing free radicals . Free radicals are unstable, highly reactive molecules that damage DNA , cause cell injury, and increase the risk of chronic disease. Beta-carotene has also been associated with reducing the risk of lung cancer . Lutein and zeaxanthin, yellow carotenoid pigments in corn and dark green leafy vegetables, may reduce the risk of macular degeneration and agerelated cataracts . Lycopene, a red carotenoid pigment in tomatoes, may help reduce the risk of prostrate cancer, cardiovascular disease, and skin damage from sunlight.

Deficiency.

Dietary deficiency of vitamin A is rare in North America and western Europe, but it is the leading cause of blindness in children worldwide. Newborn and premature infants, the urban poor, older adults, people with alcoholism or liver disease, and those with fat malabsorption syndrome are all at increased risk.

One of the earliest symptoms of vitamin-A deficiency is night blindness. It is a temporary condition, but if left untreated it can cause permanent blindness. This degeneration is called xerophthalmia, and it usually occurs in children after they are weaned. Symptoms include dryness of the cornea and eye membranes due to lack of mucus production, which leaves the eye vulnerable to surface dirt and bacterial infections. Vitamin-A deficiency can cause follicular hyperkeratosis, a condition in which hair follicles become plugged with keratin, giving a bumpy appearance and a rough, dry texture to skin.

In developing countries, the severity of infectious diseases such as measles is often correlated to the degree of vitamin-A deficiency. Providing large doses of vitamin A reduces the risk of dying from these infections. The age range of the target population for vitamin-A intervention programs is usually from birth to seven years. Administration of high-potency doses in the range of 15,000 to 60,000 micrograms (μg) are distributed to young children in targeted areas of the world to build up liver stores for up to six months. However, consumption of adequate food sources is the most important long-term solution to vitamin-A deficiency.

Toxicity.

Vitamin-A toxicity, called hypervitaminosis A, can result from long-term supplementation of two to four times the RDA for preformed vitamin A. Excess intake of preformed vitamin A is a teratogen, meaning it can cause birth defects. Birth defects associated with vitamin-A toxicity include cleft palate, heart abnormalities, and brain malfunction. Acute excess intake during pregnancy can also cause spontaneous abortions. Pregnant women should avoid prenatal supplements containing retinal, as well as medications made from retinoids, such as Accutane and Retin-A. Prolonged and excessive consumption of carotene-rich foods can lead to hypercarotenemia, a clinical condition characterized by deep orange discoloration of the skin and increased carotene levels in the blood. This condition is usually harmless.

Vitamin D (Calciferol)

In the seventeenth century, vitamin-D deficiency was so common in British children that it came to be known as "children's disease of the English." In the mid-1800s, cod liver oil became well known for treating this disease. In 1925, Elmer McCollum and coworkers determined that the "antirachitic" (antirickets) substance in cod liver oil was vitamin D. Because vitamin D is relatively stable in foods, many countries fortify milk with vitamin D to help prevent rickets. However, significant losses may result from fortified milk exposed to light.

Vitamin D from foods is absorbed from the upper part of the small intestine, along with dietary fat, and transported to the liver. In the skin, ultraviolet (UV) radiation from the sun converts a cholesterol derivative to cholecalciferol, which enters the blood stream and is transported to the liver. In the liver, vitamin D is converted to calcidiol, an inactive form that circulates in blood. Kidneys take up calcidiol and convert it to an active hormone form of vitamin D called calcitriol. People with chronic kidney failure have very low levels of calcitriol and must be routinely treated with this form of the vitamin.

The best-known function of active vitamin D is to help regulate blood levels of calcium and phosphorous. Vitamin D increases absorption of these minerals from the gastrointestinal (GI) tract. In combination with parathyroid hormone, it enhances their reabsorption from the kidneys and their mobilization from bones into the blood. Vitamin D helps maintain calcium levels even if dietary intakes are not optimal. Calcitriol affects growth of normal cells and some cancer cells. Adequate vitamin-D status has been linked to a reduced risk of developing breast, colon, and prostrate cancers.

Deficiency.

Long-term deficiency of vitamin D affects the skeletal system. In children, vitamin-D deficiency leads to rickets, a condition in which bones weaken and bow under pressure. Although vitamin-D fortification has reduced incidence of rickets in North America, it is sometimes seen in children with malabsorption syndrome and is still common in many parts of the world. In adults, vitamin-D deficiency causes osteomalacia , or "soft bones," increasing the risk for fractures in hip, spine, and other bones. Vitamin-D deficiency also contributes to osteoporosis . In elderly persons, vitamin-D supplementation reduces the risk of osteoporotic fractures.

Infants are born with stores of vitamin D that last about six months. Breast milk contains very little vitamin D, however, and infants beyond six months of age who are exclusively breastfed must obtain vitamin D via exposure to sunlight or a supplement given under the guidance of a physician.

Older adults are especially at risk for vitamin-D deficiency for several reasons. The skin, liver, and kidneys lose their capacity to synthesize and activate vitamin D with advancing age, and older adults typically drink little or no milk, a major dietary source of vitamin D. Older adults also rarely venture outdoors, and when they do, they apply sunscreen to exposed areas of the body, further contributing to the decline in vitamin-D synthesis in the skin.

Sunscreens with a sun protection factor (SPF) of 8 and above prevent vitamin-D synthesis. Sunscreen should be applied only after enough time has elapsed to provide sufficient vitamin-D synthesis. Exposure to the sun does not cause vitamin-D toxicity, and for most people, exposing the hands, face, and arms on a clear summer day for fifteen minutes a few times a week should provide sufficient Vitamin D. Dark-skinned people require longer sunlight exposure because melanin, a skin pigment, is a natural sunscreen.

Dietary recommendations assume that no vitamin D is available from exposure to sunlight. Thus, people who do not venture outdoors or who live in northern or predominantly cloudy climates need to pay attention to dietary sources. Plants are poor sources of vitamin D, so strict vegetarians must meet their vitamin-D needs through exposure to sunlight, fortification, or supplementation.

Toxicity.

Vitamin D is most likely to have toxic effects when consumed in excessive amounts through supplementation. Excess vitamin D raises blood calcium levels, resulting in calcium precipitation in soft tissues and stone formation in the kidneys, where calcium becomes concentrated in an effort to excrete it.

Vitamin K

In 1929, the Danish researcher Henrik Dam first noted that vitamin K played a critical role in blood clotting , and he named it vitamin "K" for "Koagulation." Vitamin K comprises a family of compounds known as quinones. These include phylloquinone from plants and the menaquinones from animal sources. Phylloquinone is the most biologically active form. Menaquinones are also synthesized by bacteria in the colon and absorbed, contributing about 10 percent of total vitamin-K needs. Vitamin-K absorption depends on normal consumption and digestion of dietary fat. It is primarily stored in the liver.

Vitamin K helps in the activation of seven blood-clotting-factor proteins that participate in a series of reactions to form a clot that eventually stops the flow of blood. Vitamin K also participates in the activation of bone proteins, which greatly enhances their calcium-binding properties. Low levels of circulating vitamin K have been associated with low bone-mineral density. Thus, an adequate intake of vitamin K may help protect against hip fractures.

Deficiency.

A primary deficiency of vitamin K is rare, but a secondary deficiency may result from fat malabsorption syndrome. Prolonged use of antibiotics can destroy the intestinal bacteria that produce vitamin K, precipitating deficiency in individuals at risk. Newborn infants are born with a sterile intestinal tract and those who are breastfed, may run the risk of vitamin-K deficiency, since breast-milk production takes a few days to establish and breast milk is naturally low in this vitamin. To prevent hemorrhaging, all infants in North America receive injections of vitamin K within six hours of birth.

Toxicity.

High doses of vitamin K can reduce the effectiveness of anticoagulant drugs such as warfarin (Coumadin), which is used to prevent blood clotting. People taking these drugs should maintain a consistent daily intake of vitamin K. Megadose supplements of vitamin A and E can pose a risk to vitamin-K status. Vitamin A interferes with absorption of vitamin K, and large doses of vitamin E decrease vitamin K–dependent clotting factors, thus promoting bleeding. Toxicity from food is rare, because the body excretes vitamin K much more rapidly than other fat-soluble vitamins.

Vitamin E

The link between vitamin-E deficiency and reproductive failure in rats was first discovered in 1922 by Herbert Evans and Katherine Scott Bishop. The chemical name of vitamin E, tocopherol, is derived from toco, meaning "related to childbirth."

Vitamin E comprises a family of eight naturally occurring compounds: four tocopherols and four tocotrienols, of which alpha-tocopherol is the only one to have vitamin-E activity in the human body. It is also the most common form of vitamin E in food. Vitamin E is highly susceptible to destruction by oxygen , metals, light, and deep-fat frying. As a result, prolonged food storage lowers the vitamin-E content of food.

As with other fat-soluble vitamins, absorption of vitamin E requires adequate absorption of dietary fat. In addition, the percentage of absorption declines as the amount consumed is increased. Vitamin E is stored mainly in adipose tissue, while some is stored in the muscle. The remaining vitamin E is found in cell membranes in tissue.

Vitamin E is an antioxidant and one of the body's primary defenders against oxidative damage caused by free radicals. Its activity is enhanced by other antioxidants such as vitamin C and the mineral selenium. Vitamin E interrupts free-radical chain reactions by getting oxidized, thus protecting cell membranes from free-radical attack. Scientists have implicated oxidative stress in the development of cancer, arthritis , cataracts, heart disease , and in the process of aging itself. However, it is not yet known whether supplementation with megadoses of vitamin E offers protection against heart disease and cancer beyond that provided by positive dietary and lifestyle changes.

Deficiency.

Due to the widespread use of vegetable oils, primary vitamin-E deficiency is rare. Most deficiencies occur in people with fat malabsorption syndrome. Smokers and adults on very low-fat diets are at increased risk of developing vitamin-E deficiency. Preterm infants are particularly susceptible to hemolytic anemia (anemia caused by the destruction of red blood cells) due to vitamin-E deficiency. These infants are born with limited stores of vitamin E, which are exhausted by rapid growth, and they are inefficient in absorbing vitamin E from the intestinal tract. Without vitamin E to protect against oxidation, the destruction of cell membranes causes red blood cells to burst. To prevent hemolytic anemia, special formulas and supplements containing vitamin E are prescribed for preterm infants.

Toxicity.

Large doses of vitamin E can counter the actions of vitamin K and decrease the production of vitamin K–dependent clotting factors, thus promoting serious hemorrhaging effects in adults. Individuals who are vitamin-K deficient or who are taking anticoagulant medications such as warfarin or aspirin are especially at risk from megadoses of vitamin E.

see also Vitamins, Water-Soluble.

Kiran B. Misra

Bibliography

Insel, Paul; Turner, Elaine R.; and Ross, Don (2002). Nutrition. Sudbury, MA: Jones and Bartlett.

Wardlaw, Gordon M.; Hampl, Jeffrey S.; and Disilvestro, Robert A. (2004). Perspectives in Nutrition, 6th edition. New York: McGraw-Hill.

Whitney, Eleanor Noss, and Rolfes, Sharon Rady (2002). Understanding Nutrition, 9th edition. Belmont, CA: Wadsworth/Thomson Learning.

Fat Substitutes

Since the late 1980s, fat-free and reduced-fat foods have become widely available. While not all new products survive the competitive marketplace, thousands of new reduced-fat and fat-free products have been introduced each year since 1990.

In part, these new reduced-fat food products are the result of consumer demand. But they are also a response to public health concerns and initiatives. In 1990, Healthy People 2000 asked food manufacturers to double the availability of reduced-fat food products by the year 2000, a goal that was easily met.

Dietary Fat: A Good Thing in Moderation

Despite fat's bad reputation, it is a very important nutrient . Dietary fat plays many critical roles in the body, such as providing essential fatty acids , fat-soluble vitamins , and energy . It also serves structural functions in hormones and in cells.

Fat is also a key factor in how foods taste. Fat absorbs the essence of spices and flavors and allows people to experience their full aroma. Not only does fat carry flavor, it also determines whether a cookie crunches or a muffin crumbles. In other words, fat is one of the main reasons people enjoy food.

Since the 1970s, nutrition scientists have researched the effects of diet on chronic diseases. Eating a diet lower in fat, saturated fat , and cholesterol appears to help prevent or delay the development of some serious illnesses, such as certain cancers and heart disease .

Most government health agencies and professional health organizations encourage people five years old and older to eat a diet with less than 30 percent of total calories from fat, and less than 10 percent of that from saturated fat.

Consumers are concerned about nutrition, and they want to moderate the fat in their diet but there are challenges to overcome. Nutrition, price, convenience, and product safety are important, but taste is the key driver behind food selection for most people. And many consumers still think that less fat means less taste. Fat substitutes were developed to help meet consumers' expectations about taste while providing fewer calories from fat.

What Are Fat Substitutes?

Substitutes, or fat replacers, provide the sensory and functional qualities normally provided by fat. For example, fat provides moistness in baked goods, texture in ice cream, and crispiness in potato chips. Because fat has so many diverse functions in foods, it is virtually impossible to replace it with a single compound or process. The ingredients used in place of fat depend on how a food product will be eaten or prepared. For instance, not all fat-substitute ingredients are stable when heated, so the type of fat substitute used in a fat-free salad dressing may not work well in a muffin mix.

Many fat substitutes are simply old ingredients used in new ways. For example, the Food and Drug Administration (FDA) approved polydextrose for use as a moisture-binding agent in the early 1980s, but more recently it

has been used as a fat substitute. Carrageenan has been used since the early 1960s as an emulsifier, stabilizer, and thickener, but is now commonly used to replace fat in foods, as is guar gum , which has been used as a thickener for nearly a hundred years.

Some fat substitutes are newer to the food supply, though they are made from familiar ingredients. For example, microparticulated protein is made from milk, egg, or whey protein. Other fat substitutes are new ingredients made from combinations of basic molecules .

In some cases, the FDA has approved fat-reduction ingredients as food additives . To be approved, food additives are tested extensively to assess their safety and level of use among different population groups. Examples of fat substitutes approved as food additives include carrageenan, olestra, and polydextrose.

In other instances, fat-reduction ingredients are "generally recognized as safe" (GRAS). GRAS ingredients are made from common food components and are considered by experts to be safe. For example, many spices and flavoring agents, such as sugar and salt, are GRAS ingredients. Examples of GRAS fat substitutes include guar gum and maltodextrin.

Categories of Fat Substitutes

Fat-substitute ingredients fall into three categories: carbohydrate-based, protein-based, and fat-based. Carbohydrate-based fat substitutes are the most common. They are very versatile and found in many types of food products. Carbohydrate-based fat substitutes provide between zero and four calories per gram. When used to replace fat, they may significantly lower the calorie content of a food. Most carbohydrate-based fat substitutes are GRAS substances. Some of these ingredients are only partially digestible. However, when consumed at expected levels, most carbohydrate-based fat substitutes have no digestive effects. Guar gum is an example of a carbohydrate-based fat substitute.

Protein-based fat substitutes are not as numerous as carbohydrate-based ingredients, but they have many applications and can be used in many products, including cheese, yogurt, sour cream, ice cream, mayonnaise, and salad dressing. Protein-based fat substitutes cannot be used for deep-frying. Whey protein concentrate is a protein-based fat substitute.

The last category of fat substitutes includes those that are fat-based. Because they are made from fat, they often come closest to providing fat's taste and cooking properties. Most Americans have heard of olestra, which is a fat-based fat substitute made from sucrose (table sugar) and fatty acids from vegetable oils. However, unlike sugar and vegetable oils, the body does not absorb olestra because the human digestive enzymes cannot break down such a large molecule. Olestra has the potential to inhibit absorption of some fat-soluble nutrients in the digestive tract, and, to offset any possible effects, products made with olestra have appropriate amounts of vitamins A, D, E, and K added.

Ensuring Safety

Most fat substitutes are not new to the food supply. Ingredients that are new, or used in new ways, must meet the FDA's strict criteria to be either classified as GRAS or approved as food additives. Whether they are GRAS or food additives, those ingredients approved for use in foods are considered safe for people of all ages.

Can Fat Substitutes Help to Reduce Dietary Fat?

Several studies have shown that using reduced-fat versions of food products can significantly reduce the amount of fat that people eat. For some people, eating less fat may lead to eating fewer calories and, eventually, to weight loss. As illustrated in the table above, by using reduced-fat foods, a typical lunch can be trimmed of one-third of its calories and three-fourths of its fat.

A common misconception about reduced-fat foods is that they also are low in calories. For many products, however, this is not the case. Most reduced-fat foods have had other ingredients added to replace the texture or flavor provided by fat, so that while the calories may be slightly lower in a fat-reduced product, the difference between it and a full-fat product may not be significant. With fat-modified products, as with all foods, portion size and calories still count.

Fat-modified foods can fit into a healthy eating plan. According to the American Dietetic Association, they offer a safe, feasible, and effective means to maintain the palatability of diets that are controlled in fat or calories. But they are only one of the many tools that can be used to achieve nutrition goals. Foods with fat substitutes should be consumed as part of an overall healthful eating plan, such as that outlined in the Dietary Guidelines for Americans.

see also Artificial Sweeteners; Dietary Guidelines for Americans; Fats.

Susan T. Borra

Bibliography

Diamond, L. (1997). "The Dietary Guidelines Alliance: Reaching Consumers with Meaningful Health Messages." Journal of the American Dietetic Association 97(3):247.

Hahn, N. I. (1997). "Replacing Fat with Food Technology." Journal of the American Dietetic Association 3:15–16.

Heimbach, James T.; Van Der Riet, Brooke E.; and Egan, S. Kathleen. "Impact of the Use of Reduced-Fat Foods on Nutrient Adequacy" (1997). Annals of the New York Academy of Sciences: Nutritional Implications of Macronutrient Substitutes 819:108–114.

Kurtzweil, Paula (1996). "Taking the Fat Out of Food." FDA Consumer 30(6).

Morgan, Rebecca; Sigman-Grant, Madeleine; Taylor, Dennis S.; Moriarty, Kristen; Fishell, Valerie; and Kris-Etherton, Penny (1997). "Impact of Macronutrient Substitutes on the Composition of the Diet and U.S. Food Supply." Annals of the New York Academy of Sciences: Nutritional Implications of Macronutrient Substitutes 819:70–95.

Internet Resources

American Dietetic Association (1998). "Position of the American Dietetic Association: Fat Replacers." Available from <http://www.eatright.com>

U.S. Department of Health and Human Services (1999). Healthy People 2000. Available from <http://www.health.gov/healthypeople>

U.S. Department of Health and Human Services, and U.S. Department of Agriculture (2000). Nutrition and Your Health: Dietary Guidelines for Americans, 5th ed. Available from <http://www.health.gov/dietaryguidelines>

Lipid Profile

Cardiovascular disease (CVD) is a major cause of death in the world and is mainly due to atherosclerosis (hardening of the arteries ). Abnormal blood lipids are risk factors for CVD.

Blood Lipids and Lipid Transport

Lipids are insoluble (does not dissolve) in water but are soluble (dissolves) in alcohol and other solvents. When dietary fats are digested and absorbed into the small intestine, they eventually re-form into triglycerides , which are then packaged into lipoproteins .

Dietary fats, including cholesterol , are absorbed from the small intestines and transported into the liver by lipoproteins called chylomicrons. Chylomicrons are large droplets of lipids with a thin shell of phospholipids , cholesterol, and protein . Once chylomicrons enter the bloodstream, an enzyme called lipoprotein lipase breaks down the triglycerides into fatty acid and glycerol . After a 12- to 14-hour fast, chylomicrons are absent from the bloodstream. Thus, individuals who are having a lipid profile done should fast overnight to ensure that chylomicrons have been cleared.

The liver removes the chylomicron fragments, and the cholesterol is repackaged for transport in the blood in very low-density lipoproteins (VLDLs), which eventually turn into low-density lipoproteins (LDL). LDL cholesterol (LDL-C)—the "bad cholesterol"—consists mainly of cholesterol. Most LDL particles are absorbed from the bloodstream by receptor cells in the liver. Cholesterol is then transported throughout the cells. Diets high in saturated fats and cholesterol decrease the uptake of LDL particles by the liver. LDL particles are also removed from the bloodstream by scavenger cells, or macrophages, which are white blood cells that bury themselves in blood vessels such as arteries. Scavenger cells prevent cholesterol from reentering the bloodstream, but they deposit the cholesterol in the inner walls of blood vessels, eventually leading to the development of plaque.

High-density lipoproteins (HDLs) are a separate group of lipoproteins that contain more protein and less cholesterol than LDL. HDL cholesterol (HDL-C) is also called "good cholesterol." HDL is produced primarily in the liver and intestine, and it travels in the bloodstream, picks up cholesterol, and gives the cholesterol to other lipoproteins for transport back to the liver.

Lipid Profile

A lipid profile measures total cholesterol, HDL cholesterol, LDL cholesterol, and triglycerides. A physician may order a lipid profile as part of an annual exam or if there is specific concern about CVD, especially coronary artery disease. The National Cholesterol Education Program recommends that individuals age twenty and over have a fasting lipoprotein profile every

five years. A lipid profile should be done after a nine- to twelve-hour fast without food, liquids, or medication. If fasting is not possible, the values for total cholesterol and HDL-C may still be useful. If total cholesterol is 200 milligrams per deciliter (mg/dl) or higher, or HDL-C is less than 40 mg/dl, the individual will need to have a follow-up lipoprotein profile done to determine LDL-C and triglyceride levels.

Depending on the physician's request, the lipid profile may include the ratio of cholesterol to HDL. This ratio is sometimes used in place of total blood cholesterol. The ratio is obtained by dividing the HDL cholesterol level by the total cholesterol. For example, if a person has total cholesterol of 200 mg/dl and an HDL cholesterol level of 50 mg/dl, the ratio is 4:1. The goal is to keep the ratio below 5:1, and optimally at 3.5:1. There are several over-the-counter cholesterol measuring devices on the market, but none has been endorsed by any medical organizations.

Treating Abnormal Blood Lipids

The National Cholesterol Education Program, the American College of Cardiology, and the American Heart Association recommend diet and lifestyle modification as the first line of defense against abnormal blood lipids. These recommendations include a diet low in total fat , saturated fat , and cholesterol; a diet high in fiber ; weight loss or weight management; increased physical activity; smoking cessation; increased intake of plant sterols (e.g., margarines and salad dressings made with soybean sterols); and daily use of a low-dose aspirin. Drug therapy may be required for high-risk individuals. Cholesterol-lowering drugs works to lower LDL by reducing cholesterol synthesis and by binding bile acids in the small intestines. However, there are possible side effects to these drugs that patients should be aware of.

see also Arteriosclerosis; Atherosclerosis; Cardiovascular Diseases; Fats.

Delores C. S. James

Bibliography

Birtcher, Kim K., et al. (February 2000). "Strategies for Implementing Lipid-Lowering Therapy: Pharmacy-Based Approach." American Journal of Cardiology 85(3):30–35.

National Cholesterol Education Program (2001). Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), Executive Summary. NIH Publication No. 01-3670. Washington, DC: National Institutes of Health.

Wardlaw, G.; Hampl, J.; and DiSilvestro, R. (2004). Perspectives in Nutrition, 6th edition. Boston, MA: McGraw-Hill.

Internet Resources

American Heart Association. "Cholesterol, Home Testing Devices." Available from <http:/www.americanheart.org>

Lab Tests OnLine. "Lipid Profile." Available from <http://www.labtestsonline.org>

National Heart Lung and Blood Institute. "Recommendations for Lipoprotein Measurement." Available from <http://www.nhlbi.nih.gov/prof/heart>

Lipid Profile

Definition
Purpose
Description
Recommended dosage
Precautions
Side effects
Interactions

Definition

A lipid profile includes data or results from four blood tests: total cholesterol, HDL cholesterol, LDL cholesterol and triglycerides.

WHO PERFORMS THE PROCEDURE AND WHERE IS IT PERFORMED?

• A lipid profile is typically ordered by a family doctor, internist, or geriatrician.
• A blood sample is usually obtained by a nurse, phlebotomist, or medical technologist.
• The blood sample is tested or processed by a medical technologist.
• Results are usually reviewed, returned to the person being tested and interpreted by the physician initially ordering the lipid profile.

Purpose

The purpose of a lipid profile is to help evaluate an individual’s risk of cardiovascular disease.

Description

A lipid profile quantifies four different forms of lipids that are found in the blood: total cholesterol, HDL cholesterol, LDL cholesterol and triglycerides. Dietary fats, including cholesterol, are absorbed from the small intestines. They are converted into triglycerides, which are then packaged into lipoproteins. All of these products are transported into the liver by chylomicrons. After a fast (not eating) lasting at least 12 hours, chylomicrons are absent from the bloodstream. This is the reason why persons that are having a lipid profile must fast overnight.

Humans make 75 to 80% of the cholesterol that they need. The remainder comes from their diet. Because it is important, the body stores extra cholesterol. Total cholesterol is just that: a measure of cholesterol in the blood. It is a useful measure but it can be refined, usually into the other three components of a lipid profile.

HDL stands for high density lipoproteins. HDL cholesterol is a fraction of total cholesterol. It is also known as so-called good cholesterol because high levels of HDL cholesterol seem to provide protection against a heart attack. A majority of experts feel that HDL cholesterol returns cholesterol to the liver where it is eliminated from the body. On average, 25 to 33% of all cholesterol in the blood is the HDL variety.

LDL stands for low density lipoproteins. It is also known as the so-called bad cholesterol. It slowly accumulates on the inner walls of arteries. This buildup is

QUESTIONS TO ASK YOUR DOCTOR

• Why is a lipid profile needed?
• What do the results indicate for my health?
• What treatment options do I have?

known as plaque. Over time, it creates a condition known as atherosclerosis.

Triglycerides are made (synthesized) in the body. Synthesis can be increased by being overweight, living a sedentary lifestyle (minimal to no physical activity), smoking, eating a diet that is high in carbohydrates (more than 60% of total calories) or consuming excess alcohol. People with high triglyceride levels often develop diabetes or heart disease.

Physicians calculate the ratio of HDL to LDL values to assess disease risk related to blood lipid levels.

• Very low risk: 3.3 to 3.4
• Low risk: 3.8 to 4.0
• Average risk: 4.5 to 5.0
• Moderate risk: 7.0 to 9.5
• High risk: above 11

Pharmaceutical interventions are based on the HDL to LDL ratio.

Recommended dosage

Lipid profiles can be ordered at any time. Routine lipid profiles that are used to monitor the effectiveness of drugs intended to reduce serum cholesterol are usually performed every three months.

Precautions

A fast (not eating) for a minimum of 12 hours before drawing blood contributes to a more accurate measurement of lipid in the blood. No other precautions are needed.

At the time of drawing blood, the only precaution needed is to clean the venipuncture site with alcohol.

Side effects

The most common side effects of a lipid profile are minor bleeding (hematoma) or bruising at the site of venipuncture.

KEY TERMS

Hematoma— A collection of blood that has entered a closed space.

Phlebotomist— Health care professional trained to obtain samples of blood.

Interactions

There are no interactions for a lipid profile.

Resources

BOOKS

Fischbach, F. T. and M. B. Dunning. A Manual of Laboratory and Diagnostic Tests. 8th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

McGhee, M. A Guide to Laboratory Investigations. 5th ed. Oxford, UK: Radcliffe Publishing Ltd, 2008.

Price, C. P. Evidence-Based Laboratory Medicine: Principles, Practice, and Outcomes. 2nd ed. Washington, DC: AACC Press, 2007.

Scott, M.G., A. M. Gronowski, and C. S. Eby. Tietz’s Applied Laboratory Medicine. 2nd ed. New York: Wiley-Liss, 2007.

Springhouse, A. M.. Diagnostic Tests Made Incredibly Easy!. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2008.

PERIODICALS

Amati, L., M. Chilorio, E. Jirillo, and V. Covelli. “Early pathogenesis of atherosclerosis: the childhood obesity.” Current Pharmaceutical Design 13, no. 36 (2007): 3696–3700.

Leigh-Hunt, N., and M. Rudolf. “A review of local practice regarding investigations in children attending obesity clinics and a comparison of the results with other studies.” Child Care Health and Delivery 34, no. 1 (2008): 55–58.

SHephard, M. D., B. C. Mazzachi, and A. K. Shephard. “Comparative performance of two point-of-care analysers for lipid testing.” Clinical Laboratory 53, no. 9-12 (2007): 561–566.

Wright, J. T., S. Harris-Haywood, S. Pressel, et al. “Clinical outcomes by race in hypertensive patients with and without the metabolic syndrome: Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial.” Archives of Internal Medicine 168, no. 2 (2008): 207–217.

ORGANIZATIONS

American Association for Clinical Chemistry. http://www.aacc.org/AACC/.

American Society for Clinical Laboratory Science. http://www.ascls.org/.

American Society of Clinical Pathologists. http://www.ascp.org/.

College of American Pathologists. http://www.cap.org/apps/cap.portal.

OTHER

American Clinical Laboratory Association. “Information about clinical chemistry.” 2008 [cited February 24, 2008]. http://www.clinical-labs.org/.

Clinical Laboratory Management Association. “Information about clinical chemistry.” 2008 [cited February 22, 2008]. http://www.clma.org/.

Lab Tests On Line. “Information about lab tests.” 2008 [cited February 24, 2008]. http://www.labtestsonline.org/.

National Accreditation Agency for Clinical Laboratory Sciences. “Information about laboratory tests.” 2008 [cited February 25, 2008]. http://www.naacls.org/.

L. Fleming Fallon, Jr, MD, DrPH

fat‐soluble vitamins Vitamins A, D, E, and K; they occur in food dissolved in the fats and are stored in the body to a greater extent than the water‐soluble vitamins.