Nutrition 330 Introductory Nutrition

Study Guide: Unit 9

The Antioxidant Vitamins

In this unit, we turn our attention to the antioxidant vitamins, namely vitamins A (including beta‑carotene), E, and C. We provide a brief overview of each of these vitamins, including their functions, deficiency and toxicity symptoms, and major food sources. Where appropriate, we also discuss their therapeutic uses and chemical stability. Two of these vitamins are fat soluble (A and E), while vitamin C is water‑soluble. The previous unit provides some general information on vitamins, including the key differences between water‑ and fat‑soluble vitamins.

This unit consists of three sections:

9.1—Vitamin A
9.2—Vitamin E
9.3—Vitamin C

Objectives

After completing this unit, you should be able to do the following:

1. After completing the section on vitamin A, you should be able to
   1. identify its naturally occurring and biologically active forms.
   2. identify its functions in the body.
   3. describe the symptoms of deficiency and the prevalence of deficiency in the Canadian population.
   4. discuss its therapeutic uses.
   5. list the symptoms of toxicity.
   6. list some of its major food sources.
   7. discuss its chemical stability in relation to food preparation practices and other factors.
2. After completing the section on vitamin E, you should be able to
   1. identify its function in the body as an antioxidant.
   2. describe its deficiency symptoms.
   3. discuss the claims of benefits for the use of supplements and possible toxicity symptoms.
   4. list some of its major food sources.
   5. discuss its chemical stability to food preparation practices and other factors.
3. After completing the section on vitamin C, you should be able to
   1. identify its functions in the body.
   2. describe its deficiency and toxicity symptoms.
   3. describe factors that may influence requirements.
   4. list some of its major food sources.
   5. discuss its chemical stability with respect to food preparation practices and other factors.
   6. discuss the controversies associated with its use.

9.1 Vitamin A

Reading Assignment

• Chapter 12: “The Antioxidant Nutrients—An Overview,” pages 391–392

Introduction

Vitamin A was the first vitamin to be discovered. Since its recognition in 1913 as an essential fat‑soluble nutrient required for growth in rats, subsequent research has identified multiple and diverse functions of vitamin A in vision, bone formation, and tissue formation. Recent studies have clarified some of the mechanisms of action of the different forms of vitamin A.

Objectives

After completing this section, you should be able to

• identify the naturally occurring and biologically active forms of vitamin A.
• identify its functions in the body.
• describe the symptoms of deficiency and the prevalence of deficiency in the Canadian population.
• discuss its therapeutic uses.
• list the symptoms of toxicity.
• list some of its major food sources.
• discuss its chemical stability in relation to food preparation practices and other factors.

Key Terms

After completing section 9.1, you should be able to define and use the following terms in context:

Reading Assignment

• Chapter 12: “Vitamin A and Beta‑Carotene,” pages 392–400

Vitamin A

The family of vitamin A includes a number of naturally occurring, biologically active forms, most of which are interconvertible through a series of regulated biochemical reactions, allowing the body to maintain appropriate tissue concentrations of each. This interconvertibility is important because each form of vitamin A appears to have a specific functional role, and each appears to have equal nutritional value. Forms of vitamin A include retinol, retinal, retinoic acid, and beta‑carotene. Collectively, retinol, retinal, and retinoic acid are known as retinoids.

• Retinol, the parent compound of the vitamin A group, is the alcohol form that serves as the major transport form of vitamin A in plasma. When combined with long‑chain fatty acids to form retinyl esters (e.g., retinyl palmitate), this compound becomes the major storage form of vitamin A in liver and other tissues. Retinyl esters are also the main form of vitamin A present in foods of animal origin.
• Retinal (also called retinaldehyde) is the aldehyde form used by the body in the visual process.
• Retinoic acid is the acid form that functions in cellular differentiation during growth; its presence in food is minimal.
• Beta‑carotene, a carotenoid, is a vitamin A precursor found in plants. Carotenoids are a group of red, orange, or yellow pigments, found primarily in foods of plant origin. Of the 600 (approximate) carotenoids in nature, only 50 can be converted into vitamin A; of these, only 10 have any nutritional significance. The carotenoid with the greatest vitamin A activity is beta‑carotene. Most carotenoids can combine with singlet oxygen (O) and serve as antioxidants under certain conditions. Such characteristics are not present in retinol.

Functions

Vitamin A has many roles. It is involved in vision, epithelial tissue development and maintenance, immunity, bone growth and development, and tooth development.

Vision: The best-known function of vitamin A is its involvement in the visual process, described on page 393–394. Retinal is required in the retina to combine with the protein opsin to form iodopsin (the visual pigment of the cone cells) and rhodopsin (the visual pigment of the rod cells). The cone cells are responsible for colour vision, while the rod cells are responsible for vision in dim light, and address only black and white vision. Although retinal can be regenerated to its original cis form and can recombine with opsin, repeated small losses occur—especially with rhodopsin—because sudden bright light in the dark destroys more retinal than does daylight. Consequently, night blindness (poor visual adaptation to darkness) is an early symptom of vitamin A deficiency (p. 395); it is easily reversed by supplementation.

Epithelial tissue development and maintenance: Retinoic acid is required in cellular differentiation for the development and maintenance of epithelial cells and mucus secreting cells known as goblet cells. The textbook gives a good description of the importance of soft, moist, intact mucous membranes and epithelial tissues for the prevention of infection. In vitamin A deficiency, keratin is secreted instead of mucus; as a result, the tissues become dry and hard.

Immunity: Vitamin A functions in fighting against bacterial, viral, and parasitic infections by maintaining the integrity of mucous membranes. Vitamin A also seems to be involved in the growth of the lymph glands, where antibodies are produced.

Growth and bone development: Retinoic acid is required for the differentiation of bone cells. Bone growth occurs through a balanced activity of two types of bone cells: osteoblasts (bone‑synthesizing cells) and osteoclasts (bone‑resorbing cells). Osteoblasts and osteoclasts enlarge bone through a process of simultaneous bone deposition and bone removal, a process often called bone remodelling. Faulty cell differentiation caused by a vitamin A deficiency can produce insufficient osteoclasts—bone cells with impaired enzyme function that fail to resorb the parts not needed for bone growth. As a result, stunted bone growth and thickened, abnormal bone tissue occur.

Tooth development: Through its involvement in the development of enamel‑forming epithelial cells, vitamin A also plays a role in the growth of teeth. Vitamin A deficiency may result in teeth that have a thin layer of enamel, making them susceptible to cracking, chipping, breaking, and decay.

Deficiency

Night blindness is an early stage of vitamin A deficiency. When the deficiency is more severe, it may lead to actual blindness, which is the most common cause of blindness in young children throughout the world. It is a major public health problem in many developing countries, such as parts of Asia, Latin America, and Africa, where dietary intake of vitamin A is inadequate, especially in children. Moreover, vitamin A deficiency is often associated with severe protein‑energy malnutrition (PEM), in which protein and zinc are inadequate for synthesizing the binding proteins needed to transport vitamin A throughout the body. Today we know that there are several binding proteins, each specific for a particular form of vitamin A. The major form, retinol‑binding protein (RBP), picks up retinol from the liver and transports it to various body cells. The textbook describes the connection between measles and vitamin A in children in developing countries (p. 395). Without adequate vitamin A to protect mucous membranes of the respiratory and GI tracts, measles becomes a deadly infectious disease for millions of children.

Vitamin A deficiency is rare in developed countries. The availability of fruits and vegetables, together with food fortification (e.g., milk and margarine), have made deficiency largely a thing of the past. Vitamin A deficiency, when it occurs, usually results from secondary causes, such as severe malabsorption of fat and insufficiency of bile acid, transport disorders, liver disease, and alcoholism. Symptoms of vitamin A deficiency are summarized on page 399. While actual deficiency may be quite rare, a low intake of vitamin A is found in a sizable fraction of the population of Canada (Kirkpatrick and Tarasuk, 2008).

Therapeutic Uses and Toxicity

The textbook discusses vitamin A toxicity is possible through an excessive intake of preformed vitamin A from animal sources (e.g., cod liver oil) or from supplements. Children are especially susceptible. Adolescents and adults should also be cautioned against self‑treatment of skin conditions, such as acne, with the use of over‑the‑counter oral vitamin A. In fact, supplements of vitamin A are ineffective in treating acne because they do not contain retinoic acid, the form of vitamin A effective against acne. During recent years, some vitamin A analogs (retinoids) have been tested for therapeutic use in skin disorders such as acne and psoriasis. The textbook (p. 397) identifies Accutane as an example of a synthetic analog of retinoic acid (called isotretinoin). Although effective, it is highly toxic when taken orally.

Beta‑carotene is non‑toxic; the only effect of prolonged excessive intake is hypercarotenemia. The symptom is yellowish staining of the skin, which is reversible and harmless; infants and young children are especially susceptible.

The use of vitamin A and beta‑carotene in the prevention of cancer has been an active area of research. Preformed vitamin A appears to be of very limited effectiveness in preventing cancer, and toxicity symptoms have been reported with long‑term doses as low as five to ten times the recommended levels.

Epidemiological and animal studies have shown an association between high intakes of beta‑carotene and a decreased risk of some cancers. Because beta‑carotene functions as an antioxidant, researchers hypothesized that beta‑carotene could ward off cancer through its antioxidant effect. However, several large, randomized, controlled trials have demonstrated that supplements of beta‑carotene are of no value for the prevention of cancer.

Sources

As the textbook describes, animal sources provide compounds (retinyl esters) that are easily converted to retinol in the intestine. Plant sources supply carotenoids, of which beta‑carotene is the carotenoid with the most vitamin A activity. Beta‑carotene’s absorption and conversion are less efficient than those of the retinoids. Conversion of beta‑carotene to retinol occurs in the intestine and liver.

As described on page 397, the content of vitamin A in foods is expressed as retinol activity equivalents (RAE). One microgram of retinol counts as 1 RAE, as does 12 micrograms of beta‑carotene. You should also be aware of international units (IU), an older measure of vitamin A activity. Most supplements still report vitamin A content in IU. One IU equals 0.3 micrograms of retinol or 0.3 RAE.

Plant sources of vitamin A can generally be judged by their appearance—vitamin A content is proportional to colour intensity. Dark green leafy vegetables and deep orange or yellow vegetables are usually rich sources of beta‑carotene. Canada’s Food Guide recommends consuming such foods daily. Some examples of rich food sources of vitamin A are given in Figure 12‑8 on page 398.

The major sources of vitamin A in the Canadian diet are deeply coloured fruits and vegetables, dairy products, butter, margarine, and eggs.

Stability

Little vitamin A is lost in normal food preparation. The only method of food processing that significantly affects vitamin A content is the removal of fat from such foods as milk. However, such foods are fortified with vitamin A, making the low‑fat products equivalent to the full‑fat ones in vitamin A content.

Vitamin A is sensitive to oxidation by air in the presence of light. Oxidation of fats and oils that contain fortified vitamin A can destroy fat‑soluble vitamins, including vitamin A. vitamin E, an antioxidant, can protect vitamin A.

Study Questions

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9.2 Vitamin E

Introduction

Tocopherol, the name of the family of vitamin E compounds, comes from the Greek word tokos, meaning offspring. The name was given because vitamin E was first recognized as an antisterility vitamin in both male and female rats.

Although vitamin E is identified as essential, its role in human nutrition is not yet fully understood. Despite the relative lack of knowledge, vitamin E is very popular as a supplement for a variety of ailments.

Objectives

After completing this section, you should be able to

• identify vitamin E’s function in the body as an antioxidant.
• describe its deficiency symptoms.
• discuss the claims of benefits for the use of supplements and the possible toxicity symptoms.
• list some of the major food sources for vitamin E.
• discuss its chemical stability to food preparation practices and other factors.

Key Terms

After completing section 9.2, you should be able to define and use the following terms in context:

Reading Assignment

• Chapter 12: “Vitamin E,” pages 400–401

Vitamin E

Functions

The accepted role of vitamin E is that of an antioxidant, which prevents the formation of free radicals (unstable molecules containing unpaired electrons) and the cell damage they can cause. Vitamin E functions in this way because it is oxidized instead of the polyunsaturated fatty acids or other vulnerable components of the cell and its membrane. The oxidized vitamin E loses its antioxidant activity and is excreted as a harmless compound in the bile.

Deficiency

Vitamin E deficiency produces many different symptoms, indicating that it may function in ways other than as an antioxidant.

Vitamin E deficiency is rarely seen in humans except in premature infants, who lack the ability to absorb the vitamin and are born with low stores. The symptom shown by such infants is increased capillary fragility, resulting in hemolytic anemia, a condition in which red blood cells rupture easily and spill their contents into the plasma. Low vitamin E levels in such infants probably allow the oxidation of polyunsaturated fatty acids (PUFA) in red blood cell membranes. Hemolytic anemia can be worsened by iron supplements—routinely given to premature infants—and by a high PUFA intake, once common in infant formula. Iron tends to accelerate the oxidation of vitamin E, and a high PUFA intake increases the requirement for vitamin E. The composition of formula for premature infants has now been changed to correct these problems, including the provision of adequate vitamin E; therefore, hemolytic anemia should no longer be a problem.

Primary vitamin E deficiency is rarely seen in human adults because body stores are extensive and the vitamin is widely available. However, secondary vitamin E deficiency may develop as a result of serious fat malabsorption syndromes resulting from liver, pancreatic, or gallbladder disease in infants, children, or adults.

Claims of Benefits and Toxicity

Contrary to what the textbook suggests (page 400), intervention studies have provided weak evidence (at best) that high‑dose supplements of vitamin E are of preventive value against heart disease or cancer. Research has also discredited claims that vitamin E improves physical or sexual performance, and delays the aging process. However, many people still take vitamin E supplements for all kinds of reasons—often in large doses.

Vitamin E is considered the least toxic of the fat‑soluble vitamins because absorption decreases rapidly with increased intake. However, although toxicity is rare, some signs of toxicity are now suspected. The tolerable upper intake level is 1000 milligrams. What is almost certainly a much more serious problem than actual toxicity is an increased risk of mortality. Long‑term randomized studies have reported that persons taking vitamin E supplements have a risk of death roughly 5–6% higher than subjects given a placebo (Bjelakovic et al., 2012).

Sources

As the textbook mentions, the need for vitamin E is directly proportional to the PUFA content of the diet. Fortunately, foods high in PUFA are usually high in vitamin E. Vitamin E is widespread in foods of plant origin; vegetable oils are its chief dietary source. Wheat germ oil is an especially rich source.

The vitamin E content of white bread is much lower than that of whole wheat bread. A diet consisting of fresh, unprocessed, or minimally processed foods contains considerably more vitamin E than one rich in processed and convenience foods.

Many people consume a diet with an inadequate content of polyunsaturated fats (especially omega‑3 fatty acids) in which vitamin E is often well below the RDA. For this reason, people should include some vegetable oils, such as canola and soybean oils (e.g., in soft margarine or salad dressing), in the diet. The recommendation in Canada’s Food Guide to consume a small amount of unsaturated fat each day helps to ensure that vitamin E intakes are adequate.

Stability

Vitamin E is easily destroyed by intense heating and by exposure to oxygen; thus, deep fat frying will significantly reduce the vitamin E content of both the oil used for frying and the fried food itself. Oxidation of vitamin E in foods can occur through improper storage and handling. For example, food frozen for a long time at an insufficiently low temperature may lose some of its vitamin E. The major loss of vitamin E occurs through the milling of grains.

Study Questions

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9.3 Vitamin C

Introduction

Vitamin C is also known as ascorbic acid. Ascorbic means “without scurvy.” Foods containing vitamin C were discovered to be essential in preventing and curing scurvy. Today, vitamin C is probably the best known and most controversial of all the vitamins. Linus Pauling’s 1970 book, Vitamin C and the Common Cold, popularized the use of megadoses of vitamins to cure or prevent diseases. Since then, vitamin C has been the most commonly taken single vitamin supplement, based on claims that it cures or prevents flu, colds, cold sores, cancer, atherosclerosis, arthritis, and allergies.

Objectives

After completing this section, you should be able to

• describe/discuss the following aspects related to vitamin C:
  • Identify its functions in the body.
  • Describe its deficiency and toxicity symptoms.
  • Describe factors that may influence requirements.
  • List some of its major food sources.
  • Discuss its chemical stability with respect to food preparation practices and other factors.
  • Discuss the controversies associated with its use.

Key Terms

After completing section 9.3, you should be able to define and use the following terms in context:

Reading Assignment

• Chapter 12: “Vitamin C,” pages 402–406

Vitamin C

Vitamin C is a hexose derivative (resembling a 6‑carbon monosaccharide).

Functions

Vitamin C has multiple functions in the body. Its central role is in oxidation‑reduction reactions.

Vitamin C acts as an antioxidant; it is able to donate hydrogen atoms (or electrons) to other molecules, thus acting as a reducing agent. It can also donate hydrogen atoms to oxygen molecules to form water. Without antioxidation, oxygen radicals (electrically charged oxygen, which is highly reactive) can cause extensive damage by oxidizing (inactivating) essential body compounds.

Collagen is the protein substance that holds cells together in the formation of connective tissue, cartilage, bones, teeth, skin, and tendons. The most abundant amino acid in collagen is proline, which must be hydroxylated to form hydroxyproline during collagen synthesis. The hydroxylase enzyme involved in this reaction requires vitamin C and ferrous iron (Fe++). Vitamin C serves to protect the iron from being oxidized to the ferric form (Fe+++); otherwise, hydroxylation does not occur.

Vitamin C also helps in iron absorption by reducing ferric iron (Fe+++) to ferrous iron (Fe++). The ferrous form is more readily absorbed by the body. Vitamin C also acts as a chelating agent, combining with ferrous iron to form a complex for iron storage. This storage form is resistant to oxidation.

Vitamin C participates in the conversion of some amino acids to essential body compounds:

• synthesis of epinephrine and norepinephrine, the stress hormones
• synthesis of thyroxin in the regulation of the BMR
• hydroxylation of tryptophan to serotonin, a neurotransmitter

Vitamin C contributes to the activation of folate by donating hydrogen atoms to convert folate to THF (tetrahydrofolate), its primary coenzyme form.

Vitamin C inhibits the conversion of nitrates and nitrites (food preservatives) to the carcinogenic nitrosamines.

Deficiency

Although uncommon, vitamin C deficiency is likely to occur in people who consume little or no fruit and vegetables. Susceptible groups are the elderly, alcoholics, infants consuming cow’s milk exclusively, and the severely ill. The average body pool of vitamin C is about 1500 mg, concentrated mainly in the adrenal glands and in the leucocytes (white blood cells). Early deficiency symptoms can occur during the first month of deprivation. The first physical signs are usually non‑specific, such as fatigue, weakness, shortness of breath, muscle cramps, aching bones and joints, and loss of appetite. As tissue saturation drops to about 20%, specific clinical symptoms of scurvy start to appear (see p. 404).

Toxicity

The possible health hazards of high vitamin C intake (supplements of over two grams per day) include

• nausea, abdominal cramps, and diarrhea. Ascorbic acid in the large intestine has an osmotic effect.
• interference with the testing of urinary glucose. The chemical resemblance between ascorbic acid and glucose is close. Thus, people consuming high doses of ascorbic acid can test positive for urine glucose.
• blood cell breakage, especially in certain racial groups.
• rebound scurvy. When high intakes of vitamin C are suddenly stopped, a deficiency may occur—probably caused by the body’s adaptation to a high rate of vitamin C intake.

It is important to keep these possible hazards in perspective. With the exception of nausea, abdominal cramps, and diarrhea, very few people actually suffer side effects from high vitamin C intake, even at intakes of one to two grams per day. At doses above 200 mg per day, the body has limited absorption, and blood concentration of vitamin C does not increase.

Increased Needs

Several conditions increase an individual’s requirement for vitamin C:

• smoking. Cigarette smokers show reduced plasma and leucocyte levels of vitamin C. Thirty‑five mg over the RDA is recommended for smokers.
• severe physical trauma, such as burns or surgery. A moderate increase in vitamin C intake may enhance the healing process because of the vitamin’s role in collagen formation. Infections may also increase vitamin C requirements.
• severe emotional or environmental (temperature) stress. As we have seen, vitamin C functions in the synthesis of the stress hormones, epinephrine and norepinephrine, in the adrenal glands.
• drug intake. Use of oral contraceptives, aspirin, barbiturates, sulphonamides, and tetracycline seems to increase excretion of vitamin C.

In conditions requiring extra vitamin C, the increase in vitamin C intake should not depend on vitamin C tablets. A diet rich in vitamin C from foods is the ideal way to provide the additional intake. Eating such foods also ensures a good supply of many other nutrients.

Sources

Dietary vitamin C comes almost exclusively from fruit and vegetables. As indicated in Figure 12‑12 on page 405, citrus fruits (e.g., oranges, grapefruit), strawberries, kiwis, broccoli, bell peppers, and brussels sprouts are excellent sources. Other good sources include papayas, tomatoes, potatoes, and mangos.

In Canada, several types of fruit juice are fortified with vitamin C as well as all the canned and powdered fruit drinks. Note that although fruit drinks may contain added vitamin C, they contain none of the other vitamins and minerals that natural juices contain.

Stability

Vitamin C is one of the vitamins most vulnerable to destruction. As does any water‑soluble vitamin, it dissolves readily in water during cooking. It is easily oxidized, especially in the presence of alkali, copper, or iron; copper and iron cookware therefore cause loss of vitamin C. It is also sensitive to heat. The following are some practical suggestions for conserving vitamin C and most water‑soluble nutrients in foods.

• Buy fresh fruits and vegetables in small quantities so that they can be used within a few days. Vitamin C is synthesized by enzymes in the fruit or vegetable. After harvest, the enzymes cease to function, and degradation of the vitamin begins. Refrigeration slows down the degrading process.
• Exposure to air speeds up the oxidation of vitamin C. Fruit and vegetables should therefore be cut up just before cooking or serving.
• Cook foods in as small a quantity of water as possible and for as short a time as is feasible. Steaming, baking, and microwaving are excellent ways of conserving vitamins and are preferable to boiling. Prolonged heating, such as occurs in steam tables in cafeterias or buffets, can reduce ascorbic acid content by as much as 50%. Consume food as soon as possible after cooking.
• The addition of baking soda to cooking water to soften tough vegetables and to enhance the colour is very destructive to vitamin C as well as to many of the B vitamins, especially thiamin.
• Quick freezing of food protects vitamins. Frozen vegetables should be cooked directly from the frozen state, rather than thawed first.
• Juices are best prepared fresh. They should be stored in a container with a tight lid, in a refrigerator. Even then, there may be much loss of vitamin C (and phytochemicals).

Controversies

The prophylactic (disease preventing) and therapeutic uses of vitamin C in cardiovascular disease, the common cold, flu, and cancer are highly controversial.

1. Common cold and flu: Dr. Linus Pauling made the claim around 1970 that very high doses of vitamin C can prevent and cure the common cold and flu. Clinical trials have proven that the effect of vitamin C on colds—if any—is small. Still, vitamin C is widely used in the belief that it can produce a modest reduction in duration and/or severity of the symptoms of the common cold. The weight of published evidence suggests that megadoses of vitamin C for preventing/treating the common cold is unjustified (Douglas et al., 2007). This meta‑analysis included 30 clinical trials involving 11,350 study participants taking at least 200 mg of vitamin C per day in placebo‑controlled studies. An 8% reduction in cold duration and no difference in severity of symptoms was observed. The authors of the study concluded that there is no justification for the general community to routinely use large doses of vitamin C to treat the common cold.
2. Cardiovascular disease (CVD): There are various hypotheses about the possible benefit of vitamin C supplementation in CVD. Collagen synthesis, vital in maintaining the integrity of the vascular walls, is dependent on vitamin C. Any injury to the intima (innermost layer) of the arterial walls can allow cholesterol and other lipids to be deposited, causing atherosclerotic plaque. However, there is no good evidence that supplements of vitamin C are effective for prevention or therapy.
3. Cancer: It has been speculated that vitamin C is protective against cancer, partly because of the function of vitamin C in inhibiting the formation of carcinogenic nitrosamines from nitrites in foods. Nitrates are naturally present in many fruits and vegetables, including carrots and beets. Nitrites are found in drinking water and human saliva. Even if we eat no foods preserved with nitrite, a significant amount is still present in our body, generated from nitrates. Vitamin C prevents this process.

Nevertheless, we can presume that with fewer nitrosamines, there is a reduced hazard. Therefore, the recommended practices are to

• use processed or cured meats with nitrites moderately or not at all.
• avoid overcooking meats, especially bacon, because it enhances nitrosamine formation.

include a sufficient intake of vitamin C on a daily basis, and consume some vitamin C source (e.g., orange juice) when eating nitrite‑containing foods. However, beyond this specific process, there is essentially no evidence that vitamin C is of any general value in the prevention of cancer.

Study Questions

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Antioxidant Vitamins—Summary

This unit has looked at three major antioxidants obtained from the diet: beta‑carotene and vitamins E and C. These three nutrients have much in common, aside from being antioxidants. Many epidemiological studies have shown that intake is inversely associated with risk of different diseases. In particular, a diet rich in beta‑carotene and vitamin C is associated with a lower risk of cancer. Oxidative damage is believed to play a role in the process leading to both cancer and atherosclerosis and so it has been proposed that these substances protect against these diseases. For many years, it was widely believed that beta‑carotene and vitamin C are protective against cancer, while vitamins E and C were thought to protect against atherosclerosis (and, therefore, against heart disease).

As discussed in this unit, several large, controlled trials have been carried out over the past 30 years to learn more about the effects of the antioxidant vitamins. In a typical trial, several thousand people would be randomized to one of two groups, and they would receive either an antioxidant or a placebo. Subjects were then monitored for several years to determine how many in each group developed cancer or heart disease. The major trials investigated whether beta‑carotene prevents cancer and whether vitamin E prevents heart disease. With few exceptions, findings were completely negative. An especially important finding indicated that supplements of the three antioxidants appeared to do more harm than good: people taking them increased their risk of death by roughly 5–6% over subjects given a placebo (Bjelakovic et al., 2012).

Based on these findings we can draw the following conclusions:

• Supplementation of antioxidant nutrients is probably of no benefit and may even be harmful.
• Supplementation of single antioxidants is unlikely to block the process of oxidative damage to tissues, which is of importance in causing disease.
• A combination of substances prevents disease. A diet rich in antioxidant nutrients, such as beta‑carotene and vitamin C, is also rich in a great many other substances, such as folate, dietary fibre, and thousands of different phytochemicals (non‑nutrient substances found in plants that have biological activity in the body). Combined, these substances are thought to prevent disease.
• The most appropriate dietary advice for the prevention of cancer and heart disease is to eat a healthy diet—one that has a generous content of fruit and vegetables.

References