Chapter 10.2

10.2The B Vitamins

LO 10.2

Identify the main roles, deficiency symptoms, and food sources for each of the B vitamins.

Despite supplement advertisements that claim otherwise, the vitamins do not provide the body with fuel. It is true, though, that without B vitamins the body would lack energy. The energy-yielding nutrients—carbohydrate, fat, and protein—are used for fuel; the B vitamins enable the body to use that fuel. Several of the B vitamins—thiamin, riboflavin, niacin, biotin, and pantothenic acid—form part of the coenzymes that assist enzymes in the release of energy from carbohydrate, fat, and protein. Other B vitamins play other indispensable roles in metabolism. Vitamin B6 assists enzymes that metabolize amino acids. Folate and vitamin B12 help cells to multiply. Among these cells are the red blood cells and the cells lining the GI tract—cells that deliver energy to all the others.

The vitamin portion of a coenzyme allows a chemical reaction to occur; the remaining portion of the coenzyme binds to the enzyme. Without its coenzyme, an enzyme cannot function. Thus symptoms of B vitamin deficiencies directly reflect the disturbances of metabolism caused by a lack of coenzymes. Figure 10-2 illustrates coenzyme action.

Figure 10-2Coenzyme Action

Some vitamins form parts of the coenzymes that enable enzymes either to dismantle compounds (as illustrated by the upper enzymes) or to synthesize compounds (as illustrated by the lower enzymes in this figure).

Coenzyme Action

Watch the animation and check your understanding about coenzyme action.

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The following sections describe the individual B vitamins, including their roles as coenzymes in metabolic pathways. Keep in mind that a later discussion assembles these pieces of information into a whole picture. The following sections also present the recommendations, deficiency and toxicity symptoms, and food sources for each vitamin.

Thiamin

Thiamin is the vitamin part of the coenzyme TPP (thiamin pyrophosphate) that assists in energy metabolism. The TPP coenzyme participates in the conversion of pyruvate to acetyl CoA (as Chapter 7 describes). Recall how important this step is in allowing carbohydrate metabolism to proceed through the TCA cycle, thus producing much more ATP than during glycolysis alone. The reaction removes 1 carbon from the 3-carbon pyruvate to make the 2-carbon acetyl CoA and carbon dioxide . In a similar step in the TCA cycle, TPP helps convert a 5-carbon compound to a 4-carbon compound. Besides playing these pivotal roles in energy metabolism, thiamin occupies special sites on the membranes of nerve cells. Consequently, nerve activity (and muscle activity in response to nerves) depend on thiamin.

Thiamin Recommendations

The thiamin RDA is based primarily on its role in enzyme activity. Generally, thiamin needs will be met if a person eats enough food to meet energy needs—if that energy comes from nutritious foods. The average thiamin intake in the United States meets or exceeds recommendations.

Thiamin Deficiency and Toxicity

People who fail to eat enough food to meet energy needs risk nutrient deficiencies, including thiamin deficiency. Inadequate thiamin intakes have been reported among the nation’s malnourished and homeless population. Similarly, people who derive most of their energy from empty-kcalorie foods and beverages risk thiamin deficiency. Alcohol provides a good example of how empty kcalories can lead to thiamin deficiency. Alcohol contributes energy but provides few, if any, nutrients and often displaces food. In addition, alcohol impairs thiamin absorption and hastens thiamin excretion in the urine, doubling the risk of deficiency. An estimated four out of five people who abuse alcohol have a thiamin deficiency, which damages the brain and impairs its function.

Prolonged thiamin deficiency can result in the disease beriberi, which was first observed in Indonesia when the custom of polishing rice became widespread. Rice provided 80 percent of the energy intake of the people of that area, and the germ and bran of the rice grain was their principal source of thiamin. When the germ and bran were removed in the preparation of white rice, beriberi became rampant.

Beriberi is often described as “dry” or “wet.” Dry beriberi reflects damage to the nervous system and is characterized by muscle weakness in the arms and legs. Wet beriberi reflects damage to the cardiovascular system and is characterized by dilated blood vessels, which cause the heart to overwork and the kidneys to retain salt and water, resulting in edema. Typically, both types of beriberi appear together, with one set of symptoms predominating. Figure 10-3 displays the edema of beriberi. No adverse effects have been associated with excesses of thiamin, and no UL has been determined.

Figure 10-3Thiamin-Deficiency Symptom—The Edema of Beriberi

Physical examination confirms that this person has wet beriberi. Notice how the impression of the physician’s thumb remains on the foot.

PA Images/Alamy Stock Photo

Thiamin Food Sources

Before examining Figure 10-4, you may want to read How To 10-1, which describes the content in this and similar figures found in this chapter and the next three chapters. When you look at Figure 10-4, notice that thiamin occurs in small quantities in many nutritious foods. The long red bar near the bottom of the graph shows that meats in the pork family are exceptionally rich in thiamin (see Photo 10-2). Yellow bars confirm that grains—whole grains or enriched—are a reliable source of thiamin.

Figure 10-4Thiamin in Selected Foods

Many different foods contribute some thiamin, but few are rich sources. Together, several servings of a variety of nutritious foods will help meet thiamin needs. Grain selections should be either whole grain or enriched. See How To 10-1 for more information on using this figure.

How To 10-1

Evaluate Foods for Their Nutrient Contributions

Figure 10-4 is the first of a series of figures in this and the next three chapters that present the vitamins and minerals in foods. Each figure presents the same 24 foods, which were selected to ensure a variety of choices representative of each of the food groups as suggested by the USDA Food Patterns. For example, a bread, a cereal, and a pasta were chosen from the grain group. The suggestion to include a variety of vegetables was also considered: dark green vegetables (broccoli); orange and red vegetables (carrots); starchy vegetables (potatoes); legumes (pinto beans); and other vegetables (tomato juice). The selection of fruits followed suggestions to use whole fruits (bananas); citrus fruits (oranges); melons (watermelon); and berries (strawberries). Items were selected from the milk group and protein foods in similar ways. In addition to the 24 foods that appear in all of the figures, three different foods were selected for each of the nutrients to add variety and often reflect excellent, and sometimes unusual, sources.

Notice that the figures list the food, the serving size, and the food energy (kcalories) on the left. The amount of the nutrient per serving is presented in the graph on the right along with the RDA (or AI) for adults, so you can see how many servings would be needed to meet recommendations.

The colored bars show at a glance which food groups best provide a nutrient (see the color key below). Because the USDA Food Patterns include legumes with both the protein foods group and the vegetable group and because legumes are especially rich in many vitamins and minerals, they have been given their own color to highlight their nutrient contributions.

Notice how the bar graphs shift in the various figures. Careful study of all of the figures taken together will confirm that variety is the key to nutrient adequacy.

Another way to evaluate foods for their nutrient contributions is to consider their nutrient density (their thiamin per 100 kcalories, for example). Quite often, vegetables rank higher on a nutrient-per-kcalorie list than they do on a nutrient-per-serving list (see Compare Foods Based on Nutrient Density to review how to evaluate foods based on nutrient density). The left column in the figure highlights about five foods that offer the highest nutrient density. Notice how many are vegetables.

Realistically, people cannot eat for single nutrients. Fortunately, most foods deliver more than one nutrient, allowing people to combine foods into nourishing meals.

Try It

• Calculate which food provides more riboflavin per 1-ounce serving—a pork chop (3 oz, 291 kcal, 0.25 mg riboflavin) or cheddar cheese (1½ oz, 165 kcal, 0.11 mg riboflavin). Which food is more nutrient-dense with respect to riboflavin?

How to: Evaluate Foods for Their Nutrient Contributions

Know how to read charts and graphs on evaluating foods for the nutritional contributions.

Copyright © Cengage Learning.

How to: Evaluate Foods for Their Nutrient Contributions

Know how to read charts and graphs on evaluating foods for the nutritional contributions.

Copyright © Cengage Learning.

As mentioned earlier, prolonged cooking can destroy thiamin. Also, like all water-soluble vitamins, thiamin leaches into water when foods are boiled or blanched. Cooking methods that require little or no water such as steaming and microwave heating conserve thiamin and other water-soluble vitamins.

Review Thiamin

Thiamin assists in energy metabolism as part of the coenzyme TPP. Many nutritious foods contain thiamin, with pork being an exceptionally good source. Thiamin deficiency results in beriberi. The accompanying table provides a review of thiamin facts.

Photo 10-2

Pork is the richest source of thiamin, but enriched or whole-grain products typically make the greatest contribution to a day’s intake because of the quantities eaten. Legumes such as black beans are also valuable sources of thiamin.

Angel Tucker

Riboflavin

Like thiamin, riboflavin serves as a coenzyme in many reactions, most notably in energy metabolism. The coenzyme forms of riboflavin are FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide); both can accept and then donate two hydrogens (see Figure 10-5). During energy metabolism, FAD picks up two hydrogens (with their electrons) from the TCA cycle and delivers them to the electron transport chain (as Chapter 7 describes).

Figure 10-5Riboflavin Coenzyme, Accepting and Donating Hydrogens

This figure shows the chemical structure of the riboflavin portion of the coenzyme only; the remainder of the coenzyme structure is represented by dotted lines (see Appendix C for the complete chemical structures of FAD and FMN). The reactive sites that accept and donate hydrogens are highlighted in white.

Riboflavin Recommendations

Like thiamin’s RDA, riboflavin’s RDA is based primarily on its role in enzyme activity. Most people in the United States meet or exceed riboflavin recommendations.

Riboflavin Deficiency and Toxicity

Lack of riboflavin causes inflammation of the membranes of the mouth, skin, eyes, and GI tract. Excess riboflavin appears to cause no harm, and no UL has been established.

Riboflavin Food Sources

The greatest contributions of riboflavin come from milk and milk products (see Photo 10-3 and Figure 10-6). Whole-grain or enriched grains are also valuable sources because of the quantities people typically consume. When riboflavin sources are ranked by nutrient density, many dark green, leafy vegetables (such as broccoli, turnip greens, asparagus, and spinach) appear high on the list.

Figure 10-6Riboflavin in Selected Foods

Milk and milk products (blue) are noted for their riboflavin. Several servings are needed to meet recommendations. See How To 10-1 for more information on using this figure.

Ultraviolet light destroys riboflavin. For this reason, milk is sold in cardboard or opaque plastic containers, instead of clear glass bottles. In contrast, riboflavin is stable to heat, so cooking does not destroy it.

Review Riboflavin

The coenzyme forms of riboflavin (FAD and FMN) participate in energy metabolism. Milk and milk products are notable riboflavin sources. The accompanying table provides a review of riboflavin facts.

Photo 10-3

All of these foods are good sources of riboflavin. Milk and milk products provide most of the riboflavin in people’s diets, followed by whole-grain and fortified or enriched breads and cereals.

Angel Tucker

Riboflavin

Like thiamin, riboflavin serves as a coenzyme in many reactions, most notably in energy metabolism. The coenzyme forms of riboflavin are FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide); both can accept and then donate two hydrogens (see Figure 10-5). During energy metabolism, FAD picks up two hydrogens (with their electrons) from the TCA cycle and delivers them to the electron transport chain (as Chapter 7 describes).

Figure 10-5Riboflavin Coenzyme, Accepting and Donating Hydrogens

This figure shows the chemical structure of the riboflavin portion of the coenzyme only; the remainder of the coenzyme structure is represented by dotted lines (see Appendix C for the complete chemical structures of FAD and FMN). The reactive sites that accept and donate hydrogens are highlighted in white.

Riboflavin Recommendations

Like thiamin’s RDA, riboflavin’s RDA is based primarily on its role in enzyme activity. Most people in the United States meet or exceed riboflavin recommendations.

Riboflavin Deficiency and Toxicity

Lack of riboflavin causes inflammation of the membranes of the mouth, skin, eyes, and GI tract. Excess riboflavin appears to cause no harm, and no UL has been established.

Riboflavin Food Sources

The greatest contributions of riboflavin come from milk and milk products (see Photo 10-3 and Figure 10-6). Whole-grain or enriched grains are also valuable sources because of the quantities people typically consume. When riboflavin sources are ranked by nutrient density, many dark green, leafy vegetables (such as broccoli, turnip greens, asparagus, and spinach) appear high on the list.

Figure 10-6Riboflavin in Selected Foods

Milk and milk products (blue) are noted for their riboflavin. Several servings are needed to meet recommendations. See How To 10-1 for more information on using this figure.

Ultraviolet light destroys riboflavin. For this reason, milk is sold in cardboard or opaque plastic containers, instead of clear glass bottles. In contrast, riboflavin is stable to heat, so cooking does not destroy it.

Review Riboflavin

The coenzyme forms of riboflavin (FAD and FMN) participate in energy metabolism. Milk and milk products are notable riboflavin sources. The accompanying table provides a review of riboflavin facts.

Photo 10-3

Biotin

Biotin plays a critical role in the TCA cycle: biotin delivers a carbon to 3-carbon pyruvate, thus replenishing oxaloacetate, the 4-carbon compound needed to combine with acetyl CoA to keep the TCA cycle turning (review Step 6 in Figure 7-12). The biotin coenzyme also participates in gluconeogenesis, fatty acid synthesis, and the breakdown of amino acids.

Biotin Recommendations

Biotin is needed in very small amounts. Because there is insufficient research on biotin requirements, an AI has been determined, instead of an RDA.

Biotin Deficiency and Toxicity

Biotin deficiencies rarely occur. Researchers can induce a biotin deficiency in animals or human beings by feeding them raw egg whites, which contain a protein that binds biotin and thus prevents its absorption. Biotin-deficiency symptoms include skin rash, hair loss, and neurological impairment. More than two dozen raw egg whites must be consumed daily for several months to produce these effects; cooking eggs denatures the binding protein. Because no adverse effects have been reported from high biotin intakes, a UL has not been set.

Biotin Food Sources

Biotin is widespread in foods (including egg yolks), so eating a variety of foods protects against deficiencies. Some biotin is also synthesized by GI tract bacteria, but this amount does not contribute much to the biotin absorbed.

Review Biotin

Biotin is critical in supporting the TCA cycle. Because it is widespread in foods, deficiencies are rare. The accompanying table provides a review of biotin facts.

Pantothenic Acid

Pantothenic acid is part of the chemical structure of coenzyme A—the same CoA that forms acetyl CoA, a key compound in several metabolic pathways featured in Chapter 7, including the TCA cycle. (Appendix C presents the chemical structures of these two molecules and shows that coenzyme A includes pantothenic acid as part of its structure.) It is involved in more than 100 different steps in the synthesis of lipids, neurotransmitters, steroid hormones, and hemoglobin.

Pantothenic Acid Recommendations

An AI for pantothenic acid has been set. It reflects the amount needed to replace daily losses.

Pantothenic Acid Deficiency and Toxicity

Pantothenic acid deficiency is rare. Its symptoms involve a general failure of all the body’s systems and include fatigue, GI distress, and neurological disturbances. The “burning feet” syndrome that affected prisoners of war in Asia during World War II is thought to have been caused by pantothenic acid deficiency. No toxic effects have been reported, and no UL has been established.

Pantothenic Acid Food Sources

Pantothenic acid is widespread in foods, and typical diets seem to provide adequate intakes. Beef, poultry, whole grains, potatoes, tomatoes, and broccoli are particularly good sources. Losses of pantothenic acid during food production can be substantial because it is readily destroyed by the freezing, canning, and refining processes.

Review Pantothenic Acid

Pantothenic acid is part of coenzyme A, central to many metabolic pathways. Because it is widespread in foods, deficiencies are rare. The accompanying table provides a review of pantothenic acid facts.

Vitamin B6

Vitamin occurs in three forms—pyridoxal, pyridoxine, and pyridoxamine. All three can be converted to the coenzyme PLP (pyridoxal phosphate), which is active in more than 100 reactions, including many in carbohydrate, fatty acid, and amino acid metabolism. By using PLP to transfer amino groups from an amino acid to a keto acid, the body can make nonessential amino acids (review Figure 6-11). The ability to add and remove amino groups makes PLP valuable in protein and urea metabolism as well. The conversions of the amino acid tryptophan to niacin or to the neurotransmitter serotonin also depend on PLP. In addition, PLP participates in the synthesis of heme (the nonprotein portion of hemoglobin), nucleic acids (such as DNA and RNA), and lecithin (a phospholipid).

Vitamin B6 Recommendations

The RDA for vitamin B6 is based on the amounts needed to maintain adequate levels of its coenzymes. Unlike other water-soluble vitamins, vitamin B6 is stored primarily in muscle tissue. Research does not support claims, however, that large doses of vitamin B6 enhance muscle strength or physical endurance.

Vitamin B6 Deficiency

Without adequate vitamin B6, synthesis of key neurotransmitters diminishes, and abnormal compounds produced during tryptophan metabolism accumulate in the brain. Early symptoms of vitamin B6 deficiency include depression and confusion; advanced symptoms include abnormal brain wave patterns and convulsions.

Alcohol abuse contributes to the destruction and loss of vitamin B6 from the body. As Highlight 7 describes, when the body breaks down alcohol, it produces acetaldehyde. If allowed to accumulate, acetaldehyde dislodges the PLP coenzyme from its enzymes. Once loose, PLP breaks down and is excreted.

Vitamin B6 Toxicity

The first major report of vitamin B6 toxicity appeared in the early 1980s. Until that time, most researchers and dietitians believed that, like the other water-soluble vitamins, vitamin B6 could not reach toxic concentrations in the body. The report described neurological damage in people who had been taking more than 2 grams of vitamin B6 daily (20 times the current UL of 100 milligrams per day) for 2 months or more.

Vitamin B6 Food Sources

As you can see from the colors in Figure 10-9, meats, fish, and poultry (red bars), potatoes and a few other vegetables (green bars), and fruits (purple bars) offer vitamin B6 (see Photo 10-5). Several servings of vitamin B6 –rich foods are needed to meet recommended intakes.

Figure 10-9Vitamin in Selected Foods

Many foods—including vegetables, fruits, and protein foods—offer vitamin B6. Variety helps a person meet vitamin needs. See How To 10-1 for more information on using this figure.

Foods lose vitamin B6 when heated. Information is limited, but vitamin B6 bioavailability from plant-derived foods seems to be lower than from animal-derived foods.

Review Vitamin B6

The vitamin coenzyme PLP participates in numerous reactions, perhaps most notably in amino acid metabolism. The accompanying table provides a review of vitamin facts.

Folate

Folate, also known as folacin or folic acid, has a chemical name that would fit a flying dinosaur: pteroylglutamic acid (PGA for short). Its primary coenzyme form, THF (tetrahydrofolate), serves as part of an enzyme complex that transfers 1-carbon compounds that arise during metabolism. This action converts vitamin B12 to one of its coenzyme forms, synthesizes the DNA required for all rapidly growing cells, and regenerates the amino acid methionine from homocysteine.

Figure 10-10 illustrates two forms of folate. It shows that folate in fortified foods and supplements is in its monoglutamate form (containing only one glutamate), whereas naturally occurring folate in foods contains up to six glutamates (known as a polyglutamate). During digestion, enzymes hydrolyze polyglutamate to monoglutamate and several single glutamates. The monoglutamate is then attached to a methyl group , which inactivates folate for storage in the liver and other cells. To activate folate, the methyl group must be removed by an enzyme that requires vitamin B12 . Without that help, folate remains trapped in its methyl form, unavailable to support DNA synthesis and cell growth. Figure 10-11 summarizes these actions.

Figure 10-10Forms of Folate

Chemically known as pteroylglutamic acid, folate consists of a ring structure (called a pteroyl) and one to six molecules of glutamate (an amino acid). (See Appendix C for the complete chemical structure.)

Figure 10-11Folate’s Absorption and Activation

The liver incorporates excess folate into bile that is then sent to the gallbladder and GI tract. Thus folate travels in the same enterohepatic circulation as bile (review Figure 5-14).

This complicated system for handling folate is vulnerable to GI tract injuries. Because folate is actively secreted back into the GI tract with bile, it can be reabsorbed repeatedly. If the GI tract cells are damaged, folate deficiency rapidly develops and, ironically, further damages the GI tract. Remember, folate is active in cell multiplication—and the cells lining the GI tract are among the most rapidly replaced cells in the body. When unable to make new cells, the GI tract deteriorates and absorption of all nutrients diminishes.

Folate Recommendations

The bioavailability of folate varies depending on the source, and these variations must be considered when establishing folate recommendations. The DRI committee gives naturally occurring folate from foods (polyglutamates) full credit. Synthetic folate from fortified foods and supplements (monoglutamates) is given extra credit because, on average, it is 1.7 times more available than naturally occurring food folate. Thus a person consuming 100 micrograms of folate from foods and 100 micrograms from a supplement (multiplied by 1.7) receives 270 dietary folate equivalents (DFE). The need for folate rises considerably during pregnancy and whenever cells are multiplying, so the recommendations for pregnant women are considerably higher than for other adults.

Folate and Neural Tube Defects

The brain and spinal cord develop from the neural tube, and defects in its orderly formation during the early weeks of pregnancy may result in various central nervous system disorders and death. (Figure 15-5 in Chapter 15 includes an illustration of spina bifida, a neural tube defect.)

Folate supplements taken 1 month before conception and continued throughout the first trimester of pregnancy can help prevent neural tube defects (see Photo 10-6). For this reason, all women of childbearing age who are capable of becoming pregnant should consume 0.4 milligram (400 micrograms) of folate daily—easily accomplished by eating folate-rich foods, folate-fortified foods, or a multivitamin supplement daily. Because half of the pregnancies each year are unplanned, and because neural tube defects occur early in development before most women realize they are pregnant, the Food and Drug Administration (FDA) has mandated that grain products be fortified to deliver folate to the US population. Labels on fortified products may claim that “adequate intake of folate has been shown to reduce the risk of neural tube defects.” Fortification has improved folate status in women of childbearing age and dramatically lowered the prevalence rate of neural tube defects.

Photo 10-6

This infant’s back showsspina bifida, a neural tube defectcharacterized by the incomplete closure of the spinal cord and its bony encasement. Folate helps to protect against such defects.

Newscast Online Limited/Alamy Stock Photo

Some research suggests that folate taken before and during pregnancy may also prevent congenital heart disease, birth defects such as cleft lip and cleft palate, and neurodevelopmental disorders such as autism. Such findings strengthen recommendations for women to pay attention to their folate needs.

Folate fortification raises safety concerns as well. Because high intakes of folate can mask a vitamin B12 deficiency, folate consumption should not exceed 1 milligram daily without close medical supervision. The risks and benefits of folate fortification continue to be assessed, especially when the UL for folate might be exceeded.

Folate Deficiency

Folate deficiency impairs cell division and protein synthesis—processes critical to growing tissues. In a folate deficiency, the replacement of red blood cells and GI tract cells falters. Not surprisingly, then, two of the first symptoms of a folate deficiency are anemia and GI tract deterioration.

The anemia of folate deficiency is known as macrocytic or megaloblastic anemia and is characterized by large, immature red blood cells (see Figure 10-12). Without folate, DNA strands break and cell division diminishes. This damage interferes with the synthesis of the red blood cells as they attempt to divide and mature. The result is fewer, but larger, red blood cells that cannot carry oxygen or travel through the capillaries as efficiently as normal red blood cells. Thanks to the implementation of folate fortification in the United States, the prevalence of macrocytic anemia has decreased dramatically.

Figure 10-12Normal Blood Cells and Blood Cells in Macrocytic Anemia Compared

Of all the vitamins, folate appears to be most vulnerable to interactions with drugs, which can lead to a secondary deficiency. Some medications, notably anticancer drugs, have a chemical structure similar to folate’s structure and can displace the vitamin from enzymes and interfere with normal metabolism. (Highlight 17 discusses nutrient-drug interactions, and Figure H17-1 illustrates the similarities between the vitamin folate and the anticancer drug methotrexate.)

Aspirin and antacids also interfere with the body’s folate status: aspirin inhibits the action of folate-requiring enzymes, and antacids limit the absorption of folate. Healthy adults who use these drugs to relieve an occasional headache or upset stomach need not be concerned, but people who rely heavily on aspirin or antacids should be aware of the nutrition risks.

Folate Toxicity

A UL has been established for folate from fortified foods or supplements (see p. C of the inside front cover). Commonly consumed amounts of folate from both natural sources and fortified foods appear to cause no harm. The small percentage of adults who also take high-dose folate supplements, however, can reach concentrations that are high enough to obscure vitamin B12 deficiencies and delay diagnosis of neurological damage.

Folate Food Sources

Figure 10-13 shows that folate is especially abundant in legumes, fruits, and vegetables (see Photo 10-7). The vitamin’s name suggests the word foliage, and indeed, dark green, leafy vegetables are outstanding sources. With fortification, grain products also contribute folate. The small red and blue bars in Figure 10-13 reveal that meats and milk products are poor folate sources. Heat and oxidation during cooking and storage can destroy as much as half of the folate in foods.

Figure 10-13Folate in Selected Foods

Vegetables, legumes, and fruits are rich sources of folate, as are fortified grain products. See How To 10-1 for more information on using this figure.

Review Folate

Folate’s primary coenzyme (THF) is necessary for making new cells and preventing neural tube defects. Inadequate intakes cause macrocytic anemia and excessive intakes can mask a vitamin B12 deficiency. The following table provides a review of folate facts.

Vitamin B12

Vitamin B12 and folate are closely related: each depends on the other for activation. Recall that vitamin B12 removes a methyl group to activate the folate coenzyme. When folate gives up its methyl group, the vitamin B12 coenzyme becomes activated (review Figure 10-11).

The regeneration of the amino acid methionine and the synthesis of DNA and RNA depend on both folate and vitamin B12. In addition, vitamin B12 maintains the sheath that surrounds and protects nerve fibers and promotes their normal growth. Bone cell activity and metabolism also depend on vitamin B12 .

The digestion and absorption of vitamin B12 depends on several steps. In the stomach, hydrochloric acid and the digestive enzyme pepsin release vitamin B12 from the proteins to which it is attached in foods. Then as vitamin passes from the stomach to the small intestine, it binds with a stomach secretion called intrinsic factor. Bound together, intrinsic factor and vitamin B12 travel to the end of the small intestine, where receptors recognize the complex. Importantly, the receptors do not recognize vitamin B12 without intrinsic factor. The vitamin is gradually absorbed into the bloodstream as the intrinsic factor is degraded. Transport of vitamin B12 in the blood depends on specific binding proteins.

Like folate, vitamin B12 enters the enterohepatic circulation—continuously being secreted into bile and delivered to the intestine, where it is reabsorbed. Because most vitamin B12 is reabsorbed, healthy people rarely develop deficiencies even when their intakes are minimal.

Vitamin B12 Recommendations

The RDA for adults is only 2.4 micrograms of vitamin B12 a day—just over two-millionths of a gram. (For perspective, a single grain of sugar weighs several hundred micrograms.) As tiny as this amount appears to the human eye, it contains billions of molecules of vitamin B12, enough to provide coenzymes for all the enzymes that need its help.

Vitamin B12 Deficiency and Toxicity

Most vitamin B12 deficiencies reflect inadequate absorption, not poor intake. Inadequate absorption typically occurs for one of two reasons: a lack of hydrochloric acid or a lack of intrinsic factor. Without hydrochloric acid, the vitamin is not released from the dietary proteins and so is not available for binding with the intrinsic factor. Without the intrinsic factor, the vitamin cannot be absorbed.

Vitamin B12 deficiency is common among adults who use heartburn medications to suppress gastric acid production. Deficiency is also common among older adults. Many older adults develop atrophic gastritis, a condition that damages the cells of the stomach. Atrophic gastritis may also develop in response to iron deficiency or infection with Helicobacter pylori, the bacterium implicated in ulcer formation. Without healthy stomach cells, production of hydrochloric acid and intrinsic factor diminishes. Even with an adequate intake from foods, vitamin B12 status suffers. The vitamin B12 deficiency caused by atrophic gastritis and a lack of intrinsic factor is known as pernicious anemia.

Some people inherit a defective gene for the intrinsic factor. In such cases, or when the stomach has been injured and cannot produce enough of the intrinsic factor, vitamin B12 must be given by injection to bypass the need for intestinal absorption.

Because vitamin B12 is found primarily in foods derived from animals, vegetarians, and especially vegans, are most vulnerable to vitamin B12 deficiencies. It may take several years for people who stop eating animal-derived foods to develop deficiency symptoms because the body recycles much of its vitamin B12, reabsorbing it over and over again and conserving its supply.

Because vitamin B12 is required to convert folate to its active form, one of the most obvious vitamin B12 –deficiency symptoms is the anemia commonly seen in folate deficiency. This anemia is characterized by large, immature red blood cells, which indicate slow DNA synthesis and an inability to divide (review Figure 10-12). When folate is trapped in its inactive form (methyl folate) because of vitamin B12 deficiency or is unavailable because of folate deficiency itself, DNA synthesis slows.

First to be affected in a vitamin B12 or folate deficiency are the rapidly growing blood cells. Either vitamin B12 or folate will clear up the anemia, but if folate is given when vitamin B12 is needed, the result is disastrous: devastating neurological symptoms. Remember that vitamin B12, but not folate, maintains the sheath that surrounds and protects nerve fibers and promotes their normal growth. Folate “cures” the blood symptoms of a vitamin B12 deficiency, but cannot stop the nerve symptoms from progressing. By doing so, folate “masks” a vitamin B12 deficiency.

Even marginal vitamin B12 deficiency impairs memory and cognition. Advanced neurological symptoms include a creeping paralysis that begins at the extremities and works inward and up the spine. Early detection and correction are necessary to prevent permanent nerve damage and paralysis. With sufficient folate in the diet, the neurological symptoms of vitamin deficiency can develop without evidence of anemia and the cognitive decline is especially rapid. The interactions between folate and vitamin B12 highlight some of the safety issues surrounding the use of supplements and the fortification of foods. No adverse effects have been reported for excess vitamin B12, and no UL has been set.

Vitamin B12 Food Sources

Vitamin B12 is unique among the vitamins in being found almost exclusively in foods derived from animals (see Photo 10-8). Its bioavailability is greatest from milk and fish. Anyone who eats reasonable amounts of animal-derived foods is most likely to have an adequate intake, including vegetarians who use milk products or eggs. Vegans, who restrict all foods derived from animals, need a reliable source, such as vitamin B12 –fortified soy milk or vitamin supplements. Yeast grown on a vitamin B12 –enriched medium and mixed with that medium provides some vitamin B12, but yeast itself does not contain active vitamin B12 . Similarly, neither fermented soy products such as miso (a soybean paste) nor sea algae such as spirulina provide active vitamin B12. Extensive research shows that the amounts listed on the labels of these plant products are inaccurate and misleading because the vitamin B12 is in an inactive, unavailable form.

Review Vitamin B12

Vitamin B12 supports healthy cell replication and nerve activity. It is found only in foods derived from animals, and its absorption depends on intrinsic factor. Deficiency caused by atrophic gastritis and a lack of intrinsic factor results in pernicious anemia. The accompanying table provides a review of vitamin B12 facts.

Choline

Although not defined as a vitamin, choline is an essential nutrient that is commonly grouped with the B vitamins. The body uses choline to make the neurotransmitter acetylcholine and the phospholipid lecithin. During pregnancy, choline supports the neurological development of the fetus, and during adulthood, choline may improve cognition.

Choline Recommendations

The body can make choline from the amino acid methionine, but this synthesis alone is insufficient to fully meet the body’s needs; dietary choline is also needed. For this reason, the DRI Committee established an AI for choline.

Choline Deficiency and Toxicity

Average choline intakes fall below the AI, but the impact of deficiencies are not fully understood. The UL for choline is based on its life-threatening effect of lowering blood pressure.

Choline Food Sources

Choline is found in a variety of common foods such as milk, eggs, and peanuts and as part of lecithin, a food additive commonly used as an emulsifying agent (review Figure 5-8).

Review Choline

Choline is needed in the diet, but it is not considered a vitamin. The accompanying table provides a review of choline.

Nonvitamins

Some substances have been mistaken for vitamins, but they are not essential nutrients. Among them are the compounds inositol and carnitine, both of which can be made by the body. Inositol is a part of cell membrane structures, and carnitine transports long-chain fatty acids to the mitochondria for oxidation. Other names erroneously associated with vitamins are “vitamin O” (oxygenated saltwater), “vitamin B5 ” (another name for pantothenic acid), “vitamin B15 ” (also called “pangamic acid,” a hoax), and “vitamin B17 ” (laetrile, an alleged “cancer cure” and not a vitamin or a cure by any stretch of the imagination— in fact, laetrile is a potentially dangerous substance)
Interactions Among the B Vitamins

Up to this point, this chapter has described some of the impressive ways that vitamins work individually, but their many actions in the body cannot easily be disentangled. It is often difficult to tell which vitamin is truly responsible for a given effect because the nutrients are interdependent; the presence or absence of one affects another’s absorption, metabolism, and excretion. You have already seen this interdependence with folate and vitamin B12 .

Riboflavin and vitamin B6 provide another example. One of the riboflavin coenzymes, FMN, assists the enzyme that converts vitamin B6 to its coenzyme form PLP. Consequently, a severe riboflavin deficiency can impair vitamin B6 activity. Thus a deficiency of one nutrient may alter the action of another. Furthermore, a deficiency of one nutrient may create a deficiency of another. For example, both riboflavin and vitamin B6 (as well as iron) are required for the conversion of tryptophan to niacin. Consequently, an inadequate intake of either riboflavin or vitamin B6 can deplete the body’s niacin supply. These interdependent relationships are evident in many of the roles B vitamins play in the body.

B Vitamin Roles

Figure 10-14 summarizes the metabolic pathways introduced in Chapter 7 and conveys an impression of the many ways B vitamins assist in metabolic pathways. Metabolism does all of the body’s work, and the B vitamin coenzymes are indispensable to every step. In scanning the pathways of metabolism depicted in the figure, note the many abbreviations for the coenzymes that keep the processes going.

Figure 10-14Metabolic Pathways Involving B Vitamins

These metabolic pathways are introduced in Chapter 7 and are presented here to highlight the many coenzymes that facilitate the reactions. These ­coenzymes depend on the following vitamins:

• NAD and NADP: niacin

• TPP: thiamin

• CoA: pantothenic acid

• B12: vitamin B12

• FMN and FAD: riboflavin

• THF: folate

• PLP: vitamin B6

• Biotin

Pathways leading toward acetyl CoA and the TCA cycle are catabolic, and those leading toward amino acids, glycogen, and fat are anabolic. For further details, see Appendix C.

Metabolic Pathways Involving B Vitamins

Watch the animation metabolic pathways involving B vitamins.

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Look at the now-familiar pathway of glucose breakdown. To break down glucose to pyruvate, the cells must have certain enzymes. For the enzymes to work, they must have the niacin coenzyme NAD. Cells can make NAD, but only if they have enough niacin (or enough of the amino acid tryptophan to make niacin).

The next step is the breakdown of pyruvate to acetyl CoA. The enzymes involved in this step require both NAD and the thiamin and riboflavin coenzymes TPP and FAD, respectively. The cells can manufacture the enzymes they need from the vitamins, if the vitamins are in the diet.

Another coenzyme needed for this step is CoA. Predictably, the cells can make CoA except for an essential part that must be obtained in the diet—pantothenic acid. Another coenzyme requiring biotin serves the enzyme complex involved in converting pyruvate to oxaloacetate, the compound that combines with acetyl CoA to start the TCA cycle.

These and other coenzymes participate throughout all the metabolic pathways. Vitamin B6 is an indispensable part of PLP—a coenzyme required for a crucial step in the making of the iron-containing portion of hemoglobin for red blood cells. Folate becomes THF—the coenzyme required for the synthesis of new genetic material and therefore new cells. The vitamin B12 coenzyme, in turn, regenerates THF to its active form; thus vitamin B12 is also necessary for the formation of new cells.

Thus each of the B vitamin coenzymes is involved, directly or indirectly, in energy metabolism. Some facilitate the energy-releasing reactions themselves; others help build new cells to deliver the oxygen and nutrients that allow the energy reactions to occur.

B Vitamin Deficiencies

Now suppose the body’s cells lack one of these B vitamins—niacin, for example. Without niacin, the cells cannot make NAD. Without NAD, the enzymes involved in every step of the glucose-to-energy pathway cannot function. Then, because all the body’s activities require energy, literally everything begins to grind to a halt. This is no exaggeration. The deadly disease pellagra, caused by niacin deficiency, produces the “devastating four Ds”: dermatitis, which reflects a failure of the skin; dementia, a failure of the nervous system; diarrhea, a failure of digestion and absorption; and eventually, as is the case for any severe nutrient deficiency, death. These symptoms are the obvious ones, but a niacin deficiency affects all other organs, too, because all are dependent on the energy pathways.

All of the vitamins are as essential as niacin. With any B vitamin deficiency, many body systems become deranged, and similar symptoms appear, with disastrous and far-reaching effects.

Deficiencies of single B vitamins seldom show up in isolation. After all, people do not eat nutrients singly; they eat foods, which contain mixtures of nutrients. For this reason, B vitamin deficiencies often coexist, and most typically occur among older adults, vegetarians, and those with an alcohol use disorder, heart failure, or recent bariatric surgery. Only in two cases described earlier—beriberi and pellagra—have dietary deficiencies associated with single B vitamins been observed on a large scale in human populations. Even in these cases, several vitamins were lacking even though one vitamin stood out above the rest. When foods containing the vitamin known to be needed were provided, the other vitamins that were in short supply came as part of the package.

Major deficiency diseases of epidemic proportions such as pellagra and beriberi are no longer seen in the United States, but lesser deficiencies of nutrients, including the B vitamins, sometimes occur in people whose food choices are poor because of poverty, ignorance, illness, or poor health habits like alcohol abuse. (Review Highlight 7 to fully appreciate how alcohol induces vitamin deficiencies and interferes with energy metabolism.) Remember from Chapter 1 that deficiencies can arise not only from deficient intakes (primary causes), but also for other (secondary) reasons.

In diagnosing nutrient deficiencies, the clinician keeps in mind that a particular sign or symptom may not always have the same cause. The skin and the tongue (shown in Figure 10-15) appear to be especially sensitive to B vitamin deficiencies, but focusing on these body parts gives them undue emphasis. Both the skin and the tongue are readily visible in a physical examination. The physician sees and reports the deficiency’s outward signs, but the full impact of a vitamin deficiency occurs inside the body’s cells. If the skin develops a rash or lesions, other tissues beneath it may be degenerating too. Similarly, the mouth and tongue are the visible part of the digestive system; if they are unhealthy, most likely the rest of the GI tract is as well.

Figure 10-15B Vitamin–Deficiency Symptoms—The Smooth Tongue of Glossitis and the Skin Lesions of Cheilosis

Arisara T/ Shutterstock.com; SPL/Science Source; Clinical Photography, Central Manchester University Hospitals NHS Foundation Trust, UK/Science Source

Also keep in mind that the cause of a sign or symptom is not always apparent. The review tables in this chapter show that deficiencies of riboflavin, niacin, biotin, and vitamin B6 can all cause skin rashes. So can a deficiency of protein, linoleic acid, or vitamin A. Because skin is on the outside and easy to see, it is a useful indicator of “things going wrong inside cells,” but by itself, a skin condition says nothing about its possible cause.

The same is true of anemia. Anemia is often caused by iron deficiency, but it can also be caused by a folate or vitamin B12 deficiency; by digestive tract failure to absorb any of these nutrients; or by such nonnutritional causes as infections, parasites, cancer, or loss of blood. No single nutrient will always cure a given symptom.

A person who feels chronically tired may be tempted to self-diagnose iron-deficiency anemia and self-prescribe an iron supplement. But this will relieve tiredness only if the cause is indeed iron-deficiency anemia. If the cause is a folate deficiency, taking iron will only prolong the fatigue. A person who is better informed may decide to take a multivitamin supplement with iron, covering the possibility of a vitamin deficiency. But the symptom may have a nonnutritional cause. If the cause of the tiredness is actually hidden blood loss due to cancer, the postponement of a diagnosis may threaten life. When fatigue is caused by a lack of sleep, of course, no nutrient or combination of nutrients can replace a good night’s rest. A person who is chronically tired should see a physician rather than self-prescribe. If the condition is nutrition-related, a registered dietitian nutritionist should be consulted as well.

B Vitamin Toxicities

Toxicities of the B vitamins from foods alone are unknown, but they can occur when people overuse dietary supplements. With supplements, the quantities can quickly overwhelm the cells. Consider that one small capsule can easily deliver 2 milligrams of vitamin B6, but it would take more than 3000 bananas, 6600 cups of rice, or 3600 chicken breasts to supply that amount. When the cells become oversaturated with a vitamin, they must work to eliminate the excess. The cells dispatch water-soluble vitamins to the urine for excretion, but sometimes they cannot keep pace with the onslaught. Homeostasis becomes disturbed and symptoms of toxicity develop.

B Vitamin Food Sources

Significantly, deficiency diseases, such as beriberi and pellagra, were resolved by providing foods. Dietary supplements advertise that vitamins are indispensable to life, but human beings obtained their nourishment from foods for centuries before supplements existed. If the diet lacks a vitamin, the first solution is to adjust food intake to obtain that vitamin.

The bar graphs of selected foods in this chapter, taken together, sing the praises of a balanced diet. The grains deliver thiamin, riboflavin, niacin, and folate. The fruit and vegetable groups excel in folate. Protein foods meet thiamin, niacin, vitamin B6, and vitamin B12 needs. The milk group stands out for riboflavin and vitamin B12 . A diet that offers a variety of foods from each group, prepared with reasonable care, serves up ample B vitamins.

Review

The B vitamins serve as coenzymes that facilitate the work of every cell. They are active in carbohydrate, fat, and protein metabolism and in the making of DNA and thus new cells. Historically famous B ­vitamin-deficiency diseases are beriberi (thiamin), pellagra (niacin), and pernicious anemia (vitamin B12 ). Pellagra can be prevented by an adequate protein intake because the amino acid tryptophan can be converted to niacin in the body. A high intake of folate can mask the blood symptoms of a vitamin B12 deficiency, but it will not prevent the associated nerve damage. Vitamin B61` participates in amino acid metabolism and can be harmful in excess. ­Biotin and pantothenic acid serve important roles in energy metabolism and are common in a variety of foods. Many substances that people claim as B vitamins are not. Fortunately, a ­variety of foods from each of the food groups provides an adequate supply of all of the B vitamins