Unit 8: The B Vitamins Flashcards
General Characteristics of Vitamins
The vitamins are organic, essential nutrients required in tiny amounts to perform specific functions that promote growth, reproduction, or the maintenance of health and life.
• vita = life
• amine = containing nitrogen (the first vitamins discovered contained nitrogen)
Structure: Vitamins are individual units; they are not linked together (as are molecules of glucose or amino acids). presents the chemical structure for each of the vitamins.
•Function: Vitamins do not yield usable energy when metabolized; many assist the enzymes that participate in the release of energy from carbohydrates, fats, and proteins.
•Food contents: The amounts of vitamins people ingest daily from foods and the amounts they require are measured in micrograms (pg) or milligrams (mg)
**The vitamins are similar to the energy-yielding nutrients, though, in that they are vital to life, organic, and available from foods
Define Bioavailability
The amount of vitamins and minerals available from foods depends not only on the quantity provided by a food but also on the amount absorbed and used by the body—referred to as bioavailability. Vitamins and minerals differ in the amounts the body can absorb and the extent to which they must be specially handled.
Determining the bioavailability of a vitamin or mineral is a more complex task because it depends on many factors, including:
• Efficiency of digestion and time of transit through the GI tract
• Previous nutrient intake and nutrition status
• Method of food preparation (raw, cooked, or processed)
• Source of the nutrient (synthetic, fortified, or naturally occurring)
• Other foods consumed at the same time
• Naturally occurring binders found in foods, such as phytates present in legumes and whole grains and oxalates found in some vegetables, chemically combine with minerals preventing their absorption
• Fibres present in foods can reduce mineral absorption by trapping them and carrying them out of the body with other waste products
Define Precursors
Some of the vitamins are available from foods in inactive forms known as precursors, or provitamins. Once inside the body, the precursor is converted to an active form of the vitamin.
Define Coenzyme
is a small organic molecule that associates closely with certain enzymes; many B vitamins form an integral part of coenzymes.
Water-Soluble Vitamins
Water-Soluble Vitamins: B Vitamins and Vitamin C
Absorption: Directly into the blood
Transport: Travel freely
Storage: Circulate freely in water-filled compartments of the body
Excretion: Kidneys detect and remove excess in urine
Toxicity: Possible to reach toxic levels when consumed from supplements
Requirements: Needed in frequent doses (perhaps 1 to 3 days)
Water‑soluble vitamins are generally less stable than fat‑soluble ones during cooking. Water‑soluble vitamins can easily be dissolved in cooking water and can be destroyed by over‑cooking or poor storage techniques.
Fat-Soluble Vitamins
Fat-Soluble Vitamins: Vitamins A, D, E, and K
Absorption: First into the lymph, then the blood
Transport: Many require transport proteins
Storage: Stored in the cells associated with fat
Excretion: Less readily excreted; tend to remain in fat-storage sites
Toxicity: Likely to reach toxic levels when consumed from supplements
Requirements: Needed in periodic doses (perhaps weeks or even months)
Although each fat‑soluble vitamin—A, D, E, and K—has distinct physiological functions in the body, all share the following characteristics:
- They are present in fatty or oily portions of foods; bile and digestive enzymes are required to release them.
- Once released, they form aggregates (micelles) with long‑chain dietary fatty acids for absorption. Any condition that interferes with fat absorption will also reduce absorption of the fat‑soluble vitamins.
- After absorption into the intestinal mucosal cells, the fat‑soluble vitamins are incorporated into chylomicrons, which then travel through the lymphatic system into the general blood supply. The fat‑soluble vitamins are then taken up by the liver where they are stored or changed into biologically active forms to be transported by special protein carriers to various body sites.
- Since the fat‑soluble vitamins are insoluble in water, they cannot be excreted in the urine. Only small losses may occur through the bile and then through the feces. In excess of need, most fat‑soluble vitamins remain in the liver and adipose tissue; the body draws on these stores when dietary intakes are low. Hence, deficiency symptoms may take a long time to develop. When intake is high, stores can accumulate to toxic levels.
- They are generally more resistant than water‑soluble vitamins to loss during the cooking and processing of foods. They are fairly stable to heat and are not lost in cooking liquid. The fat‑soluble vitamin most susceptible to destruction is vitamin E.
The B vitamins are often referred to as a group or complex, because they were originally thought to be a single vitamin. Later work demonstrated that “vitamin B” actually consists of several distinct chemicals, now known as different B vitamins. However, the term B‑complex has remained part of nutrition jargon because these vitamins are often referred to as a group and share various characteristics:
- *They act as coenzymes, which serve as “helpers” to the enzymes involved in the metabolism of carbohydrates, lipids, and proteins.
- *They help cells to multiply (e.g., red blood cells and cells of the digestive and nervous systems).
- *They are widely distributed in all food groups; B12 is an exception: it is found only in food of animal origin.
- *They tend to be concentrated in the outer coating of seeds and grains; therefore, milling causes major vitamin loss.
- *They are all water‑soluble, not stored in the body to any appreciable extent (except B12), relatively non‑toxic, and excreted via the urine when consumed in excess.
Thiamin
The main coenzyme form of thiamin is thiamin pyrophosphate (TPP), which is a molecule containing thiamin and two phosphate groups.
Functions
TPP functions in several types of reactions. A major one is oxidative decarboxylation, the removal of a carbon atom in the presence of oxygen to form carbon dioxide. An example of this reaction has been mentioned in the discussion of energy metabolism (Unit 7), where pyruvate is converted to acetyl‑CoA. Oxidative decarboxylation requiring TPP also occurs within the TCA cycle. As you can see, whenever energy is needed or is being produced, an adequate supply of thiamin is essential. The text also identifies a role for thiamin in maintaining nerve cell membranes.
Deficiency
As described in the textbook, prolonged or severe thiamin deficiency (beriberi) is common in parts of Asia where highly polished, unenriched rice is the staple food. In North America, thiamin deficiency is uncommon. Borderline cases may show mild symptoms, such as loss of appetite, weakness, and numbness of legs, indigestion, constipation, and increased pulse rate. Alcoholics can develop a secondary thiamin deficiency because of
poor absorption caused by alcohol‑induced injury to the GI tract cells;
decreased activation of thiamin to TPP resulting from liver damage by alcohol; and
increased need for thiamin to metabolize alcohol.
Alcoholics may also have a poor dietary thiamin intake, so thiamin deficiency can develop quickly. The main symptoms of secondary thiamin deficiency are altered mental state, characteristic eye movements, and ataxia (lack of muscular coordination). Reversal is rapid when oral thiamin is administered.
Toxicity
Thiamin is generally non‑toxic, unless high doses are injected.
Sources
As demonstrated in Figure 10‑5 on page 326, thiamin is present in small quantities in nearly all nutritious foods. Diets that include all four food groups can easily meet the recommended levels of intake for thiamin. In the Grain Products group, it is important to choose whole-grain or enriched products—the major contributors of thiamin. In Canada, it is mandatory for white flour to be enriched with thiamin, riboflavin, niacin, folacin, and iron.
Stability
Thiamin is one of the vitamins most easily lost in food preparation.
Dry heating at high temperatures, such as occurs when ready‑to‑eat cereals are puffed or toasted or when bread is toasted, can cause significant loss. Depending on time and temperature, meat loses 20–60% of its thiamin in roasting, while broiling results in a 30% loss. Baking bread results in only a 5–15% loss.
Cooking cereals and vegetables for moderate lengths of time in small amounts of water results in a small loss. If liberal amounts of water are used and then discarded, thiamin loss increases substantially.
Thiamin is also destroyed by the use of baking soda (alkali) in cooking or by the use of sulphite additives to prevent browning of dried fruits.
Certain foods (e.g., raw fish and tea leaves) contain an enzyme which has an anti‑thiamin activity. However, cooking inactivates the enzyme. The
Riboflavin
The two coenzyme forms of riboflavin are flavin adenine dinucleotide (FAD), and flavin mononucleotide (FMN).
Functions
By functioning as hydrogen carriers, FAD and FMN are essential coenzymes for many oxidation‑reduction reactions in the cells. FAD and FMN are essential during carbohydrate, lipid, and protein metabolism; in the TCA cycle; and in the electron transport chain, where energy is produced. FAD and FMN are also essential for other B‑vitamin activities, such as the activation of vitamin B6 in the conversion of tryptophan to niacin (this process is discussed more fully in the next section) and the conversion of folate to its coenzyme forms. These examples show the interdependence of B vitamins.
Riboflavin is essential for growth, serving multiple functions in adrenal and thyroid gland function, collagen formation, immune function, red blood cell formation, and gluconeogenesis.
Deficiency
The symptoms of riboflavin deficiency include tissue inflammation and breakdown, as described in the textbook. Such symptoms are non‑specific, probably because riboflavin deficiency seldom occurs in isolation but is usually linked with deficiencies of other B‑complex vitamins. Riboflavin deficiency takes several months to develop because the liver and kidney are capable of storing FAD and FMN. Severe riboflavin deficiency is rarely seen in the Western world, thanks to mandatory enrichment of white flour, breads, and baked goods. However, some borderline deficiency does occur in people who have a very low intake of enriched foods and dairy products, and also in alcoholics.
Toxicity
Riboflavin toxicity is rare, because excess riboflavin can be excreted by the kidneys. Supplementation with large amounts of riboflavin may cause the urine to become a fluorescent yellow (the colour of riboflavin).
Sources
As shown in Figure 10‑7 on page 328, the dominant sources of riboflavin are milk and milk products. Whole-grain and enriched breads and cereals also contribute appreciably to the total daily intake, though they provide lesser amounts of riboflavin than many other sources.
Stability
Riboflavin is fairly stable in general handling, storage, and cooking procedures. It is water‑soluble and may therefore be lost when large amounts of water are used to cook vegetables, and are then discarded. However, vegetables are not the primary source of riboflavin in the diet. The major loss of riboflavin occurs when food is exposed to ultraviolet or visible light. Milk should therefore be stored in a cool, dark place, preferably in an opaque container.
Niacin
The two coenzyme forms of niacin are nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP).
Functions
Like riboflavin, the coenzyme forms of niacin (NAD and NADP) function as hydrogen carriers in oxidation‑reduction reactions during the metabolism of carbohydrates, lipids, proteins, and alcohol.
The most significant role of NAD is in the electron transport chain, where hydrogen atoms are transferred successively from NAD to FAD and finally to oxygen to form water and ATP. Thus, an adequate supply of niacin is essential for energy production.
NAD and NADP are involved in the synthesis of triglycerides, non‑essential amino acids, and glycogen. Niacin is therefore essential to the health of all body cells.
NAD is also required in the activation of folate to its coenzyme forms.
Deficiency
As described in the textbook, pellagra is characterized by the symptoms of the four Ds: dermatitis, diarrhea, dementia, and eventually, death. Pellagra is generally caused by a low intake of niacin as well as a low intake of tryptophan, an amino acid that can be converted to niacin. It is also suspected that a large intake of leucine (another amino acid) can create an amino acid imbalance, which is crucial to the development of pellagra. Corn, which is high in leucine and low in free niacin, can, if used as the staple grain in low-protein diets, precipitate pellagra. However, the Mexican and South American practice of soaking corn in a solution of lime (alkali) before grinding it into flour releases enough niacin to prevent pellagra.
Toxicity
The textbook describes the use of high doses of niacin in the form of nicotinic acid to treat people with a high blood‑cholesterol level. This therapy for hypercholesterolemia is effective for some individuals but has the uncomfortable side‑effect of “flushing.” Other symptoms of excess niacin intake are listed on page 330.
Sources
The sources of niacin are those foods which contain preformed niacin, tryptophan, or both. Sixty milligrams of tryptophan are equivalent to one milligram of niacin. Food composition tables give milligrams of preformed niacin. To reflect the body’s ability to convert tryptophan to niacin, the RDA for niacin is expressed in niacin equivalents (NE):
NE = mg of performed niacin \+ mg of tryptophan* 60
*mg of tryptophan in excess of the body’s need (RDA) for protein
As indicated in Figure 10‑9 on page 331, meat, fish, and poultry are the major sources of niacin.
Stability
Niacin is the most stable of all the B vitamins, in both the dry and liquid forms. It resists destruction by heat, oxygen, and light, as well as by acid or alkali. The most significant loss occurs through leaching of the vitamin into cooking water.
Vitamin B6
The most active coenzyme form of vitamin B6 is pyridoxal phosphate (PLP).
Functions
Vitamin B6 is involved in every step of protein and amino acid metabolism, but it also plays a role in carbohydrate and lipid metabolism. Its functions are
absorption and transport of amino acids across the membrane of the intestinal mucosa.
transamination—the transfer of amino groups from one compound to another. Vitamin B6 is essential for the synthesis of non‑essential amino acids.
deamination—the removal of nitrogen groups from amino acids. Vitamin B6 is essential in the catabolism of amino acids to produce energy.
decarboxylation, a process required in the synthesis of neurotransmitters (e.g., serotonin from the amino acid, tryptophan). Serotonin is important in sleep, sensory perception, and mood regulation.
production of niacin from tryptophan.
hemoglobin synthesis.
Deficiency
A primary deficiency of vitamin B6 with clinical symptoms is rare in humans because of the wide distribution of the vitamin in food. Secondary deficiency, however, is found in people using drugs that are vitamin B6 antagonists and in alcoholics. When the body metabolizes alcohol, acetaldehyde is produced. Acetaldehyde is a toxic compound that can destroy vitamin B6 and that promotes its loss from the body.
Deficiency symptoms are generally non‑specific and similar to other B‑vitamin deficiencies; they include muscle weakness, irritability, insomnia, dermatitis, and weight loss. The only specific symptom is small‑cell type anemia (microcytic anemia), which results from impaired hemoglobin synthesis.
Evidence of sub‑clinical deficiency (i.e., deficiency without outward signs) has been reported in the elderly, especially those with a limited food intake, and in some pregnant and lactating women—again, those with a poor food intake.
Toxicity
High doses of vitamin B6 (in the range of two grams or more) have been reported to produce toxicity resulting in neurological damage. The text describes some of the conditions for which vitamin B6 supplementation has been used, but cautions against self‑medication. The potential dangers of toxicity are obvious; furthermore, toxicity can occur even with relatively low levels taken on a long‑term basis, and may be irreversible.
Sources
Vitamin B6 is present in most foods in variable amounts. Figure 10‑10 on page 334 lists some of its major sources. Legumes, meats, certain fruits (e.g., banana, watermelon, fig, cantaloupe), and certain vegetables (e.g., potato, spinach, broccoli) all contribute some B6. Milk and dairy products as well as bread and cereals are less significant sources. The milling of grain causes substantial losses of B6 (up to 90%). Enrichment of foods with B6 is currently done on a voluntary basis only. Some ready‑to‑eat cereals in Canada may contain added B6, but white flour and breads are not enriched with this vitamin. Accordingly, whole-grain bread and flour are better sources of vitamin B6 than are white bread and flour.
Stability
Vitamin B6 is fairly stable to heat (except severe heat treatments, such as sterilization) and oxygen, but relatively sensitive to light and alkaline conditions. Freezing of vegetables can lead to a 20% loss of the vitamin.
Folate
The primary coenzyme form of folate is tetrahydrofolate (THF). Absorbed folate is reduced (by adding hydrogen) to form THF. Ascorbic acid, vitamin B12, and NAD are required for the activation of folate to THF by the liver.
Functions
THF acts as a carrier of methyl (CH3) groups from one substance to another.
THF is required for the synthesis of nucleic acids (DNA and RNA) that are essential for cell division and protein synthesis. Furthermore, THF is involved in the synthesis of some non‑essential amino acids, such as glycine, serine, and histidine. Thus, folate is involved in protein synthesis in two ways: through DNA and RNA production, and in the synthesis of certain amino acids.
THF participates in the methylation process during the synthesis of acetylcholine, the neurotransmitter for nerve impulses.
THF is also essential for the formation of both red and white blood cells.
Deficiency
A poor nutritional folate status is common in humans. It is often found in
the low‑income elderly, as a result of poor dietary intake.
pregnant and lactating women, infants, and children, because of their increased need.
alcoholics and individuals with GI tract damage and impaired absorption (e.g., in celiac or Crohn’s disease).
people using drugs such as oral contraceptives, aspirin, certain cancer drugs, and anti‑convulsants.
Deficiency symptoms include
macrocytic or megaloblastic anemia (i.e., large‑cell type). The red blood cells are large, immature, and contain a nucleus. Normal, mature red blood cells are small and anucleated. The megaloblastic cells do not contain their full complement of enzymes, nor do they have full oxygen‑carrying capacity. This leads to anemia, with symptoms identical to the anemia seen in vitamin B12 deficiency (which we discuss in the next section).
changes in the epithelial tissues of the GI tract, tongue, stomach, vagina, and cervix, where there is rapid turnover of cells. The mucosal lining of the intestine becomes flattened instead of convoluted, thereby reducing absorption surface area and impairing enzyme secretions and absorption of nutrients. Symptoms such as diarrhea, heartburn, and smooth red tongue are the results of the cell changes.
behavioural changes, such as fatigue, mild depression, abnormal nerve reflexes, disorientation, poor memory, and confusion. These neurological effects are probably related to the metabolism of amino acids affected by folate deficiency, which in turn may alter the synthesis of neurotransmitters in the brain and nervous system. However, these symptoms are reversible, with no real damage to nerve cells.
decreased and abnormal white blood cells, probably caused by impaired DNA synthesis in the formation of white blood cells. This decrease results in reduced immunity to infectious disease.
neural tube defects (NTD). Conditions such as spina bifida may occur in babies when the mother’s folate intake is deficient early in pregnancy. For this reason, pregnant women, or those who are trying to get pregnant, are advised to take a daily folate supplement of 400 ug.
Toxicity
The only probable risk of high dosages of folate may be the masking of vitamin B12 deficiency symptoms, which we discuss later.
Sources
Folate derives its name from the Latin word folium, meaning foliage or leaf, because it was first isolated from spinach leaves and was known to be concentrated in green, leafy plants. Some outstanding sources are shown in Figure 10‑14 on page 340. They include dark green leafy vegetables such as spinach, asparagus, and broccoli, and legumes such as beans and lentils.
The food group making the largest contribution to folate intake in the Canadian diet is Vegetables and Fruits, particularly dark green vegetables. Canada’s Food Guide now includes a specific recommendation to include at least one serving of a dark green vegetable daily to ensure an adequate intake of folate. Many foods, including many varieties of breakfast cereals, are “enriched” with folic acid (synthetic folate). Despite the addition of folic acid to many foods, sections of the population, especially women, still consume an inadequate amount of this vitamin (Kirkpatrick and Tarasuk, 2008). In this respect, folate seems to be the most commonly problematic of the B‑vitamin family.
Precise calculation of folate in food is complicated. Most of the folate in foods in mixed Canadian diets is in bound form, as described on pages 334–335. Bioavailability of dietary folate can vary from 25–50%, depending on food sources and physiological factors. The value for total folate, as presented in nutrient databases, is usually an overestimate of the actual amount available to the body. Folate added to supplements and fortified foods, on the other hand, is more available than that in naturally occurring food sources; databases do not account for this, either. The “how to” on page 335 goes through the calculation of estimating folate equivalents (you will not be tested on this).
Stability
Losses of folate in foods during home cooking or industrial processing may range from 50–90%, depending on the temperature used. Storing leafy vegetables at room temperature can result in considerable loss of folate, caused by the action of oxygen and ultraviolet light. Cooking with large amounts of water can cause folate to leach out, while milling removes the majority of folate from grain products.
Vitamin B12
Vitamin B12 is a complex molecule with several biologically active forms. As do most other B vitamins, it functions as a coenzyme. You need not remember the specific names for the coenzyme forms of this vitamin; they are more commonly known as cobamide coenzymes.
Functions
Two general functions are attributed to vitamin B12. It serves as a carrier of single carbon methyl groups and as a carrier of hydrogen atoms.
Vitamin B12 is needed to remove the methyl group from methyl folate to convert it to the physiologically active form of THF.
Vitamin B12 and folate work cooperatively in the synthesis of DNA and RNA during cellular reproduction. Accordingly, tissues that have a high turnover, such as red blood cells and cells of the GI tract, are affected by both B12 and folate deficiencies.
Vitamin B12 (on its own) is required for the synthesis and maintenance of the myelin sheath of nerve fibres. Myelin is mainly lipid in composition, and vitamin B12 deficiency produces demyelination of nerve fibres (i.e., serious nerve damage).
Vitamin B12 also acts as a hydrogen carrier in carbohydrate metabolism to produce energy, especially for the brain cells.
Deficiency
Primary deficiency of vitamin B12 is mainly confined to strict vegans (persons living exclusively on foods of plant origin) since this vitamin is present only in foods derived from animals. The main cause of secondary deficiency is the lack of intrinsic factor as a result of an inherited disorder that usually shows up in middle age: atrophy of stomach cells. Malabsorption of vitamin B12 in disorders of the small intestine such as celiac and Crohn’s disease may also induce deficiency. However, deficiency may take a long time to develop (up to three years) because the liver maintains a large store of the vitamin.
In the stomach, vitamin B12 is released from protein complexes in food by hydrochloric acid. Gastric secretion also contains a glycoprotein called intrinsic factor, which combines with vitamin B12 and attaches to receptors on the mucosa of the ileum where absorption of B12 takes place. Without the intrinsic factor, insufficient B12 is absorbed even if a normal amount is present in the diet. However, when extremely large amounts of B12 are ingested, small amounts diffuse across the intestinal mucosa and are absorbed. The historic treatment for pernicious anemia—feeding large quantities (one pound per day) of raw liver—was effective because of this “flooding” of the GI tract with B12. Vitamin B12 injection is the only practical option for treating pernicious anemia.
Many health professionals recommend a dietary supplement of B12 for people over 60 years old. This is because of progressive gastric atrophy that occurs with aging and that reduces the body’s ability to absorb B12.
Vitamin B12 deficiency is associated with the well‑defined syndrome pernicious anemia. More accurately, pernicious anemia is caused by a lack of intrinsic factor, rather than lack of B12. Pernicious anemia is characterized by
macrocytic or megaloblastic anemia, identical to the anemia seen in folate deficiency. With high doses of folate, the anemic symptom of vitamin B12 deficiency is corrected. However, such treatment masks a B12 deficiency because the vitamin acts independently in the nervous system.
neurologic damage. Peripheral systems are affected first causing numbness and tingling in hands and feet. Damage progresses to the spinal column, resulting in paralysis, and finally to the brain, resulting in “megaloblastic madness.” Beginning with mental confusion and agitation, the symptoms progress to depression, and finally to psychotic changes, such as delusions, hallucinations, and paranoia. The neurological degeneration seen in B12 deficiency is different from the behavioural changes in folate deficiency, because irreversible nerve damage also results from demyelination of nerves.
oral and gastrointestinal effects. The early stages of B12 deficiency are accompanied by inflammation and atrophy of the tongue or oral mucosa—also commonly found in other B‑vitamin deficiencies.
Toxicity
Vitamin B12 has no reported toxicity and no associated symptoms.
Sources
Vitamin B12 is microbial in origin. Bacteria in the rumen of some animals (e.g., cattle and sheep) synthesize B12, which is absorbed and incorporated into their tissues and milk. Hence, the only source of B12 in the human diet is from foods of animal origin. Since liver is the storage site for B12, it is obviously an excellent source. Meat, milk, and eggs are other good sources.
Shellfish, such as clams and oysters that filter water containing B12‑synthesizing micro‑organisms, can acquire fairly high concentrations of the vitamin in their tissues. Some fermented cheeses, such as Camembert, contain moderate amounts of B12. Fruits, vegetables, and grains do not contain B12 unless they are unwashed and contaminated with organic fertilizer (human and animal feces). Although micro‑organisms in the human GI tract synthesize large amounts of the vitamin, this process occurs too far down in the colon for the vitamin to be absorbed.
Stability
Vitamin B12 is relatively stable to heat, except at very high temperatures, such as in sterilization and microwaving. Although B12 is water‑soluble, its major food sources are not usually subjected to cooking in large amounts of water. Generally, about 70–90% of the vitamin activity is retained during cooking.
