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    • Introduction Vitamins are defined as essential micronutrients that are not synthesized by mammals. Most vitamins are essential for the metabolism of all living organisms, and they are synthesized by microorganisms and plants. Coenzymes (and/or prosthetic groups) are defined as organic compounds with low molecular weight that are required to show enzyme activity by binding with their apoenzymes. Many coenzymes are biosynthesized from vitamins and contain a nucleotide (or nucleoside) moiety in their molecules. Besides their functions as vitamins and coenzymes, most of vitamins and coenzymes have been shown to have various other biofunctions. Accordingly, it is more appropriate to understand both as effective biofactors.
    • Most vitamins and related compounds are now industrially produced and widely used as food or feed additives, medical or therapeutic agents, health aids, cosmetic and technical aids, and so on. Thus, vitamins and related compounds are important products for which many biotechnological production processes (i.e., fermentation and microbial/enzymatic transformation) as well as organic chemical synthetic ones have been reported; some of them are now applied for large-scale production. Industrial production methodology, annual production amounts, and fields of application for these vitamins and related compounds are summarized here In this chapter, some of the vitamins and related compounds are described from the viewpoint of their microbial production.
    • TYPES OF VITAMINS
      • They are of two types
      • Water Soluble Vitamins
      • These vitamins are readily soluble in water.
      • Fat Soluble Vitamins
      • These vitamins are readily soluble in fatty compounds
    • WATER SOLUBLE VITAMINS Introduction of Water-Soluble Vitamins Water-soluble vitamins are alike in that, with the exception of B12, they can be supplied by plants in the diet. These vitamins are not stored in the body for very long and therefore need to be consumed regularly. Primarily the water-soluble vitamins serve as coenzymes in metabolic reactions. The majority of the water-soluble vitamins are 'B' vitamins and these play a major role in energy metabolism. The following vitamins will be described: thiamin, riboflavin, niacin, pyridoxine, folic acid, vitamin B12, and vitamin C.
    • Summary of some water soluble vitamins Function Thiamin, or vitamin B1, plays a major role in carbohydrate metabolism. Thiamin acts as a coenzyme along with phosphorus in important cellular reactions such as decarboxylation and transketolation. Thiamin pyrophosphate (TPP), a coenzyme, allows pyruvate to enter the citric acid cycle (Krebs' cycle) to produce energy for cellular functions. TPP acts in fat synthesis by transketolation, providing glyceraldehyde for the conversion of glucose to fat. Absorption and excretion Thiamin is absorbed quite easily in the jejunum and ileum. Thiamin is transported to the liver in the blood. High amounts of thiamin are stored in the skeletal muscles, heart, liver, kidneys, and brain. Approximately one-half of the thiamin is stored in the muscles. The half-life of thiamin in the body is 9 to 18 days. Thiamin is mainly excreted in the urine.
    • Clinical conditions Thiamin deficiency, called beriberi, effects the nervous system due to its dependence on glucose for energy. Insufficient thiamin can result in diminished alertness and reflexes, apathy, and fatigue. Thiamin deficiency affects lipogenesis and results in degeneration of the lipid myelin sheaths covering the nerve fibers. Clinical symptoms include pain and prickly sensations, and in a severe deficiency paralysis can result. Gastrointestinal symptoms include indigestion, constipation, gastric atony, deficient hydrochloric acid secretion, and anorexia. Thiamin deficiency also can weaken the heart muscle, leading to cardiac failure and edema in the extremities. A disease called Wernicke-Korsakoff syndrome results in ocular motor signs, ataxia, and deranged mental function. Most patients with Wernicke-Korsakoff syndrome are alcoholics, but few alcoholics actually develop the disease. Food Sources Thiamin is found in small quantities in many plant and animal foods. Sources include lean pork, beef, liver, yeast, whole grains, enriched grains, and legumes. Supplementation Supplementation Thiamin therapy is used in the treatment of alcoholics. Malnutrition often develops from alcohol and a poor diet, leading to neurological disorders. Infections increase cellular energy requirements and therefore thiamin requirements. Thiamin administration to beriberi patients ranges from 50-100 mg given intravenously or intramuscularly for one or two weeks. The dose can then be dropped to 10 mg until the patient recovers.
    • Riboflavin Function Riboflavin, or B2, is a constituent of enzymes called flavoproteins. Flavin mononucleotide (FMN) and flavin-adenine dinucleotide (FAD) are vital in the respiratory chain of cellular energy metabolism. FMN is used in deamination, which is the process of removing the amino group from amino acids. FAD is used in the deamination of glycine, an amino acid. FAD is also involved in the oxidation of some fatty acids. Absorbtion and Excretion The coenzymes FAD and FMN are released from proteins by the acid in the upper gut. Riboflavin is absorbed in the proximal small intestine. Bile salts facilitate the uptake of riboflavin. In human blood, riboflavin is primarily bound to proteins. The immunoglobulin IgG binds readily to the free form of riboflavin. Conversion of riboflavin to coenzymes occurs in cellular cytoplasm of tissues, primarily in the small intestine, liver, heart, and kidney. Lactoflavin is contained in the milk of lactating women. The synthesis of the coenzymes is tightly regulated and dependent on riboflavin status. Little riboflavin is actually stored in the body; it is excreted through the urine.
    • Clinical conditions Riboflavin deficiency, also known as ariboflavinosis, occurs in areas with long periods of low intake. Deficiency is usually accompanied by deficiency of other B vitamins. Symptoms include the inflammation and breakdown of tissue, swollen and cra cked lips, swollen tongue, and red, itchy eyes. Newborn infants with jaundice that are treated with phototherapy have shown signs of riboflavin deficiency. Excess excretion occurs in catabolic patients undergoing nitrogen loss. Toxicity is non-existent. Excess riboflavin is readily excreted in the urine. Food Sources Milk is the most abundant source of riboflavin. Other sources include organ meats, whole grains, enriched grains, and broccoli. Riboflavin is easily lost in cooking due to its water solubility. Supplementation Riboflavin therapy is rarely used, despite its important bodily functions.
    • Niacin Niacin, also called nicotinic acid, is involved in oxidation-reduction reactions as coenzymes that convert protein and glycerol from fats to glucose, and oxidize glucose to release energy. Niacin is involved in the synthetic pathway of adenosine tri-phosphate (ATP) and in ADP-ribose transfer reactions. The two niacin coenzymes involved in these processes are nicotinamide-adenine dinucleotide (NAD) and nicotinamide-adenine dinucleotide phosphate (NADP). NAD is a substrate for the enzyme poly (ADP-ribose) polymerase (PARP) which is involved in DNA repair. Absorption and excretion Niacin is absorbed into the intestine by diffusion. Approximately 15-30% of niacin is bound to protein and taken up by the tissues. Niacin metabolites are excreted in the urine. Tryptophan is a precurser to niacin. The amount of tryptophan converted to niacin is dependent on diet and hormonal factors. If there is a deficiency in both tryptophan and niacin, tryptophan will be used for protein synthesis rather than niacin production.
    • Clinical conditions Niacin deficiency leads to a disorder called pellagra. Pellagra is characterized by the 3 "D"s: dermatitis, diarrhea, and dementia. Skin exposed to sunlight develops dark, scaly dermatitis. There is a characteristic "necklace" lesion on the neck. Niacin deficiency can lead to inflammation of the mucous membranes of the tongue, esophagus, urethra, prostate, and vagina. Intestinal inflammation leads to diarrhea. Long-term niacin deficiency leads to central nervous system dysfunction manifested as confusion, apathy, disorientation and neuritis. Individuals may be predisposed to niacin deficiency if they are also consuming low levels of vitamin B6, copper, and riboflavin. Niacin deficiency can also lead to a disease called Hartnup's syndrome. This is due to impaired synthesis of niacin from tryptophan. Food Sources Meat is an excellent source of niacin. Legumes, milk, eggs, and yeast are good sources. Grains are commonly enriched with niacin. Milk and eggs are actually low in niacin, but high in tryptophan, a precursor to niacin. The measure of niacin equivalents takes into account the tryptophan that may be converted to niacin. Corn is high in tryptophan and niacin, but also contains the amino acid leucine which inhibits the synthesis of NAD in red blood cells.
    • Supplementation Niacin is used for the treatment of hyperlipidemia. Niacin decreases very low-density lipoprotein (VLDL) and increases high density lipoprotein (HDL) leading to a regression in artherosclerotic plaques. The recommended dose is gradually increased to 1.5-2 grams/day if the modified-release form of niacin is taken and 3 grams/day for the regular crystalline niacin form. Side effects of niacin therapy have included flushing, pruritus, urticaria, nausea, vomiting, diarrhea, bloating, and constipation. Research is being conducted to examine the potential effect of niacin therapy for the prevention of non-insulin dependent diabetes.
    • Pyridoxine Function Pyridoxine, or vitamin B6, is a coenzyme in reactions of amino acid, carbohydrate, and fat metabolism. Vitamin B6 is actually a term used for a group of vitamins with similar functions: pyridoxine, pyridoxal, and pyridoxamine. All are precursors to pyridoxine coenzyme pyridoxalphosphate (PLP). This coenzyme is involved in reactions involving many systems within the body. PLP has a role in gluconeogenesis through transaminase reactions. The conversion of tryptophan to niacin utilizes an enzyme that requires PLP. In red blood cells PLP is a coenzyme for transaminases. PLP is also involved in the synthesis of several neurotransmitters, such as serotonin, taurine, dopamine, gamma-aminobutyric, and norepinephrine. Intake of vitamin B6 has been associated with immune function. Low intake of B6 results in a decrease of interleukin-2 and lymphocyte proliferation. The effect of B6 on lipid metabolism is still under debate but it may be involved in the conversion of linoleic acid to arachidonic acid. Absorption and excretion Pyridoxine is absorbed passively into the jejunum. The bioavailability of vitamin B6 is quite good, more than 75% from foods. Fiber may limit availability. Pyridoxine is transported in the blood bound to albumin and hemoglobin. The majority of B6 is stored in the muscle.
    • Clinical conditions Vitamin B6 metabolism is affected by an alteration in tryptophan metabolism or plasma PLP concentration. Many conditions result in altered tryptophan metabolism. These include asthma, breast cancer, diabetes, and rheumatoid arthritis. PLP plasma concentration is decreased in asthma, alcoholism, breast cancer, diabetes, renal disease, sickle-cell anemia, and smoking. Drugs that have been shown to effect B6 metabolism include isoniazid, ethinylestradiol, penicillamine, theophylline, and caffeine. Megadoses of vitamin B6, one gram or more per day, have been reported to cause nerve damage. Food Sources Good sources of vitamin B6 are meats, grains, and nuts. Supplementation Vitamin B6 has been used for Down's syndrome, autism, gestational diabetes, diabetic neuropathy, and depression. Some beneficial effects have been reported in the literature. Therapeutic dosages range from 50 to 100 mg. Doses over 2000 mg have been associated with nerve toxicity exhibited by tingling feet, loss of muscle coordination, and degeneration of nerve tissue.
    • Folic acid Function Folic acid, also called folate, is involved in DNA and protein synthesis. It has a role in the synthesis of the amino acid methionine which is involved in lipid metabolism. Folic acid has a primary role in systems involved with the transfer of single carbon units to other substances. Such reactions include: purine synthesis, pyrimidine nucleotide synthesis, and the conversion of three amino acids. These conversions include the interconversion of the nonessential amino acids serine and glycine, the catabolism of histidine to glutamic acid, and the conversion of homocysteine to methionine. Absorption and excretion Folic acid is absorbed primarily in the proximal third portion of the small intestine. Folate in food is in the form of polyglutamate. Excess glutamates must be split off to make folate absorbable. Approximately one-half of the stored folate is in the liver. Folate is excreted in the urine and bile.
      • Clinical conditions
      • Folic acid deficiency has six major causes:
      • <I>inadequate diet</I> of fresh fruits and vegetables, the consumption of over-processed foods in which the heat has destroyed folate, or alcoholism that is often associated with a poor diet;
      • 2) <I>inadequate absorption</I> due to malabsorption diseases such as gluten-induced enteropathy, tropical sprue, or drugs such as anticonvulsants, barbiturates, ethanol, cholestyramine, or azulfidine;
      • 3) <I>inadequate use</I> by metabolic block due to folic acid antagonistic drugs, enzyme deficiencies, vitamin B12 deficiency, alcohol, ascorbic acid deficiency, and dietary amino acid excess of glycine and methionine;
      • 4) <I>increased requirement</I> due to extra tissue demand by the fetus or malignant tissue, infancy, increased metabolism, and increased *hematopoiesis**;
      • 5) <I>increased excretion</I> due to vitamin B12 deficiency, liver disease, and kidney dialysis; and
      • 6) <I>increased destruction</I> due to excess of antioxidant supplements.
      Food Sources Primary folate sources include yeast, liver, fresh green vegetables, and fresh fruits such as oranges. Folate is a heat-labile substance that is easily destroyed by cooking, especially in water. Up to 50-90% of folate may be destroyed by cooking.
    • Supplementation Folate supplementation is primarily used to prevent neural tube defects. The recommendation for fertile women is 400 mcg and increases to 600 mcg during pregnancy. The Food and Drug Administration has mandated the fortification of grain products with folate. Up to 15 mg of folate per day will not cause toxicity. Very high doses may have a convulsant effect, and a dose of 350 mg per day has been reported to cause zinc deficiency
    • Vitamin C Function Vitamin C is a generic descriptor for all compounds exhibiting the biological activity of ascorbic acid, and the vitamin is often called ascorbic acid. Vitamin C has three main functions: to provide reducing equivalents for biochemical reactions, to serve as a cofactor for reactions requiring reduced metal ions, and to serve as a protective antioxidant. Vitamin C is a reductive cofactor in the hydroxylation of the amino acids proline and lysine during the formation of collagen. It also has an influence on other connective tissue components, elastin, fibronectin, and bone matrix. As an antioxidant, vitamin C can donate electrons to decrease free radicals, and can easily return to its reduced state. Vitamin C protects against the peroxidation of plasma lipid and low-density lipid protein (LDL), provides antioxidant protection in the eye, and protects DNA from oxidative damage. Vitamin C has many other functions in the body. It is involved in the neurotransmitter synthesis. Vitamin C is involved in the regulation of iron metabolism. Dietary vitamin C enhances the absorption of nonheme iron, but can also interact with iron to promote oxidative damage. Vitamin C and iron play a role in the synthesis of carnitine. Vitamin C enhances vasodilatory and anticlotting effects.
    • Absorption and excretion The absorption of vitamin C into the intestinal tract is an active process requiring energy. Absorption is dose dependent, being greater with low dietary intake of vitamin C. Only 50% of vitamin C is absorbed when intakes are as high as 1 to 1.5 grams. Vitamin C is found in the body in the pituitary and adrenal glands, leukocytes, eye lenses, and the brain. As plasma ascorbic acid increases, the ability of the renal tubules to absorb it maximizes (called renal threshold). Unabsorbed excess is excreted in the urine. Clinical conditions Vitamin C deficiency results in a disease called scurvy. Many symptoms of the disease are due to defects in connective tissue formation. Symptoms include inflammed and bleeding gums, bleeding into joints and peritoneal cavity, arthralgia, impaired wound healing, weakness, fatigue, depression, and vasomotor instability. Scurvy is rare in developed countries but it is seen in cases of alcohol and drug abuse, which usually coincide with a poor diet. Food Sources Vitamin C is found most abundantly in citrus fruits and juices, green vegetables, tomatoes, tomato juice, and potatoes.
    • Supplementation The effects of vitamin C supplementation on disease states has been studied extensively but still remain controversial. Vitamin C alters the immune system, specifically lymphocyte proliferation and natural killer cell activities. The vitamin inhibits and inactivates viruses, but no clinical efficacy has been proven. Vitamin C supplementation trials have not shown that it reduces the incidence of colds, but some studies have seen a decrease in the duration and severity of colds with supplementation. Vitamin C blocks carcinogenic processes through antioxidant activity. Epidemiological studies have shown a strong association of vitamin C supplementation with decreased risk of cancer of the oral cavity, esophagus, stomach, and pancreas. Less strong associations were found with lung, cervix, rectum, and breast cancer. Epidemiological studies have shown mixed results of the efficacy of vitamin C for heart disease. It has been suggested that vitamin C may decrease risk of heart disease due to the inhibition of plasma LDL oxidation and vasodilatory and anticlotting activity.
    • Vitamin B12 Function Vitamin B12, or cobalamin, is a coenzyme for methylmalonyl-CoA mutase and methionine synthetase. Methionine synthetase is involved in the synthesis of DNA and RNA via purine and pyrimidines. The enzyme influences the entry of folate into cells. Folate demethylates by the conversion of homocysteine to methionine via methionine synthetase. The enzyme methylmalonyl-CoA mutase is involved in the conversion of propionic to succinic acid, a factor of fatty acid metabolism. Absorption and excretion Vitamin B12 has a high affinity for glycoproteins. Intrinsic factor is a glycoprotein that is secreted by the gastric cells and is required for absorption of vitamin B12. It moves into the ileum where it is absorbed. The vitamin is transported to cells by a protein carrier called transcobalamin I. Clinical conditions Megaloblastic anemia is a condition that results from a deficiency in B12. It is actually a deficiency in intracellular folate accompanied by B12 deficiency. Vitamin B12 deficiency can also result in neuropathy and with high homocysteine levels. Causes of B12 deficiency are: malabsorption, pancreatic insufficiency, pernicious anemia, AIDS, and an abnormal connection between the colon and small intestine.
    • Food Sources Vitamin B12 is only found in animal tissue. Liver is the primary source of vitamin B12. Other sources are meat and fish. Supplementation Vitamin B12 injections are commonly given intramuscularly by physicians to prevent pernicious anemia. Oral vitamin B12 can be used effectively in raising serum vitamin B12 levels. Other indications for which supplemental B12 has been used are AIDS, Alzheimer's disease, asthma, and depression, although scientific information is limited.
    • FAT SOLUBLE COMPOUNDS Introduction of Fat-Soluble Vitamins Vitamins have been discovered over the last century as a result of the investigations into what caused certain diseases. Vitamins are defined by two essential characteristics. A vitamin must be a vital organic dietary substance that is not carbohydrate, fat, or protein, and is necessary in very small quantities to perform a metabolic function or prevent a deficiency state. A vitamin cannot be manufactured by the body and therefore must be supplied by food. The discovery of vitamin D has lead to the belief that it is more a hormone than a vitamin, but still is discussed with vitamins.
    • Vitamin A Vitamin A is a term used to describe a family of essential, fat-soluble compounds structurally related to, and sharing the biological activity of, the lipid alcohol retinol. Vitamin A includes provitamin A carotenoids that are dietary precursers of retinol. Function Vitamin A is vital to normal vision. In the retina, vitamin A is responsible for the transduction of light into neural signals. Vitamin A has an important role in cellular differentiation, responsible for the integrity of epithelial tissues. Vitamin A is involved in embryonic development. It is thought that vitamin A has a role in immune function, both cell-mediated immunity and humoral immunity. Vitamin A deficiency is associated with a decrease in resistance to infection. Interventions with vitamin A have demonstrated an association with decreased severity of measles and diarrhea. Absorption and excretion Most of dietary preformed vitamin A is absorbed into the intestine, and absorption remains high with increased intake. Vitamin A is packaged along with lipids into chylomicrons for transport through the lymph and plasma to the liver. The liver is the principal storage site of vitamin A and the majority of retinol oxidation and catabolism takes place here. Too little dietary fat and factors that interfere with lipolysis or emulsification may decrease absorption of vitamin A.
    • Clinical conditions A deficiency of vitamin A leads to epithelial keratinization, appetite changes resulting in poor growth, and xerophthalmia. Each year approximately 3 to 10 million children in developing countries become xerophthalmic and 250,000 to 500,000 become blind. Overconsumption of vitamin A by ten times the RDA results in a condition called hypervitaminosis A. Symptoms include headache, vomiting, diplopia, alopecia, dry mucous membranes, desquamation, bone and joint pain, liver damage, hemorrhage, and coma. Too much dietary vitamin A may be teratogenic. Spontaneous abortions and birth defects have occurred with the consumption of the 13-cis RA form of vitamin A, such as found in the acne drug Accutane. Food Sources Plants synthesize provitamin A carotenoids, which humans convert to retinol. Preformed vitamin A is found in animal foods only. The best sources of vitamin A include liver, yellow and green leafy vegetables, eggs, and whole milk products. Supplementation The safe upper limit of vitamin A is 8000 to 10000 IU, or 3000 mcg RE. Supplements of 50,000 to 200,000 IU have been utilized to protect children from developing xerophthalmia for a period of four to six months. Retinoids are used in topical agents for hyperkeratoic disorders, acne, and skin cancer, due to their influence on epithelial cell proliferation. Vitamin A has also been used in cancer prevention. Epidemiological studies have shown an association of total vitamin A to reduced risk of epithelial cancer.
    • Vitamin E Vitamin E is a term used for molecules that exhibit the biological activity of alpha-tocopherol. Function Vitamin E is an antioxidant that prevents free radical damage in biological membranes. It is a potent scavenger of peroxyl radicals and protects polyunsaturated fatty acids within phospholipids in membranes and in plasma lipoproteins. Vitamin E has an effect on several enzyme activities and membrane properties. It is involved in the regulation of vascular smooth muscle cell proliferation and protein kinase C activity. Absorption and excretion Vitamin E absorption into the intestinal lumen requires bile and pancreatic secretions. Vitamin E is incorporated into chylomicrons and secreted from the intestine to the lymph. The chylomicrons are taken up by lipoproteins, such as high-density lip oproteins (HDL), and travel to the liver. Vitamin E is secreted by the liver in very low-density lipoproteins (VLDL). VLDL form low-density lipoproteins (LDL) and the vitamin E is transferred to HDL. Most of the vitamin E in the body is stored in adipose tissue. Vitamin E is excreted in the bile, urine, feces, and through the skin. Vitamin C and other hydrogen donors regenerate oxidized vitamin E in the body, restoring the antioxidant activity of vitamin E.
    • Clinical conditions Vitamin E deficiency is very rare and almost never occurs due to a dietary deficiency. A genetic defect in hepatic alpha-tocopherol transfer protein causes a vitamin E deficiency characterized by peripheral neuropathy. Vitamin E supplements o f 800-1200 milligrams (mg) per day can prevent neurological problems in people with this defect. Vitamin E deficiency can also be caused by a genetic defect in lipoprotein synthesis. People with this defect have an impaired ability to absorb dietary fat. Symptoms include steatorrhea, retarded growth, retinitis pigmentosa, and neurological disorders with ataxia. Vitamin E deficiency can also result from fat malabsorption. Fat malabsorption can be caused by a resection of the small bowel, Crohn's disease, celiac disease, and chronic pancreatitis. Children with cystic fibrosis can become vitamin E deficient due to impaired secretion of pancreatic digestive enzymes. Vitamin E supplementation is less effective for patients with fat malabsorption due to the role of fat in absorption of vitamin E. Food Sources Vegetable oils are the best sources of vitamin E. Unprocessed cereal grains and nuts are good sources. Meats containing animal fat also contain vitamin E.
    • Supplementation Supplemental vitamin E may be beneficial for the following indications: retinopathy in premature infants, anemia in infants, cardiovascular disorders, immune function, and cataracts. The National Academy of Sciences has set a tolerable upper inta ke level of 1000 mg for adults but such a limit has not been determined for infants. Supplemental vitamin E is available in two forms. The natural form is designated as d-alpha-tocopherol ; the synthetic form is dl-alpha-tocopherol. Natura l vitamin E is more beneficial than the synthetic version.
    • Vitamin D Vitamin D is produced in the epidermis and dermis of the skin by a small band of radiation from the sun (UV-B radiation). Function The primary function of vitamin D is to maintain serum calcium and phosphorus concentrations to support cellular processes, neuromuscular function, and bone ossification. Vitamin D enhances the efficiency of the small intestine in absorbing dietary calcium and phosphorus, and mobilizes calcium and phosphorus stores from the bone. Vitamin D has also been shown to have an effect on the immune system. Leukemic cells have receptors for 1,25(OH)2D3, responding to it by differentiating into macrophages. Absorption and excretion Vitamin D is incorporated into chylomicron. Approximately 80% is absorbed into the lymphatic system. Vitamin D is bound to vitamin D-binding protein in the blood and carried to the liver where it undergoes its first hydroxylation into 25-hydroxyvitamin D. This is then hydroxylated in the kidney into 1,25(OH)2D. When there is a calcium deficiency, parathyroid hormone is produced, which increases the tubular reabsorption of calcium and renal production of 1,25(OH)2D. The 1,25(OH)2D travels to the small intestine and increases the efficiency of calcium absorption.
    • Clinical conditions The classic vitamin D deficiency is called rickets, a disease that used to be seen in children. This is a bone-deforming disease characterized by enlargement of the epiphyses of long bones and the rib cage, bowing of the legs, bending of the spine, and weak and toneless muscles. Vitamin D deficiency can result in a secondary hyperparathyroidism which accelerates osteoporosis and a mineralization defect in bones resulting in an adult rickets or osteomalacia. This results in weakened bones and an increased risk of fractures. Chronic intestinal malabsorption syndromes such as liver disease, cystic fibrosis, Crohn's disease, and sprue may also result from a deficiency in vitamin D. Food Sources Few foods contain vitamin D naturally. Some are fish liver oil and fatty fish. Milk is fortified with vitamin D and is the primary source of dietary vitamin D. Some cereals, breads, and infant formulas are fortified with vitamin D, too. Supplementation Vitamin D deficiency in the elderly is treated with a dose of 50,000 IU for eight weeks followed by a maintenance dose of 400 IU.
    • Vitamin K The several existing forms of vitamin K have similar biological activity in blood clotting. Phylloquinone is the major form found in plants. Menaquinone is synthesized by intestinal bacterial flora. Menadione is a water-soluble vitamin K analog. Function Vitamin K functions in the clotting of blood. There are seven vitamin K dependent coagulation proteins, or factors, that are proenzymes. All require calcium for activation. A prothrombinase complex on the platelet membrane converts prothrombin (vitamin K clotting protein) to thrombin, which converts fibrinogen to fibrin. There are two vitamin K dependent bone proteins that serve an unclear role in bone metabolism. Absorption and excretion Vitamin K is absorbed into the small intestine and incorporated in chylomicrons. It then enters the lymphatic system and is transported through the body. In the liver, some vitamin K is stored, some is oxidized, and some is re-secreted with very low density lipoprotein (VLDL). Most vitamin K is excreted in the feces. Fat malabsorption syndromes result in decreased vitamin K absorption. Hyperlipidemia decreases the transfer of vitamin K to tissues.
    • Clinical conditions Vitamin K deficiency is rare in adults and is more likely to occur in breast-fed newborns. Vitamin K deficiency results in easy bruising and bleeding, such as gastrointestinal hemorrhage, menorrhagia, and hematuria. Newborns are susceptible to vitamin K deficiency because the placenta is a poor transmittor of lipids, the neonatal liver is immature with respect to prothrombin synthesis, breastmilk is low in vitamin K, and the infant gut is sterile in the first few days of life. Vitamin K deficiency in newborns is called Hemorragic Disease of the Newborn. Malabsorption syndromes and other gastrointestinal disorders decrease vitamin K. Liver disease can result in hypoprothrombinemia whereby the liver is unable to use vitamin K to synthesize vitamin K-dependent factors. Drug therapy can result in a vitamin K deficiency. Drugs such as coumarin, salicyclates, some antibiotics, and megadoses of vitamin A and vitamin E antagonize the action of vitamin K. Food Sources Phylloquinone is widely distributed in plant foods, especially high in green leafy vegetables such as spinach, kale, turnip greens, and green tea leaves. Menaquinone is found in liver and some cheeses. Supplementation To prevent hemorrhagic disease, 1 mg of the phyolloquinone form of vitamin K is injected into newborns at birth. No toxicity has been seen at intakes 500 times the RDA.
    •