A vitamin is now generally accepted to be an organic compound that is a component of a natural food, but is distinct from other nutrients such as carbohydrates, fats, proteins, minerals and water.
A vitamin is now generally accepted to be an organic compound that is (1) a component of a natural food, but is distinct from other nutrients such as carbohydrates, fats, proteins, minerals and water; (2) present in most foods in a minute amount; (3) essential for normal metabolism in physiological functions such as growth, development, maintenance and reproduction; (4) a cause of a specific deficiency disease or syndrome if absent from the diet or if improperly absorbed or utilized; and (5) not always synthesized by the host in sufficient amounts to meet physiological demands and therefore must be obtained from the diet. Vitamins are differentiated from the trace elements, also present in the diet in small quantities, by their organic nature.
Some vitamins deviate from the preceding definition in that they do not always need to be constituents of food (McDowell, 2000). Vitamin C (ascorbic acid), for example, can be synthesized by companion animals and farm livestock with the exception of fish. Nevertheless, a deficiency has been reported in some species that synthesize vitamin C, and supplementation with this vitamin has been shown to have therapeutic value for certain disease conditions or for maximizing performance. For example, swine, poultry and ruminants can synthesize vitamin C, but there is a favorable response to supplemental C when these animals are under stress. Also, some swine have been shown to have a genetic defect that limits synthesis of the vitamin. Likewise, for most species, niacin can be synthesized from the amino acid tryptophan (but not by the cat or by the fish species studied to date) and choline from the amino acid methionine. The fact that niacin deficiency can be induced easily in various fish suggests that most fish do not have the capacity to synthesize niacin.
Vitamin D can be synthesized from the action of ultraviolet (UV) light on a precursor compound in the skin. This is not true, however, for dogs and cats (and possibly other carnivores), which derive little or no vitamin D from UV light activity on skin (How et al., 1994a, b; 1995). Although there is often synthesis of niacin and vitamin D, these normally will be supplemented in modern animal diets. Except for fish, vitamin C supplementation is considered only under special circumstances, such as environmental stress, for other farm livestock and companion animals.
Classically, vitamins have been divided into two groups based on their solubilities in fat solvent or in water (Table 1). Thus, fat-soluble vitamins include A, D, E and K, while vitamins of the B complex and vitamin C are classified as water soluble. Fat-soluble vitamins are found in feedstuffs in association with lipids. The fat-soluble vitamins are absorbed along with dietary fats, apparently by mechanisms similar to those involved in fat absorption.
Conditions favorable to fat absorption, such as adequate bile flow and good micelle formation, also favor absorption of the fat-soluble vitamins (Scott et al., 1982; McDowell, 2000). Water-soluble vitamins are not associated with fats and alterations in fat absorption do not affect their absorption. The fat-soluble vitamins A and D and, to the lesser extent, E are generally stored in appreciable amounts in the animal body. Water-soluble vitamins are not stored and excesses are rapidly excreted, except for vitamin B12 and perhaps biotin. Table 2 lists solubility characteristics of 16 vitamins classified as either fat or water soluble. Although metabolically essential, not all of these vitamins would be dietary essentials for all species.
The history of the discovery of the vitamins is an inspirational and exciting account of the ingenuity, dedication and self-sacrifice of many individuals. Excellent reviews of this history and accompanying references can be found in Funk (1922), Harris (1955), McCollum (1957) and Wagner and Folkers (1962). A recent review highlights the early history of vitamins (McDowell, 2006). This history section draws on those reviews, sometimes without specific citations, and readers are encouraged to refer to the reviews. The development of the concept of vitamins can be roughly divided into four, broadly overlapping periods: 1) empirical healing of some diseases through the administration of certain foods; 2) development of analytical capabilities to identify classes of nutrients in foods; 3) experimental induction of dietary diseases in animals; and 4) administration of synthetic diets to discover essential nutritional factors.
Most of the history of vitamins is linked to efforts to find cures for human diseases such as night blindness, xerophthalmia, scurvy, beriberi, rickets and pellagra. Experiments with animals including rats, mice, chickens, pigeons, guinea pigs and dogs contributed greatly to the advances made in vitamin research between 1900 and the 1930s.
The first phase of developing the concept of vitamins began many centuries ago, and gradually led to the recognition that night blindness, xerophthalmia, scurvy, beriberi and rickets are dietary diseases. These diseases had long plagued humankind and they were mentioned in the earliest written records. Records of medical science from antiquity attest to the fact that researchers had already made a link between certain foods and diseases or infirmities, postulating that food constituents played either a causal or a preventive role. These are considered the nebulous beginnings of the concept of essential nutrients (Wagner and Folkers, 1962).
Beriberi is probably the earliest documented deficiency disorder, being recognized in Chinaas early as 2697 B.C. By 1500 B.C., scurvy, night blindness and xerophthalmia were described in Egypt. Two books of the Bible contain accounts that point to vitamin A deficiency (McDowell, 2006). Jeremiah 14:6 states: “and the asses did stand in high places, their eyes did fail because there was no grass.” In addition, the Bible mentions that fish bile was used to cure a blind man named Tobias.
In 400 B.C., the Greek physician Hippocrates, known as the Father of Medicine, reported using raw ox liver dipped in honey to prevent night blindness. He also described soldiers afflicted with scurvy. Scurvy took a heavy toll on the Crusades because the soldiers travelled far from home and their diet was deficient in vitamin C.
During the long sea voyages that took place between 1492 and 1600, scurvy posed a serious threat to the health of sailors and undermined world exploration. For example, Magellan lost 80% of his crew to the disease while sailing around the world. Vasco de Gama, another great explorer, lost 60% of his 160-man crew while mapping the coast of Africa. In 1536, during Jacques Cartier’s expedition to Canada, 107 out of 110 men became sick with scurvy. However, the expedition was saved when the Indians shared their knowledge of the curative value of pine needles and bark. In 1593, British Admiral Richard Hawkins wrote: “I have seen some 10,000 seamen die of scurvy, some sailors tried treating themselves by trimming the rotting, putrid black flesh from their gums and washing their teeth in urine.”
In 1747, James Lind, a British naval surgeon, carried out the first controlled clinical experiment aboard a ship aimed at finding a cure for scurvy (Lind 1757). Twelve patients with scurvy were divided into six treatment groups. Two sailors received a dietary supplement of oranges and lemons while the other treatment groups were given nutmeg, garlic, vinegar, cider and sea water, respectively. The two men who had received the citrus fruit were cured of scurvy. Where did Lind get the idea that scurvy was related to nutrition? He had been told a story of an English sailor with scurvy who was left to die on a desolate island with no food. Feeling hungry, the man nibbled a few blades of beach grass. The next day, he felt stronger and ate some more grass. After a few weeks on this “diet,” he was completely well.
Prior to the beginning of the 20th century, there was a growing body of evidence that nutritional factors, which later became known as vitamins, were implicated in certain diseases. Louis Pasteur was the chief opponent of the “vitamin theory,” which held that certain diseases resulted from a shortage of specific nutrients in foods. Pasteur believed there were only three classes of organic nutrients: carbohydrates, fats and proteins. His research showing that microorganisms caused disease made scientists with medical training reluctant to believe the vitamin theory. It has been said that the immensely successful “germ theory” of disease, coupled with toxin theory and the successful use of antisepsis and vaccination, convinced scientists of the day that only a positive agent could cause disease (Guggenheim, 1995). Right up to the mid-1930s, the majority of U.S. doctors still believed that pellagra was an infectious disease (McDowell, 2006).
In the second half of the 19th century, a disease other than scurvy was killing sailors in the Japanese navy. In 1880, the Japanese navy numbered 4,956; within a year, 1,725 men had died of beriberi. In three years, almost 5,000 Japanese sailors died of beriberi. Patients with beriberi became weak and eventually partially paralyzed, lost weight and died. Doctors tried to find the germ that was causing beriberi. Finally, they listened to Japanese naval surgeon Kamekiro Takaki, who believed that the sailors’ diet was causing beriberi. Takaki noted a 60% incidence of beriberi on a ship returning from a one-year voyage during which the sailors’ diet had been mostly polished rice and some fish. He sent out a second ship under the same conditions, but this time substituted barley, meat, milk and fresh vegetables for some of the rice. The dietary change eliminated beriberi but Takaki incorrectly concluded that the beriberi was prevented by the additional protein. Regardless, the Japanese now knew that they could prevent beriberi by not relying on polished rice as the only dietary staple.
Beginning in the mid-1850s, German scientists were recognized as leaders in the field of nutrition. In the late 1800s, Professor C. von Bunge, who worked at the German university in Dorpat, Estonia and then at Basel, had some graduate students conduct experiments with purified diets for small animals (Wolf and Carpenter, 1997). In 1881, N. Lunin, a Russian student studying in von Bunge’s laboratory, observed that some mice died after 16 to 36 days when fed a diet composed solely of purified fat, protein, carbohydrate, salts and water. Lunin suggested that natural foods such as milk contain small quantities of “unknown substances essential to life.”
In 1896, Dutch physician and bacteriologist Christian Eijkman made a historic finding in relation to a cure for beriberi. Eijkman was conducting research in Indonesia in an effort to identify the causal pathogen of beriberi. He astutely observed that a polyneuritis condition in chickens produced clinical signs similar to those seen in humans with beriberi. This chance discovery was made when a new head cook at the hospital discontinued the supply of “military” rice (polished rice), and the chickens were fed the whole-grain “civilian” rice recovered from the polyneuritis. Many great advances in science have come about as a result of chance observations like this being made by men and women of inspiration. After extensive experimentation, Eijkman proved that both polyneuritis and beriberi were caused by eating polished white rice and that both of these afflictions could be prevented or cured when the outer portions of the rice grain (e.g. rice bran) were eaten. Thus, Eijkman became the first researcher to produce a vitamin deficiency disease in an experimental animal (Eijkman, 1890-1896). He also noted that prisoners with beriberi who had been eating polished rice tended to get well when they were fed a less milled product. In 1901, Grijns, one of Eijkman’s colleagues inIndonesia, was the first to come up with a correct interpretation of the connection between the excessive consumption of polished rice and the etiology of beriberi. He concluded that rice contained “an essential nutrient” found in the outer layers of the grain.
In 1902, a Norwegian scientist named Holst conducted some experiments on “ship-beriberi” (actually scurvy) using poultry, but the experiments failed. In 1907, Holst and Frolich produced experimental scurvy in guinea pigs. Later it was learned that poultry can synthesize vitamin C, while guinea pigs cannot.
In 1906, Frederick Hopkins, who was working with rats in England, reported that “no animal can live upon a mixture of pure protein, fat and carbohydrate and even when the necessary inorganic material is supplied, the animal cannot flourish.” Hopkins found that small amounts of milk added to purified diets allowed rats to live and thrive. He suggested that unknown nutrients were essential for animal life, calling them “accessory food factors.” Hopkins’ experiments were similar to those of Lunin; however, they were more in-depth, and he played an important role by recording his views in such memorable terms that they received wide recognition (McCollum, 1957). Hopkins also expressed the belief that various disorders were caused by diets deficient in unidentified nutrients (e.g., scurvy and rickets). He was responsible for opening up a new field of discovery that largely depended on the use of experimental rats.
In 1912, Casimir Funk, a Polish biochemist working at the Lister Institute in London, proposed the “vitamin theory” (Funk 1922). He had reviewed the literature and made the important conclusion that beriberi could be prevented or cured by a protective factor present in natural food, which he successfully isolated from rice by-products. What he had isolated was given the name “beriberi vitamin” in 1912. This term “vitamin” denoted that the substance was vital to life and it was chemically an amine (vital + amine). In 1912 Funk proposed the theory that other “deficiency diseases” in addition to beriberi were caused by a lack of these vital substances, namely scurvy, rickets, sprue and pellagra. He was apparently the first to suggest that pellagra was a nutrient deficiency disease.
In 1907, Elmer McCollum arrived in Wisconsin to work on a project to determine why cows fed wheat or oats (versus yellow corn) gave birth to blind or dead calves. The answer was found to be that wheat and oats lacked the vitamin A precursor carotene. In 1913-1915, McCollum and Davis discovered two growth factors for rats, “fat-soluble A” and “water-soluble B.” By 1922, McCollum had identified vitamin D as a substance independent of vitamin A. He bubbled oxygen through cod liver oil to destroy its vitamin A; the treated oil remained effective against rickets but not against xeropthalmia. Thus, “fat-soluble vitamin A” had to be two vitamins, not just one.
In 1923, Evans and Bishop discovered that vitamin E deficiency caused reproductive failure in rats. Steenbock (1924) showed that irradiation of foods as well as animals with ultraviolet light produced vitamin D. In 1928, Szent-Györgyi isolated hexuronic acid (later renamed “ascorbic acid”) from foods such as orange juice. One year later, Moore proved that the animal body converts carotene to vitamin A. This experiment involved feeding one group of rats carotene and finding higher levels of vitamin A in their livers compared to controls. By 1928, Joseph Goldberger and Conrad Elvehjem had shown that vitamin B was more than one substance. After the “vitamin” was heated, it was no longer effective in preventing beriberi (B1), but it was still good for rat growth (B2). The 1930s and 1940s were the golden age of vitamin research. During this period, the customary approach was to: 1) study the effects of a deficient diet; 2) find a food source that prevents the deficiency; and 3) gradually concentrate the particular nutrient (vitamin) in a food and test potency. Laboratory animals were used in these procedures.
Henrick Dam of Denmarkdiscovered vitamin K in 1929 when he noted hemorrhages in chicks fed a fat-free diet. Ironically one year earlier, Herman Almquist, working in the United States, had discovered both forms of the vitamin (K1 and K2) in studies with chicks. Unfortunately university administrators delayed the review of his paper, and when it was finally submitted to the journal Science, it was rejected. Therefore, only Henrick Dam received a Nobel prize for the discovery of vitamin K.
Vitamin B12 was the last traditional vitamin to be identified in 1948. Shortly thereafter it was discovered that cobalt was an essential component of the vitamin. Simple monogastric animals were found to require the vitamin, whereas ruminants and other species with large microbial populations (e.g., horses) require dietary cobalt rather than vitamin B12.
Compared with the situation for night blindness, xeropthalmia, beriberi, scurvy and rickets, there were no records from the ancient past of the disease of pellagra. The disease was found to be caused by niacin deficiency in humans, a problem prevalent mainly in cultures where corn (maize) was a key dietary staple (Harris, 1919). Columbus took corn to Spain from America. Pellagra was not recognized until 1735, when Gaspar Casal, physician to King Philip V of Spain, identified it among peasants in northern Spain. The local people called it mal de la rosa, and Casal associated the disease with poverty and spoiled corn. The popularity of corn spread eastward from Spain to southern France, Italy, Russia and Egypt, and so did pellagra. Babcock, of Columbia, South Carolina, who identified pellagra in the United States by establishing a link with the disease in Italy, studied the case records of the South Carolina State Hospital and concluded that the disease had occurred there as early as 1828. Most of the cases occurred in low-income groups, whose diet was limited to inexpensive foodstuffs. Diets characteristically associated with the disease were referred to as the three M’s, specifically meal (corn), meat (backfat) and molasses.
The word pellagra means rough skin, which relates to dermatitis. Other descriptive names for the condition were mal de sol (illness of the sun) and “corn bread fever.” In the early 1900s in the United States, particularly in the South, it was common for 20,000 deaths to occur annually from pellagra. It was estimated that for every death due to pellagra, there were at least 35 cases of the disease. Even as late as 1941, five years after the cause of pellagra was known, 2,000 deaths were attributed to the disease. The clinical signs and mortality associated with pellagra can be referred to as the four D’s: dermatitis (of areas exposed to the sun), diarrhea, dementia (mental problems) and death. Several mental institutions in the United States, Europe and Egypt were primarily devoted to the care of pellagra sufferers, or pellagrins.
In 1914, Goldberger, a bacteriologist with the United States Public Health Service, was assigned the task of identifying the cause of pellagra. In his studies, he observed that the disease was associated with poor diet and poverty and that well-fed persons did not contract the disease (Carpenter, 1981). In orphanages, prisons and mental institutions in South Carolina, Georgia and Mississippi the therapeutic value of good diets was demonstrated. In order to prove that pellagra was not an infectious disease, Goldberger, his wife and 14 volunteers constituted a “filth squad” who ingested and were injected with various biological materials and/or excreta from pellagrins. These extreme measures did not result in pellagra, thus demonstrating the non-infectious nature of pellagra. At the time, researchers and physicians did not want to believe that pellagra resulted from poor nutrition, and they sought to link it to an infection in keeping with the popular “germ theory” of diseases (McDowell, 2006). An important step toward isolating the preventive factor for pellagra involved the discovery of a suitable laboratory animal for testing its potency in various concentrated preparations. It was found that a pellagra-like disease (blacktongue) could be produced in dogs. Elvehjem and his colleagues (1937) isolated nicotinamide from liver and identified it as the factor that could cure blacktongue in dogs. Reports of the dramatic therapeutic effects of niacin in human cases of pellagra quickly followed from several clinics.
In 1824, Combe first discovered fatal anemia (pernicious anemia) and suggested that it was linked to a digestive disorder. Minot and Murphy reported in 1926 that large amounts of raw liver would alleviate the symptoms of pernicious anemia. In 1948, Rickes and his colleagues in the United States and Smith in England isolated vitamin B12and identified it as the anti-pernicious anemia factor (McDowell, 2006).
Much earlier, in 1929, Castle had shown that pernicious anemia resulted from the interaction between a dietary factor (extrinsic) and a mucoprotein substance produced by the stomach (intrinsic factor). Castle used an unusual, but effective, method to relieve the symptoms of pernicious anemia patients. He ate some beef and after allowing enough time for the meat to mix with gastric juices, he regurgitated the food and mixed his vomit with the patients’ food. With this treatment, the patients were able to recover because they received both the extrinsic (vitamin B12) and intrinsic (a mucoprotein) factors from Castle’s incompletely digested beef meal.
Definite vitamin requirements are given in the National Research Council (NRC) publications for swine (NRC, 1998), poultry (NRC, 1994) and fish (NRC, 2011). Thirteen vitamins are listed as required for swine and poultry: the four fat-soluble vitamins of A, D, E and K, and the water-soluble vitamins of thiamin, riboflavin, niacin, pantothenic acid, vitamin B6, biotin, folic acid, vitamin B12 and choline.
Poultry raised in intensive production systems are particularly susceptible to vitamin deficiencies (Scott et al., 1982). Reasons for this susceptibility are that (1) poultry derive little or no benefit from microbial synthesis of vitamins in the gastrointestinal tract; (2) poultry have high requirements for vitamins; and (3) the high-density concentration of modern poultry operations places many stresses on the birds that may increase their vitamin requirements. Typical grain-oilseed meal poultry diets (e.g., corn-soybean meal) are generally supplemented with vitamins A, D3, E, K, riboflavin, niacin, pantothenic acid, B12 and choline (Scott et al., 1982). Thiamin and vitamin B6 are usually present in adequate quantities in the major ingredients of corn-soybean meal-based diets. More attention is now being given to circumstances where supplemental biotin and folic acid are justified. Carnitine has been found to be of value in some studies.
Vitamin D and B12 are almost completely absent from diets based on corn and soybean meal. Vitamin K is generally added to poultry diets more than to other species’ diets because birds have less intestinal synthesis due to a shorter intestinal tract and faster rate of food passage. Birds in cages have less access to feces (coprophagy) and therefore need higher levels of supplemental vitamins. Supplemental vitamins (e.g. vitamin C) alleviate heat stress in poultry (Shain et al., 2004; Roussan et al., 2008). A number of vitamins, including vitamins, A, E, D and C have been shown to improve the immune responses in poultry (Puthpongsiriporn et al., 2001) and swine (Shankar, 2006). Some vitamins are administered in excess of traditional requirements (e.g., vitamin E and C). They play a role as antioxidents in order to improve immunity and health of poultry and swine (McDowell, 2000).
Vitamin supplementation of swine diets is obviously necessary, with vitamin needs having become more critical in recent years as complete confinement feeding has increased. Swine in confinement, without access to vitamin-rich pasture, and housed on slatted floors, which limit vitamins available from coprophagy, have a greater need for supplemental vitamins. For swine the vitamins most likely to be marginal or deficient in corn-soybean diets are vitamins A, D3, E, riboflavin, niacin, pantothenic acid and B12.
Almost all swine diets in the United Statesare now fortified with vitamins A, D3, E, K, B12, riboflavin, niacin, pantothenic acid, biotin and choline. An increasing number of feed manufacturers are adding folic acid and B6 for specific management and feeding regiments. Diets are fortified with these vitamins even though not all experiments indicate a need for each of them. Most feed manufacturers add them as a precaution to take care of stress factors, subclinical disease levels and other conditions on the average farm that may increase vitamin needs (Cunha, 1977). It appears that carnitine supplementation of weaning pigs has potential to improve performance (Newton and Burtle, 1992; Rincker et al., 2003; Rehfeldt and Kuhn, 2006).
Feeding fish in their aqueous environment involves considerations beyond those for feeding land animals. These aspects include the nutrient contribution of natural aquatic organisms in pond culture and the loss of nutrients if feed is not consumed immediately. Fish feeds require processing methods that provide special physical properties to facilitate feeding in water, and variation in feeding behavior requires special feeding regiments for various species (NRC, 2011). One problem with feeding fish relates to finding stable forms of vitamin C when feed is administered on the water.
Fish require 15 vitamins, the same 13 as poultry and swine require, as well as vitamin C and myo-inositol. The quantitative requirements for most of the vitamins have been established for chinook salmon, rainbow trout, common carp, channel fish and yellowtail, while only some of the requirements are known for other fish species. For warm-water fish, intestinal microorganisms are a source of certain B vitamins and presumably vitamin K. In cold-water carnivorous fish, however, microorganisms are not a significant source of vitamins (Hepher, 1988; NRC, 2011). However, vitamin B12 can be synthesized by intestinal microorganisms in catfish when an adequate dietary source of cobalt is available (Li et al., 2004).
Vitamins for which definite requirements are given in the Cattle (NRC, 2000, 2001), Sheep and Goats (NRC, 2007b) National Research Council (NRC) publications are A, D3 and E. It is well known that microorganisms in the rumen synthesize most B vitamins and vitamin K (Lardinois et al., 1944; Hungate, 1966). Rumen synthesis of the B vitamins and vitamin K develops rapidly in the young ruminant once solid feed is introduced into the diet. The rumen contents subsequently pass through parts of the digestive tract that are ideally suited for digestion and absorption of microbial products. Consequently, B vitamins and vitamin K synthesized in the rumen are readily available to the animal.
Although rumen microorganisms normally synthesize B vitamins and vitamin K in sufficient quantities to meet requirements, under special circumstances deficiencies have occurred and hence supplementation has proved beneficial for thiamin, niacin, biotin, vitamin B12, choline, carnitine, folic acid and vitamin K. Supplemental biotin has been found beneficial for ruminants, particularly high producing transitional dairy cows for both improving hoof integrity and increasing milk production (Seymour, 2001; Girard and Matte, 2006). Vitamin C can by synthesized in tissues by ruminants and most other animals under normal conditions; however, clinical cases of scurvy in ruminants have been described and supplemental vitamin C may be beneficial under certain conditions (e.g., stress). Since the conditions in which supplemental vitamin C may be beneficial are not well defined, recommended requirements are not included in the ruminant NRC publications.
Supplemental choline is readily destroyed by ruminal microorganisms, however, a by-pass choline supplement has increased lactational performance (Emanuele et al., 2007; Toghdory et al., 2007) and growth performance of finishing cattle (Bryant et al., 1999; Bindel et al., 2000). Vitamin E at high dietary concentrations counteracted detrimental reproductive effects for bulls fed high gossypol diets (Velasquez-Pereira et al., 1998). High levels of supplemental vitamin E prior to slaughter can improve meat quality and color (Yang et al., 2002; Formanek et al., 2003) while high dietary concentrations of vitamin D3 has increased meat tenderness (Foot et al., 2004; Gutierrez et al., 2007). Several vitamins (e.g., vitamin E) administered to ruminants have increased immune response (NRC, 2000; Abdukalykova et al., 2008).
Digestive systems of young ruminants, before full development of the rumen and its microflora, resemble those of monogastric animals. A reasonable assumption is that ruminants, at the tissue level, require the same vitamins as monogastric animals. Similarity of requirements has been shown for young ruminants before development of the rumen (usually 6 to 8 weeks of age). Deficiencies of thiamin, riboflavin, vitamin B6, pantothenic acid, choline, biotin, niacin and vitamin B12 have been produced experimentally in young ruminants prior to the development of the rumen (Miller, 1979).
Vitamin B deficiency signs can be easily produced in young ruminants prior to development of a functioning rumen. However, natural milk given to young ruminants provides adequate B vitamins in addition to vitamin A and E for good health and adequate performance. Levels of various vitamins in colostrum and whole milk of cows are show in Table 3. When young ruminants are fed milk replacers, however, it is advisable to verify the adequacy of vitamin intakes because supplementation may be needed until their rumens are functional. Such a determination is particularly important when a milk replacer contains appreciable quantities of non-milk protein. In pre-ruminants receiving milk replacers, the reticulo-rumen develops slowly, and rumen synthesis of various nutrients, including B complex vitamins, may be limited.
There is a lack of experimental information on the level of vitamins required for well-balanced horse diets, as well as on which vitamins are needed to be added (Cunha, 1991; Frape, 2004). The vitamins most likely deficient for all classes of horses are vitamins A and E, with vitamin D also deficient for horses in confinement. Racehorses that are exercised only briefly in the early morning, with little exposure to sunlight, may be receiving inadequate vitamin D. Also, it is not unusual for show horses to be housed indoors for extended periods of time during summer daylight hours in order to avoid dulling of the hair coat; thus loosing the opportunity of obtaining vitamin D activity from the sun. Requirements for vitamin A, D, and E can be met with high quality (e.g., green color) sun-cured hay. Deficiencies of vitamin K and the B vitamins appear to be less likely in the mature horse than in the other monogastric species, as many vitamins are synthesized in the cecum of the horse. It is not known, however, what quantities of the vitamins synthesized in the cecum are absorbed in the large intestine. Since it is unreliable to depend on intestinal synthesis, many horse owners use B vitamin supplementation of diets for the young horse and those being developed for racing or performance purposes (Cunha, 1991).
Horses grazing high-quality pastures are likely to need little or no supplementation because forages are rich sources of most fat- and water-soluble vitamins. In recent years however, vitamin supplementation has become more critical to the horse as the trend toward total confinement has increased. Currently, few horses receive high levels of vitamin intake from a lush green pasture or from a high-quality, leafy, green hay. Cunha (1991) suggested that a vitamin premix for horses contain vitamins A, D3, E, K, thiamin, riboflavin, niacin, B6, biotin, pantothenic acid, folic acid, B12and choline. Biotin supplementation is recommended as research has shown benefit of the vitamin for hoof integrity (Comben et al., 1984; Reilly et al., 1998, 1999).
Vitamin requirements have been recommended for dogs and cats (NRC, 2006; AAFCO, 2007). Despite the lack of precise information on the requirements of many vitamins for dogs and cats and the almost complete lack of information on vitamin bioavailability in important pet foods, there is a baseline of information on vitamin nutrition. Apparently dogs have some general similarities in vitamin requirements with other monogastric species (e.g., swine). Cats, however, show a specialization consistent with the evolutionary influence of a strict carnivorous diet. Cats lack the ability to synthesize taurine, cannot convert linoleic acid and are unable to cope with high levels of dietary carbohydrate. With regard to vitamins, cats cannot synthesize niacin from tryptophan or convert carotene to vitamin A. Unlike humans and most animals studied, both dogs and cats, as previously mentioned, have a nutritional requirement for vitamin D because insufficient quantities are synthesized in the skin from UV irradiation (How et al., 1994a, b; 1995). It is concluded that the cat, unlike the dog, is an obligate carnivore and is dependent on at least some animal derived materials in its diet. Diets that do provide more animal protein (particularly organ meats) will likewise often provide more bioavailable vitamins for companion animals. A cat diet must not only be nutritious but also highly palatable (Zaghini and Biagi, 2005).
Approximately 75% of nonaccidental deaths in dogs are due to cancer, kidney failure and heart disease. Data are accumulating that suggest that many “age related” diseases such as cancer and heart disease are caused in part by free-radical damage. Free radicals can be generated by stress factors including weaning, housebreaking, rapid gains and disease conditions. Supplementing pet diets with antioxidants such as vitamin E, vitamin C and beta-carotene can prevent or reduce the negative impact of free radical damage and thereby increase length and quality of life for companion animals.
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