DSM in Animal Nutrition & Health
Factors Affecting Vitamin Requirements and Vitamin Utilization
A. Physiological Make-Up and Production Function
Vitamin needs of animals and humans depend greatly on their physiological make-up, age, health and nutritional status and function, such as producing meat, milk, eggs, hair or wool, or carrying a fetus (Roche, 1979). For example, dairy cows producing greater volumes of milk have higher vitamin requirements than dry cows or cows producing low quantities. Breeder hens have higher vitamin requirements for optimum hatchability, since vitamin requirements for egg production are generally less than for egg hatchability. Higher levels of vitamins A, D3 and E are needed in breeder hen diets than in feeds for rapidly growing broilers. Selection for faster growth rate may allow animals to reach much higher weights at much younger ages with less feed consumed. Dudley-Cash (1994) concludes that since genetic potential has improved the rate of feed conversion 0.8% yearly and most of the NRC vitamin requirement data are 20 to 40 years old, vitamin requirements determined several decades ago may not apply to today’s poultry. Genetic selection of swine for faster weight gains and increased numbers of litters per year also increase vitamin requirements (Cunha, 1980, 1984b). Assuming the vitamin needs per unit of body protein accretion are relatively constant, Stahly et al., 2007 hypothesized that pigs with high capacities for lean tissue growth would require 2 to 4 times the daily B vitamin needs currently defined by NRC (1998). Stahly et al. (2007) compared dietary B-vitamin needs of strains of pigs with high and moderate lean growth, supplemented with an additional 0 to 400% of NRC requirements. Pigs from the high lean strain consumed less feed and grew faster and more efficiently than pigs of the moderate lean strain. In both lean strains, the rate and efficiency of growth were improved as dietary B-vitamin concentrations were increased.
Milk production per dairy cow in the United Stateshas more than doubled since the early 1960s. Individual cows that produce 13,000 to 15,000 kg (28,600 to 33,000 lbs) per 305-day lactation are becoming more common. It is logical to expect that such increases in production will have some impact on vitamin requirements for no other reason than the vitamin content of milk. Milk is an excellent source of most vitamins. Table 13 illustrates milk composition comparisons among three ruminants species, mares and sows.
Different breeds and strains of animals have been shown to vary in their vitamin requirements. In swine, apparently there is a wide variation in pantothenic acid requirements among breeds and among animals within the same breed. Data from Michigan suggest that in one-half of growing pigs studied, 9.13 mg pantothenic acid per kg (4.2 mg per lb) was sufficient for growth, whereas the remaining half required more than this but less than 13.5 mg per kg (6.1 mg per lb) (Luecke et al., 1953). Vitamin needs of new strains developed for improved production are higher (Stahly et al., 2007). Leg problems seen in fast-growing strains of broilers can be corrected in part by higher levels of biotin, folacin, niacin and choline (Roche, 1979). Improved genetic potential (breed, type and strain) for companion animals with different conformation (e.g., more lean mass), as needed for working or racing dogs, will influence vitamin requirements.
B. Confinement Rearing without Access to Pasture
The trend toward rearing livestock in complete confinement has had a profound effect on vitamin nutrition. Pasture could be depended on to provide significant quantities of most vitamins, since young, lush, green grasses or legumes are good vitamin sources. More available forms of vitamins A and E are present in pastures and green forages, which contain ample quantities of beta-carotene and alpha-tocopherol versus those found in grains, which are lower in bioavailability. Confinement rearing, to include poultry in cages and swine on slatted floors, provides limited animal access to feces (coprophagy), which is rich in many vitamins. Confinement rearing requires producers to pay more attention to higher vitamin requirement (Cunha, 1984).
C. Antioxidant and Immunity Role of Vitamins
Immunological response and disease conditions are intimately related to the requirements of certain vitamins. The antioxidant vitamins (vitamin E, vitamin C and beta-carotene) are particularly influenced by disease conditions. These nutrients play important roles in animal health by inactivating harmful free radicals produced through normal cellular activity from various stressors. Free radicals can be extremely damaging to biological systems (Padh, 1991). Free radicals, including hydroxy, hypochlorite, peroxy, alkoxy, superoxide, hydrogen peroxide and singlet oxygen, are generated by autoxidation, or radiation or from activities of some oxidases, dehydrogenases and peroxidases. Also, phagocytic granulocytes undergo respiratory bursts to produce oxygen radicals to destroy pathogens. However, these oxidative products can, in turn, damage healthy cells if they are not eliminated. Antioxidants serve to stabilize these highly reactive free radicals, thereby maintaining the structural and functional integrity of cells (Chew, 1995; McDowell, 2006). Therefore, antioxidants are very important to immune defense and health of humans and animals.
Tissue defense mechanisms against free-radical damage generally include vitamin C, vitamin E and beta-carotene as the major vitamin antioxidant sources. In addition, several metalloenzymes, which include glutathione peroxidase (selenium), catalase (iron) and superoxide dismutase (copper, zinc and manganese), are also critical in protecting the internal cellular constituents from oxidative damage. The dietary and tissue balance of all these nutrients are important in protecting tissues against free-radical damage.
In fish, vitamin C appears to protect phagocytic cells and surrounding tissues from oxidative damage. An increased immune response resulted from high dietary levels of vitamin C in channel catfish (Durve and Lovell, 1982; Li and Lovell, 1985), rainbow trout (Blazer and Wolke, 1984; Wahli et al., 1986; Navarre and Halver, 1989) and golden shiners (Chen et al., 2003). However, Lall et al., (1990) observed no differences in humoral response in Atlantic salmon.
Both in vitro and in vivo studies show that the antioxidant vitamins generally enhance different aspects of cellular and non-cellular immunity. The antioxidant function of these vitamins could, at least in part, enhance immunity by maintaining the function and structural integrity of important immune cells. A compromised immune system will result in reduced animal production efficiency through increased susceptibility to disease, thereby leading to animal morbidity and mortality. In data with rats, vitamin C was required for an adequate immune response in limiting lung pathology after influenza virus infection (Li et al., 2006). One of the protective effects of vitamin C may partly be mediated through its ability to reduce circulating glucocorticoids (Degkwitz, 1987). The suppressive effect of glucocorticoids on neutrophil function in cattle was alleviated with vitamin C supplementation (Roth and Kaeberle, 1985). In addition, ascorbate can regenerate the reduced form of alpha-tocopherol, perhaps accounting for the observed sparing effect of these vitamins (Jacob, 1995; Tanoka et al., 1997). In the process of sparing fatty acid oxidation, tocopherol is oxidized to the tocopheryl free-radical. Ascorbic acid can donate an electron to the tocopheryl free-radical, regenerating the reduced antioxidant form of tocopherol.
Vitamin C is the most important antioxidant in extracellular fluids and can protect biomembranes against lipid peroxidation damage by eliminating peroxyl radicals in the aqueous phase before the latter can initiate peroxidation (Frei et al., 1989). Vitamin C and E supplementation resulted in a 78% decrease in the susceptibility of lipoproteins to mononuclear cell-mediated oxidation (Rifici and Khachadurian, 1993).
In guinea pigs, vitamin C was shown to be important in maintaining normal primary and secondary antibody responses and was important for neutrophil function (Anderson and Lukey, 1987). Ascorbic acid is reported to have a stimulating effect on phagocytic activity of leukocytes, on function of the reticuloendothelial system and on formation of antibodies. Vitamin C can stimulate the production of interferons, the proteins that protect cells against viral attack (Siegel. 1974).
As an effective scavenger of reactive oxygen species, ascorbic acid minimizes the oxidative stress associated with the respiratory burst of activated phagocytic leukocytes, thereby functioning to control the inflammation and tissue damage associated with immune responses (Chien et al., 2004). Ascorbic acid is very high in phagocytic cells with these cells using free-radicals and other highly reactive oxygen containing molecules to help kill pathogens that invade the body. In the process, however, cells and tissues may be damaged by these reactive species. Ascorbic acid helps to protect these cells from oxidative damage.
Vitamin A, although it has less antioxidant potential than beta-carotene, has a strong influence on immunological response. Animals deficient in vitamin A will show increased frequency and severity of bacterial, protozoal and viral infections as well as other disease conditions. Part of the disease resistance, as a function of vitamin A, is related to maintenance of mucous membranes and normal functioning of the adrenal gland for production of corticosteroids needed to combat disease. An animal’s ability to resist disease depends on a responsive immune system. A vitamin A deficiency causes a reduced immune response.
Vitamin A deficiency affects immune functions, particularly the antibody response to T-cell-dependent antigens (Ross, 1992). The RAR-alpha mRNA expression and antigen-specific proliferative response of T-lymphocytes are influenced by vitamin A status in vivo, and directly modulated by retinoic acid (Halevy et al., 1994). Vitamin A deficiency affects a number of cells of the immune system, and that repletion with retinoic acid effectively reestablishes the number of circulating lymphocytes (Zhao and Ross, 1995).
Vitamin E is perhaps the most studied nutrient related to the immune response (Meydani and Han, 2006). Evidence accumulated over the years and in many species indicates that vitamin E is an essential nutrient for normal function of the immune system. Furthermore, studies suggest that beneficial effects of certain nutrients, such as vitamin E on reducing disease risk, can be through their effects on the immune response. Deficiency in vitamin E impairs B- and T-cell-mediated immunity. Vitamin E acts in part by reducing prostaglandin synthesis and by preventing the oxidation of PUFAs in cell membranes (Shankar, 2006).
A diminished primary antibody response could also increase the severity and/or duration of and episode of infection, whereas a diminished secondary response could increase the risk of developing a second episode of infection. Vitamin A deficiency causes decreases in phagocytic activity in macrophages and neutrophils. The secretory immunoglobulin A (IgA) system is an important first line of defense against infections of mucosal surfaces (McGhee et al., 1992). Several studies in animal models have shown that the intestinal IgA response is impaired by vitamin A deficiency (Davis and Sell, 1989; Wiedermann et al., 1993; Stephensen et al., 1996).
An optimal vitamin A range exists for enhancement of vitamin A responses, because both deficient and excessive levels suppress immune function. In many experiments with laboratory and domestic animals, the effects of both clinical and subclinical deficiencies of vitamin A on the production of antibodies and on the resistance of different tissues to microbial infection or parasitic infestation have frequently been demonstrated (Kelley and Easter, 1987). Supplemental vitamin A improved the health of animals infected with roundworms, hens infected with the genus Capillaria and rats with hookworms (Herrick, 1972). Vitamin A is valuable in treating ringworm (Trichphyton verrucosum) infection in cattle.
A combination of vitamin A (15,000 IU per kg or 6,818 IU per lb diet) and vitamin E (250 ppm) was more effective than either vitamin alone in reducing heat stress (32°C)-related decreases in broiler performance (Sahin et al., 2001a). High environmental temperature not only has an adverse effect on laying performance but also can impede disease resistance (Lin et al., 2006). Vitamin A supplementation at high levels (2-3 times the NRC requirement) to commercial layer hens under heat stress was beneficial to laying performance and immune function (Lin et al., 2002). Hens suffering heat-stress immediately after Newcastle disease vaccination need higher dietary vitamin A intake to obtain the maximal level of antibody production (Davis and Sell, 1989). Vitamin A could alleviate the oxidative injuries induced by heat exposure and immune challenge (Wang et al., 2002).
Vitamin A-deficient chicks showed rapid loss of lymphocytes and deficient rats showed atrophy of the thymus and spleen and reduced response to diphtheria and tetanus toxoids (Krishnan et al., 1974). Mortality from fowl typhoid (Salmonella gallinarum) was reduced in chicks fed vitamin A levels greater than the normal levels in a high protein diets. Serum antibody levels in chicks were increased two- to five-fold by high dietary vitamin A concentrations. The immune response from introduced Newcastle disease virus was higher for broiler chicks receiving 2,500 IU of vitamin A compared to controls and the best for those receiving 20,000 IU (Serman and Mazija, 1985). Harmon et al. (1963) studied the effect of a vitamin A deficiency on antibody production by baby pigs and found a high correlation coefficient between serum vitamin A and antibody titer. Baby pigs infected with Trichuris suis responded to supplemental vitamin A by an enhanced immunological response compared to controls (Bebravicius et al., 1987).
Animal studies indicate that certain carotenoids with antioxidant capacities, but without vitamin A activity, can enhance many aspects of immune functions, can act directly as antimutagens and anticarcinogens, can protect against radiation damage, and can block the damaging effects of photosensitizers. Also, carotenoids can directly affect gene expression and this mechanism may enable carotenoids to modulate the interaction between B-cells and T-cells, thus regulating humoral and cell-mediated immunity (Koutsos, 2003). Lack of carotenoids was reported to increase parameters of systemic inflammation in growing chicks (Koutsos et al., 2006).
Considerable attention is presently being directed to the role vitamin E and selenium play in protecting leukocytes and macrophages during phagocytosis, the mechanism whereby animals immunologically kill invading bacteria. Both vitamin E and selenium may help these cells survive the toxic products that are produced to effectively kill ingested bacteria (Badwey and Karnovsky, 1980). Macrophages and neutrophils from vitamin E-deficient animals have decreased phagocytic activity (Burkholder and Swecher, 1990). Large doses of vitamin E protected chicks and poults against Escherichia coli with increased phagocytosis and antibody production (Tengerdy and Brown, 1977). Vitamin E supplementation of the feed, at levels of 150 to 300 IU per kg (68.2 to 136.4 IU per lb.), decreased chicks mortality due to E. coli challenge from 40%, in the birds not supplemented with vitamin E, to 5% in supplemented birds (Tengerdy and Nockels, 1975). Chicks fed vitamin E at 100 IU per kg diet (45 IU per lb) had increased weight gains and reduced mortality during coccidiosis challenge (Colnago et al., 1984). Heat stress severely reduced growth performance and immune response of broilers, whereas the immune response of broilers was improved by vitamin E (Niu et al., 2009). Broiler chicks fed 80 IU vitamin E per kg (36.4 IU per lb) had increased innate and humoral immune response against coccidiosis vaccine and an Eimeria (protozoan parasites) challenge (Perez-Carbajoal et al., 2010).
Since vitamin E acts as a tissue antioxidant and aids in quenching free radicals produced in the body, any infection or other stress factor may exacerbate depletion of the limited vitamin E stores from various tissues. With respect to immunocompetency, dietary requirements may be adequate for normal growth and production; however, higher levels have been shown to positively influence both cellular and humoral immune status of ruminant species. The former two responses are generally used as criteria for determining the requirements of a nutrient. During stress and disease, there is an increase in production of glucocorticoids, epinephrine, eicosanoids, and phagocytic activity. Eicosanoid and corticoid synthesis and phagocytic respiratory bursts are prominent producers of free-radicals that challenge the antioxidant systems. Vitamin E has been implicated in stimulation of serum antibody synthesis, particularly IgG antibodies (Tengerdy, 1980). The productive effects of vitamin E on animal health may be involved with its role in reduction of glucocorticoids, which are known to be immunosuppressive (Golub and Gershwin, 1985). In rats, in vivoinflammatory challenge decreased vitamin E blood and liver concentrations (Fritsche and McGuire, 1996). Vitamin E also most likely has an immuno-enhancing effect by virtue of altering arachidonic acid metabolism and subsequent synthesis of prostaglandin, thromboxanes and leukotrienes. Under stress conditions, increased levels of these compounds by endogenous synthesis or exogenous entry may adversely affect immune cell function (Hadden, 1987).
The effects of vitamin E and selenium supplementation on protection against infection by several types of pathogenic organisms, as well as antibody titers and phagocytosis of pathogens, have been reported for calves (Cipriano et al., 1982; Reddy et al., 1987a) and lambs (Reffett et al., 1988; Finch and Turner, 1989; Turner and Finch, 1990). As an example, calves receiving 125 IU of vitamin E daily were able to maximize their immune responses compared to calves receiving low dietary vitamin E (Reddy et al., 1987b). In sows, vitamin E restriction depressed lymphocytes and polymorphonuclear cells for immune function (Wuryastuti et al., 1993). Dogs with vitamin E deficiency had a depressed proliferative lymphocyte responsiveness (Langweiler et al., 1983). Antioxidants, including vitamin E, play a role in resistance to viral infection. Vitamin E deficiency allows a normally benign virus to cause disease (Beck et al., 1994). In mice, enhanced virulence of a virus resulted in myocardial injury that was prevented with vitamin E adequacy. A selenium or vitamin E deficiency leads to a change in viral phenotype, such that an avirulent strain of a virus becomes virulent and a virulent strain becomes more virulent (Beck, 1997; Sheridan and Beck, 2008).
Vitamin E alone or in combination with selenium is suggested to be essential for the development of resistance to diseases such as influenza and tetanus in horses (Hintz, 1996). The increased requirements of vitamin E for immune responses was an important consideration for the horse NRC committee. It increased estimated requirements for vitamin E from 15 to 50-80 IU per kg (from 6.8 to 22.7-36.4 IU per lb).
Studies by Tiege et al. (1978) have shown that susceptibility of pigs to dysentery resulting from exposure to the spirochete Treponema hyodysenteriae was greatly increased by the combined dietary deficiencies of vitamin E and selenium. In studies with young pigs, supplemental vitamin E has been beneficial in increasing the humoral response against sheep red blood cells (Peplowski et al., 1981; Morrow et al., 1987). In vitamin E-restricted sows there were depressed peripheral blood lymphocytes and polymorphonuclear cell immune functions (Wuryastuti et al., 1993).
There have been more recent reports on benefits of vitamin E supplementation for livestock than any other vitamin (McDowell et al., 1996). Vitamin E was originally supplemented to poultry and livestock for prevention of exudative diathesis, encephalomalacia, white muscle disease, liver degeneration and other degenerative diseases. Recent research has revealed the benefits of improving disease resistance. Supplementing vitamin E in well-balanced diets has been shown to increase humoral immunity for ruminants (Hoffmann-La Roche, 1994) and monogastric species (Langweiler et al., 1983; Wuryastuti et al., 1993). These results suggest that the criteria for establishing requirements based on overt deficiencies or growth do no consider optimal health.
In a series of 25-day feedlot receiving trials, Lee et al. (1985) observed an improvement in early performance of newly arrived growing cattle supplemented with 450 IU vitamin E (as dl-alpha-tocopheryl acetate) per head per day for the first 21 days and 800 IU vitamin E for the remaining 7 days of a 28-day trial. Average daily gain and gain-to-feed ratios were improved by 23.2% and 28.6%, respectively, for vitamin E-supplemented stressed cattle. The number of sick pen days per head was reduced by 15.6%, and morbidity was reduced by 13.4% with vitamin E supplementation. The growth response to vitamin E could be related to the fact that young, rapidly growing animals are in a metabolically demanding state resulting from overall tissue growth, which has a high energy demand. Vitamin E is an integral part of this response via its ability to quench free-radicals, which are generated during the course of metabolism.
D. Stress, Disease or Adverse Environmental Conditions
Intensified production increases stress and subclinical disease level conditions because of higher densities of animals in confined areas. Stress and disease conditions in animals may increase the basic requirement for certain vitamins. A number of studies indicated that nutrient levels that are adequate for growth, feed efficiency, gestation, and lactation may not be adequate for normal immunity and for maximizing the animal’s resistance to disease (Cunha, 1985; Nockels, 1988, 1991; Ward, 1994). Diseases or parasites affecting the gastrointestinal tract will reduce intestinal absorption of vitamins, both from dietary sources and those synthesized by microorganisms. If they cause diarrhea or vomiting, this will also decrease intestinal absorption and increase vitamin needs. Vitamin A deficiency is often seen in heavily parasitized animals that supposedly were receiving an adequate amount of the vitamin (McDowell, 2004).
Although B-vitamins are synthesized in the rumen, some feedlot operators find it beneficial to provide injections of B-vitamins to animals upon their arrival. This is likely beneficial as newly arrived animals have been severely stressed with rumen function often severely reduced. Lee et al. (1985) reported that rate and efficiency of gain of stressed beef calves was improved over a 28-day period by addition of a combination of vitamin E and a mixture of B-vitamins to a feedlot diets. In one study, supplemental B-vitamins given to feedlot calves tended to reduce morbidity of animals (Zinn et al., 1987).
Any disease that includes bleeding of the intestinal wall increases both vitamin loss and vitamin requirements for tissue regeneration. Likewise, a condition that causes a loss in appetite, and thus feed intake, increases the level of vitamins per unit of feed consumed to meet daily body needs. Diseases that adversely affect the integrity of the intestinal wall may interfere with vitamin A conversion from carotene and, therefore, increase the animal’s vitamin A needs. Cunha (1987) suggested that the conversion of vitamin D to its functional forms in the liver and kidney would be affected by diseases of these organs.
Mycotoxins are known to cause digestive disturbance, such as vomiting and diarrhea, as well as internal bleeding, and interfere with absorption of dietary vitamins A, D, E and K. In broiler chickens, moldy corn containing mycotoxins has been associated with deficiencies of vitamin D (rickets) and vitamin E (encephalomalacia) despite of the fact that these vitamins were supplemented at levels regarded as satisfactory.
In recent years, a malady dubbed “spiking syndrome” in broilers caused a sharp rise in mortality at about 14 days of age. Some nutritionists feel that this problem may be associated with Fusarium mycotoxins, although the exact cause is not clearly defined. Increased levels of thiamin reduce the rate of mortality, and it is suggested that when either corn quality is poor or mycotoxin levels and/or mold counts are high, thiamin should be increased by 1.11 to 1.65 mg per kg (0.50 to 0.75 mg per lb) in the starter feed (Gadient, 1986).
Mortality from fowl typhoid (Salmonella gallinarum) was reduced in chicks fed vitamin levels greater than normal (Hill, 1961). Vitamin E supplementation at a high level decreased chick mortality due to Escherichia coli challenge from 40% to 5% (Tengerdy and Nockels, 1975). Scott et al. (1982) concluded that coccidiosis produces a triple stress on vitamin K requirements as follows: (1) coccidiosis reduces feed intake, thereby reducing vitamin K intake; (2) coccidiosis injures the intestinal tract and reduces absorption of the vitamin; and (3) sulfaquinoxaline treatment and other coccidiostats causes an increased requirement for vitamin K.
Shell quality can be severely depressed by various stresses, including disturbance and heat stress. Vitamin C has been found to promote vitamin D metabolism and is also known to counter effects of various stresses. Heat stress depresses a range of egg production and quality characteristics. Ascorbic acid supplementation has been shown to result in improvements in these traits (Cheng et al., 1990). Ascorbic acid can also alleviate nutritional stress. Balnave et al.(1994) showed that poor shell quality of hens given saline drinking water could be overcome by addition of ascorbic acid to the water (1 g/l). Although vitamin C is commonly associated with alleviation of the effects of heat stress in laying hens, recent work has demonstrated that vitamin E can also play an important role. Depression in egg production in laying hens brought about by heat stress can be partially prevented by dietary supplementation with vitamin E (Utomo et al., 1994). Evidence was obtained that the mechanisms might involve a restoration of the supply in the circulation of egg yolk precursors, particularly vitellogenin. It was found to be important to feed the vitamin E prior to and throughout the period of stress to maintain tissue concentration sufficiently high to provide the best protective effect (Whitehead, 1998). Vitamin E enhances the immune status of layers during heat stress and potentially during other stress periods such as transport, vaccination, molt, etc. (Scheideler, 1998). There was a positive correlation between enhanced immunity and a positive effect on production parameters such as egg production and egg mass during stress in layers.
To compare the potential effects of stress conditions on vitamin requirements, Ward (1994) fed five levels of vitamins to 9,600 broilers over a 42-day period. NRC; The five levels were: low 25% industry (Ward, 1993); average industry; high 25% industry; and high 25% + 25%. Birds were subjected to three levels of stress (minimum, moderate and relatively high) based on different levels of coccidia, E. coli, placement density, and nutritional plane. The results showed that as degree of stress increased, bird performance declined. Furthermore, although the highest level of vitamins did not completely overcome the detrimental effect of stress, clearly the higher levels of vitamins did improve performance over the lower levels (Table 14).
Companion animals can be under stress when confined to a small living space. This stress is intensified when pets are forced to remain in kennels for long periods of time. Under these conditions, stress and subclinical disease level conditions increase because of closer and more frequent contact between animals in confinement. Animals are stressed when they are forced to remain in overheated houses or are left out in the cold and rain.
The efficiency of beta-carotene in meeting the vitamin A requirements of trout and salmon apparently is dependent on water temperature. Cold-water fish utilize precursors of vitamin A at 12.4° to 14°C, but do not at 9°C (Poston et al., 1977). Activity of beta-carotene-15, 15’-dioxygenase, which oxidizes beta-carotene to retinal in the intestinal mucosa, may be restricted at cold temperatures.
E. Vitamin Antagonists
Vitamin antagonists (anti-metabolites) interfere with the activity of various vitamins, and Oldfield (1987) summarized the action of antagonists. The antagonist could cleave the vitamin molecule and render it inactive, as occurs with thiaminase and thiamin; it could bind with the metabolite, with similar results, as happens between avidin and biotin; or by reason of structural similarity it could occupy reaction sites and thereby deny them to the vitamin, as with dicumarol and vitamin K. The presence of vitamin antagonists in animal and human diets should be considered when adjusting vitamin allowances, as most vitamins have antagonists that reduce their utilization. Some common antagonists are as follows:
- Thiaminase found in raw fish and some feedstuffs, is a thiamin antagonist. Pyrrithiamin is another thiamin antagonist.
- Dicumarol, found in certain plants, interferences with blood clotting by blocking the action of vitamin K.
- Avidin, found in raw egg white, and streptavidin, from Streptomyces mold, are biotin antimetabolites.
- Rancid fats inactivate biotin and destroy vitamins A, D and E and possibly others.
Mycotoxins are antagonists in feed that can substantially decrease antioxidant nutrient assimilation and increase their requirements to prevent damaging effects of free radicals and toxic products. It is now increasingly recognized that at least 25% of the world’s grains are contaminated with mycotoxins (Surai, 2002). Mycotoxins are known to cause digestive disturbances such as vomiting and diarrhea as well as internal bleeding, and interfere with absorption of dietary vitamin A, as well as vitamins D, E and K (McDowell, 2006). In broiler chickens moldy corn (mycotoxins) has been associated with deficiencies of vitamins D (rickets) and E (encephalomalacia) in spite of the fact that these vitamins were supplemented at levels regarded as satisfactory.
Toxic minerals may be antagonists and will likewise increase vitamin requirements. Vitamin E is known to protect against toxicity of certain heavy metals (e.g., cadmium, mercury, leads), which increases the requirement for the vitamin (McDowell, 2000). Lead, for example, has been shown to increase riboflavin requirements (Donaldson, 1986). For chicks, 6.7 mg riboflavin per kg (3.0 mg per lb) was more effective in suppressing lead toxicity than was 3.0 mg per kg (1.4 mg per lb).
Specific vitamins can likewise be antagonistic to other vitamins. Excess vitamin A can be detrimental to the metabolism (e.g., absorption) of other far-soluble vitamins. Large excesses of vitamin E have been shown to result in hemorrhages in some species, apparently by reducing vitamin K absorption. The problem can be eliminated with additional dietary vitamin K.
Other substances that are less well defined have been reported to be antagonistic to certain vitamins. Alfalfa juice protein concentrate (AJPC) has been shown to be antagonistic to vitamins B6 and K. Depressed growth, decreased antibody responses to red blood cells of sheep and increased blood-clotting times result from the use of AJPC. Vitamins B6 and K have been found to be crucial to counteracting the toxicity (Tsiagble et al., 1987).
F. Use of Antimicrobial Drugs
Some antimicrobial drugs will increase vitamin needs of animals by altering intestinal microflora and inhibiting synthesis of certain vitamins. Certain sulfonamides may increase requirements of biotin, folic acid, vitamin K and possibly others when intestinal synthesis is reduced. This may be of little significance except when drugs that are antagonistic towards a particular vitamin are added in excess, i.e., sulfaquinoxaline versus vitamin K, and sulfonamide potentiators versus folic acid (Perry, 1978).
G. Levels of Other Nutrients in the Diet
Level of fat in the diet may affect absorption of the fat-soluble vitamins A, D, E and K, as well as the requirements for vitamin E and possibly other vitamins. Fat-soluble vitamins may fail to be absorbed if digestion of fat is impaired. The high cost of fat as an energy source has resulted in minimal fat levels in current, least-cost feed formulations, which may result in reduced absorption of fat-soluble vitamins (Hoffmann-La Roche, 1991).
Type (e.g., animal fats, vegetable oils and blends) and quality (e.g., cis versus trans, saturated versus polyunsaturated fatty acids [PUFA], and oxidized sources) of fats can influence individual vitamin allowances. For example, high dietary PUFA increase the vitamin E requirements by 3 IU per gram of PUFA (Bieber-Wlaschny, 1988). This could particularly be a problem for cats, which may receive diets high in fish oils. High dietary trans-fatty acid content disrupts arachidonic acid metabolism and marginal biotin levels exacerbate this condition (Watkins, 1989).
Many interrelationships of vitamins with other nutrients exist and, therefore, affect requirements. For example, prominent interrelationships exist for vitamin E with selenium, vitamin D with calcium and phosphorus, choline with methionine, and niacin with tryptophan.
H. Body Vitamin Reserves
Body storage of vitamins from previous intake will affect daily requirements of these nutrients. An animal tends to store reserves of certain vitamins in its body so that a daily intake is not required. This is true for the fat soluble vitamins A, D and E, and vitamin B12. The fat-soluble vitamins A, D and E, but not vitamin K, are more inclined to remain in the body. This is especially true of vitamin A and/or carotene, which may be stored by an animal in its liver and fatty tissue in sufficient quantities to meet its requirements for varying periods of time. Lactating animals fed adequate quantities of vitamins transfer more of these nutrients though the milk, allowing the neonate a better opportunity to survive. Small fish have not yet developed substantial tissue vitamin stores and they grow rapidly; hence, vitamin deficiency signs appear more rapidly in small fish than in larger fish when they are fed a deficient diet (Hardy, 2001).