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6 Vitamins INTRODUCTION take of 2 percent of BW for maintenance, breeding, gesta- tion, and light work; 2.25 percent of BW for moderate work; Vitamins are defined as a group of complex unrelated fat- and 2.5 percent of BW in DM intake for all other feeding and water-soluble organic compounds present in minute classes. For example, the vitamin E requirement for lacta- amounts in natural foodstuffs. They are essential to normal tion in the previous revision is 80 IU/kg DM and has been metabolism and their lack in the diet causes deficiency dis- transformed to 2 IU/kg BW, assuming a DM intake of 2.5 eases (McDowell, 2000). Vitamin requirements of horses percent of BW (i.e., 80 IU vitamin D/kg DM Ã 2.5 kg have been estimated using several response variables (e.g., DM/100 kg BW). prevention of specific deficiency symptoms, maximizing tis- sue stores, and optimization of various biological functions). It should be noted that the requirement for a vitamin may VITAMIN A differ depending upon the response variable used. For ex- Function ample, 0.233 international units (IU) of vitamin E/kg body weight (BW) was determined to be the minimum require- The classical function of vitamin A is its role in night vi- ment necessary to maintain erythrocyte stability in growing sion (Wald, 1968). Vitamin A in the form of 11-cis-retinal horses (Stowe, 1968a), whereas approximately 1 IU/kg BW combines with opsin to produce rhodopsin, which breaks was reported to have an immunostimulatory effect in adult down in the presence of light-yielding energy that is trans- horses when compared to controls fed approximately 0.315 ported to the brain by the optic nerve in the process of sight. IU/kg BW (Baalsrud and Overnes, 1986). Vitamin A functions in cell differentiation by the regulation Requirements for vitamins A, D, E, thiamin, and ri- of gene expression via nuclear retinoic acid receptors, and as boflavin have been estimated. The basis for these estimates a result plays crucial roles in reproduction and embryogen- is discussed below along with information regarding dietary esis (Solomons, 2001). Additionally, vitamin A is important sources and consequences of deficiency and toxicity. Al- for maintaining the innate and adaptive immune response to though limited, information regarding vitamin nutrition for infection (Stephensen, 2001). vitamin K, niacin, biotin, folate, vitamin B12, vitamin B6, pantothenic acid, and vitamin C (ascorbic acid) is discussed. Dietary Sources However, insufficient information exists to estimate dietary requirements of these vitamins for horses. In addition to re- Vitamin A refers to a subgroup of retinoids possessing quirements, an attempt was made to estimate the presumed the biological activity of all-trans-retinol (Solomons, 2001). upper safe levels of intake for each vitamin. The presumed Retinol does not occur naturally in feedstuffs commonly upper safe level is defined as the estimated (based on litera- used for horses (e.g., forages, cereal grains, plant protein ture) upper range of vitamin intake that can be presumed to supplements), but is derived from pro-vitamin A compounds be safe, and is not necessarily the maximum tolerance level (carotenoids). Retinol is present in vitamin A supplements of vitamin intake (NRC, 1987). as retinyl-ester (e.g., retinyl-acetate, retinyl-palmitate). Many of the vitamin requirements in the previous revi- The biological activity of various retinoids and pro- sion of this document were expressed per unit of dry matter vitamin A compounds differs and must be taken in account (DM) intake, and have been transformed to a BW basis in when evaluating and formulating equine diets. The interna- the current revision. The transformation assumes a (DM) in- tional unit is used to express vitamin A activity of different 109
110 NUTRIENT REQUIREMENTS OF HORSES sources on an equivalent basis. One IU of vitamin A is vitamin A. The amount of Î²-carotene metabolized into vita- equivalent to the biological activity of 0.300 Âµg of all-trans- min A is dependent upon Î²-carotene intake (Ullrey, 1972; retinol. Solomons, 2001). Kienzle et al. (2002) found a water- Beta-carotene is the primary naturally occurring pro- dispersible Î²-carotene source, different from the aforemen- vitamin A source in feedstuffs used for horses. Beta- tioned studies, was effective at increasing plasma Î²-carotene carotene can be metabolized into a retinyl ester (retinyl- concentration, but vitamin A status was not measured. Inter- palmitate or retinyl-stearate) within the mucosa of the small estingly the dosage of Î²-carotene used by Kienzle et al. was intestine, and the liver to some extent (Ullrey, 1972; Napoli, approximately half that (0.8 vs. 1.8 mg Î²-carotene/kg BW) 2000). Retinyl esters formed in the small intestinal mucosa used by Watson et al. (1996). Therefore, effectiveness of are then transported to the liver for storage or distributed to synthetic Î²-carotene as sources of pro-vitamin A for horses other tissues for further metabolism. Previous NRC publica- remains to be determined. tions have assumed 1 mg of Î²-carotene is equivalent to no Retinyl-palmitate and -acetate are supplemental forms of more than 400 IU of vitamin A (NRC, 1989). Different con- vitamin A used in diets for horses (NRC, 1989). These es- version rates for pregnant mares and growing horses have terified forms are more stable than retinol making them less been suggested (1 mg Î²-carotene = 555 and 333 IU vitamin vulnerable to degradation during storage as compared to un- A, respectively) based on an extrapolation of conversion esterified forms (McDowell, 2000). Retinyl-esters are hy- rates established in rats (McDowell, 1989). The aforemen- drolyzed within the lumen of the small intestine to retinol, tioned conversion efficiencies are higher than reported for which is then absorbed. One IU of vitamin A is equivalent other monogastric species. In typical swine diets 1 mg total to the biological activity of 0.550 Âµg of all-trans-retinyl carotene was calculated to be equivalent to 267 IU vitamin palmitate, or 0.344 of all-trans-retinyl acetate. A (Ullrey, 1972). Reference dietary intakes used for humans consider 1 mg Î²-carotene equivalent to 275 IU vitamin A ac- Deficiency tivity. Additionally the effect of Î²-carotene intake can influ- ence the conversion rate. An inverse relationship between Night blindness is a classical vitamin A deficiency symp- the amount of Î²-carotene metabolized into vitamin A and tom reported in horses, as well as other species (McDowell, Î²-carotene intake has been reported for several species (Ull- 1989). Extremely low vitamin A intake is necessary for the rey, 1972; Solomons, 2001), but has not been investigated in condition to occur. Induction of night blindness in Percheron horses. Clearly more work is necessary to establish accurate horses occurred after rations consisting of barley, oats, bran, estimates of the vitamin A value of naturally occurring and straw containing low concentrations of total carotene (5 Î²-carotene and other carotenoids. to 10 Âµg/kg BW; no more than 2 to 4 IU vitamin A/kg BW) Beta-carotene concentrations derived from back- were fed for 265 to 627 days (Guilbert et al., 1940). Semi- calculation of vitamin A values published in NRC (1989) purified diets devoid of vitamin A activity were necessary to (i.e., 400 IU of vitamin A is equivalent to 1 mg Î²-carotene) induce clinical signs of vitamin A deficiency in orphaned vary widely among forages. Forages contain from 30â385 foals (Stowe, 1968b). Greiwe-Crandell (1997) reported no mg Î²-carotene/kg DM. Pasture (nondormant) contains the clinical signs of vitamin A deficiency and a plateau effect in greatest concentration of Î²-carotene, while mature grass hay vitamin A status in mares consuming hay, previously stored has the lowest concentrations. Several factors, such as de- for 2 years, containing less than 4 mg Î²-carotene/kg DM for gree of maturity, conditions at harvest, and length of storage, 22 months. The authors interpreted the results as an adaptive can influence Î²-carotene concentrations of forages (Ullrey, response to very low levels of carotene intake. These results 1972). Among cereal grains, corn contains the greatest con- suggest that horses are somewhat resilient to vitamin A de- centration of Î²-carotene (approximately 6 mg/kg DM), ficiency, at least when common clinical deficiency symp- which is considerably less than that of forages. toms are used as indicators of deficiency. Impaired growth Synthetic Î²-carotene has been evaluated as a source of and hematopoiesis were reported in growing ponies fed ra- provitamin A. Watson et al. (1996) suggested that a water- tions marginally deficient in vitamin A (Donoghue et al., dispersible form of Î²-carotene was not well absorbed by 1981). Therefore, parameters associated with growth and ponies as indicated by a lack of effect on plasma Î²-carotene hematopoiesis appear to be more sensitive indicators of vi- concentration following supplementation, but vitamin A sta- tamin A deficiency as compared to clinical symptoms such tus of the ponies was not evaluated. Greiwe-Crandell et al. as night blindness. (1997), using this same form of Î²-carotene, found it was not In addition to clinical signs, serum total vitamin A con- effective at maintaining vitamin A status in mares over a 20- centration has been used as an indicator of vitamin A defi- month period as compared to retinyl-palmitate or naturally ciency. Total serum vitamin A concentration of less than 10 occurring Î²-carotene from pasture and hay. However, it Âµg/dl is considered deficient (Lewis, 1995). However, total should be noted that the Î²-carotene used in this study was serum vitamin A is not a sensitive indicator of marginal vi- administered in two large doses per week rather than daily, tamin A status due to mobilization of retinol from the liver which may have influenced the conversion of Î²-carotene to into blood in response to inadequate vitamin A intake (Jar-
VITAMINS 111 rett and Schurg, 1987). The relative dose response test al., 1981; Jarrett and Schurg, 1987). Toxicity due to Î²- (RDR), an indirect measure of liver vitamin A stores, has carotene has not been reported. Additionally, it should be been suggested as a more accurate indicator of marginal vi- noted that the previously mentioned assumption that 1 mg of tamin A status in horses than either serum total vitamin A or Î²-carotene contains 400 IU of vitamin A may yield vitamin serum retinol (Greiwe-Crandell et al., 1995). The RDR is A concentrations above the presumed upper safe level of expressed as the percentage increase in serum retinol fol- 16,000 IU/kg DM, which is most likely erroneous based on lowing oral administration of a vitamin A bolus. The time the absence of toxicity in horses consuming these amounts. period between the initial and final measures of serum retinol used to determine its percent increase coincide with Requirements peak serum retinol concentration. The basis for the RDR is that during vitamin A sufficiency, a relatively large propor- Vitamin A requirements for horses of different physio- tion of newly absorbed vitamin A is stored in the liver due logical states are not well defined. Limited information ex- to relatively low production and concentration of retinol ists regarding vitamin A nutrition as it pertains to mainte- binding protein (RBP), which is necessary for transport of nance (Guilbert et al., 1940), reproduction (Stowe, 1967), vitamin A from the liver to peripheral tissues. In contrast, gestation (Greiwe-Crandell et al., 1997; Maenpaa et al., during vitamin A deficiency, RBP synthesis and concentra- 1988a,b), lactation (Stowe, 1982; Schweigert and Gottwald, tion increase and newly absorbed vitamin A is transported 1999), growth (Donoghue et al., 1981), and work (Abrams, from the liver to peripheral tissues resulting in a relative in- 1979). crease in serum retinol concentration after administration of an oral bolus; therefore, RDR increases. Relative dose re- Maintenance sponse values greater than 20 percent have been observed in horses consuming rations deficient in vitamin A (Greiwe- The vitamin A requirement for horses with maintenance- Crandell et al., 1995; Lewis, 1995; Greiwe-Crandell et al., only requirements is based on the intake of vitamin A nec- 1997). However, an RDR ranging from 20â30 percent was essary to prevent night blindness, plus an allowance deemed reported in reproductively sound mares with no clinical sufficient to maximize tissue storage (NRC, 1989). This rec- symptoms of vitamin A deficiency (Greiwe-Crandell et al., ommendation is based on the work of Guilbert et al. (1940) 1997), suggesting more work is necessary to define exact and has been the basis for maintenance vitamin A require- thresholds for vitamin A deficiency using RDR. Since vita- ments since the first publication on recommended nutrient min A can be stored in the liver (McDowell, 2000), it is pos- allowances for horses in 1949. Guilbert et al. (1940) used 9 sible that the lack of clinical deficiency symptoms were due Percheron horses ranging in age from 119â444 days in a to liver stores of vitamin A covering dietary deficits. depletion-repletion experiment that was aimed at determin- Immunity and reproduction are two other physiological ing the minimum intake of either total carotene or vitamin functions influenced by vitamin A status. Respiratory infec- A, from alfalfa and cod-liver oil, respectively, which was tion in weanlings was associated with low vitamin A status necessary to prevent clinical signs of night blindness. Daily as measured by RDR (Greiwe-Crandell et al., 1995). Im- consumption of 17â22 IU/kg BW was the minimum neces- paired function of the immune system during vitamin A de- sary to prevent clinical signs of night blindness. However, ficiency has been documented in several species (McDow- previous work conducted by these authors on rats indicated ell, 1989; Stephensen, 2001). Vitamin A deficiency in swine that 3 times the minimum vitamin A requirement, or 51â66 has been shown to increase early embryonic mortality (Mc- IU/kg BW, was necessary for significant tissue storage. Dowell, 1989). The effect of vitamin A status on both im- Using data from the manuscript of Guilbert et al. (1940), munity and reproduction in horses require further study. mean vitamin A intakes (Â± SD) of horses showing no signs of night blindness, partial night blindness, and total night blindness were calculated to be 22.9 Â± 5.1 (n = 10), 17.5 Â± Toxicity 2.6 (n = 5), and 4 Â± 2.7 (n = 10) IU vitamin A/kg BW, re- Vitamin A toxicity has been reported to result in bone spectively. When the mean vitamin A intake of horses show- fragility, hyperostosis, exfoliated epithelium and teratogen- ing no signs of night blindness is increased by two standard esis (NRC, 1987). In addition, excess vitamin A has been deviations, the vitamin A intake is 33.1 IU/d, which is ap- implicated in developmental orthopedic disease in growing proximately equal to NRC (1989) requirement for mainte- horses (Donoghue et al., 1981; Kronfeld et al., 1990). The nance (30 IU/kg BW). Based on this information, 30 IU/kg presumed upper safe level of vitamin A in the diet is 16,000 BW is recommended as the maintenance vitamin A require- IU/kg DM (NRC, 1987). Plasma total vitamin A concentra- ment. tions greater than 40â60 Âµg/dl are indicative of toxicosis (Lewis, 1995). Retinyl-ester concentration of plasma in- creases relative to retinol during toxicosis and may also be an indicator of excess vitamin A consumption (Donoghue et
112 NUTRIENT REQUIREMENTS OF HORSES Growth al., 1997). Some of the seasonal variation was most likely due to change in diet (i.e., pasture vs. preserved forage) and The role of vitamin A in the growing horse is not well deterioration of Î²-carotene in preserved forage (Fonnesbeck studied. Daily vitamin A requirements for growth in the sec- and Symons, 1967). However, Maenpaa (1988a) stated the ond through fourth revisions of the NRC publications (NRC, seasonal decline in pregnant mares was greater than previ- 1966, 1973, 1978) remained the same at 40 IU/kg BW, but ously reported in nonpregnant adult horses (Maenpaa et al., were increased slightly in the fifth revision (NRC, 1989) to 1987: approximately 36 and 8.9 percent, respectively) and 45 IU/kg BW. The basis for this change in vitamin A re- suggested the difference may be due to increased utilization quirement was unclear. Guilbert et al. (1940) observed of vitamin A during gestation. Interestingly, supplementa- growth and development was normal in horses consuming tion with 18â36 IU vitamin A/kg BW (source not reported) 22.9 Â± 5.1 IU vitamin A/kg BW and ranging in age from did not prevent the seasonal decline in the pregnant mares 119â444 days. Donoghue et al. (1981) suggested that a (Maenpaa et al., 1988b). Seasonal declines in vitamin A sta- range from 60â200 IU/kg BW resulted in optimization of tus have been reported in broodmares maintained in a dry- seven different response variables, which included growth lot setting both with retinyl-palmitate supplementation (125 rate, serum biochemistry, and hematologic criteria in ponies IU vitamin A/kg BW) and without vitamin A supplementa- ranging in age from 4â12 months. However, the authors tion (< 0.8 IU/kg BW) (Greiwe-Crandell et al., 1997), which noted that this conclusion is based on interpolation and re- supports the idea that the seasonal decline in vitamin A sta- quires further definition in growing horses. Interpolation tus is not completely due to changes in vitamin A intake and was made across an extremely wide range, i.e., 12â1,200 Âµg may be influenced by gestation. Stowe (1982) provided ev- retinol/kg BW/d, which may detract from the accuracy of idence that metabolism of vitamin A increases at parturition the estimate. Stowe (1968b) reported a minimum vitamin A due to increased secretion of vitamin A in colostrum. requirement in growing horses (9.5â11 IU/kg BW) that was Greiwe-Crandell et al. (1997) also reported that mares main- considerably less than that of Donoghue et al. (1981), albeit tained on pasture with no other vitamin A supplementation using younger horses (orphaned foals) and different re- (i.e., Î²-carotene from pasture was the only source of vitamin sponse variables (maintenance of appetite). Based on the in- A activity) had a greater vitamin A status (as measured by a formation available, there is no justification for changing the relative dose response test) than mares maintained on dry-lot requirement from that established by previous NRC com- and receiving a dose of vitamin A equivalent to 125 IU /kg mittees, i.e., 45 IU/kg BW. This value is similar to average BW/d from retinyl-palmitate. It was further suggested that if values required by finishing swine (NRC, 1998). the vitamin A status of horses on pasture is viewed as opti- mum, then supplementation with approximately twice the Breeding, Gestation, and Lactation NRC (1989) requirement is below optimum. However, it should also be noted that horses used in this study were only The vitamin A requirement for pregnant and lactating supplemented with vitamin A two times per week using a vi- mares was reported to be 60 IU/kg BW (NRC, 1989). Bar- tamin A dose equivalent to a daily supplementation of 125 ren Standardbred mares supplemented orally with 100,000 IU/kg BW/d. Although vitamin A status of unsupplemented IU vitamin A/day + 100 IU vitamin E/day had improved re- mares without access to pasture declined in these studies, no productive status (e.g., more serviced heats, greater number negative effects due to declining status were reported in of live foals) compared to unsupplemented controls, or these mares. At present, no evidence suggests vitamin A re- horses consuming either 100,000 IU vitamin A/day or 100 quirements for broodmares are different from those previ- IU vitamin E/day (Stowe, 1967). The vitamin A activity of ously recommended, i.e., 60 IU/kg BW (NRC, 1989). the unsupplemented control ration was not reported. How- Several studies have investigated the hypothesis that Î²- ever, this experiment was somewhat biased because mares carotene, or provitamin A, improves reproductive status, but receiving the control ration and vitamin A-only ration were results are equivocal (Watson et al., 1996). Some have sug- older than the other two groups. The average age of mares in gested the water-dispersible form of Î²-carotene used in the control, vitamin A only, vitamin E only, and vitamins A these studies was not well absorbed and does not increase plus E was 19.8, 16.5, 14, and 14.8 years, respectively. How- blood concentrations of Î²-carotene or retinol (Watson et al., ever, a separate experiment reported in the manuscript by 1996; Greiwe-Crandell et al., 1997), while others provided Stowe (1967), where age of the mares was balanced across evidence to the contrary (Kienzle et al., 2002). Therefore the treatments, indicated that a parenteral dose of vitamins A effect of Î²-carotene, independent of vitamin A activity, on and E, approximately equivalent to the oral dose used in the reproduction in mares remains uncertain. first experiment, also resulted in improved reproductive sta- tus. These results suggest an interaction between vitamins A and E may enhance reproductive status. Seasonal variation Work in vitamin A status has been reported in broodmares in sev- Vitamin A requirements specific to work have not been eral studies (Maenpaa et al., 1988a,b; Greiwe-Crandell et established. Previous editions of the NRC nutrient require-
VITAMINS 113 ments of horses consider the requirement for work to be Deficiency somewhere between maintenance (30 IU/kg BW) and that Rickets, a disease characterized by bone deformities re- for gestation and lactation (60 IU/kg BW). The fifth edition sulting from decreased concentration of calcium (Ca) and of the NRC (1989) Nutrient Requirements of Horses stated phosphorus (P) in the organic matrices of cartilage and the vitamin A requirement for work as 45 IU/kg BW. bone, is the classical vitamin D deficiency symptom in ani- In a search of the literature, only one report dealing with mals and humans (McDowell, 2000). Bone growth and de- vitamin A supplementation to working horses was identi- velopment were affected in ponies deprived of sunlight and fied. Abrams (1979) hypothesized that vitamin A supple- dietary vitamin D as compared to two other groups of ponies mentation to Thoroughbred racehorses in training would as- either fed diets containing 1,000 IU/d and having no expo- sist in the maintenance of connective tissue integrity, sure to sunlight, or fed diets containing no supplemental vi- thereby reducing tendon injury. Horses were supplemented tamin D and having exposure to sunlight; however, exter- with 50,000 IU/d (approximately 111â125 IU/kg BW/d; nally visible bone deformities typifying rickets were not source not provided) over a 2-year period. Vitamin A- evident (Elshorafa et al., 1979). Although vitamin D status supplemented horses completed more races with a greater of horses has been reported to be low relative to other number of wins and a lower incidence of tendon injuries as species (Maenpaa et al., 1988a), and supplemental vitamin compared to controls. However, the design of the experi- D has been reported to promote calcium and phosphorus ab- ment precludes definitive conclusions in that the opportunity sorption in horses (Hintz et al., 1973), there are no reports of to race was not afforded equally to all horses. vitamin D deficiency to date in horses maintained in practi- In conclusion, additional experiments are required to es- cal settings with some exposure to sunlight. tablish vitamin A requirements specific to work. Vitamin A requirements for exercising horses in this edition are un- changed from the previous addition (i.e., 45 IU/kg BW) due Toxicity to the lack of new information. Toxicity of vitamin D is associated with calcification of soft tissue (Harrington, 1982; Harrington and Page, 1983) VITAMIN D and death (Hintz et al., 1973). The presumed upper safe level is 44 IU/kg BW/d (NRC, 1987). Function Vitamin D plays an important role in calcium homeosta- Requirements sis. Vitamin D3 does not possess any direct biological activ- In the first edition of the NRC (1949), it was stated that ity, but is metabolized into 25 (OH)D3, 1,25 (OH)2D3, and 24,25 (OH)2D3. The classical target organs for vitamin D ac- Under normal farm conditions, where horses are worked tion are intestine, kidney, and bone. Vitamin D facilitates regularly and are exposed to sunshine, they probably do not calcium absorption from the intestine and reabsorption of need added amounts of vitamin D. Where they are confined calcium from the kidney, and influences both mobilization or where exposure to sunshine is restricted, or if they are fed and accretion of calcium (and phosphorus) from bone. Vita- for rapid growth and development of bone such as for racing min Dâs role in calcium homeostasis is its most well- at an early age, there may be some basis for supplying extra recognized function; however, vitamin D has also been amounts of vitamin D. Experimental information on the re- demonstrated to influence cell growth and differentiation quirements of the horse for vitamin D is not available. On (Norman, 2001). the basis of information on other species 300 I.U. of vitamin D per 100 pounds live weight daily should be adequate to meet the needs of horses. Dietary Sources Vitamin D is found in both plants (ergocalciferol, vitamin Although a true minimum vitamin D requirement for D2) and animals (cholecalciferol, vitamin D3). However, its horses exposed to sunshine is unknown, the value of 300 IU presence in feeds commonly used for horses is relatively vitamin D/100 lb BW was maintained through subsequent low. Some vitamin D2 is found in sun-cured hay, particularly revisions, albeit expressed as 6.6 IU/kg BW in the third edi- alfalfa (McDowell, 2000). Vitamin D is synthesized in the tion (NRC, 1973) and expressed as 300 IU/kg DM in the skin from the ultraviolet irradiation of 7-dehydrocholesterol fifth revision. The fifth revision qualifies this recommenda- (McDowell, 2000). Vitamin D3 is the most common supple- tion further by stating in footnote b of Table 5-3 that ârec- mental form of vitamin D for horses. ommendations are for horses not exposed to sunlight or to artificial light with an emission spectrum of 280â315 nm.â This recommendation (6.6 IU/kg BW) is maintained in the present edition for all feeding classes except growing horses. In the fifth revision (NRC, 1989), additional infor-
114 NUTRIENT REQUIREMENTS OF HORSES mation from an experiment conducted in growing ponies de- forms. Concentration of naturally occurring vitamin E activ- prived of sunlight (Elshorafa et al., 1979) was used to esti- ity varies considerably in typical feeds used for horses (NRC, mate vitamin D requirements of 800 IU/kg DM for horses in 1989; Lynch, 1996b). Fresh forages and those harvested at an the early stages of growth deprived of sunlight, but indicated immature state generally contain the highest concentrations that 500 IU/kg DM may be sufficient for later stages of of vitamin E activity (30â100 IU/kg DM), while grains (e.g., growth. Using BW, mature BW, average daily gain (ADG), corn, oats, and barley) tend to have lesser concentrations and month of age values, from Tables 5-1A-G (NRC, 1989), (20â30 IU/kg DM). Naturally occurring vitamin E declines and the NRC (1989) model software; vitamin D require- over time in stored feeds. For example, losses of 54â73 per- ments for growing horses were estimated across a range of cent of vitamin E have been reported in alfalfa stored at 33Â°C BW, mature BW, and ages. These estimates were then con- for 12 weeks (Lynch, 1996b). Therefore, the intake of vita- verted from a diet concentration (i.e., IU/kg DM) to a BW min E can vary considerably depending on the horseâs diet. basis (i.e., IU/kg BW). The converted estimates are as fol- Many commercial horse feeds account for this variation and lows: 22.2, 17.4, 15.9, and 13.7 IU/kg BW for 0â6, 7â12, are formulated with supplemental vitamin E (generally, all- 13â18, and 19â24 months of age, respectively. In conclu- rac-Î±-tocopheryl acetate) to compensate for potentially lim- sion, the true minimum dietary vitamin D requirement for iting concentrations in forages and other raw ingredients horses exposed to sunlight has not been defined. The meta- used in horse feed manufacture. Supplemental vitamin E bolic requirement for vitamin D is assumed to be met by ex- used in commercial feeds and vitamin supplements are esters posure to sunlight. The above estimates may be useful for of Î±-tocopherol (e.g., Î±-tocopheryl acetate) and is termed horses with limited exposure to sunlight (e.g., horses main- natural-source or synthetic depending upon whether it exists tained predominantly indoors). as the RRR stereoisomer (e.g., RRR-Î±-tocopheryl acetate) or a racemic mixture of the eight stereoisomers (e.g., all-rac- Î±-tocopheryl acetate). The natural-source RRR-Î±-tocopheryl VITAMIN E acetate contains 1.36 IU/mg, whereas the synthetic all-rac- Î±-tocopheryl acetate contains 1 IU/mg. Natural-source Function vitamin E appears more efficient at increasing serum Vitamin Eâs most widely accepted function is that of a bi- Î±-tocopherol as compared to synthetic vitamin E. Gansen et ological antioxidant (Sies, 1993). Its lipophilic nature allows al. (1995) reported a similar increase in serum Î±-tocopherol it to incorporate into cell membranes where it serves to pro- in horses fed diets for 6 weeks supplemented with natural- tect unsaturated lipids and other susceptible membrane com- source vitamin E (212 mg RRR-Î±-tocopheryl acetate, 252 ponents against oxidative damage. Vitamin E donates a hy- mg RRR-Î³-tocopheryl acetate, and 116 mg RRR-Î´-tocopheryl drogen atom from its phenolic group to lipid peroxyl acetate) as compared to those fed diets supplemented with a radicals produced during auto-oxidation of membrane synthetic form (672 mg all-rac-Î±-tocopheryl acetate), but polyunsaturated fatty acids forming a more stable lipid per- they noted that the natural source contained approximately oxide and stable tocopheryl radical. The subsequent lipid one-third the Î±-tocopherol as compared to the synthetic peroxides are further degraded by selenium-dependent glu- form. Pagan et al. (2005) reported that a synthetic source of tathione peroxidase. A detailed description of vitamin Eâs vitamin E (all-rac-Î±-tocopheryl acetate) was less effective at antioxidant function is described by Pryor (2001). elevating plasma Î±-tocopherol concentrations than natural- source vitamin E and that natural-source micellized vitamin E was superior at elevating plasma Î±-tocopherol during Dietary Sources short-term administration (~ 14 d) as compared to either the Vitamin E activity originates from eight different natu- synthetic or natural-source vitamin E. rally occurring compounds, four tocopherols (Î±, Î², Î³, Î´) and four tocotrienols (Î±, Î², Î³, Î´). Both tocopherols and to- Deficiency cotrienols consist of a chromanol ring and a 16-C side chain. Tocopherols have a saturated side chain, whereas to- White muscle disease (also known as nutritional muscu- cotrienols contain an unsaturated side chain. The Î±, Î², Î³, and lar dystrophy) is a noninflammatory degenerative disease Î´ forms differ due to placement and number of methyl that affects skeletal and cardiac muscle of foals ranging in groups on the chromanol ring, which accounts for some of age from birth to 11 months of age (Lofstedt, 1997). Al- the differences in vitamin E activity among the different though vitamin E deficiency has been implicated in white forms (Lynch, 1996a). The side chain of Î±-tocopherol con- muscle disease (Schougaard et al., 1972; Wilson et al., tains three asymmetric carbons resulting in eight different 1976), available evidence points to selenium deficiency as stereoisomers. Naturally occurring tocopherols exist as the the primary cause rather than vitamin E deficiency (Lofst- 2R 4â²R 8â²R (commonly referred to as RRR) stereoisomer. edt, 1997). However, vitamin E along with selenium has Naturally occurring RRR-Î±-tocopherol contains the greatest been used in treatment of white muscle disease. biological activity (1.49 IU/mg) of the different vitamin E
VITAMINS 115 Equine degenerative myeloencephalopathy (EDM) is an ditionally, some dietary sources of PUFA contain relatively idiopathic, diffuse, degenerative disease of the spinal cord high concentrations of vitamin E (Hoffman et al., 1998). and selected parts of the brain in young horses (generally Vitamin C and selenium status may also influence vita- < 2 years of age) that results in gait deficits (Blythe and min E status and subsequent requirements. Evidence from Craig, 1997). Some evidence suggests a role for vitamin E species other than horses suggests vitamin C status can in- in the pathophysiology of EDM (Liu et al., 1983; Mayhew fluence vitamin E status (Halpner et al., 1998; Lauridsen et al., 1987; Gandini et al., 2004); however, an unidentified and Jensen, 2005). The mechanism by which vitamin C in- familial factor is a prerequisite of the disease (Blythe et al., fluences vitamin E status may involve either recycling of the 1991). Based on this evidence, EDM does not appear to be Î±-tocopheroxyl radical back to Î±-tocopherol, or a sparing a primary vitamin E deficiency symptom. effect whereby vitamin C quenches free radicals that would Equine motor neuron disease (EMND) is a neurodegen- otherwise consume Î±-tocopherol (Halpner et al., 1998). Se- erative disorder of the somatic lower motor neurons affect- lenium is a component of the antioxidant enzyme glu- ing horses 2 years of age and older (Divers, 2005). Clinical tathione peroxidase and has also been demonstrated to spare findings include an acute onset of trembling, almost con- vitamin E (Combs, 1996). However, the effect of vitamin C stant shifting of weight in the rear legs when standing, pro- and selenium status on vitamin E status in horses remains to longed recumbency, and muscle wasting (Divers, 2005), as be determined. well as ocular manifestations (Riis et al., 1999). Several lines of evidence support the hypothesis that EMND occurs Toxicity following a prolonged period of vitamin E deficiency (Divers, 2005). Evidence includes serum Î±-tocopherol con- Vitamin E does not appear to be toxic to horses even at centration in affected horses that is often < 1 Âµg/ml, and in- relatively high intakes, and the upper safe diet concentration duction of equine motor neuron disease in horses fed diets is set at 1,000 IU/kg DM (NRC, 1987). However, this pre- low in vitamin E (concentration not reported, but it was < 50 sumed upper safe level is based on observations in other to 80 IU/kg DM) for 18â22 months. species. Coagulopathy and impaired bone mineralization Serum Î±-tocopherol is commonly used as an indicator of have been reported in other species consuming diets above vitamin E status. Craig et al. (1992) found single serum the upper safe level (1,000 IU/kg DM) (NRC, 1987). samples an unsatisfactory indicator of vitamin E status in horses, and stated this finding may have clinical application Requirements in the evaluation of horses suspected to be affected with EDM, or other vitamin E-related conditions. Within horse Maintenance serum, Î±-tocopherol concentrations fluctuated considerably The first published vitamin E requirement for horses was over a 72-hour period in 12 different horses (25 samples/ 15 IU vitamin E/kg diet DM (NRC, 1978), and was based on horse taken at 3-hour intervals). The mean coefficient of concentrations required to maintain erythrocyte stability in variation (CV) for Î±-tocopherol in all horses was 12 percent vitamin E-deficient foals (i.e., 0.233 IU/kg BW) (Stowe, and ranged from 7â17 percent in individuals. In some in- 1968a). In the fifth revision (NRC, 1989), the maintenance stances, serum Î±-tocopherol within an individual horse fluc- vitamin E requirement was increased to 50 IU/kg DM or ap- tuated over a 72-hour period from concentrations considered proximately 1 IU/kg BW, based on a report of enhanced hu- by the authors as adequate (> 2 Âµg/ml) through those con- moral immune function in mature horses supplemented with sidered marginal (1.5â2 Âµg/ml) and deficient (< 1.5 Âµg/ml). 1 IU vitamin E/kg BW (Baalsrud and Overnes, 1986). The Addition of dietary fat containing relatively high concen- change in vitamin E requirement was also supported by the trations of polyunsaturated fatty acids (PUFA, such as corn finding of Roneus et al. (1986) that 1.4â4.4 IU vitamin E/kg oil and soybean oil) has been suggested to decrease vitamin BW was necessary to maximize tissue stores of vitamin E. E status in several species (Muggli, 1989; McDowell, 2000). To date there is no new information suggesting maintenance Based on work in animals and humans, a ratio of 0.6 mg vitamin E requirement is different from that of the fifth re- Î±-tocopherol to 1 g PUFA was predicted as a minimum to vision of this document (NRC, 1989). protect against vitamin E deficiency (Harris and Embree, 1963); however, as the degree of fatty acid unsaturation in- Growth creases, the ratio of Î±-tocopherol:PUFA may be even greater (Muggli, 1989). Information regarding the relationship be- Vitamin E requirements specific to growth have not been tween vitamin E status and PUFA in horses is limited. Addi- defined. A vitamin E requirement of 0.233 IU/kg BW was tion of soybean oil (6.4 percent of the total diet; approxi- estimated for foals using erythrocyte stability as a response mately 20 percent of the total DE intake) to the diet did not variable (Stowe, 1968a), which is approximately 11 IU vita- negatively affect serum Î±-tocopherol concentrations in 2- min E/kg DM assuming a DM intake of 2.5 percent of BW. year-old horses over a 90-day period, and, in fact, mean Nutritional muscular dystrophy was identified in neonatal serum Î±-tocopherol concentration was greater on day 90 in foals whose dams consumed diets containing low concen-
116 NUTRIENT REQUIREMENTS OF HORSES trations of vitamin E (approximately 6â8 IU vitamin E/kg and exertional rhabdomyolysis, and the potential for oxida- DM); however, this finding was confounded by low sele- tive damage to skeletal muscle during exercise. nium intake in the mares (Wilson et al., 1976). A relationship between vitamin E (and selenium) defi- More work is necessary to determine the requirements ciency and exertional rhabdomyolysis was initially sug- for vitamin E specific to growth. Based on the information gested (Hill, 1962); however, subsequent studies did not available, 80 IU/kg DM recommended in the 1989 NRC is support this idea (Roneus and Hakkarainen, 1985) and more than adequate for growing horses. Vitamin E require- pointed to multifactorial etiologies (Beech, 1994). ments of growing horses in the current revision are ex- The relationship between vitamin E and exercise- pressed as IU/kg BW (2 IU/kg BW), which is equivalent to induced oxidative stress has been investigated in horses. 80 IU/kg DM assuming 2.5 percent BW as DM intake. There is evidence that exercise induces some degree of lipid oxidation in horses (McMeniman and Hintz, 1992; Williams et al., 2004a,b), yet its contribution toward oxida- Breeding, Gestation, and Lactation tive damage of tissues and subsequent health of the horse is Stowe (1967) reported a beneficial effect of a low level of uncertain (McMeniman and Hintz, 1992; Siciliano et al., oral vitamin E supplementation (100 IU/d, approximately 1997). Exercise conditioning has been demonstrated to in- 10 percent of the current requirement) on reproduction in fluence vitamin E status. Petersson et al. (1991) reported barren mares. Ott and Asquith (1981) did not find any ad- that plasma, but not middle gluteal muscle, vitamin E con- vantage of supplementing 46 IU of additional vitamin E/d to centration was lower over a 4-month period in exercised a ration already containing vitamin E concentration equiv- horses compared with nonexercised controls when they alent to NRC (1978) requirements (i.e., 15 IU/kg DM) on re- consumed a diet deficient in vitamin E (NRC, 1989) con- breeding efficiency in foaling mares. Supplementation of sisting of grain (7.8 IU E/kg DM) and free choice straw 200â400 IU vitamin E/d to gestating mares was ineffective (18.5 IU E/kg DM). When the ration was supplemented at maintaining serum Î±-tocopherol concentrations of mares with vitamin E (grain and straw containing 85.6 and 17 IU fed a base diet of preserved forage (Maenpaa et al., 1988b), E/kg DM, respectively), there was no difference in plasma yet no outward signs of deficiency were reported. Libido vitamin E between exercised and nonexercised groups. Ad- and seminal characteristics were not affected when stallions ditionally, there was a trend toward an inverse relationship were supplemented with 5,000 IU vitamin E/d, as compared between middle gluteal muscle vitamin E concentration and to an unsupplemented ration consisting of grain mix and an indicator of lipid oxidation (thiobarbituric acid reactive grass hay (Rich et al., 1983). These results suggest that even substances) in skeletal muscle. Although these horses were the maintenance requirement for vitamin E recommended in fed a vitamin E-deficient diet over a 4-month period, no the NRC (1989), i.e., 50 IU/kg DM, is sufficient for repro- clinical signs of vitamin E deficiency were observed, nor duction in both stallions and mares. Therefore, the require- were blood variables indicative of deficiency altered (red ment for reproduction remains unchanged from the previous cell hemolysis, muscle enzyme leakage). It should be noted revision (i.e., 50 IU/kg DM or 1 IU/kg BW assuming a DM that the exercise protocol used in this experiment was rela- intake of 2 percent of BW). tively light. Vitamin E status of horses performing rigorous Hoffman et al. (1999) reported that foals suckling mares endurance type exercise was improved with levels of sup- fed diets containing approximately 160 IU vitamin E/kg plementation exceeding the current NRC requirement (240 DM, or twice that recommended for broodmares (NRC, IU/kg DM or approximately 6 IU/kg BW assuming DM in- 1989), tended to have greater serum immunoglobulin G take of 2.5 percent of BW: Hoffman et al., 2001; 11.1 IU/kg (IgG) titers than those suckling mares fed 80 IU vitamin BW: Williams et al., 2004b). Siciliano et al. (1997) reported E/kg DM. This response was thought to be a reflection of the a decline in both serum (approximately 30 percent) and significantly greater IgG concentration of the colostrum middle gluteal muscle vitamin E concentration (approxi- from those mares. Vitamin E used in the aforementioned ex- mately 20 percent) over a 90-day exercise conditioning pe- periment was supplied both from the base ration (mixed riod when horses were fed a basal diet (15â44 IU/kg DM, grass hay plus a grain-mix-concentrate) and from a supple- or 0.3â0.88 IU/kg BW) or 80 IU/kg DM (1.6 IU/kg BW), mental source containing all-rac-Î±-tocopheryl acetate. but not in horses fed 300 IU/kg DM (6 IU/kg BW). This Whether or not the difference in antibody titers reported in result suggests that dietary concentrations of vitamin E these foals results in improved health remains to be deter- greater than 80 IU/kg DM and potentially approaching 300 mined. The current vitamin E requirement for lactation is IU/kg DM are necessary to maintain blood and skeletal unchanged from the previous revision (i.e., 80 IU/kg DM or muscle concentrations undergoing exercise conditioning. 2 IU/kg BW assuming a DM intake of 2.5 percent BW). This finding is in agreement with Saastamoinen and Juusela (1993), who found that approximately 150â250 IU of vita- min E/kg DM was necessary to prevent serum vitamin E Work concentration from declining in horses receiving regular ex- Interest in the vitamin E requirement for work was stim- ercise. Vitamin E supplementation (5,000 IU/d or approxi- ulated by a possible relationship between vitamin E status mately 11.1 IU/kg BW) decreased white blood cell apopto-
VITAMINS 117 sis and plasma creatine kinase activity during and after a Deficiency treadmill-simulated 55-km endurance race (Williams et al., Vitamin K deficiency results in the production of under- 2004b). carboxylated Gla-proteins, such as undercarboxylated os- Although the above findings suggest that vitamin E sup- teocalcin, that lack biological activity. Impairment of blood plementation exceeding current recommendations may coagulation is the major clinical sign of vitamin K defi- improve vitamin E status of exercising horses in some situ- ciency in all species (McDowell, 1989). Vitamin K defi- ations, more work using varied dietary vitamin E concentra- ciency has also been implicated in diseases affecting bone tions and differing exercise protocols is required to establish and vascular health in humans (Vermeer et al., 2004). optimum requirements necessary to maintain vitamin E Vitamin K deficiency in horses due to inadequate vitamin status during exercise. The current requirements are un- K consumption has not been identified. Vitamin K antago- changed from the previous revision, but are expressed per nists such as dicumarol and other coumarin derivatives (e.g., unit of BW assuming a DM intake of 2, 2.25, and 2.5 per- warfarin) can impair vitamin K metabolism and result in de- cent of BW for light, moderate, and all other levels of work, ficiency symptoms. Dicumarol is produced in moldy sweet respectively (i.e., 80 IU/kg DM is equivalent to 1.6, 1.8, and clover hay and has been reported to impair blood coagula- 2 IU/kg BW for light, moderate, and all other levels of work, tion, according to a single report in one horse (McDonald, respectively). 1980). Additionally, therapeutic administration of warfarin to horses can interfere with vitamin K metabolism and im- pair blood coagulation. Prothrombin time increased in VITAMIN K horses receiving warfarin administration (0.08 mg/kg BW/d for 4â5 days) and was restored in 24 hours by either intra- Function venous or subcutaneous administration of 300â500 mg vita- Vitamin K serves as a cofactor for vitamin K-dependent min K1 (Byars et al., 1986). carboxylase, which catalyzes the post-translational synthe- sis of Î³-carboxyglutamic acid (Gla) from glutamic acid Toxicity residues contained in precursor proteins (Ferland, 2001). The resulting vitamin K-dependent proteins, also referred to Excess intake of phylloquinone appears to be essentially as Gla-proteins, are involved in blood clotting, bone metab- innocuous. Molitor and Robinson (1940) administered 25 olism, and vascular health (Dowd et al., 1995; Vermeer et g/kg BW orally or parenterally to laboratory animals with al., 1996, 2004). Vitamin K has also been suggested to play no adverse effect. Menaquinones and menadione in the diet a role in brain sphingolipid metabolism through mecha- probably also have low toxicity. The NRC (1987) proposed nisms that are not well understood (Denisova and Booth, that oral toxic levels are at least 1,000 times the dietary re- 2005). quirement. However, Rebhun et al. (1984) administered single doses of menadione bisulfite to horses in amounts of 2.1â8.3 mg/kg BW via intramuscular or intravenous routes. Dietary Sources These dosages conformed to manufacturerâs recommenda- tions, but resulted in renal colic, hematuria, azotemia, and Vitamin K occurs naturally as phylloquinone (K1; electrolyte abnormalities consistent with acute renal failure. 2-methyl-3-phytyl-1,4-napthoquinone) and the group of At necropsy, lesions of renal tubular nephrosis were found. compounds known as menaquinone (K2; 2-methyl-1,4- Because phylloquinone injectables appear safer than mena- napthoquinones) (Ferland, 2001). Phylloquinone is the form dione injectables for the human newborn (American Acad- of vitamin K found in plants. Menaquinone is produced by emy of Pediatrics, 1971), use of the former seems prefer- intestinal bacteria. Menadione (K3) is a synthetic form of vi- able when parenteral vitamin K is administered to the tamin K used as a feed supplement and is metabolized in the horse. body to an active form, i.e., menaquinone-4. Among typical feedstuffs used for horses, forages con- Requirements tain the greatest concentration of vitamin K (2.73â21.6 mg/kg DM) and cereals contain relatively low concentra- Dietary vitamin K requirements have not been deter- tions (0.2â0.4 mg/kg DM) (McDowell, 1989; Siciliano et mined for the horse (NRC, 1989). Phylloquinone content of al., 2000a). Menaquinones produced by intestinal bacteria pasture, hay, or both, along with menaquinones synthesized may also provide the horse with some vitamin K, but the by intestinal bacteria, presumably meet requirements in all exact contribution is unknown. Menaquinones derived from but the most unusual of circumstances. intestinal bacteria can be absorbed in humans and rodents, Limited reports exist regarding factors influencing vita- but the overall contribution toward meeting vitamin K re- min K requirements of horses. Vitamin K status, as mea- quirements may be limited by the capacity for absorption in sured by undercarboxylated osteocalcin, was not affected by the lower bowel (Suttie, 1995) and may be inadequate to the initiation of exercise training in young horses (18â24 maintain optimum status in humans (Ferland, 2001). months of age) while consuming a diet containing 2.73 mg
118 NUTRIENT REQUIREMENTS OF HORSES phylloquinone/kg DM, nor was it correlated to exercise as- Requirements sociated changes in bone mineral or bone pathology (Sicil- The NRC (1989) requirement for thiamin is 5 mg/kg DM iano et al., 2000a). Vitamin K status, as measured by under- for working horses and 3 mg/kg DM for all others, and was carboxylated osteocalcin, of foals and weanlings increased based on diet concentrations necessary to maintain appetite with age possibly reflecting increased forage consumption (Carroll et al., 1949), increase growth rate (Jordan, 1979), and increased capacity for intestinal microbial synthesis of improve thiamin balance, and improve biochemical mea- menaquinone (Siciliano et al., 2000b). Serum undercar- sures reflective of thiamin function in exercising horses boxylated osteocalcin was not correlated with medial radi- (Topliff et al., 1981). ographic bone density in these foals and weanlings. The ef- Carroll et al. (1949) provided evidence of microbial thi- fect of lower vitamin K status on bone health in foals amin synthesis in the gastrointestinal tract of horses, partic- remains to be determined. ularly the anterior portion of the large colon. In a follow-up experiment, evidence indicated microbial thiamin synthesis THIAMIN alone was inadequate to prevent deficiency symptoms as thi- amin deficiency symptoms (e.g., loss of appetite, weight Function loss, ataxia) were reported in two Percheron horses (2 years of age, approximately 600-kg BW) fed the same semi- Thiamin is required by pyruvate dehydrogenase, Î±- purified diet containing 1.1 mg thiamin/kg DM (total DM ketoglutarate dehydrogenase, and transketolase, all of which intake approximately 1.25â1.5 percent of BW) over a 16- are involved in carbohydrate metabolism (Bates, 2001). week period (Carroll et al., 1949). One horse died following Pyruvate dehydrogenase and Î±-ketoglutarate dehydrogenase 19 weeks of the low-thiamin diet and the other improved are involved in the metabolism of substrates used for adeno- over a 12-week period when supplemented with 30 mg sine triphosphate (ATP) synthesis (e.g., glucose), whereas thiamin/d (approximately 5.5 mg thiamin/100 kg BW). transketolase is involved in the pentose phosphate pathway. Jordan (1979) reported that weanling ponies (110â130 days of age) fed diets containing 6.6 mg thiamin/kg DM (70 Dietary Sources percent corn, 30 percent alfalfa meal) gained more BW (89.5 percent increase) as compared to those consuming the Thiamin is found in relatively high concentrations in ce- basal diet only. Feed intake was not different between the real grains (e.g., corn, 3.5; oats, 5.2; wheat, 5.5; barley, 5.7 two groups. No clinical signs of thiamin deficiency were re- mg/kg DM), cereal grain byproducts (wheat bran, 8; wheat ported in the unsupplemented group. middlings, 12; rice bran, 23 mg/kg DM), protein supple- Topliff et al. (1981) concluded that 3 mg thiamin/kg DM ments (e.g., cottonseed meal, 6.4; peanut meal, 12 mg/kg may not be adequate for exercising horses. This conclusion DM), and is particularly high in brewerâs yeast (95.2 mg/kg) was based on the finding that the mean blood thiamin concen- (McDowell, 1989). Thiamin is supplemented as either thi- trations of horses fed diets containing either 4 or 28 mg amin hydrochloride or mononitrate. thiamin/kg DM were greater than in horses fed diets contain- ing 2 mg thiamin/kg DM. Additionally, an indicator of pyru- Deficiency vate dehydrogenase activity suggested greater activity follow- ing 30 minutes of exercise in horses fed diets containing 4 or The classical deficiency symptom for thiamin is beriberi 28 mg thiamin/kg DM as compared to 2 mg thiamin/kg DM. (Bates, 2001). Anorexia, bradycardia, muscle fasciculations, There is no new evidence to suggest that thiamin re- and ataxia have been reported in cases of thiamin deficiency quirements are different from NRC (1989). Thiamin re- in horses (Carroll et al., 1949; Roberts et al., 1949; Cym- quirements in the previous revision, expressed per kg DM, baluk et al., 1978). Carroll et al. (1949) reported thiamin de- have been transformed to a BW basis assuming a DM intake ficiency symptoms in two horses fed semi-purified diets of 2 percent of BW for maintenance, breeding stallions, ges- containing approximately 1.1 mg/kg for a 16-week period. tation, and light work; 2.25 percent of BW for moderate Thiamin deficiency symptoms have been reported in horses work; and 2.5 percent of BW for all other feeding classes. due to ingestion of bracken fern (Roberts et al., 1949) and For example, a maintenance requirement previously ex- the coccidiostat amprolium (Cymbaluk et al., 1978), both of pressed as 3 mg/kg DM is now expressed as 0.06 mg/kg BW which interfere with thiamin metabolism. Thiamin defi- (i.e., 3 mg/kg DM Ã 2 kg DM/100 kg BW). ciency in horses fed typical feed ingredients, in the absence of interfering substances, has not been reported. RIBOFLAVIN Toxicity Function Thiamin toxicity in horses does not seem likely and has Riboflavin is a precursor to the coenzymes flavin adenine not been reported (NRC, 1989). dinucleotide (FAD) and flavin mononucleotide (FMN). Both FAD and FMN are involved in oxidation-reduction re-
VITAMINS 119 actions used in ATP synthesis, drug metabolism, lipid me- was based on the work of Pearson et al. (1944a,b) who re- tabolism, and antioxidant defense mechanisms (i.e., glu- ported that 44 Âµg riboflavin/kg BW (approximately 2.2 tathione redox cycle) (Rivlin, 2001). mg/kg air dried feed) was adequate based on measurements of growth and whole body riboflavin status in Shetland ponies. However, in another report two horses fed a ration Dietary Sources low in B vitamins containing 0.4 mg/kg air-dried feed for 19 Relative to dietary requirements for horses, values pub- weeks did not demonstrate deficiency symptoms attributed lished in the U.S. Canadian Feed tables suggest that ri- to the low-riboflavin content of the diet (Carroll et al., boflavin is found in high concentration in legumes such as 1949). In the fifth NRC revision (1989), the requirement re- alfalfa and clover (13â17 mg/kg DM). However, slightly mained similar and was suggested to be no more than 2 lesser concentrations are found in some grass hays (7â10 mg/kg DM air-dried feed. At the time of this writing, no new mg/kg DM), and relatively low concentrations occur in ce- information regarding riboflavin requirements of horses ex- real grains (1.4â1.7 mg/kg DM) (NRC, 1982). Naturally oc- ists. Horses fed forage-based diets should have a riboflavin curring riboflavin present in feedstuffs is generally in the intake well above 2 mg/kg air-dried feed based on estimates form of FAD and FMN, both of which are coenzyme deriv- of riboflavin concentration in feedstuffs previously dis- atives of riboflavin. cussed. Riboflavin requirements in the previous revision, Riboflavin synthesis in the intestine of the adult horse or expressed per kg DM, have been transformed to a BW basis pony has been demonstrated by Jones et al. (1946), Carroll assuming a DM intake of 2 percent of BW for maintenance, et al. (1949), and Linerode (1966). When Carroll and col- breeding stallions, gestation, and light work; 2.25 percent leagues (1949) fed a riboflavin-deficient diet containing 0.4 for moderate work; and 2.5 percent of BW for all other feed- mg of riboflavin/kg DM, riboflavin concentrations (mg/kg ing classes. For example, a maintenance requirement previ- ingesta DM) in the various intestinal sections were as fol- ously expressed as 2 mg/kg DM is now expressed as 0.04 lows: duodenum, 3.8; ileum, 1.1; cecum, 7; anterior large mg/kg BW (i.e., 2 mg/kg DM Ã 2 kg DM/100 kg BW). colon, 9.2; and anterior small colon, 12.2. The increased concentrations occurring in the cecum and large colon rel- NIACIN ative to the foregut are indicative of microbial riboflavin synthesis. Function Niacin is essential for the coenzymes nicotinamide ade- Deficiency nine dinucleotide (NAD) and nicotinamide adenine dinu- Although riboflavin deficiency has not been described in cleotide phosphate (NADP), which are involved in many im- horses, signs in other species include rough hair coat; atro- portant biological oxidation-reduction reactions. phy of the epidermis, hair follicles, and sebaceous glands; Additionally, NAD has been reported to provide the sub- dermatitis; vascularization of the cornea; catarrhal conjunc- strate for three classes of enzymes that transfer ADP-ribose tivitis; photophobia; and excess lacrimation. Some years units to proteins involved in DNA processing, cell differen- ago, it was suggested that periodic ophthalmia (recurrent tiation, and cellular calcium mobilization (Jacob, 2001). uveitis or moon blindness) is a consequence of riboflavin deficiency (Jones, 1942; Jones et al., 1945). However, the Dietary Sources linkage between the two is not substantial, and invasions of the cornea by leptospira (Roberts, 1958) or microfilaria Niacin is a generic term for nicotinic acid (pyridine-3- (Onchrocera cervicalis) (Cello, 1962) have been implicated carboxylic acid) and nicotinamide (nicotinic acid amide). in the production of periodic ophthalmia. Both nicotinic acid and nicotinamide are equivalent in terms of their vitamin activity. Naturally occurring niacin present in feedstuffs is in the Toxicity form of NAD and NADP (Jacob, 2001). Both NAD and Little evidence exists of oral toxicity of riboflavin in any NADP are hydrolyzed in the intestinal mucosa to yield species. Schumacher et al. (1965) reported a reduction in nicotinaminde. Niacin is widely distributed in the diet, but pups born to rats supplemented with 104 mg of riboflavin/kg varies in availability depending upon whether it is in a diet. Estimates of the rat LD50 for intraperitoneal, subcuta- bound form (NRC, 1982; McDowell, 1989). Corn, oats, and neous, and oral administration are 0.56, 5, and more than 10 barley have been reported to contain 28, 16, and 94 mg g of riboflavin/kg BW, respectively. niacin/kg DM, respectively; however, 85â90 percent may be in an unavailable bound form. Therefore, McDowell (1989) suggested niacin from cereal grain sources should be ig- Requirements nored or at least given a value of no greater than one-third of The first NRC riboflavin allowance estimated for horses the total niacin. Other reported niacin concentrations for was 2.2 mg/kg air-dried feed (NRC, 1949). This estimate feedstuffs include: soybean meal, 31 mg/kg DM; alfalfa, 42
120 NUTRIENT REQUIREMENTS OF HORSES mg/kg DM; and timothy hay, 24 mg/kg DM (NRC, 1982). Requirements Approximately 40 percent of niacin in oilseeds is in a bound No dietary requirement for niacin has been established form (McDowell, 1989). No estimate of the percentage of for horses. bound niacin is available for soybean meal or forages com- monly fed to horses. Niacin appears to be produced by microbial fermentation BIOTIN in the hindgut of the horse. Carroll et al. (1949) fed a diet containing 3 mg of nicotinic acid/kg DM and found the fol- Function lowing nicotinic acid concentrations (mg/kg DM) in ingesta: Biotin is a co-enzyme for four carboxylase enzymes: duodenum, 55; ileum, 58; cecum, 121; anterior large colon, acetyl-CoA carboxylase, pyruvate carboxylase, propionyl- 96; and anterior small colon, 119. Linerode (1966) also con- CoA carboxylase, and Î²-methylcrotonyl-CoA carboxylase cluded that appreciable microbial niacin synthesis occurs in (Zempleni, 2001). These carboxylase enzymes are involved the cecum and colon of the adult pony. in fatty acid synthesis (acetyl-CoA carboxylase), gluconeo- Niacin can be synthesized from tryptophan in the horseâs genesis (pyruvate carboxylase), amino acid metabolism hepatic tissues (Schweigert et al., 1947). The Food and Nu- (propionyl-CoA carboxylase and Î²-methylcrotonyl-CoA trition Board (1998) uses a tryptophan to niacin conversion carboxylase), and metabolism of cholesterol and odd-chain of 60 mg tryptophan to 1 mg niacin. fatty acids (propionyl-CoA carboxylase). As a result biotin plays an important role in intermediary metabolism. Deficiency Biotin is essential for cell proliferation. Biotinâs role in intermediary metabolism (i.e., carboxylase enzymes), along Niacin deficiency has not been described in the horse. with roles in gene expression and biotinylation of histones, Niacin deficiency in other species results in severe meta- have been suggested as the basis for the role of biotin in cell bolic disorders that manifest as lesions of the skin (e.g., pel- proliferation (Zempleni and Mock, 2001). lagra) and digestive system (McDowell, 1989). Dietary Sources Toxicity Biotin is 2-keto-3, 4-imadazilido-2-tetrahydrothiophene- Effects of niacin excess have not been described in the valeric acid and has eight possible isomers of which only d- horse. However, high oral intakes of nicotinic acid have pro- biotin contains vitamin activity (McDowell, 1989). Informa- duced vasodialation, itching, sensations of heat, nausea, tion regarding biotin concentration of feedstuffs for horses is vomiting, headaches, and occasional skin lesions in humans limited. That which is available indicates relatively high con- (Robie, 1967; Hawkins, 1968). In addition, Winter and centrations for alfalfa (0.2 mg/kg DM, hay; 0.49 mg/kg DM, Boyer (1973) reported hepatotoxicity from high nicoti- fresh); intermediate concentrations for oats (0.11â0.39 namide intake. Research with laboratory animals suggests mg/kg DM), barley (0.13â0.17 mg/kg DM), and soybean that daily oral intake greater than 350 mg of nicotinic acid meal (0.18â0.5 mg/kg DM); and low concentrations for corn equivalents/kg BW can be toxic (NRC, 1987). Nicotinic (0.06â0.1 mg/kg DM) (NRC, 1982; McDowell, 1989). Bi- acid may be tolerated somewhat better than nicotinamide. otin availability has not been assessed for horses, but that for Limits for parenteral administration could be lower than poultry and swine suggests corn and soybean meal are rela- those for oral intake. tively high at 75â100 percent and 100 percent, respectively Because niacin toxicity has been reported to inhibit the (Baker, 1995). Most naturally occurring biotin exists in a mobilization of free fatty acids (FFA) from adipose tissue form bound to protein, i.e., Îµ-N-biotinyl-L-lysine (biocytin), of humans during exercise (Heath et al., 1993; Murray et making availability dependent upon digestibility of the spe- al., 1995), Parker et al. (1997) investigated the effect of 6 cific binding proteins (Baker, 1995). weeks of nicotinic supplementation (3 g/d) on niacin status Biotin is also synthesized by intestinal microbes. Carroll and plasma FFA concentrations associated with a standard- et al. (1949) fed a diet containing less than 0.01 mg of ized exercise test. Niacin status was not affected by either biotin/kg DM and found the following biotin concentrations nicotinic acid supplementation or exercise conditioning, in ingesta (mg/kg of DM): duodenum, less than 0.1; ileum, nor was plasma FFA concentration associated with a stan- 0.1; cecum, 0.2; anterior large colon, 3.8; and anterior small dardized exercise test affected by nicotinic acid supplemen- colon, 2.3. tation. Interestingly niacin number (the ratio of NAD to NADP) used as an indicator of niacin status in this experi- Deficiency ment ranged from 75 to 100, which is lower than the refer- ence range for healthy humans (i.e., 127 to 223) (Jacob, Severe dermatitis is the most common deficiency symp- 2001). tom seen in livestock (McDowell, 1989). No unequivocal
VITAMINS 121 evidence of biotin deficiency in the horse has been pub- proving hoof integrity in certain horse populations, particu- lished. Signs in other species include inflammation and larly those affected with poor hoof quality. However, no de- cracks of the plantar surface of the feet (Cunha et al., 1946, finitive requirement for biotin has been determined. 1948). Biotin deficiency has been implicated in some popula- FOLATE tions of horses chronically affected with poor hoof quality, such as soft white line and crumbling, fissured horn at the Function bearing border of the hoof wall (Josseck et al., 1995; Zenker et al., 1995). Daily supplementation with 20 mg biotin im- Folate is required for numerous biosynthetic pathways proved hoof wall integrity (via macroscopic assessment) fol- involving transfer and utilization of single carbon units. lowing at least 9 months of supplementation, but not growth Among them are reactions necessary for DNA, purine, and rate (Josseck et al., 1995), and improved hoof structure (via methionine synthesis (Bailey et al., 2001). Therefore, folate histological assessment) and hoof wall tensile strength fol- is particularly important for tissues in which rapid cell lowing 33 and 38 months of supplementation (Zenker et al., growth, turnover, or some combination is occurring. 1995). Previous observations from uncontrolled field studies suggested 10â30 mg biotin/d for not less than 6â9 months Dietary Sources improved hardness and integrity of hooves previously of poor quality (Comben et al., 1984; Kempson, 1987). Using Folate is a generic term referring to folic acid and natu- scanning electron microscopy, Kempson (1987) identified rally occurring folate (Bailey et al., 2001). Folic acid is the two types of defects in hoof samples from horses having thin synthetic form of folate and consists of a pteridene bicyclic friable horn. The first type of defect was characterized by a ring system, p-aminobenzoic acid and glutamic acid. Natu- loss of structure and horn in the stratum externum of the rally occurring dietary folate differs from folic acid in that it hoof wall, whereas the second was characterized by a loss of contains 5 to 8 glutamic acids joined in Î³-peptide linkages, tubular structure in the inner layers of the hoof wall. The i.e., polyglutamate form. first defect appeared responsive to biotin supplementation (~ Reported values for folate concentration of typical horse 15 mg/d). The second defect, which consisted of approxi- feed ingredients are limited. Those available are for alfalfa mately 94 percent of the affected horses studied, was (2.5â4.1 mg/kg DM), timothy hay (2.3 mg/kg DM), and ce- thought due to dietary protein and calcium deficiency. This real grains (corn, 0.3; oats, 0.4; barley, 0.6 mg/kg DM) work suggests that some horses with thin friable hoof wall (NRC, 1982). Horses consuming fresh forage have greater may benefit from dietary biotin supplementation, while oth- serum folate concentrations compared to horses consum- ers may not. ing preserved forages, grains, and grain byproducts, which Buffa et al. (1992) reported increased hoof wall growth presumably reflects greater folate concentrations of fresh rate and hoof hardness in Thoroughbred and Thoroughbred- forage. cross horses fed 15 mg biotin/d for 10 months as compared Folic acid appears to be produced in the digestive tract by to controls fed 0.81 mg biotin/d. Reilly et al. (1998) reported microbial synthesis. Carroll et al. (1949) fed a diet contain- a 15 percent higher hoof wall growth rate in ponies supple- ing less than 0.1 mg folic acid/kg DM and found the fol- mented with 0.12 mg biotin/kg BW/d for 5 months as com- lowing folic acid concentrations in ingesta (mg/kg of DM): pared to controls fed 0.0015 mg naturally occurring biotin/ duodenum, 0.9; ileum, 0.5; cecum, 3; anterior large colon, kg BW/d. 4.7; and anterior small colon, 2.7. Bioavailability estimates of folic acid and naturally oc- curring dietary folate in humans are 85 and 50 percent, re- Toxicity spectively (Food and Nutrition Board, 1998). However, Effects of excess biotin have not been described in the Allen (1984) found that orally administered folic acid was horse. Fetal resorption has been reported in rats injected absorbed poorly in the horse. subcutaneously with 50 to 100 mg biotin/kg BW. Poultry and swine can tolerate at least 4 to 10 times their dietary re- Deficiency quirement and probably much more (NRC, 1987). Folate deficiency has not been described in the horse (NRC, 1989). Megaloblastic anemia and leukopenia are Requirements common findings in other species. In addition, tissues hav- No controlled studies have been published establishing a ing a rapid rate of cell growth or tissue regeneration (e.g., dietary biotin requirement above that supplied by intestinal gastrointestinal tract epithelial lining, epidermis, and bone synthesis. As stated in the deficiency section, there is some marrow) are also affected (McDowell, 1989). Folate defi- evidence that biotin supplementation may be useful in im- ciency in pregnant women is associated with increased risk
122 NUTRIENT REQUIREMENTS OF HORSES of preterm delivery, infant low birth weight, fetal growth re- serum folate concentration of horses on pasture was approx- tardation, and neural tube defects (Bailey et al., 2001). imately 3-fold that of stabled horses fed preserved forage Sulfadiazine and pyrimethamine are antimicrobials used and suggested that exercise may increase folate needs of to treat equine protozoal myeloencephalitis (EPM). Both of some horses in training. these drugs can impair folate status. Sulfadiazine inhibits The effect of folate status on athletic performance is rel- microbial synthesis of folate by preventing dihydroteroic atively uninvestigated. Physiological response to exercise acid formation from para-aminobenzoic acid. Pyrimeth- and time to fatigue during a stepwise exercise test carried amine inhibits dihydrofolate reductase, which is necessary out to exhaustion on a high-speed treadmill was not influ- for folate absorption and metabolism. Colahan et al. (2002) enced when serum folate was decreased from 8 to 6 ng/ml reported a 2 ng/ml reduction in serum folate (5-methyl- following oral administration of sulfadiazine and pyri- tetrahydrofolate) from approximately 8 to 6 ng/ml follow- methamine (Colahan et al., 2002). The duration of this ex- ing 4 days of sulfadiazine and pyrimethamine administra- periment was relatively short (i.e., 4 days of sulfadiazine and tion. Piercy et al. (2002) reported clinical findings pyrimethamine administration) and longer-term effects of compatible with folate deficiency in a horse treated with sulfadiazine and pyrimethamine administration on folate sulfadiazine and pyrimethamine for EPM over a 9-month status and exercise performance were not evaluated. period. The findings included hematological defects, hy- Ordakowski-Burk et al. (2005) reported folate status in poplastic bone marrow, and dysphagia caused by oral ul- mares and foals from foaling through 6 months of lactation ceration and glossitis. Serum folate concentration was ap- and concluded folate supplementation was not necessary. proximately 4.5 ng/ml. Folic acid supplementation (19.2 The mares consumed folate from natural sources only (pas- mg/d) accompanied the treatment and was hypothesized to ture, hay, and supplemental feed) in amounts ranging from exacerbate the deficiency by competing for absorption with 30â80 mg folate/d. the active, reduced form of folate (5-methyl tetrahydrofo- The current lack of information regarding folate require- late). A similar hypothesis was put forth and supported by ments of horses precludes accurate estimation of a true re- the finding of congenital defects in newborn foals born of quirement. Based on the absence of reports of folate defi- mares treated with sulfadiazine and pyrimethamine for ciency in horses maintained in practical settings, naturally equine protozoal myeolencephalitis during pregnancy, and occurring folate in feeds and that of microbial origin appear also supplemented with folic acid (40 mg/day) for periods to satisfy the requirement. However, further investigation of ranging from the last 3 months of gestation to 2 years folate requirements for horses not having access to pasture (Toribio et al., 1998). is warranted, particularly for horses with potentially high re- quirements, e.g., gestation, lactation, growth, and intense exercise. Toxicity Folate is generally regarded as nontoxic (NRC, 1987). OTHER B-VITAMINS However, single parenteral doses about 1,000 times greater than the dietary requirement have been reported to induce Information regarding dietary requirements for vitamin epileptic convulsion and renal hypertrophy in the rat. B12, pantothenic acid, and vitamin B6 of horses is either ex- As discussed above, folic acid supplementation is not tremely limited or not available (NRC, 1989). All of these recommended in horses treated with dihydrofolate reductase vitamins appear to be synthesized in the gastrointestinal inhibitors (e.g., pyrimethamine) (Toribio et al., 1998; Piercy tract of horses ( Carroll et al., 1949; Linerode, 1966; Alexan- et al., 2002). der and Davies, 1969; Davies, 1971). Vitamin B12 (cyanocobalamin) is a component of several enzyme systems involved in purine and pyrimidine synthe- Requirements sis, transfer of methyl groups, protein synthesis, carbohy- Folate requirements of horses have not been determined. drate, and fat metabolism (McDowell, 2000). Vitamin B12 is Folate originating from microbes in the gastrointestinal tract not present in plants, but is synthesized by microorganisms and that occurring naturally in feeds appears to meet the present in the digestive tract. Synthesis of vitamin B12 re- needs of most horses. However, Seckington et al. (1967) re- quires the trace mineral cobalt. Supplemental cobalt (15 mg ported lower serum folate concentration in stabled Thor- cobalt chloride) has been reported to influence serum and oughbred racehorses and postpartum mares (mean 7.5 and fecal vitamin B12 concentrations (Alexander and Davies, 7.4 ng/ml, respectively) as compared to mature horses at 1969). Stillions et al. (1971b) fed adult horses a semi- pasture (mean 11.5 ng/ml). Likewise, serum folate was purified diet containing about 1 Âµg of vitamin B12 and about lower in race horses undergoing training for 6 months with- 5 mg cobalt/kg air-dry feed. Although serum vitamin B12 out access to pasture (range 1.5â6.1 ng/ml) as compared to concentration and daily urinary vitamin B12 excretion were unexercised horse and pony mares maintained on pasture lower than with a diet containing 90 Âµg of vitamin B12/kg, (range 6.4â15.8 and 7.4â16.6 ng/ml, for horses and ponies, daily vitamin B12 excretion was about 500 Âµg or five times respectively: Allen, 1978). Roberts (1983) also reported greater than intake on the low- or high-vitamin B12 diet, re-
VITAMINS 123 spectively. No evidence of vitamin B12 deficiency was seen, 2001). Vitamin C concentrations of typical feedstuffs for and hemoglobin and hematocrit values were normal over an horses are not available. experimental period of 11 months. Horses have remained in Ascorbic acid, ascorbyl palmitate, and calcium ascorbyl- good health while grazing pastures so low in cobalt that ru- 2-monophosphate have been used as vitamin C supplements minants confined to them have died (Filmer, 1933). Evi- for horses. Ascorbyl palmitate has been reported to be more dence of absorption of vitamin B12 from the cecum and efficient at raising plasma ascorbic acid concentration than colon was reported by Stillions et al. (1971b) and Salminen ascorbyl-2-monophosphate (Deaton et al., 2003) or ascorbic (1975). Caple et al. (1982) examined several hundred horses acid (Snow and Frigg, 1987, 1990). and reported plasma vitamin B12 concentrations of 1.8â7.3 Vitamin C can be synthesized from glucose in several Âµg/L. Intramuscular injections of vitamin B12 were cleared species (Chatterjee, 1973). Horses also appear to have the rapidly from the plasma, and large amounts were excreted in ability to synthesize vitamin C from glucose (Pearson et al., the feces via the bile when vitamin B12 was administered in- 1943; Stillions et al., 1971a). travenously in foals. Colostrum contributed significantly to the vitamin B12 status of the foal during the first 24 hours Deficiency after birth. Much of the vitamin was stored in the liver. In a survey of 88 horses in various states of physiology and train- Scurvy, resulting from impaired collagen synthesis, is the ing, Roberts (1983) found no evidence of vitamin B12 defi- classical vitamin C deficiency symptom. Classic vitamin C ciency based on serum vitamin B12 concentrations or cellu- deficiency has not been reported in horses. However, some lar hematology. No evidence of a dietary vitamin B12 authors have reported a relationship between decreased requirement above that supplied by intestinal synthesis has blood ascorbic acid concentrations in horses and several dis- been reported. Vitamin B12 deficiency or toxicity has not eases, including post-operative and post-traumatic wound been described in the horse (NRC, 1989). infections, epistaxis, strangles, acute rhinopneumonia, and Pantothenic acid is a constituent of coenzyme A and acyl- performance insufficiency (Jaeschke and Keller, 1978b; carrier protein, which are involved in numerous metabolic Jaeschke, 1984). Serum ascorbic acid concentrations reflec- pathways involving carbohydrates, proteins, lipids, neuro- tive of deficiency have not been established in horses; how- transmitters, steroid hormones, porphyrins, and hemoglobin ever, several values for healthy horses have been reported. (McDowell, 2000). Pantothenic acid is widely distributed in Jaeschke and Keller (1978a) reported mean serum ascorbic the diet (McDowell, 2000). No signs of deficiency were ob- acid concentration of 488 healthy adult horses was 5.9 Â± 1.4 served in adult horses fed diets containing 0.8 mg of pan- Âµg/ml. Snow et al. (1987) reported mean plasma ascorbic tothenic acid or less than 0.2 mg pantothenic acid/kg DM acid concentrations in a group of approximately 20 unsup- (Carroll et al., 1949). Likewise, no signs of deficiency were plemented Thoroughbred racehorses over the period from observed by Pearson and Schmidt (1958) in growing ponies February to October ranged from 2â4.2 Âµg/ml. Mean plasma fed a diet containing 3.2 mg pantothenic acid/kg air-dried ascorbic acid concentrations reported in endurance racing feed. No dietary pantothenic acid requirement has been es- horses ranged from 0.8â4.6 Âµg/ml (Hargreaves et al., 2002; tablished for horses, nor has a deficiency or toxicity been re- Marlin et al., 2002; Williams et al., 2004a). Pearson et al. ported in horses (NRC, 1989). (1943) reported a mean plasma ascorbic acid concentration Vitamin B6 is a component of numerous enzymes in- of 3.2 Â± 1.3 Âµg/ml in unsupplemented Shetland ponies. volved in the metabolism of protein, fats, and carbohydrates, and it is widely distributed in the diet (McDowell, 2000). No Toxicity dietary vitamin B6 requirement has been established, nor has a deficiency or toxicity been reported in horses (NRC, 1989). Excess ascorbic acid intakes in humans and laboratory animals have been reported to produce allergic responses, oxaluria, uricosuria, and interference with mixed function VITAMIN C oxidase systems; however, there is insufficient information on the tolerance and toxicity of ascorbic acid in most do- Function mestic animals (NRC, 1987). Daily doses of 20 g (approxi- Vitamin C functions as a biological antioxidant within mately 44 mg ascorbic acid/kg BW) have been administered the redox system and as a cofactor for mixed function oxi- to horses over a period of approximately 8 months with no dases involved in the synthesis of collagen, carnitine, and apparent negative effect (Snow et al., 1987). norepinephrine (Johnston, 2001). Requirements Dietary and Other Sources Dietary vitamin C requirements for the horse have not Vitamin C activity originates from two compounds, L- been determined and are assumed to be met by endogenous ascorbic acid and dehydro-L-ascorbic acid, which are equiv- synthesis (Pearson et al., 1943; Stillions et al., 1971a). Sev- alent in biological activity (McDowell, 1989; Johnston, eral factors, including disease (Jaeschke, 1984), transport
124 NUTRIENT REQUIREMENTS OF HORSES (Baucus et al., 1990a,b), recurrent airway obstruction (Dea- Byars, T. D., C. E. Greene, and D. T. Kemp. 1986. Antidotal effect of vita- ton et al., 2004), old age (> 20 years of age: Ralston et al., min-K-1 against warfarin-induced anticoagulation in horses. Am. J. Vet. Res. 47:2309â2312. 1988), and endurance exercise (Hargreaves et al., 2002; Caple, I. W., G. G. Halpin, J. K. Azuolas, G. F. Nugent, and R. J. Cram. Marlin et al., 2002) have been demonstrated to decrease 1982. Studies of selenium, iodine and vitamin B12 nutrition of horses in plasma or serum concentrations of ascorbic acid in horses, Victoria. Pp. 57â68 in Proc. 4th Bain-Fall Memorial Lecture. Sydney, which may suggest an increased consumption of ascorbic Australia: Sydney University. acid pools within the body in the presence of these factors. Carroll, F. D., H. Goss, and C. E. Howell. 1949. The synthesis of B vita- mins in the horse. J. Anim. Sci. 8:290â299. However, it is important to note that others have reported an Cello, R. M. 1962. Recent findings in periodic ophthalmia. P. 39 in 8th increase in plasma ascorbic acid concentration (adjusted for Annu. Assoc. Equine Practitioners, San Francisco, CA. changes in plasma volume) following endurance exercise Chatterjee, I. B. 1973. Evolution and biosynthesis of ascorbic-acid. Science (Williams et al., 2004a), or transient increases over a 12- 182:1271â1272. week period in physically conditioned Thoroughbred race- Colahan, P. T., J. E. Bailey, M. Johnson, B. L. Rice, C. C. Chou, J. P. Cheeks, G. L. Jones, and M. Yang. 2002. Effect of sulfadiazine and horses (de Moffarts et al., 2005), and no apparent difference pyrimethamine on selected physiological and performance parameters between aged and younger horses (Deaton et al., 2004). Fur- in athletically conditioned Thoroughbred horses during an incremental ther investigation is required to determine whether endoge- exercise stress test. Vet. Ther. 3:49â63. nous ascorbic acid synthesis is adequate to meet require- Comben, N., R. J. Clark, and D. J. B. Sutherland. 1984. Clinical observa- ments for all horses. tions on the response of equine hoof defects to dietary supplementation with biotin. Vet. Rec. 115:642â645. Combs, G. F. 1996. Nutritional interrelationship of vitamin E and selenium. REFERENCES Pp. 37 in Vitamin E in Animal Nutrition and Management, 2nd rev. ed., M. B. Coelho, ed. Mount Olive, NJ: BASF. Abrams, J. T. 1979. The effect of dietary vitamin A supplements on the Craig, A. M., L. L. Blythe, K. E. Rowe, E. D. Lassen, R. Barrington, and clinical condition and track performance of racehorses. Bibliotheca Nu- K. C. Walker. 1992. Variability of alpha-tocopherol values associated tritio et Dieta 27:113â120. with procurement, storage, and freezing of equine serum and plasma Alexander, F., and M. E. Davies. 1969. Studies on vitamin B12 in horse. Br. samples. Am. J. Vet. Res. 53:2228â2234. Vet. J. 125:169â176. Cunha, T. J., D. C. Lindley, and M. E. Ensminger. 1946. Biotin deficiency Allen, B. V. 1978. Serum folate levels in horses, with particular reference syndrome in pigs fed desiccated egg white. J. Anim. Sci. 5:219â to the English Thoroughbred. Vet. Rec. 103:257â259. 225. Allen, B. V. 1984. Dietary intake and absorption of folic acid in the horse. Cunha, T. J., R. W. Colby, L. K. Bustad, and J. F. Bone. 1948. The need for P. 118 in Proc. Assoc. Vet. Clin. Pharmacol. Ther. and interrelationship of folic acid, anti-pernicious anemia liver extract, American Academy of Pediatrics, Committee on Nutrition. 1971. Vitamin and biotin in the pig. J. Nutr. 36:215â229. K supplementation for infants receiving milk substitute infant formulas Cymbaluk, N. F., P. B. Fretz, and F. M. Loew. 1978. Amprolium-induced and for those with fat malabsorption. Pediatrics 48:483â487. thiamine deficiency in horses: clinical features. Am. J. Vet. Res. Baalsrud, K. J., and G. Overnes. 1986. 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Treating and preventing chronic intermittent rhabdomyoly- 25:238â240. sis. Vet. Med. 89:458â461. Donoghue, S., D. S. Kronfeld, S. J. Berkowitz, and R. L. Copp. 1981. Vit- Blythe, L. L., and A. M. Craig. 1997. Degenerative myeloencephalopathy. amin A nutrition of the equine: growth, serum biochemistry and hema- P. 319 in Current Therapy in Equine Medicine, N. E. Robinson, ed. tology. J. Nutr. 111:365â374. Philadelphia: W. B. Saunders. Dowd, P., S. W. Ham, S. Naganathan, and R. Hershline. 1995. The mecha- Blythe, L. L., A. M. Craig, E. D. Lassen, K. E. Rowe, and L. H. Appell. nism of action of vitamin K. Annu. Rev. Nutr. 15:419â440. 1991. Serially determined plasma alpha-tocopherol concentrations and Elshorafa, W. M., J. P. Feaster, E. A. Ott, and R. L. Asquith. 1979. Effect of results of the oral vitamin E absorption test in clinically normal horses vitamin-D and sunlight on growth and bone-development of young and in horses with degenerative myeloencephalopathy. Am. J. Vet. 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VITAMINS 125 Fonnesbeck, P. V., and L. D. Symons. 1967. Utilization of the carotene of Jaeschke, G. 1984. Influence of ascorbic acid on physical development and hay by horses. J. Anim. Sci. 26:1030â1038. performance of racehorses. P. 139 in Proc. of Ascorbic Acid in Domes- Food and Nutrition Board. 1998. Dietary reference intakes for thiamin, ri- tic Animals, I. Wegger, F. J. Tagwerker, and J. Moustgaard, eds. Copen- boflavin, niacin, vitamin B6, folate, vitamin B12, pantothenic acid, bi- hagen: Danish Agriculture Society. otin, and choline. Washington, DC: National Academy Press. Jaeschke, G., and H. Keller. 1978a. Ascorbic-acid status of horses. 1. Meth- Gandini, G., R. Fatzer, M. Mariscoli, A. Spadari, M. Cipone, and A. Jaggy. ods and normal values. Berliner und Munchener Tierarztliche Wochen- 2004. Equine degenerative myeloencephalopathy in five Quarter schrift 91:279â286. horses: clinical and neuropathological findings. Equine Vet. J. Jaeschke, G., and H. Keller. 1978b. Ascorbic-acid status in horses. 2. Clin- 36:83â85. ical aspects and deficiency symptoms. Berliner und Munchener Tier- Gansen, S., A. Lindner, and A. Wagener. 1995. Influence of a supplemen- arztliche Wochenschrift 91:375â379. tation with natural and synthetic vitamin E on serum Î±-tocopherol con- Jarrett, S. H., and W. A. Schurg. 1987. Use of a modified relative dose re- tent and V4 of Thoroughbred horses. Page 68 in Proc. 14th Equine Nutr. sponse test for determination of vitamin A status in horses. Nutr. Rep. Physiol. Soc. Symp., Ontario, CA. Int. 35:733â742. Greiwe-Crandell, K. M., D. S. Kronfeld, L. A. Gay, and D. Sklan. 1995. Johnston, C. S. 2001. Vitamin C. P. 175 in Present Knowledge in Nutrition, Seasonal vitamin A depletion in grazing horses is assessed better by the B. A. Bowman and R. M. Russel, eds. Washington, DC: ILSI Press. relative dose response test than by serum retinol concentration. J. Nutr. Jones, T. C. 1942. Equine periodic ophthalmia. Am. J. Vet. 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