Subcommittee on Dairy Cattle Nutrition, Committee on Animal Nutrition, National Research Council 408 pages
Vitamin D is a pro-hormone, a necessary precursor for the production of the calcium regulating hormone 1,25-dihydroxyvitamin D. Vitamin D can be produced within the skin of most mammals, including cattle, as a result of the photochemical conversion of 7-dehydrocholesterol to vitamin D3. In plants, ultraviolet irradiation causes photochemical conversion of ergosterol to vitamin D2. Vitamin D, supplied by the skin or the diet, is rapidly transported to and sequestered by the liver. The rapid removal of vitamin D from circulation prevents concentrations of vitamin D in blood from becoming very high; the normal concentration is 1 to 2 ng vitamin D/ml plasma (Horst and Littledike, 1982). Within the liver, vitamin D can be converted to 25-hydroxyvitamin D by vitamin D 25-hydrox-ylase and released into the blood. The production of 25-hydroxyvitamin D within the liver is dependent on the vitamin D content of the diet. Thus plasma 25-hydroxy-vitamin D concentration is the best indicator of vitamin D status of an animal (Horst et al., 1994).
The 25-hydroxyvitamin D then circulates to the kidney where it can be converted to the hormone 1,25-dihydroxy-vitamin D. This hormone acts to increase the active transport of calcium and phosphorus across the intestinal epithelial cells, and potentiates the action of parathyroid hormone to increase bone calcium resorption. Both functions are vital for calcium and phosphorus homeostasis. In addition to calcium and phosphorus homeostasis, 1,25-dihydroxyvi-tamin D is involved in maintaining immune function (Rein-hardt and Hustmyer, 1987); generally it promotes Th2 (humoral) immunity while inhibiting Th1 (cell mediated) immunity (Daynes et al., 1995).
Renal production of 1,25-dihydroxyvitamin D is tightly regulated. The 25-hydroxyvitamin D-1-a-hydroxylase activity of the kidney is stimulated by parathyroid hormone, which is released in response to declining concentrations of calcium in blood (DeLuca, 1979). In the absence of parathyroid hormone, when an animal is in positive Ca balance, 25-hydroxyvitamin D can be hydroxylated in the kidney to 24,25-dihydroxyvitamin D as a primary step in the inactivation and catabolism of vitamin D. The vitamin D catabolic enzymes also function to deactivate 1,25-dihy-droxyvitamin D. These catabolic enzymes exist in tissues throughout the body. In these tissues the catabolic pathway is generally stimulated by 1,25-dihydroxyvitamin D as a negative feedback to reduce high concentrations of 1,25-dihydroxyvitamin D in plasma (Goff et al., 1992; Reinhardt and Horst, 1989).
A low concentration of phosphorus in blood also can enhance renal production of 1,25-dihydroxyvitamin D, even when the concentration of calcium in plasma is normal or above normal (Tanaka and DeLuca, 1973; Gray and Napoli, 1983). Also, higher than normal concentrations of phosphorus in blood can inhibit renal production of 1,25-dihydroxyvitamin D, which can be a factor contributing to milk fever in the periparturient cow (Barton et al., 1987). Pharmacologic doses of vitamin D have been utilized with limited success to prevent milk fever. This is discussed in the section on milk fever (Chapter 9).
Vitamin D2, the form associated with plants, and vitamin D3, the form associated with vertebrates are both used for supplementation of diets. The biologic activity of the two forms is generally considered equal in cattle; however Horst and Littledike (1982) demonstrated an apparent discrimination against the vitamin D2 form in cattle. Presumably this discrimination is the result of reduced binding of vitamin D2 metabolites to vitamin D-binding proteins in blood leading to more rapid clearance of vitamin D2 metabolites from plasma. However, the subcommittee does not recommend adjusting the vitamin D requirement based on the form of vitamin D used as a supplement.
Vitamin D deficiency reduces the ability to maintain calcium and phosphorus homeostasis, resulting in a decline for phosphorus and less often a decrease for calcium in plasma. This eventually causes rickets in young animals and osteomalacia in adults; both are bone diseases in which the primary lesion is failure to mineralize the organic matrix of bone. In young animals rickets causes enlarged and painful joints; the costochondral joints of the ribs are often readily palpated. In adults, lameness and pelvic fracture are a common sequelae of vitamin D deficiency.
The amount of dietary vitamin D required to provide adequate substrate for production of 1,25-dihydroxyvita-min D is difficult to define. Animals exposed to sunlight at the lower latitudes may not require any dietary vitamin D. Sun-cured hay also may provide enough vitamin D to prevent symptoms of vitamin D deficiency (Thomas and Moore, 1951).
The movement away from pasture feeding systems and toward confinement and feeding of stored feeds and byproducts has increased the need for dietary supplementation of vitamin D for dairy cows. As a general rule, the contribution of sunlight and forage to the supply of vitamin D for the cow is not considered when describing the vitamin D requirement. The vitamin D requirement in this publication will consider the "requirement" to be the amount of supplemental vitamin D that should be added to the diet.
Horst et al. (1994) determined that plasma 25-hydroxyvi-tamin D concentrations below 5 ng/ml are indicative of vitamin D deficiency and concentrations of 200 to 300 ng/ ml would indicate vitamin D toxicosis. Normal cows have concentrations of 25-hydroxyvitamin D in plasma between 20 and 50 ng/ml.
Dry, pregnant cows housed indoors and fed a corn silage based diet had plasma concentrations of 25-hydroxyvitamin D in plasma of 19 ng/ml at 14 days prior to parturition and 10.5 ng/ml at 35 days into lactation. Supplementation of the diet with 5,000 (7.5 IU vitamin D/kg BW) or 10,000 IU vitamin D (15 IU vitamin D/kg BW) maintained plasma concentrations between 25 and 31 ng/ml throughout the dry period and early lactation (Vinet et al., 1985).
Ward et al. (1971) reported that cows fed an alfalfa hay-concentrate diet receiving 300,000 IU vitamin D3 once each week («=> 43,000 IU/day) returned to estrus 16 days earlier than cows given no supplement. Ward et al. (1972) also demonstrated that cows receiving 300,000 IU vitamin D3/week had improved absorption of dietary calcium. Hibbs and Conrad (1983) summarized the results of several Ohio State University trials and concluded that cows supplemented with 40,000 IU vitamin D2/day (50 to 70 IU vitamin D/kg BW) produced more milk and generally ate more than cows fed the same diets with no vitamin D supplementation or supplemented with 80,000 or more IU vitamin D/day. Reduced milk production, which could be interpreted as the beginning of vitamin D intoxicosis, was observed when cows were fed 80,000 IU vitamin D/day (1204.40 IU/kg BW).
McDermott et al. (1985) fed an orchard grass-corn silage based ration supplemented with 0, 10,000, 50,000, or 250,000 IU vitamin D3/day to Holstein cows in late gestation and for the first 12 weeks of lactation. Cows had no access to sunlight from 2 weeks before calving until 4 days postpartum. Thereafter they were outside and exposed to sunlight 1 to 2 h/day. Plasma 25-hydroxyvitamin D concentrations in unsupplemented cows were below 20 ng/ml during late gestation and the first 4 weeks of lactation. Plasma 25-hydroxyvitamin D concentrations in cows receiving 10,000 or 50,000 IU vitamin D/day (16-80 IU/ kg) were similar (between 30 and 45 ng 25-hydroxyvitamin D/ml). Cows receiving 250,000 IU vitamin D/day had elevated plasma 25-hydroxyvitamin D concentrations (60-80 ng/ml). The rapid changes in plasma concentrations of 25-hydroxyvitamin D, 24,25-dihydroxyvitamin D, and vitamin D suggested that at 250,000 IU/day the capacity of the liver to store vitamin D had been exceeded, which was interpreted as excessive vitamin D supplementation though no outward clinical signs of vitamin D intoxication were noted.
Under most circumstances 10,000 IU/day (16 IU vitamin D/kg BW) should provide adequate vitamin D for dairy cows during late gestation. Astrup and Nedkvitne (1987) reported that lactating cows producing about 20 kg of milk/ day required about 10 IU vitamin D/kg body weight to maintain normal concentrations of calcium and phosphorus in blood. These studies were conducted in Norway in winter and spring when effective sunlight exposure should have been minimal.
The 1989 Nutrient Requirements of Dairy Cattle (National Research Council, 1989) requirement for vitamin D for adult dairy cows was set at 30 IU/kg body weight. This is more vitamin D than many studies suggest is necessary for maintenance of normal plasma concentrations of 25-hydroxyvitamin D (17 IU/kg BW) (McDermott et al.,1985) or calcium and phosphorus (10 IU/kg BW) (Astrup and Nedkvitne, 1987) in plasma. However, Ward et al. (1971, 1972) and Hibbs and Conrad (1983) suggested that milk production and reproductive and health benefits were potentially improved when diets were supplemented with as much as 70 IU/kg BW. Based on all available data, the requirement of 30 IU/kg BW established previously (National Research Council, 1989) seems justified.
(VitaminDWiki: 30 IU/kg = 66 IU per pound, 150 pound person =10,000 IU)
The maximum tolerable amount of vitamin D is inversely related to dietary concentrations of calcium and phosphorus. The studies of McDermott et al. (1985) suggest that 50,000 IU D3/day (80 IU/kg BW) is well tolerated while 250,000 IU vitamin D3/day (400 IU/kg BW) is not. Hibbs and Conrad (1983) reported a slight decline in milk production when cows were fed 80,000 IU D2/day («=> 160 IU/kg BW). The 1987 National Research Council committee on vitamin tolerance of animals (National Research Council, 1987) suggested the maximal tolerable level of vitamin D is 2,200 IU/kg diet when fed for long periods (more than 60 days) and 25,000 IU/kg diet when fed for short periods of time. Vitamin D intoxication is associated with reduced feed intake, polyuria initially followed by anuria, dry feces, and reduced milk production. Upon necropsy calcification of kidneys, aorta, abomasum, and bronchioles is evident (Littledike and Horst, 1980).
Some of the dietary vitamin D is degraded in the rumen by bacteria to inactive metabolites (Sommerfeldt et al., 1983; Gardner et al., 1988). Injection of vitamin D avoids this problem; however, the maximal tolerable dose of par-enterally administered vitamin D is at least 100-fold lower than the maximal tolerable oral dose and repeated injections can be especially toxic (Littledike and Horst, 1980).
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