Because natural foods are low in this vitamin, most commercially prepared pet foods are enriched with vitamin D to ensure that dogs and cats receive adequate amounts of this vitamin. This is particularly important since recent studies have shown conclusively that neither dogs nor cats receive a significant benefit from synthesis of vitamin D in the skin through exposure to UV irradiation (How, et al.,1994a, b; 1995).
Vitamin D deficiency in dogs and cats receiving commercially prepared foods is not common. Rickets is more common with diets that are low in vitamin D and have an accompanying deficiency in dietary calcium and/or phosphorus, or with diets that are imbalanced with respect to calcium and phosphorus (where calcium percentage is less than phosphorus). A number of studies have shown that more vitamin D is required to correct an imbalance of calcium and phosphorus.
Kealy et al. (1991), in studies with weanling pups, suggested that supplementation of nonpurified, commercially available dog foods with vitamin D may not be necessary. However, this study did not analyze the vitamin D content of the commercial diet, which did contain some animal products potentially rich in the vitamin (e.g., meat and bone meal). Pet foods that contain high protein animal by-products (e.g., blood meal and liver) would likely not need supplemental vitamin D. Cat foods, in particular, that contain fish products would be receiving substantial amounts of vitamin D. Although less than for vitamins A and B12, body storage of vitamin D occurs. During times of low dietary vitamin D concentrations in pet foods, puppies and kittens may be relying on previous stores of the vitamin.
Both synthetic D2 and D3 are quite stable when stored at room temperature. In complete feeds and mineral-vitamin premixes, Schneider (1986) reported activity losses of 10% to 30% after either four or six months of storage at 22ƒC. However, pure vitamin D3 crystals or vitamin D3 resin is very susceptible to degradation upon exposure to heat or contact with mineral elements. In fact, the resin is stored under refrigeration with nitrogen gas. Dry, stabilized supplements retain potency much longer and can be used in high mineral supplements. It has been shown that vitamin D3 is much more stable than D2 in feeds containing minerals.
Stabilization of the vitamin can be achieved by (a) rapid compression of the mixed feed, for example, into pellets so that air is excluded; (b) storing feed under cool, dry, dark conditions; (c) preventing close contact between the vitamin and potent metallic oxidation catalysts (e.g., manganese); (d) including natural or synthetic antioxidants in the mix. The vitamin can also be protected by enclosing it in durable, gelatin beadlets.
Stability of dry vitamin D supplements is affected most by high temperature, high moisture content and contact with trace minerals such as ferrous sulfate, manganese oxide and others. Hirsch (1982) reports the results of a "conventional" or non-stabilized vitamin D3 product being mixed into a trace mineral premix or into animal feed and stored at ambient room temperature (20°to 25°C) for up to 12 weeks. The feed had lost 31% of its vitamin D activity after 12 weeks, and the trace mineral premix had lost 66% of its activity after only six weeks in storage.
Vitamin D deficiencies may result from (a) errors in vitamin addition to diets, (b) inadequate mixing and distribution in feed, (c) separation of vitamin D particles after mixing, (d) instability of the vitamin content of the supplement or (e) excessive length of storage of diets under environmental conditions causing vitamin D loss (Hirsch, 1982).
Supplementation considerations are dependent on other dietary ingredients. As previously noted, the requirements for vitamin D are increased several fold by inadequate levels of calcium and/or phosphorus or by improper ratios of these two elements in the diet. A number of reports have indicated that molds in feeds interfere with vitamin D (Cunha, 1977); for example, when corn contains the mold Fusarium roseum, a metabolite of this mold prevents vitamin D3 in the intestinal tract from being absorbed by the chick. A similar deleterious effect on vitamin D metabolism would be expected in dogs and cats.
Other factors that influence vitamin D status are diseases of the endocrine system, intestinal disorders, liver malfunction, kidney disorders and drugs. Liver malfunction limits production of the active forms of the vitamin, while intestinal disorders reduce absorption.
In veterinary medicine, there are clinical conditions for which the judicious employment of vitamin D analogues may be warranted. Evidence suggests that impaired intestinal absorption of calcium due to an acquired defect in vitamin D metabolism plays a significant role in the development of hypocalcemia and bone disorders in chronic renal insufficiency and uremia. Chronic renal disease interferes with the production of 1,25-(OH)2D3 by the kidney, thereby diminishing intestinal calcium transport and resulting in development of hypocalcemia. Plasma levels of 25-OHD3 were lower following massive resection of the distal small bowel (75%) in adult beagle dogs (Imamura and Yamaguchi, 1992). In dogs with chronic renal disease, 1,25-(OH)2D3 has been advocated for use as a therapeutic agent in the prevention of hypocalcemia and osteodystrophy, with daily dosages as high as 0.1 µg per kg (0.05 µg per lb) body weight (Lewis et al., 1987). Because toxic manifestations of hypervitaminosis D are associated with hypercalcemia, serum calcium levels must be closely monitored when 1,25-(OH)2D3 is given (NRC, 1985; Lewis et al., 1987).