Synthesis of vitamin D3 in the skin of poultry, through exposure to UV radiation in direct sunlight, is limited because poultry in commercial production are confined to houses. In addition, feedstuffs supply negligible amounts of vitamin D activity. Consequently, all poultry diets should be supplemented with vitamin D3 (cholecalciferol from D-activated animal sterol). The D3 form of the vitamin has high bioavailability for poultry and all other food-producing animals, while the D2 form (ergocalciferol) has very limited bioavailability for poultry; thus, vitamin D3 is the commercially available form for use in poultry rations.
Some irradiated sterol resins, used as the source of vitamin D3 in various vitamin D3 products for feed use, may contain excessive amounts of biologically inactive impurities, such as tachysterol and isotachysterol. The vitamin D3 activity in low purity vitamin D3 resins and supplements (Baker, 1978) can be overestimated by the USP Chemical Assay, which does not correct for these biologically inactive compounds. A commercially available vitamin product containing stabilized, high-purity vitamin D3 for feed or drinking water use should be used to assure the vitamin D3 levels needed to prevent deficiency and allow optimal performance. Continued irradiation eventually destroys the vitamin D that is produced, but the chief cause of loss from feeds is oxidation. Higher vitamin D levels in freeze-dried fish meals suggest less destruction during drying, possibly because of decreased atmospheric oxygen (Scott and Latshaw, 1994). Pure vitamin D crystals and vitamin D resin are 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 products retain potency much longer and can be used in supplements with high mineral content. It has been shown that vitamin D3 is more stable than D2 in feeds containing minerals.
As vitamin D3 is more available than the D2 form, likewise the metabolites of vitamin D, 25-(OH)D3 and 1,25-(OH)2D3 are the most potent sources of vitamin D. The most potent form of vitamin D, 1,25-(OH)2D3 is not approved to be added to feeds by the FDA. Feeding studies with 25-(OH)D3 suggest it has nearly twice the activity of D3 (Soares et al., 1995). Grunder et al. (1990) suggest that 5 µg of 1,25-(OH)2D3 per day (2.27 µg per lb) of diet can replace 27.5 µg of D3 per kg (12.5 µg per lb). Mireles et al. (1996) concluded that the use of 25-(OH)D3 under commercial-type environments utilizing commercial broiler strains significantly improved performance and body weight and reduced the incidence and severity of bone disorders. They recommended that for maximum performance 25-(OH)D3 should be fed from day 1 of age at a rate of 68.9 µg per kg (31.3 µg per lb) diet.
Considerable research has been conducted over the past few years evaluating the efficacy of vitamin D3 metabolites for poultry. As well as improving inorganic calcium and phosphorus utilization, much like vitamin D3 (Biehl and Baker, 1997a), these vitamin D3 metabolites when supplemented to diets already adequate in vitamin D3 are very effective in improving leg disorders and in enhancing the utilization of phytate-phosphorus and trace minerals. For example, Tsang (1992) concluded that substituting 1,25-(OH)2D3 for D3 in the diet can significantly reduce egg breakage. Also, the primary plasma metabolite of vitamin D3, 25-(OH)D3, is capable of reducing the incidence of tibial dyschondroplasia (Rennie and Whitehead, 1996) when provided at high concentrations in diets for growing broilers.
More potent vitamin D3 metabolites, 1,25-(OH)2D3 (the active body metabolite of vitamin D3) and 1-alpha-OH D3 [the precursor of 1,25-(OH)2D3] also have been shown to improve tibial dyschondroplasia when added at low dietary concentrations (5 to 10 µg per kg or 2.3 to 4.5 µg per lb) to vitamin D3-adequate corn-soybean meal diets (Edwards, 1990: Rennie et al., 1993; Elliot and Edwards, 1997; Mitchell et al., 1997). However, Mitchell et al. (1997) suggested that 1,25-(OH)2D3 may not prevent tibial dyschondroplasia for a large portion of the population.
Vitamin D metabolites improve phosphorus utilization from phytate. Intestinal brush border phytase could possibly contribute to phytate-phosphorus digestibility and may be subject to regulation by the vitamin D3 and phosphorus status of the chicken (Maenz and Classen, 1998; Carlos and Edwards, 1998). Hydroxylation at the 1-alpha position of vitamin D3 appears important to the vitamin's efficacy in improving phytate utilization (Biehl and Baker, 1997b; Biehl et al., 1998). Yet, though both 1,25-(OH)2D3 and 1-alpha-OH D3 markedly improve the release of phytate-bound phosphorus, Biehl and Baker (1997a) report that it is apparently not caused by increased intestinal phytase activity. The response of vitamin D is much like the response that occurs when microbial phytase is added to these same diets (Biehl et al., 1997a; Denbow et al., 1995; Yi et al., 1996). The ability of 1,25-(OH)2D3 and 1-alpha-(OH)D3 to improve phytate-phosphorus utilization is potentially very important to the poultry industry. Phosphorus is the third most expensive ingredient in poultry diets, behind energy and protein, and phosphorus excretion in waste products is becoming a major concern, especially in countries where intensive livestock production is practiced.
Stabilization of vitamin D can be achieved by: (1) rapid compression of the mixed feed, for example, into cubes, so that air is excluded; (2) storing feed under cool, dry, dark conditions; (3) preventing close contact between the vitamin and potent metallic oxidation catalysts, for example, manganese; and (4) including natural or synthetic antioxidants in the mix. The vitamin can also be protected by enclosing it in durable gelatin micropellets.
Stability of dry vitamin D supplements is affected most by high temperature, exposure to moisture and contact with trace minerals such as ferrous sulfate, manganese oxide and others. In complete feeds and mineral-vitamin premixes, Schneider (1986) reported activity losses of 10% to 30% after either four or six months' storage at 22†C (72†F). Hirsch (1982) reports the results of a conventional or nonstabilized vitamin D3 product being mixed into a trace mineral premix or into animal feed and stored at ambient room temperature (20†C or 72†F) for up to 12 weeks. The mash 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 of storage.
Cost of vitamin D supplementation to animal and poultry feeds is very nominal (Rowland, 1982). In contrast, the cost of not adding enough vitamin D to prevent deficiencies is very high. Supplemental levels of vitamin D3 administered to poultry through the feed or drinking water should be adjusted to provide the margin of safety needed to offset the factors influencing the vitamin D needs of poultry. This is important to prevent deficiency and allow optimum performance. Factors that increase the amount of vitamin D needed to maximize productive and reproductive responses often are not reflected in the NRC requirements. Consequently, nutritionists often use more than the minimum levels of vitamin D in feeds. Successful nutrition programs contain two to five times the NRC minimum of vitamin D. However, no amount of vitamin D can make up for lack of enough calcium or phosphorus in the diet.
Rowland (1982) noted that diets for young, rapidly growing chickens must contain liberal amounts of vitamin D to prevent field problems. He further observed that the NRC level of 200 IU per kg (90.9 IU per lb) of feed for young chickens is extremely unrealistic for broilers. Even under low-stress research conditions, three to five times the NRC level is required to support maximum weight gain of broilers, and under commercial conditions, 10 times the NRC level is prudent for broiler feed. The NRC vitamin D levels for laying hens and turkeys are somewhat more realistic, with a factor of five times the NRC level generally supporting optimum performance and providing some margin of safety (Rowland, 1982). The most logical approach is to adjust supplemental vitamin D levels to expected production conditions.
Besides inadequate quantities of dietary vitamin D3, deficiencies may result from (1) errors in vitamin addition to diets; (2) inadequate mixing and distribution in feed; (3) separation of vitamin D particles after mixing; (4) instability of the vitamin content of the supplement; or (5) excessive length of storage of diets under environmental conditions causing vitamin D loss (Hirsch, 1982).
Supplementation considerations are dependent on other dietary ingredients. 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 absorption from the intestinal tract in chicks. Other molds may also be involved, and may result in a large percentage of birds with bone disorders. A number of flocks have been successfully treated by adding water-dispersible forms of vitamin D to drinking water at three to five times the normally recommended vitamin D levels. This "field rickets syndrome" in poultry is apparently not cured by adjusting vitamin D3 allowances in the feed, but it is frequently cured (clinical signs) by administering high levels of vitamin D3 from a water-dispersible vitamin product in the drinking water.
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. The possibility exists that poultry with certain diseases or heavy infestation of internal parasites might be unable to synthesize the metabolically active forms of the vitamin D as a result of liver or kidney damage. Unknown factors in feeds may increase vitamin D requirements. For example, there is also evidence of a factor in rye and in soybean fractions that can produce malabsorption of this vitamin in the intestine (Mac-Auliffe and McGinnis, 1976). Vitamin D supplementation may be needed for an optimum immune response. Vitamin D deficiency results in a marked depression in the cellular immune responses of young broiler chicks with negligible apparent impact on humoral immunity (Aslam et al., 1998).
