The stability of vitamin A in feeds and premixes has been improved tremendously in recent years by chemical stabilization as an ester and by physical protection using antioxidants, emulsifying agents, and stabilized materials in spray-dried, beadlet or prilled products (Bauernfeind and DeRitter, 1972; Hoffmann-La Roche, 1988). These vitamin A product forms result in not only enhanced chemical and physical stability, but also excellent biologic availability. Nevertheless, vitamin A supplements should not be stored for long periods prior to use and feeding.
Several factors can influence the loss of vitamin A from feedstuffs during storage. The trace minerals in feeds and supplements, particularly copper, are detrimental to vitamin A stability. Dash and Mitchell (1976) reported the vitamin A content of 1,293 commercial feeds over three years. The loss of vitamin A was over 50% in one year's time. Vitamin A loss in commercial feeds was evident even if the commercial feeds contained stabilized vitamin A supplements.
There is evidence that yellow corn may lose carotene rapidly during storage. For instance, a hybrid corn high in carotene lost about half of its carotene in eight months' storage at 25°C and approximately 75% in three years. Less carotene was lost during storage at 7°C (Quackenbush, 1963). Because of vitamin A variability in feeds and losses during processing and storage, most animal nutritionists tend to ignore vitamin A activity in feedstuffs and rely exclusively on dietary fortification to arrive at vitamin allowances for swine.
Vitamin A and carotene destruction also occurs during processing of feeds with steam and pressure. Pelleting effects on vitamin A in feed are caused by die thickness and hole size, which produce frictional heat and a shearing effect that can expose the vitamin to destructive processes. In addition, steam application exposes feed to heat and moisture.
Diseases and mycotoxins increase the need for supplemental vitamin A. Furthermore, diseases can interfere with the absorption and utilization of vitamin A (i.e., enteric diseases such as malabsorption syndrome, mycotoxins and diarrhea). The effect of mycotoxins in the feed should also be considered, since aflatoxin is known to interfere with protein synthesis (Doerr, 1987). Thus, it can be seen how mycotoxins may interfere with RBP synthesis and the transport of vitamin A.
Short-term administration of vitamin A in drinking water or by injection is recommended to support any specific measures used in treatment of diseased and convalescent animals. This is true particularly for swine in which vitamin A stores may have been depleted by fever and in animals suffering from intestinal disorders when vitamin A absorption is seriously impaired.
The decision for vitamin A supplementation should be based mainly on whether a deficiency could be a practical problem. As with most nutrients, a borderline deficiency is much more likely than a severe deficiency. Likewise, a marginal deficiency adversely affecting performance by a few percentage points is not easily detected. Based on the positive results that may be derived and taking into account that vitamin A supplementation is inexpensive and no toxicity problems have been reported when it is given at recommended levels, it seems beneficial to supplement vitamin A at all times for swine and to increase the supplementation amounts substantially for pigs that are diseased or under stress.
The amount of vitamin A added to swine diets is usually in excess of the requirements in the NRC publication because no safety factors are built into the NRC values (Olson, 1984). Additional vitamin A is added to allow for loss of activity due to oxidative destruction of the vitamin A ester during feed processing and storage, variability of carotenes in feedstuffs, changes in feed consumption, genetic differences in animals and stress due to disease and other environmental factors. Stahly et al. (1997) reported evidence that requirements for one or more antioxidant vitamins, i.e., vitamin A, E and C, are greater than NRC (1988) estimates when pigs are exposed to a high level of antigens.
