To offset losses of vitamin E activity in feedstuffs, rations should be adequately fortified using dl-alpha-tocopheryl acetate, the most stable source of vitamin E activity available for feed use. Methods of providing supplemental vitamin E are: (1) as part of a concentrate or liquid supplement, (2) as an injectable product and (3) in drinking water preparations. Commercially, the dl- and d-alpha-tocopheryl acetates are available in purified form or in various dilutions and include (1) a highly concentrated oil, for further processing; (2) emulsions incorporated in powders for use in dry premixes or water-dispersible preparations; and (3) adsorbates or absorbates of the tocopheryl acetate oil on selected carriers, in free flowing, "dry" powders, or granules. The dry type is for use in feeds only.
Vitamin E in the acetate form is highly stable in vitamin premixes, with 98% retention after six months but in the alcohol form is completely destroyed during that time period. Vitamin E acetate is stable in feeds with neutral or slightly acidic pH. However, even slightly alkaline conditions may affect the stability, such as when limestone carrier is used or in the presence of large quantities of magnesium oxide. Rate of oxidation of natural tocopherols is increased in diets containing increased levels of copper, iron, zinc or manganese (Dove and Ewan, 1991).
The need for supplementation of vitamin E is dependent on the requirement of individual species, conditions of production and in relation to available vitamin E in food or feed sources. The primary factors that influence the need for vitamin E supplementation in poultry include: (1) vitamin E- and (or) selenium-deficient concentrates; (2) diets that contain predominantly non-alpha-tocopherols and thereby are less biologically active; (3) diets that include ingredients that increase vitamin E requirements (e.g., unsaturated fats, waters high in nitrates); (4) harvesting, drying or storage conditions of feeds that result in destruction of vitamin E and (or) selenium; (5) accelerated rates of gain, production and feed efficiency that increase metabolic demands for vitamin E; and (6) intensified production that also indirectly increases vitamin E needs of animals by elevating stress, which often increases susceptibility to various diseases.
For breeding birds, consideration may be given to the effect of vitamin E on progeny. Haq et al. (1996) fed broiler breeders a diet containing 300 IU per kg (136.4 IU per lb) of vitamin E. Other antioxidants were fed as well. Only vitamin E appeared to improve the immune status of the chicks hatched when measured by seven-day post-hatch antibody titers. Likewise, in turkey poults, McKnight et al. (1996) reported that when hens were fed 140 IU per kg (63.6 IU per lb) of vitamin E, their progeny had superior performance vs. poults from hens fed 40 IU per kg (18.2 IU per lb) of vitamin E. Both these levels may seem excessive when compared to the NRC (1994) level of 25 IU per kg (11.4 IU per lb). However, the study this level was based upon (Jensen and McGinnis, 1958) has little resemblance to today's turkey industry as breeders were raised on the range and allowed to mate naturally. Thus, one can only assume that the actual need of the turkey breeder for vitamin E has increased over the years. The same may be said for commercial laying hens. Miles et al. (1994) gave evidence showing that pullets responded to levels of vitamin E from 25 to 50 IU per kg (11.4 to 22.7 IU per lb) diet in terms of improved feed efficiency and reduced tracheal lesions due to infectious bronchitis challenge.
High levels of supplemental vitamin E to broiler flocks with subclinical infectious bursal disease (IBD) have proved beneficial (McIlroy et al., 1993). The birds were fed either 48 or 178 mg vitamin E per kg of diet (21.8 or 89.9 mg per lb) throughout the life cycle. Flocks with subclinical IBD that were fed the higher level of vitamin E showed a 1.45% improvement in feed efficiency and a 2.2% increase in weight gains. These flocks produced 10.3% greater net income than flocks receiving the lower level of supplemental vitamin E. These researchers concluded that the increased performance in the vitamin E supplemented flocks was due to the increased immunocompetence and increased disease resistance. Gore and Quereshi (1997) injected turkey and chicken embryos with vitamin E three days prior to hatching. The results from this study demonstrated an enhanced antibody and macrophage response and suggest that in-ovo exposure with vitamin E may improve post-hatch poult and broiler performance. The effect of vitamin E supplementation to the parent hen on peroxidation susceptibility was examined and it was concluded that the high peroxidative susceptibility of the chick's brain can be normalized by supplementation of the parent hen with vitamin E (Surai et al., 1999).
Chronic heat stress is well known to have adverse effects on laying hens, depressing feed intake, egg number and weight and shell thickness. After heat stress, poultry may have reductions in alpha-tocopherol concentrations in certain tissues. Supplemental vitamin E may be required after stress to restore alpha-tocopherol in tissues (Nockels et al., 1996). Whitehead (1998) reported that yolk precursors were elevated by vitamin E in hens subjected to heat stress. Both during and following heat stress, the circulating levels of vitellogenin were higher in hens fed 500 IU per kg (227.3 IU per lb) of vitamin E. Similarly, Scheideler (1998) reported that hens fed 45 or 65 IU per kg (20.5 to 29.5 IU per lb) of vitamin E held their production levels through a period of heat stress while hens fed a lower level of vitamin E (25 IU per kg or 11.4 IU per lb) declined in egg production. Bollengier-Lee et al. (1998; 1999) studied the effects of different dietary concentrations of vitamin E (tocopherol acetate) on laying hens exposed to chronic heat stress at 32†C (90°F) from 26 to 30 weeks of age. Egg production and egg weight were significantly higher for vitamin E-supplemented birds. It was concluded that a dietary supplement of 250 mg per kg (113.6 mg per lb) of vitamin E provided before, during and after heat stress is optimum for alleviating, at least in part, the adverse effects of chronic heat stress in laying hens.
A survey of the literature suggests a positive effect of vitamin E on performance and immune functions in poultry. Although the National Research Council guidelines recommend 5 to 25 IU of vitamin E per kg (2.3 to 11.4 IU per lb) of diet (NRC, 1994), poultry producers are supplementing vitamins up to 10 times the NRC requirements (Ward, 1993). Supplemental levels as high as 25 times NRC have increased antibody response in turkeys (Ferket et al., 1993). In addition, it is generally observed that nutrient levels considered adequate for growth may not be adequate for optimal immune response and disease resistance (Nockels, 1988).
Field trials have shown a positive influence of vitamin E supplementation on immunity. Improving the health of broiler flocks produces a quantifiable positive economic benefit for broiler producers. On the basis of field trials, Chung and Boren (1999) recommend vitamin E at 240 mg per kg (109.1 mg per lb) of diet in broiler starter diets to achieve optimum health, production and processing performance. Vitamin E has proved beneficial for inclusion in inactivated vaccines (Franchini et al., 1991; 1995). Results show that vaccines with vitamin E, especially when it replaced 20% or 30% of mineral oil, induced a more rapid and higher antibody response in broilers than control vaccines.
Kennedy et al. (1992) reported net income as a comparative index of broiler performance. He reported that broiler flocks fed a 180 mg per kg (81.8 mg per lb) vitamin E diet had a 1.3% significantly heavier (P < 0.05) weight per bird and a 0.84% significantly better (P < 0.05) feed efficiency than controls fed 44 mg per kg (20 mg per lb) vitamin E. Net income for the flock on high vitamin E was 2.7% more than for the control flocks.
In a commercial broiler trial, 1,524,000 birds received either 33 or 240 mg vitamin E per kg of diet (15 or 109 mg per lb) in a starter diet for only the first 20 days of the life cycle (Boren and Bond, 1996). At slaughter the feed:gain ratio for the higher vitamin E supplementation level was 2.3% higher. Whole-bird disease condemnations, septicemia/toxemia, air sacculitis and inflammatory process (cellulitis) were 34%, 25%, 25% and 61% lower for the group that originally had received the higher vitamin E supplementation.
Vitamin E/selenium deficiencies are found in specific world regions and are characterized by low concentrations of vitamin E and selenium in feedstuffs. Regions that rely on concentrate importations from these areas deficient in selenium and (or) vitamin E (e.g., the Midwest and eastern coastal United States) likewise must provide these nutrients to poultry. Adverse conditions such as poor weather (drought and early frost), molds and insect infestation will reduce the vitamin E value of feedstuffs. The vitamin E activity in blighted corn was 59% lower than that in sound corn, and the vitamin E activity in lightweight corn averaged 21% below that in sound corn (Adams et al., 1975). Feed spoilage will also promote vitamin E/selenium deficiencies; therefore, to prevent loss of vitamin E in diets, the producer should use fresh feed at all times because the vitamin is rapidly destroyed under hot, humid conditions. Also, the producer should use an antioxidant in the diet to prevent the destruction of the vitamin E. Losses during storage increase as the duration and temperature of storage increase.
Results of numerous studies have shown that feeding high supplemental vitamin E levels prior to slaughter increased the shelf life and delayed rancidity development in chicken and turkey meat, thus preventing off-odors and off-flavors (Marusich, 1984; 1978a,b). These high supplemental vitamin E levels provided allowances greater than those needed for adequate growth, feed conversion or reproduction. Supplemental vitamin E extended the shelf life of fresh and frozen whole carcasses, as well as further-processed meat products.
Sheldon et al. (1997) reported that vitamin E supplementation at 20 times and 25 times NRC diets produced the most typical and acceptable turkey meat flavors with the fewest oxidized off-flavor notes for both fresh and frozen samples as opposed to the more oxidized flavor notes detected in the control samples. Mean color scores increased, indicative of less pale meat, as the level and duration of feeding dietary vitamin E increased. Morrissey et al. (1997) found that feeding 200 mg alpha-tocopheryl acetate per kg (90.9 mg per lb) diet to broiler chicks for at least four weeks prior to slaughter is necessary to optimize muscle content and stability against lipid peroxidation. When feeding oxidized sunflower oil to broiler chicks, Galvin et al. (1997) concluded that supplementation with 200 to 400 mg alpha-tocopherol acetate per kg (90.9 to 181.8 mg per lb) may be necessary to achieve an optimum muscle alpha-tocopherol concentration.
