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Companion Animals: Vitamin E

Fortification Considerations

Several tocopherols in plants and certain vegetable oils are the naturally occurring sources of vitamin E activity. Alpha-tocopherol provides the highest vitamin E biological activity. However, the stability of all naturally occurring tocopherols is poor, and substantial losses of vitamin E activity occur in natural ingredients when processed and stored as well as in manufacturing and storage of finished pet foods. To offset losses of vitamin E activity in ingredients, pet foods should be adequately fortified using dl-alpha-tocopheryl acetate, the most stable source of vitamin E activity available for pet food use. Alpha-tocopherol, an alcohol, is stabilized by conversion to the acetate ester namely, dl-alpha-tocopheryl acetate. For pets, the major methods of providing supplemental vitamin E are as part of the complete diet or as an injectable product if a vitamin E-responsive disease condition is expected.

Commercially, the acetate esters of vitamin E are available in purified form or in various dilutions and include (a) a highly concentrated oily form, for further processing; (b) emulsions incorporated in powders for use in dry premixes or water-dispersible preparations and (c) adsorbates or absorbates of the oily tocopheryl acetate on selected carriers, in free-flowing, "dry" powder, meal or granules. Vitamin E as the acetate form is highly stable in vitamin premixes, with 98% retention after six months but in the alcohol form is completely destroyed during the time period (Gadient, 1986).

Injectable vitamin E preparations are also available that contain free d- or dl- alpha-tocopherol. Liquid emulsions of appropriate types can be used for injection. In this form, alpha-tocopherol is more efficiently absorbed from intramuscular injection sites than is a water miscible preparation containing alpha-tocopheryl acetate or either form dissolved in an oily base (Machlin, 1991). Products containing vitamin E and selenium can often be given intramuscularly to dogs exhibiting clinical signs of muscular degeneration. Response to treatment of this condition is extremely variable depending on degree of muscular degeneration.

The need for supplementation of vitamin E is dependent on the requirement of individual species, conditions of production and the amount of available vitamin E in food or feed sources. The most important consideration for pet diets is the feed ingredients. If diets have relatively large quantities of meat and slaughterhouse by-products (e.g., fat and internal organs), good sources of vitamin E will be provided. If, however, grains make up a large proportion of the diet, little available vitamin E will be provided. 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. Losses during storage increase as the duration and temperature of storage increase.

For pet foods, the most important feed ingredient that will dictate the need for supplementation is fat source and the stability of the fat source. Large amounts of PUFA can quickly precipitate vitamin E deficiency. Fats from oilseeds are normally not highly detrimental because the oils, in addition to containing high amounts of predominantly linoleic acid (18:2), are likewise sources of vitamin E. Fish oils, however, contain little vitamin E and are highly destructive to vitamin E stores, greatly increasing the requirements of the vitamin. As previously mentioned, a diet that contains high levels of fish oil may cause a three- to fourfold increase in a cat's daily requirement for vitamin E. Rancid fats should never be fed to pets as they will quickly bring about destruction of fat-soluble vitamins.

It has been suggested that a fixed ratio of vitamin E to PUFA should be maintained in the diet to assure adequate vitamin E intake in the presence of high levels of unsaturated fats, particularly in cat foods containing fish products or added fish oil. In counteracting high levels of PUFA in pet diets, Harris and Embree (1963) recommended a dietary alpha-tocopherol:PUFA ratio of 0.6:1. This is a good approach but does not differentiate between the major oilseed PUFA of linoleic acid (18:2) and linolenic acid (18:3) from the more highly unsaturated fatty acids of fish oil, including the fatty acids arachidonic (20:4), docosapentaenoic (22:5) and docosahexanenoic (22:6). A more appropriate method to provide sufficient quantities of vitamin E is to follow the AAFCO (1992) recommendation of adding 10 IU vitamin E above the vitamin E requirement per gram of fish oil per kg of diet (4.55 IU per g per lb of diet).

Supplementing vitamin E in well-balanced diets has been shown to increase humoral immunity in a number of species (Badwey and Karnovsky 1980; Cipriano et al., 1982; Burkholder and Swecker, 1990). These results suggest that the criteria for establishing requirements based on overt deficiencies or growth do not consider optimal health (Hoffmann-La Roche, 1991). Additional supplemental vitamin E to dog and cat diets would provide an insurance of an optimum health for these pets.

Longevity of pets and reduction of "age-related" diseases, such as cancer and heart disease, have a relationship to free radical damage, which can be minimized by antioxidant vitamin supplementation. Vitamin E appears to lengthen life span (Strombeck, 1999). When animals are given vitamin E from a young age, the onset slows for some age-related problems, such as cataracts, cancer, cardiovascular disease and decreased immune function. Dogs with dilated cardiac myopathy have increased oxidative stress compared with normal dogs, and vitamin E concentrations decrease as the disease progresses (Freeman, 1998). Therefore, antioxidant therapy of dogs and cats with cardiac disease is recommended.

Recommendations for daily antioxidant fortification rates for dogs and cats of vitamin E, vitamin C, and beta-carotene have been suggested by Parr (1996). For example, the daily vitamin E supplemental level for a 13.6 kg (30 lb) dog is 90 IU and for a 2.7 kg (6 lb) cat is 18 IU.

Marks et al. (1994) suggest that vitamin E may be beneficial for the management of dogs and cats with copper-associated liver damage because of the antioxidant effects that protect against lipid peroxidation. Vitamin E should be supplemented at levels of 500 mg per day for dogs and 100 mg per day for cats.

The amount of vitamin E required to produce milk is much less than the amount needed to produce milk containing optimum concentrations of the vitamin. Since placental transfer of vitamin E to puppies and kittens is expected to be low, based on studies with other species (Mahan, 1990; Nockels, 1991; Njeru et al., 1994), providing colostrum and later-produced milk high in vitamin E is essential. In sheep, ewes receiving supplemental vitamin E produced colostrum almost threefold higher in vitamin E than did non-vitamin E supplemented animals (Njeru et al., 1994). Also, after the nursing period, dogs, and particularly cats, do sometimes receive cow's milk as part of their diet. Cows receiving higher levels of dietary vitamin E likewise produce milk containing more vitamin E. Feeding supplemental vitamin E as dl-alpha-tocopheryl acetate, providing an equivalent of 500 mg of dl-alpha-tocopherol per cow per day, increased the vitamin E content and oxidative stability of milk (Dunkley et al., 1967).

Vitamin E fed to meat-producing animals will result in a more stable meat product, including stability of the red meat color. Dramatic effects of vitamin E supplementation (500 IU per head daily) to finishing steers on the stability of beef color have been observed (Faustman et al., 1989a). Loin steaks of control steers discolored two to three days sooner than those supplemented with vitamin E. Supplemental dietary vitamin E extended the color shelf life of loin steaks from 3.7 to 6.3 days. In a subsequent report, Faustman et al. (1989b) observed that vitamin E stabilized the pigments and lipids of meat from the supplemented steers. Except for increased stability of pet foods, the effect of meat color would seem completely unimportant from a nutritional standpoint. Color is an extremely critical component of fresh red meat appearance and greatly influences the customer's (pet owner's) perception of meat quality. This would only be a consideration for pet diets that are predominantly meat (particularly beef).

Vitamin E therapy has a role in certain skin disorders in dogs. Apparently, subclinical vitamin E deficiency causes suppression of the immune system, which increases a dog's susceptibility to certain skin conditions. Vitamin E evidently has an anti-inflammatory effect that may be related to stabilization of cell and lysosomal membranes against damage resulting from free radicals and peroxides (Bissett et al., 1990). Favorable responses to vitamin E supplementation with varying levels of success have resulted from the skin conditions of demodicosis, primary acanthosis nigricans, discoid lupus erythematosus and dermatomyositis (Werner and Harvey, 1995). Vitamin E deficiency in dogs has also been associated with other cutaneous abnormalities (Sheffy, 1979; Worden, 1958). The dermatosis was poorly characterized but included "sores" on the feet and over wear areas as well as generalized scaling and "denudation" (Scott and Sheffy, 1987).

Many dogs with acanthosis nigricans and other skin disorders respond favorably to treatment with systemic glucocorticoids. However, concern with the immediate and long-term side effects of glucocorticoid therapy dictates the need to find alternative treatments, one of which may be supplementation with vitamin E. In many cases, skin disorders are chronic and persistent, and therapy is directed toward control rather than cure.

Quantities of therapeutic vitamin E administered to alleviate skin disorders are experimental and highly variable. For discoid lupus erythematosus, the therapeutic dosage in dogs was 100 to 400 mg of dl-alpha-tocopheryl acetate given orally twice daily (Codner and Thatcher, 1993). For primary acanthosis nigricans, dachshunds showed improvement after 60 days of vitamin E therapy (200 mg twice daily) (Scott and Walton, 1985). A vitamin E supplemented level of 200 mg five times daily was curative for demodicosis for 147 of 149 cases (Fiqueriredo, 1985).

Naturally occurring vitamin E deficiency in cats is usually reported when diets containing excessive amounts of canned red tuna or cod liver oil are fed. The prognosis for steatitis in untreated cats can be grave. Therapy consists of dietary correction, oral vitamin E supplementation (dl-alpha-tocopherol, 25 to 75 mg twice daily), anti-inflammatory doses of corticosteroids [e.g., prednisone, 0.5 to 1.0 mg per kg (0.23 to 0.45 mg per lb) of body weight twice daily] and supportive care (Codner and Thatcher, 1993). The corticosteroid therapy, in addition to decreasing inflammation will reduce pain in the cat. Severely affected cats may fail to improve. However, prognosis for recovery from steatitis is usually very good, but it may be slow in advanced cases.

 

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