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The importance of Vitamin E in your horse’s diet

Summary

• Vitamin E serves as major component of the antioxidant defence mechanism
• Vitamin E also serves to enhance the immune system; is essential for cellular respiration; is involved in DNA synthesis; acts as a cofactor in the synthesis of vitamin C; reduces signs of zinc deficiency; has a protective function against the harmful effects of lead, mercury and silver; decreases platelet aggregation; and enhances vitamin A absorption and storage
• d-alpha-tocopherol is the major and most active form of vitamin E in feeds and the only significant form in the horse’s body
• Synthetic forms of vitamin E (dl-isomers) have 74% of the biological activity of their d-isomers
• Grinding, storage, and heat, all greatly decrease the vitamin E content of a feed
• Lower tissue vitamin E levels not only increase the risk of exercise-induced muscle damage but may also decrease performance.
• Green growing forage contains good levels of vitamin E but grains and hay/chaff contain poor levels
• According to recommended levels of vitamin E, supplementation for all horses is required except those on adequate pasture during plant growth, since other horse feeds generally contain only 5 to 60 IU/kg dry matter.

Functions of vitamin E

Vitamin E, and selenium function jointly in protecting body tissue – particularly cell membranes, enzymes, and other intracellular substances from oxidation-induced damage. Oxidation is the process by which fats, carbohydrates, and proteins are converted to carbon dioxide, water, and energy, i.e. are burned to produce the energy needed for body functions. However, oxidation of the body’s structural and functional components is harmful. A simple analogy is that petrol is burned to provide the energy needed to run the car, but we don’t want to burn up the car itself. The body must have an antioxidant defence mechanism to protect it from oxidation-induced damage and Vitamin E and selenium function as major components of this defence mechanism.

In the process of oxidizing nutrients for energy, oxygen is used and carbon dioxide and water are produced. In the process of reducing oxygen to water, free radicals are produced. These free radicals are powerful oxidizing agents which, if they aren’t destroyed, damage living cells. Vitamin E helps prevent this from occurring by blocking these free radicals from attacking living cells. Inadequate amounts of either vitamin E or selenium result in increased oxidation-induced damage and, therefore, similar effects; giving either tends to treat or alleviate these effects.

Vitamin E serves a number of other functions: it enhances the immune system; is essential for cellular respiration; is involved in DNA synthesis; acts as a cofactor in the synthesis of vitamin C; reduces signs of zinc deficiency; has a protective function against the harmful effects of lead, mercury and silver; decreases platelet aggregation; and enhances vitamin A absorption and storage (Coelho, 1991).

Vitamin E requirements and sources

There are eight forms of naturally occurring vitamin E, however d-alpha-tocopherol is the major and most active form in feeds and the only significant form in the horse’s body (Roneus et al., 1986). Synthetic forms of vitamin E used for administration and diet supplementation are the dl forms, rather than the naturally occurring ring d-isomers of alpha-tocopherol or alpha-tocopheryls. The dl-isomers have 74% of the biological activity of their d-isomers (Wooden and Papas, 1991). To function effectively as an antioxidant, vitamin E must be easily oxidized; as a consequence, naturally occurring forms and synthetic alcohol forms (tocopherols) are relatively unstable. Commercial synthetic forms that have been esterified, such as tocopheryl acetates or acid succinates do not have antioxidant activity until their ester linkage is broken in the digestive tract. As a result, tocopheryl esters are quite stable. Dl-alpha tocopheryl acetate is the form most widely used commercially. Moisture in stored feeds sufficient for fermentation and mould growth to occur (over 13%), as well as grinding, storage, and heat, all greatly decrease the vitamin E content of a feed.

Green growing forage contains 100 to 450, average quality grass or legume hays 10 to 60, dehydrated Lucerne pellets 20 to 80, and cereal grains 5 to 30 IU of vitamin E/kg dry matter (Ott, 1989; Staurt, 1987). The amount in forages decreases with plant maturity: by 70 to 90% from early growth to maturity in grasses, and 35 to 65% in lucerne from bud to post-flowering (Lynch, 1991). Whole oilseeds are good sources of vitamin E, but most vitamin E has been removed from oilseed meals. From 30 to 80% of vitamin E activity is lost between cutting to baling hay; another 54 to 73% loss occurred in Lucerne hay stored at 33°C for 12 weeks (Lynch, 1991). Although no ill effects are observed in idle mature horses consuming less than 15 IU/kg diet dry matter (Roneus et al., 1986), higher amounts appear to be beneficial and are recommended (45IU/kg feed, or about 400IU per day for a 500kg idle horse). 100IU/kg diet dry matter is needed to maintain maximum liver and muscle vitamin E levels (Roneus et al., 1986).

Higher tissue vitamin E levels give greater antioxidant protection against tissue damage. This may be beneficial when nutrient oxidation increases in order to satisfy energy needs that occur with exercise or exertion. This benefit was demonstrated by the absence of muscle soreness and lameness in horses and zebras following their capture and restraint when their diets contained 100IU vitamin E/kg, whereas soreness and lameness occurred when their diet contained only 50IU/kg (Ott, 1989).

Lower tissue vitamin E levels not only increase the risk of exercise-induced muscle damage but may also decrease performance.

While not demonstrated in horses, exercise endurance of vitamin E-deficient rats was found to be 40% lower than controls (Quintanilha and Packer, 1983).

The National Research Council recommends 50IU vitamin E/kg diet dry matter for the idle mature horse and 80 to 100 for foals, pregnant and lactating mares, and working horses (Ott, 1989).

These recommendations seem appropriate, but they require vitamin E supplementation for all horses except those on adequate pasture during plant growth, since other horse feeds generally contain only 5 to 60 IU/kg dry matter.

Supplemental vitamin E (usually at 6 to 20 times that recommended in the diet of the healthy animal) has been shown to enhance both cellular and humoral immunity in many different species of animals (Hayek et al., 1991). As a result, when a herd or flock is infected with an infectious pathogen, vitamin E supplementation appears to lessen clinical signs of the disease, and the administration of vitamin E as an adjuvant to vaccination may improve efficacy of the vaccine (Hayek et al., 1991).

Unlike other fat soluble vitamins A and D, there are few available or mobilisable vitamin E stores in the body. There is inadequate vitamin E storage to maintain optimum body vitamin E status over the winter, or for more than a few weeks at the most. If there is inadequate vitamin E in the horse’s diet, then daily, or at a maximum weekly, supplementation is needed to correct it. A periodic vitamin E injection is not sufficient.

Also, unlike the other fat-soluble vitamins A and D, excess vitamin E is relatively non-toxic. Signs or detrimental effects of vitamin E toxicosis have not been reported or produced in horses. Dietary levels of at least 1000 to 2000 IU/kg of diet dry matter can apparently be fed for prolonged periods without harm to rates and chicks (Ott, 1989). However, because very high intakes of vitamin E may interfere with utilization of other fat-soluble vitamins, a conservative maximum tolerable level or 1000IU/kg diet dry matter has been recommended.

Vitamin E deficiencies

A mild deficiency of either vitamin E or selenium may cause a decrease in the animal’s immune response to infectious diseases. More severe deficiencies of selenium, vitamin E or both in foals, cause myopathies, steatites, or varying severities of both. Foals in which white muscle damage is the major effect (which is the most common syndrome) may be stillborn, alive but affected at birth, or appear normal at birth but during the first weeks of life become stiff, weak and listless, develop a stilted hopping gait in the rear legs and have muscle pain. The tongue may be involved, resulting in difficulty in nursing and swallowing; which may result in aspiration pneumonia. Less commonly, generalized steatites, instead of myopathy, may be the predominant effect of primarily a vitamin E, but also a selenium deficiency (Foreman et al., 1986). This occurs particularly in older foals up to several months of age and may manifest as progressive emaciation and debilitation in spite of a good appetite. Affected horses have multiple indurated subcutaneous swellings composed of mineralized and necrotic adipose tissue, with sensitive, hardened nuchal ligaments. A rough, shaggy haircoat may also be present.

A vitamin E deficiency also results in neuronal degeneration, without muscle or fat involvement. Equine Degenerative Myeloencephalopathy (EDM) is a diffuse, degenerative disease of the spinal cord and brain stem. In horses it occurs in both sexes of many different breeds. It most commonly affects foals 1 to 14 months old, however EDM may occur in horses from 12 to 10 years of age. The onset of gait abnormalities may occur abruptly or, more commonly, progress solely and stabilise for long periods. All four legs are affected, although the hind legs commonly are more affected than the front. EDM is one of the most common causes of wobblers syndrome.

Vitamin E and Reproduction

A vitamin E deficiency is known to impair reproduction in both males and females of many species of animals. The impairments include repeat breeding, early embryonic death, abortion, retained placenta, and degenerative changes in the testes. However, these effects have never been reported in horses, and, as the National Research Council reports, there is no substantial evidence to indicate that vitamin E supplementation helps resolve reproductive problems in horses, vitamin E is occasionally recommended and given to improve horses’ reproductive efficiency. Numerous studies, however, have failed to confirm any benefit of vitamin E supplementation on the stallion’s or mare’s reproductive performance or libido.

Source: Lewis, L.D., 1995. Equine Clinical Nutrition, Feeding and Care. Williams & Wilkins, USA.

Further References:

Coelho, M.B., 1991. Functions of Vitamin E. In: Vitamin E in Animal Nutrition and Management. Edited by MB Coelho. BASF Corp, 100 Cherry Hill Rd, Parsippany, NJ, pp11-17.
Foreman, J.H., Potter, K.A., Bayly, W.M. et al., 1986. Generalised steatites associated with selenium deficiency and normal vitamin E status in a foal. J. Am. Vet. Med. Assoc. 189, 83-86.
Hayek, M.G., Boissonneault, G.A., Mitchell, G.E., 1991. Influence of vitamin E on the immune response of livestock and poultry. In Vitamin E in Animal Nutrition and Management. Edited by MB Coelho. BASF Corp, 100 Cherry Hill Rd, Parsippany, NJ, pp105-110.
Lynch, G.L., 1991. Natural occurrence and content of vitamin E in feedstuffs. In: Vitamin E in Animal Nutrition and Management. Edited by MB Coelho. BASF Corp, 100 Cherry Hill Rd, Parsippany, NJ, pp43-48.
Ott, E.A., 1989. Chair Subc on Horse Nutr of National Research Council: Nutrient Requirements of Horses. 5th ed. National Academy Press, Washington, DC.
Roneus, B.O., Hakkarainen, J., Lindholm, C.A., et al., 1986. Vitamin E requirements of adult Standardbred horses evaluated by tissue depletion and repletion. Eq. Vet. J. 18, 50-58.
Staurt, R.L., 1987. Factors affecting the vitamin E status of beef cattle. In The Role of Vitamins in Animal Performance and Immune Response. Proc Riche Tech Symp, Hoffman-La Roche, Nutley, NJ, pp67-79.
Quintanilha, A.T., Packer, L., 1983. Vitamin E, physical exercise and tissue oxidative damage. In Biology of Vitamin E. Ciba Found Symp 101, Pitman Books, London, pp56-69.
Wooden, G.R., Papas, A.M., 1991. Utilisation of various forms of vitamin E by horses. Proc Equine Nutr & Physiol Soc Symp, p265.