Difference between revisions of "Vitamin E (α-Tocopherol) - Nutrition"
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== Consequences of Vitamin E Deficiency == | == Consequences of Vitamin E Deficiency == | ||
====Dogs:==== | ====Dogs:==== | ||
| − | Vitamin E deficiency in dogs can develop anorexia, reproductive failure, skeletal and endocardial muscle degeneration, retinal degeneration, dermatitis, and subcutaneous [[oedema]]<ref>Elvehjem CA, et al. The effect of vitamin E on reproduction of dogs on milk diets. J Pediatr 1944;24:436-441.</ref><ref>Van Vleet JF. Experimentally induced vitamin E-selenium deficiency in the growing dog. JAVMA 1975; 166:769-774.</ref><ref name="Davidson">Davidson MG, et al. Retinal degeneration associated with vitamin E deficiency in hunting dogs. JAVMA 1998;213:645-651.</ref>. Dogs with concurrent intestinal disease affecting absorption of dietary fat (i.e. a [[Protein Losing Enteropathy|protein-losing enteropathy]]) as well as dogs with [[ | + | Vitamin E deficiency in dogs can develop anorexia, reproductive failure, skeletal and endocardial muscle degeneration, retinal degeneration, dermatitis, and subcutaneous [[oedema]]<ref>Elvehjem CA, et al. The effect of vitamin E on reproduction of dogs on milk diets. J Pediatr 1944;24:436-441.</ref><ref>Van Vleet JF. Experimentally induced vitamin E-selenium deficiency in the growing dog. JAVMA 1975; 166:769-774.</ref><ref name="Davidson">Davidson MG, et al. Retinal degeneration associated with vitamin E deficiency in hunting dogs. JAVMA 1998;213:645-651.</ref>. Dogs with concurrent intestinal disease affecting absorption of dietary fat (i.e. a [[Protein Losing Enteropathy|protein-losing enteropathy]]) as well as dogs with [[Liver - Pathology|liver disease]] are at a higher risk of developing relative α-tocopherol deficiencies despite adequate dietary intake. |
====Cats:==== | ====Cats:==== | ||
| − | Clinical signs of vitamin E deficiency in cats and kittens include anorexia, depression, myopathy, and pansteatitis (i.e. | + | Clinical signs of vitamin E deficiency in cats and kittens include anorexia, depression, myopathy, and pansteatitis (i.e. painful nodular inflammation of adipose tissue)<ref>Gershoff SN and Norkin SA. Vitamin E deficiency in cats. J Nutr 1962;77:303-308.</ref><ref>Dennis JM and Alexander RW. Nutritional myopathy in a cat. Vet Rec 1982;111:195-196.</ref><ref name="Niza">Niza MM, et al. Feline pansteatitis revisited: hazards of unbalanced home-made diets. J Feline Med Surg 2003;5:271-277.</ref>. The level of vitamin E required to prevent clinical sign of deficiency is directly related to the level of dietary PUFAs. |
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====Influence of Diet:==== | ====Influence of Diet:==== | ||
The metabolic requirement for vitamin E is dependent on the PUFA concentration in the diet as well as the degree of peroxidation that occurs during processing and storage<ref name="Chow"/><ref name="NRC"/>. '''Diets high in fat and specifically high in long-chain omega-3 PUFAs will increase the tocopherol requirements in the diet'''<ref name="Davidson"/><ref name="Niza"/><ref>Hendricks WH, et al. Vitamin E requirement of adult cats increased slightly with high dietary intake of polyunsaturated fatty acids. J Nutr 2002;132:1613S-1615S.</ref>. Recycling of α-tocopherol is also impaired with concurrent high intakes of vitamin C (a water-soluble vitamin that is not a dietary requirement for dogs and cats); supplementation with vitamin C may increase vitamin E requirements<ref>Chen LH. Interaction of vitamin E and ascorbic acid (review). In Vivo 1989;3:199-209.</ref>. | The metabolic requirement for vitamin E is dependent on the PUFA concentration in the diet as well as the degree of peroxidation that occurs during processing and storage<ref name="Chow"/><ref name="NRC"/>. '''Diets high in fat and specifically high in long-chain omega-3 PUFAs will increase the tocopherol requirements in the diet'''<ref name="Davidson"/><ref name="Niza"/><ref>Hendricks WH, et al. Vitamin E requirement of adult cats increased slightly with high dietary intake of polyunsaturated fatty acids. J Nutr 2002;132:1613S-1615S.</ref>. Recycling of α-tocopherol is also impaired with concurrent high intakes of vitamin C (a water-soluble vitamin that is not a dietary requirement for dogs and cats); supplementation with vitamin C may increase vitamin E requirements<ref>Chen LH. Interaction of vitamin E and ascorbic acid (review). In Vivo 1989;3:199-209.</ref>. | ||
==Toxicity== | ==Toxicity== | ||
| − | There are no published reports of vitamin E toxicity in dogs, though in cats high levels of dietary vitamin E can result in prolonged bleeding times<ref>Strieker MJ, et al. Vitamin K deficiency in cats fed commercial fish-based diets. J Small Anim Prac 1996;37:322-326.</ref>. High dosage of vitamin E supplementation in people has also been associated with increased risk of mortality<ref>Bjelakovic G, et al. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention systematic review and meta-analysis. JAMA 2007;297:842-857.</ref>, though this effect has not been studied in dogs and cats. | + | There are no published reports of vitamin E toxicity in dogs, though in cats high levels of dietary vitamin E can result in prolonged [[Coagulation Tests|bleeding times]]<ref>Strieker MJ, et al. Vitamin K deficiency in cats fed commercial fish-based diets. J Small Anim Prac 1996;37:322-326.</ref>. High dosage of vitamin E supplementation in people has also been associated with increased risk of mortality<ref>Bjelakovic G, et al. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention systematic review and meta-analysis. JAMA 2007;297:842-857.</ref>, though this effect has not been studied in dogs and cats. |
==Dietary Sources== | ==Dietary Sources== | ||
Nuts, seeds and seed oils have high concentration of α-tocopherol. | Nuts, seeds and seed oils have high concentration of α-tocopherol. | ||
| − | Mixed-tocopherols (i.e. | + | Mixed-tocopherols (i.e. combination of δ- and α-tocopherol) are used in commercial pet foods due to increased stability with processing and storage compared to α-tocopherol alone. The concentration of the biologically active α-tocopherol in mixed-tocopherol can range from 10-40% of the total vitamin E content. Mixed-tocopherols are effective at preventing lipid oxidation that occurs during the processing and storage of foods, but depending on the source may not provide adequate concentrations of α-tocopherol to the diet. |
==Diagnosing Vitamin E Deficiency== | ==Diagnosing Vitamin E Deficiency== | ||
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==References== | ==References== | ||
<references/> | <references/> | ||
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| + | {{Reviewed Nutrition 1 | ||
| + | |date = 22 May 2015}} | ||
| + | {{Waltham}} | ||
| + | {{OpenPages}} | ||
[[Category:Vitamins]] | [[Category:Vitamins]] | ||
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Latest revision as of 08:48, 11 May 2016
What is Vitamin E (α-Tocopherol)?
Vitamin E is a category of essential fat-soluble vitamins referred to as tocopherols. There are four stereoisomers of tocopherols found in nature (α, β, γ, and δ). Of these, α-tocopherol has the highest biological activity. Similar to other fat-soluble vitamins, vitamin E is incorporated into mixed micelles along with dietary fat and absorbed by diffusion across the mucosal surface of the small intestine. Absorbed vitamin E is then incorporated into chylomicrons and released into the lymphatics for transport to the liver, though some absorption into the portal circulation occurs as well. Within the liver selective α-tocopherol-binding proteins will incorporate α-tocopherol into very low density lipoproteins (VLDLs); α-tocopherol-binding proteins have only limiting binding of β-, γ-, or δ-isomers[1]. The resultant α-tocopherol laden VLDLs transport α-tocopherol throughout the body. Vitamin E is primarily excreted through bile in faeces, though significant amounts of the metabolite α-tocopheric acid can also lost through urine[2].
Why is it Important?
Vitamin E is an antioxidant that protects cellular membranes lipid peroxidation by free radicals.
Roles in the Body
- Antioxidant: Reactive oxygen species (e.g. peroxide, superoxide, and nitric oxide radicals) are formed during normal cellular respiration. These free radicals can cause damage to membrane-bound polyunsaturated fatty acids (PUFAs) as well as deoxyribonucleic acid (DNA). Membrane and intracellular vitamin E is able to donate a hydrogen electron to help prevent or stop propagation of this cellular damage. Oxidized α-tocopherols can be regenerated within the cell by other antioxidant systems, such as glutathione and vitamin C[1].
- Cell Signalling: Aside from its role as an antioxidant, α-tocopherol is also an inhibitor of protein kinase C in platelets. The presence of high concentrations of α-tocopherol in endothelial cells also down-regulates the intracellular and vascular cell adhesion molecules. The combination of these two effects can result in inhibition of platelet aggregation[3].
Consequences of Vitamin E Deficiency
Dogs:
Vitamin E deficiency in dogs can develop anorexia, reproductive failure, skeletal and endocardial muscle degeneration, retinal degeneration, dermatitis, and subcutaneous oedema[4][5][6]. Dogs with concurrent intestinal disease affecting absorption of dietary fat (i.e. a protein-losing enteropathy) as well as dogs with liver disease are at a higher risk of developing relative α-tocopherol deficiencies despite adequate dietary intake.
Cats:
Clinical signs of vitamin E deficiency in cats and kittens include anorexia, depression, myopathy, and pansteatitis (i.e. painful nodular inflammation of adipose tissue)[7][8][9]. The level of vitamin E required to prevent clinical sign of deficiency is directly related to the level of dietary PUFAs.
Influence of Diet:
The metabolic requirement for vitamin E is dependent on the PUFA concentration in the diet as well as the degree of peroxidation that occurs during processing and storage[1][2]. Diets high in fat and specifically high in long-chain omega-3 PUFAs will increase the tocopherol requirements in the diet[6][9][10]. Recycling of α-tocopherol is also impaired with concurrent high intakes of vitamin C (a water-soluble vitamin that is not a dietary requirement for dogs and cats); supplementation with vitamin C may increase vitamin E requirements[11].
Toxicity
There are no published reports of vitamin E toxicity in dogs, though in cats high levels of dietary vitamin E can result in prolonged bleeding times[12]. High dosage of vitamin E supplementation in people has also been associated with increased risk of mortality[13], though this effect has not been studied in dogs and cats.
Dietary Sources
Nuts, seeds and seed oils have high concentration of α-tocopherol. Mixed-tocopherols (i.e. combination of δ- and α-tocopherol) are used in commercial pet foods due to increased stability with processing and storage compared to α-tocopherol alone. The concentration of the biologically active α-tocopherol in mixed-tocopherol can range from 10-40% of the total vitamin E content. Mixed-tocopherols are effective at preventing lipid oxidation that occurs during the processing and storage of foods, but depending on the source may not provide adequate concentrations of α-tocopherol to the diet.
Diagnosing Vitamin E Deficiency
Confirmation of Vitamin E deficiency is made by measuring plasma α-tocopherol concentration, although this is not routinely available in most veterinary reference laboratories. Physical examination may reveal skin lesions and a diagnosis may be confirmed via biopsy of nodules. A suspicion of a deficiency may arise when there is a presence of clinical signs consistent with deficiency and evaluation of diet demonstrates a deficiency.
References
- ↑ 1.0 1.1 1.2 Chow CK. Vitamin E. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p.584-598.
- ↑ 2.0 2.1 National Research Council (NRC). Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.205-210.
- ↑ Brigelius-Flohe R and Traber MG. Vitamin E: function and metabolism. FASEB 1999;13:1145-1155.
- ↑ Elvehjem CA, et al. The effect of vitamin E on reproduction of dogs on milk diets. J Pediatr 1944;24:436-441.
- ↑ Van Vleet JF. Experimentally induced vitamin E-selenium deficiency in the growing dog. JAVMA 1975; 166:769-774.
- ↑ 6.0 6.1 Davidson MG, et al. Retinal degeneration associated with vitamin E deficiency in hunting dogs. JAVMA 1998;213:645-651.
- ↑ Gershoff SN and Norkin SA. Vitamin E deficiency in cats. J Nutr 1962;77:303-308.
- ↑ Dennis JM and Alexander RW. Nutritional myopathy in a cat. Vet Rec 1982;111:195-196.
- ↑ 9.0 9.1 Niza MM, et al. Feline pansteatitis revisited: hazards of unbalanced home-made diets. J Feline Med Surg 2003;5:271-277.
- ↑ Hendricks WH, et al. Vitamin E requirement of adult cats increased slightly with high dietary intake of polyunsaturated fatty acids. J Nutr 2002;132:1613S-1615S.
- ↑ Chen LH. Interaction of vitamin E and ascorbic acid (review). In Vivo 1989;3:199-209.
- ↑ Strieker MJ, et al. Vitamin K deficiency in cats fed commercial fish-based diets. J Small Anim Prac 1996;37:322-326.
- ↑ Bjelakovic G, et al. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention systematic review and meta-analysis. JAMA 2007;297:842-857.
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This article was: Date reviewed: 22 May 2015 |
| Endorsed by WALTHAM®, a leading authority in companion animal nutrition and wellbeing for over 50 years and the science institute for Mars Petcare. | 
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