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Vitamin E constitutes a family of 8 tocopherols and tocotrienol fat soluble compounds. Members of the vitamin E family are hydrophobic fat-soluble compounds found in a variety of food sources such as corn oil, peanuts, vegetable oils, fruits and vegetables consumed through diet. Dietary habits thus play a significant role in which vitamin E isoform is primarily consumed; a Mediterranean diet, for example contains a significant amount of leafy greens, which contain high levels of α-tocopherol. The health benefits of consuming vitamin E through diet or supplementation are believed to be for its antioxidant properties as a peroxyl radical scavenger.
Fat malabsorption as well as metabolic defects can lead to vitamin E deficiency and some dietary intake surveys suggest people, mainly females, do not meet their vitamin E requirements through diet alone.
Vitamin E has been studied in relation to liver disease. When the liver is diseased and bile salts are unable to reach the intestine for digestion, malabsorption of fat occurs. When fat is not broken down properly, stools become pale, yellow, loose, greasy, foul smelling or frothy and floating –‘steatorrhoea’. As fat contains vitamins, including Vitamin E, patients with liver disease may become deficient in this vitamin.
Patients with non-alcoholic-steatohepatitis (NASH) have been found to have reduced plasma levels of vitamin E.
Vitamin E is an antioxidant that protects against toxic liver injury in animals. It reduces the production of tumour growth factor (TGFβ)[3,4] and reduces the activity of hepatic stellate cells. Vitamin E has already been shown to improve or stabilise hepatic fibrosis scores in NASH.
A trial in hepatitis patients gave those in the active treatment group a daily antioxidant supplementation (vitamin E 800 mg, C 500 mg and zinc 40 mg) for six months. The supplements protected patients against the oxidative effects of the hepatitis C. In 69 hepatitis B patients, serum vitamin E, as well as other antioxidants, was found to be lower in concentration and oxidative stress was found to be higher, than in 20 healthy controls. In a randomised controlled trial, investigators evaluated 51 patients with alcoholic hepatitis. Twenty-five patients received daily supplementation with 1000 mg of vitamin E and 26 took a placebo for three months. Patients showed improvement in serum hyaluronic acid levels.
Age-related cataracts (ARC’s)
A meta-analysis was undertaken to evaluate the relationship between vitamin E and ARC’s. Studies involved samples of people of all ages. Dietary vitamin E intake, dietary and supplemental vitamin E intake, and high serum tocopherol levels were significantly associated with decreased risk of ARC. The risk of ARC decreased with dietary vitamin E intake from 7 mg/d. The findings of the meta-analysis indicated that dietary vitamin E intake, dietary and supplemental vitamin E intake, and high level of serum tocopherol might be significantly associated with reduced ARC risk.
There is some evidence to suggest that any excess vitamin E may be harmful. Data from recent observational studies raised the concerns of a possible increase in all-cause mortality in patients taking doses of vitamin E higher than 400 IU/d. Moreover a meta-analysis that included 9 trials suggested that vitamin E might increase the risk of hemorrhagic stroke. More recently, an extended follow-up of a large RCT observed a significant increase in prostate cancer incidence in healthy men taking vitamin E 400 IU daily for over 7 years.
- Grant JP, Chapman G, Russell MK. Malabsorption associated with surgical procedures and it’s treatment. Nutr Clin Pract 1996; 11: 43-52.
- Erhardt A., Stahl W., Sies H., Lirussi F., Donner A., Haussinger D. Plasma levels of vitamin E and carotenoids are decreased in patients with nonalcoholic steatohepatitis (NASH) Eur. J. Med. Res. 2011;16:76–78.
- Parola M, Leonarduzzi G, Biasi F, Albano E, Biocca ME, Poli G, Dianzani MU. Vitamin E dietary supplementation protects against carbon tetrachloride-induced chronic liver damage and cirrhosis. Hepatology. 1992;16:1014–1021.
- Parola M, Muraca R, Dianzani I, Barrera G, Leonarduzzi G, Bendinelli P, Piccoletti R, Poli G. Vitamin E dietary supplementation inhibits transforming growth factor beta 1 gene expression in the rat liver. FEBS Lett. 1992;308:267–270.
- Hasegawa T, Yoneda M, Nakamura K, Makino I, Terano A. Plasma transforming growth factor-beta1 level and efficacy of alpha-tocopherol in patients with non-alcoholic steatohepatitis: a pilot study. Aliment Pharmacol Ther. 2001;15:1667–1672.
- Harrison SA, Torgerson S, Hayashi P, Ward J, Schenker S. Vitamin E and vitamin C treatment improves fibrosis in patients with nonalcoholic steatohepatitis. Am J Gastroenterol. 2003;98:2485–2490.
- Sanyal AJ, Chalasani N, Kowdley KV, McCullough A, Diehl AM, Bass NM, Neuschwander-Tetri BA, Lavine JE, Tonascia J, Unalp A, et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med. 2010;362:1675–1685.
- Farias MS, Budni P, Ribeiro CM et al. Antioxidant supplementation attenuates oxidative stress in chronic hepatitis C patients. Gastroenterol Hepatol. 2012;35(6):386-94.
- Tasdelen Fisgin N, Aydin BK, Sarikaya H, et al. Oxidative stress and antioxidant defense in patients with chronic hepatitis B. Clin Lab. 2012;58(3-4):273-80.
- Mezey E, Potter JJ, Rennie-Tankersley L, Caballeria J, Pares A. A randomized placebo controlled trial of vitamin E for alcoholic hepatitis. J Hepatol. 2004;40:40–46.
- Zhang Y, Jiang W, Xie Z, Wu W, Zhang D. Vitamin E and risk of age-related cataract: a meta-analysis. Public Health Nutr. 2015 Oct;18(15):2804-14. doi: 10.1017/S1368980014003115. Epub 2015 Jan 16.
- Schürks M, Glynn RJ, Rist PM, Tzourio C, Kurth T. Effects of vitamin E on stroke subtypes: meta-analysis of randomised controlled trials. BMJ. 2010;341:c5702.
- Klein EA, Thompson IM, Tangen CM, Crowley JJ, Lucia MS, Goodman PJ, Minasian LM, Ford LG, Parnes HL, Gaziano JM, et al. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT) JAMA. 2011;306:1549–1556.