Vitamin E – the food stabiliser and important antioxidant in your body (part 2).

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In the first part of the article, we focused on chemical forms of Vitamin E. Now, let’s look into active forms of Vitamin E in the human body and their functions. This part is a scientific review of Vitamin E deficiency symptoms and issues caused by its excessive amount.

 

The presence of Vitamin E in the body.

Serum concentrations of Vitamin E (alpha-Tocopherol) depend on the liver functioning. Vitamin E is absorbed in the various forms (but mainly as Tocopherol or Tocotrienol) from the small intestine. Vitamin E molecules are transported to a liver. There any esterified forms of Vitamin E are transformed to alcohol form (especially alpha-Tocopherol). (1)

Among all forms of Vitamin E in the body, alpha-Tocopherol is preferentially retained in the liver by the binding to alpha-Tocopherol transfer protein (alpha-TTP), which incorporates alpha-Tocopherol into lipoproteins for delivery to extrahepatic tissues. Other forms of Vitamin E are actively metabolised and mostly excreted. (2)

 

Functions of Vitamin E in the body.

Alpha-Tocopherol seems to be the most important lipid-soluble antioxidant. It protects cell membranes from oxidation by reacting with free radicals produced in the lipid oxidation chain reaction. In this process from Tocopherol molecule tocopheroxyl radical is formed. Next, Tocopherol molecule undergoes further oxidation to other products, as it is presented below.

The oxidised alpha-tocopheroxyl radicals produced in this process may be however recycled back to the active, reduced form, through reduction by other antioxidants, such as ascorbate, retinol or ubiquinol. So, Tocopherol is a part of the antioxidative mechanism presented below.

Fatty soluble alpha-Tocopherol protects from oxidation not only cell membranes, but also other important molecules like for example low-density lipoproteins (LDLs). LDLs specifically transport cholesterol from the liver to the tissues of the body. It is known, that oxidised LDLs are implicated in the development of cardiovascular diseases, so sufficient level of Vitamin E is here very important.

In addition to its activities as an antioxidant, Vitamin E involves immune functions like cell signalling, regulation of gene expression and other metabolic processes. For example, alpha-Tocopherol inhibits the activity of protein kinase C, an enzyme involved in cell proliferation and differentiation in smooth muscle cells, platelets and monocytes.

Vitamin E also increases the expression of two enzymes that suppress arachidonic acid metabolism, thereby increasing the release of prostacyclin from the endothelium, which, in turn, dilates blood vessels and inhibits platelet aggregation. (3)

Alfa-Tocopherol may also have an influence on the activity of specific membrane proteins and enzymes. (4)

Although all forms of Vitamin E are known to be potent antioxidants, the functions of the other than alpha-Tocopherol forms of Vitamin E are less known.

Researchers have found that Tocotrienols and γ-Tocopherol are better scavengers of peroxyl radicals and reactive nitrogen species than alpha-Tocopherol. However, in the body mainly alpha-Tocopherol is used. (5)

Some studies have indicated that gamma-Tocopherol and its major metabolite, gamma-carboxyethylhydroxychroman, may play a role in protecting the animal body from free radical-induced damage in various conditions of oxidative stress and inflammation. However, a potential anti-inflammatory effect of gamma-Tocopherol in humans has not been proved. (5)

Gamma-Tocopherol has been found helpful in improving of vascular endothelial function during smoking cessation. There is also a chance that gamma-Tocopherol, as a nucleophile, may react with electrophilic mutagens. (6)

Tocotrienols have special roles in protecting neurones from damage, cancer prevention and cholesterol reduction. Numerous preclinical studies have also suggested that Tocotrienols might be beneficial in the prevention of chronic diseases, but the effectiveness of their supplemental in humans was not fully checked. (7)

 

Health claims of Vitamin E.

Main healthy functions of Vitamin E are based on its properties as an antioxidant and its roles in anti-inflammatory processes, inhibition of platelet aggregation and immune enhancement. So, in general, we can say that Vitamin E can be successfully applied to promote health, as well as, prevent and treat diseases, like coronary heart disease, eye disorders, cancer and cognitive decline. More about medical claims you can read in Ahsan's review. (8)

Deficiency of Vitamin E.

Typical symptoms of deficiency of vitamin E include peripheral neuropathy, ataxia, skeletal myopathy, retinopathy, and impairment of the immune response. (9)

Prolonged deficiency of Vitamin E can cause problems as poor transmission of nerve impulses, muscle weakness and retinal degeneration that leads to blindness. (10)

Because Vitamin E deficiency is usually rare or not obvious, deficiency symptoms have not been often found in healthy people who obtain little Vitamin E from their diets. However, recently scientist published information that only 21% of the populations reached a serum alpha-Tocopherol concentration above 30 micromol/L (the minimum value recommended by experts). The study found that Vitamin E intake also differed regionally. It has been found that about 27% of the American, 80% of the Middle East/African, 62% of the Asian, and 19% of the European populations are below mentioned above recommended value. (11)

Deficiency of vitamin E can be also found in premature babies of very low birth weight (<1,500 grams). Vitamin E supplementation in these infants might reduce the risk of some complications, such as those affecting the retina and the risk of infections. (12)

Children with severe Vitamin E deficiency at birth also rapidly experience irreversible neurologic symptoms, if not treated quickly with Vitamin E. (13)

We have to remember that the digestive tract requires fat to absorb Vitamin E. Therefore, people with fat-malabsorption disorders, Crohn's disease, cystic fibrosis, abetalipoproteinemia or an inability to secrete bile from the liver into the digestive tract, are more likely to become deficient with Vitamin E. They sometimes require water-soluble forms of Vitamin E, such as Tocopheryl polyethylene glycol-1000 succinate.

Severe Vitamin E deficiency has been associated with specific genetic defects affecting the transport of alpha-Tocopherol by alpha-Tocopherol transfer protein (alpha-TTP) and lipoproteins. (13)

Also, smokers might be at increased risk of deficiency compared with non-smokers. (14)

 

Health risk from an excessive amount of Vitamin E.

Vitamin E is relatively non-toxic and research studies have not found any adverse effects from consuming Vitamin E in food. Sometimes high doses of Vitamin E can cause a headache, muscle weakness, double vision, tiredness and bowel looseness, and there is a theoretical risk of over-thinning the blood which could increase the risk of haemorrhagic stroke. (3)

Uptake of high doses of Vitamin E (400 IU/day (equivalent to 180 mg/day of RRR-alpha-Tocopherol ) or higher) significantly increases mortality risk. That level of Vitamin E supplementation may also harm adult men by increasing their risk of prostate cancer. (15)

Some physicians recommend discontinuing high-dose Vitamin E supplementation two to four weeks before elective surgery and dental procedures to decrease the risk of haemorrhage. (16)

It has been also published, that in some patients with common forms of retinitis pigmentosa after taking 400 IU/day of synthetic Vitamin E (equivalent to 180 mg/day of RRR-alpha-Tocopherol) was observed modest, but significant, acceleration of the loss of retinal function compared to placebo. (17)

 

Read also other parts of the article: part 1part 2part 3part 4part 5.

 

If you are a supplier of Vitamin E present your products to the IngredientsHub expo visitors.

 

Literature

  1. (Traber MG. Vitamin E. In: Shils ME, Shike M, Ross AC, Caballero B, Cousins R, eds. Modern Nutrition in Health and Disease. 10th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2006;396-411., Traber MG. Vitamin E regulatory mechanisms. Annu Rev Nutr 2007;27:347-62)
  2. (Food and Nutrition Board, Institute of Medicine. Vitamin E. Dietary reference intakes for Vitamin C, Vitamin E, selenium, and carotenoids. Washington, D.C.: National Academy Press; 2000:186-283)
  3. (Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoids., Washington, DC: National Academy Press, 2000)
  4. (Davis S, Davis BM, Richens JL, et al. alpha-Tocopherols modify the membrane dipole potential leading to modulation of ligand binding by P-glycoprotein. J Lipid Res. 2015;56(8):1543-1550., Marko MG, Ahmed T, Bunnell SC, et al. Age-associated decline in effective immune synapse formation of CD4(+) T cells is reversed by Vitamin E supplementation. J. Immunol. 2007;178(3):1443-1449., Molano A, Meydani SN. Vitamin E, signalosomes and gene expression in T cells. Mol Aspects Med. 2012;33(1):55-62)
  5. (Jiang Q. Natural forms of Vitamin E: metabolism, antioxidant, and anti-inflammatory activities and their role in disease prevention and therapy. Free Radic Biol Med. 2014;72:76-90)
  6. (Jiang Q. Natural forms of Vitamin E: metabolism, antioxidant, and anti-inflammatory activities and their role in disease prevention and therapy. Free Radic Biol Med. 2014;72:76-90)
  7. (Mah E, Pei R, Guo Y, et al. γ-Tocopherol-rich supplementation additively improves vascular endothelial function during smoking cessation. Free Radic Biol Med. 2013;65:1291-1299, Mah E, Pei R, Guo Y, et al. Greater γ-Tocopherol status during acute smoking abstinence with nicotine replacement therapy improved vascular endothelial function by decreasing 8-iso-15(S)-prostaglandin F2alpha. Exp Biol Med (Maywood). 2015;240(4):527-533)
  8. (Ahsan H, Ahad A, Iqbal J, Siddiqui WA. Pharmacological potential of Tocotrienols: a review. Nutr Metab (Lond). 2014;11(1):52)
  9. (Ahsan H, Ahad A, Iqbal J, Siddiqui WA. Pharmacological potential of Tocotrienols: a review. Nutr Metab (Lond). 2014;11(1):52); http://lpi.oregonstate.edu/mic/Vitamins/Vitamin-E#introduction)
  10. (Kowdley KV, Mason JB, Meydani SN, Cornwall S, Grand RJ. Vitamin E deficiency and impaired cellular immunity related to intestinal fat malabsorption. Gastroenterology 1992;102:2139-42)
  11. (Tanyel MC, Mancano LD. Neurologic findings in Vitamin E deficiency. Am Fam Physician 1997;55:197-201)
  12. (Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoid. Washington, DC: National Academy Press, 2000; Péter S, Friedel A, Roos FF, Wyss A, Eggersdorfer M, Hoffmann K, Weber P., A Systematic Review of Global Alpha-Tocopherol Status as Assessed by Nutritional Intake Levels and Blood Serum Concentrations., Int J Vitam Nutr Res. 2016 Jul 14:1-21)
  13. (Brion LP, Bell EF, Raghuveer TS. Vitamin E supplementation for prevention of morbidity and mortality in preterm infants. Cochrane Database Syst Rev;4:CD003665)
  14. (Leonard SW, Bruno RS, Ramakrishnan R, Bray T, Traber MG. Cigarette smoking increases human Vitamin E requirements as estimated by plasma deuterium-labelled CEHC. Ann N Y Acad Sci. 2004;1031:357-360, Wright ME, Lawson KA, Weinstein SJ, et al. Higher baseline serum concentrations of Vitamin E are associated with lower total and cause-specific mortality in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Clin Nutr. 2006;84(5):1200-1207).
  15. (Miller ER 3rd, Pastor-Barriuso R, Dalal D, Riemersma RA, Appel LJ, Guallar E. Meta-analysis: high-dosage Vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2005;142:37-46., Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA 2007;297:842-57; Klein EA, Thompson Jr. IM, Tangen CM, Crowley JJ, Lucia MS, Goodman PJ, et al. Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT). JAMA 2011;306:1549-1556)
  16. (Hendler SS, Rorvik DR, eds. PDR for Nutritional Supplements. 2nd edition ed: Thomson Reuters; 2008)
  17. (Berson EL, Rosner B, Sandberg MA, et al. A randomized trial of Vitamin A and Vitamin E supplementation for retinitis pigmentosa. Arch Ophthalmol. 1993;111(6):761-772)