EPI LIFE COACH articles
|DATE||Friday, March 03|
|AUTHOR||Dr. Carlos Orozco (BSc, MSc, ND, MD, PhD, FPAMS)|
Vitamin E is a mixture of several related compounds known as tocopherols. The -tocopherol molecule is the most potent of these tocopherols.
Vitamin E is absorbed from the intestines packaged in chylomicrons. It is delivered to the tissues via chylomicron transport and then to the liver through chylomicron remnant uptake. The liver can export vitamin E in very low density lipoproteins known as VLDLs. Due to its lipophilic nature, vitamin E accumulates in cellular membranes, fat deposits and other circulating lipoproteins. The major site of vitamin E storage is in adipose tissue.
The major biological function of vitamin E is to act as a natural antioxidant by scavenging free radicals and molecular oxygen. In particular vitamin E is important for preventing peroxidation of polyunsaturated membrane fatty acids. The vitamins E and C are interrelated in their antioxidant capabilities. Active a-tocopherol can be regenerated by interaction with vitamin C following scavenge of a peroxy free radical. Alternatively, a-tocopherol can scavenge two peroxy free radicals and then be conjugated to glucuronate for biliar excretion.
The main function of alpha-tocopherol in humans appears to be that of an antioxidant. Free radicals are formed primarily in the body during normal metabolism and also upon exposure to environmental factors such as cigarette smoke or pollutants. Fats, which are an integral part of all cell membranes, are vulnerable to destruction through oxidation by free radicals. The fat-soluble vitamin, alpha-tocopherol, is uniquely suited to intercepting free radicals and preventing a chain reaction of lipid destruction. Aside from maintaining the integrity of cell membranes throughout the body, alpha-tocopherol also protects the fats in low density lipoproteins (LDLs) from oxidation. Lipoproteins are particles composed of lipids and proteins, which are able to transport fats through the blood stream. LDL transport cholesterol from the liver to the tissues of the body. Oxidized LDLs have been implicated in the development of cardiovascular diseases. When a molecule of alpha-tocopherol neutralizes a free radical, it is altered in such a way that its antioxidant capacity is lost. However, other antioxidants, such as vitamin C, are capable of regenerating the antioxidant capacity of alpha-tocopherol (2).
Several other functions of alpha-tocopherol have been identified, which likely are not related to its antioxidant capacity. Alpha-tocopherol is known to inhibit the actvity of protein kinase C, an important cell signaling molecule, as well as to affect the expression and activity of immune and inflammatory cells. Additionally, alpha-tocopherol has been shown to inhibit platelet aggregation and to enhance vasodilation(3,4).
Signs and Symptoms of Vitamin E Deficiency:
Deficiency of vitamin E may be associated with areflexia, ceroid deposition in muscle, chronic liver disease, cirrhosis of gall bladder, creatinuria, cystic fibrotic symptoms, pulmonary embolism, gall disturbances, involuntary eye movements, muscle wasting and weakness, nerve damage, neuromuscular deficit, autoimmune diseases, poor coordination, red blood cell fragility, red blood cell hemolysis, renolytic anemia, spinocerebral disease.
- Traber MG. Utilization of vitamin E. Biofactors. 1999;10(2-3):115-120. (PubMed).
- Traber MG. Vitamin E. In: Shils M, Olson JA, Shike M, Ross AC, eds. Nutrition in Health and Disease. 9th ed. Baltimore: Williams & Wilkins; 1999:347-362.
- Food and Nutrition Board, Institute of Medicine. Vitamin E. Dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. WashingtonD.C.: NationalAcademy Press; 2000:186-283. (National Academy Press).
- Traber MG. Does vitamin E decrease heart attack risk? summary and implications with respect to dietargy recommendations. J Nutr. 2001;131(2):395S-397S. (PubMed)