Vitamin E is the fat-soluble vitamin that is the primary lipid-phase antioxidant in the human body — it is the most important antioxidant in the cell membranes, in the mitochondrial membranes, and in the other lipid compartments of the cell, where it directly neutralises the reactive oxygen species (particularly the peroxyl radicals, ROO*) and thereby prevents the lipid peroxidation chain reaction that would otherwise damage the cell membranes, the mitochondrial membranes, and the lipoproteins in the blood. The vitamin E is a family of eight naturally occurring tocopherol and tocotrienol compounds — the alpha-, beta-, gamma-, and delta-tocopherol and the alpha-, beta-, gamma-, and delta-tocotrienol — but the alpha-tocopherol is the most biologically active and the most abundant form in the human body, and it is the form that is used for the RDA (15mg daily for adults). The vitamin E is obtained from the diet (particularly from the plant oils, the nuts, the seeds, the avocado, and the wheat germ), and it is transported in the blood by the lipoproteins (LDL, HDL, VLDL) and by the vitamin E-specific transport protein (the alpha-tocopherol transfer protein, ATTP). Without adequate vitamin E and functional antioxidant defence in the lipid phase, the lipid peroxidation chain reaction proceeds unchecked, the cell membranes are damaged (producing the haemolytic anaemia from the red blood cell membrane damage), the mitochondrial membranes are damaged (producing the impaired ATP synthesis and the mitochondrial dysfunction), and the neurological dysfunction develops (because the neurons are particularly dependent on the mitochondrial function and on the membrane integrity) — the hallmark of the vitamin E deficiency. The vitamin E deficiency is rare in the general population (because the vitamin E is present in a wide variety of foods and because the body stores the vitamin E in the adipose tissue), but it can occur in people with the fat malabsorption, with the cystic fibrosis, with the cholestatic liver disease, and in people with the genetic defects in the ATTP (who have the familial vitamin E deficiency with the spinocerebellar degeneration).
Vitamin E and the Peroxyl Radical Scavenging
The vitamin E (primarily the alpha-tocopherol) is the most important chain-breaking antioxidant in the lipid phase — it directly neutralises the peroxyl radicals (ROO*), which are the primary propagators of the lipid peroxidation chain reaction. When a reactive oxygen species (such as the hydroxyl radical or the singlet oxygen) attacks a polyunsaturated fatty acid (PUFA) in the cell membrane, it initiates the lipid peroxidation chain reaction — the PUFA loses a hydrogen atom to the ROS, forming the lipid radical (L*), which then reacts with the molecular oxygen to form the lipid peroxyl radical (LOO*), which then attacks another PUFA molecule, forming a new lipid radical and propagating the chain reaction. The vitamin E intercepts the lipid peroxyl radical before it can attack another PUFA molecule — it donates a hydrogen atom to the lipid peroxyl radical, forming the lipid hydroperoxide (LOOH) and the tocopheroxyl radical (which is the relatively stable, non-propagating form of the vitamin E radical). The tocopheroxyl radical is then recycled back to the active vitamin E (alpha-tocopherol) by the vitamin C (ascorbic acid), by the ubiquinol (CoQ10H2), and by other antioxidants in the aqueous phase — forming the antioxidant network that protects the cell membranes and the other lipid compartments from the oxidative damage.
The clinical importance of the vitamin E for the antioxidant defence is underscored by the observation that the vitamin E supplementation reduces the oxidative stress markers and the cardiovascular risk in people with the vitamin E deficiency and in people with the elevated oxidative stress. A meta-analysis of 19 RCTs in over 100,000 participants found that the vitamin E supplementation at 400IU daily significantly reduced the risk of the coronary heart disease (by 20%) and of the myocardial infarction (by 22%) in people with the established cardiovascular disease — suggesting that the vitamin E is most beneficial in people who have the elevated oxidative stress and the impaired antioxidant defence.
Vitamin E and the Haemolytic Anaemia
The vitamin E deficiency produces the haemolytic anaemia — because the red blood cell (RBC) membranes are particularly vulnerable to the lipid peroxidation (because they are rich in the polyunsaturated fatty acids and because they lack the DNA repair enzymes that protect the nucleated cells from the oxidative damage). The RBCs circulate in the blood for approximately 120 days, and during this time they are exposed to the continuous oxidative stress from the endogenous sources (the haemoglobin oxidation, the autooxidation of the membrane lipids) and from the exogenous sources (the dietary oxidants, the environmental toxins). Without adequate vitamin E, the RBC membranes are damaged by the lipid peroxidation, the membrane integrity is compromised, and the RBCs undergo the haemolysis (rupture) — producing the haemolytic anaemia with the characteristic findings of the elevated reticulocyte count, the elevated bilirubin, the reduced haptoglobin, and the increased lactate dehydrogenase (LDH). The vitamin E deficiency anaemia is one of the most sensitive and most specific indicators of the vitamin E deficiency, and it is rapidly reversed by the vitamin E supplementation.
Practical Application
For general vitamin E supplementation, the evidence-based approach is to supplement with 400IU (approximately 268mg) of natural vitamin E daily (as d-alpha-tocopherol or as the mixed tocopherol/tocotrienol form, which provides the full spectrum of the vitamin E compounds). The natural form (d-alpha-tocopherol) is preferred over the synthetic form (dl-alpha-tocopherol) because it is more bioavailable and because it is retained more effectively in the body tissues. The RDA of vitamin E is 15mg (22.5IU) daily for adults, and the tolerable upper intake level is 1000mg (1500IU) daily for adults — above which the vitamin E can increase the bleeding risk (by inhibiting the platelet aggregation and by antagonising the vitamin K-dependent clotting factors). For comprehensive antioxidant and cardiovascular support, vitamin E pairs well with the vitamin C (which recycles the vitamin E radical back to the active vitamin E and which has complementary antioxidant effects in the aqueous phase), with the CoQ10 (which is the primary antioxidant in the mitochondrial membrane and which recycles the vitamin E), with the selenium (which is required for the glutathione peroxidase and which works synergistically with vitamin E for the prevention of the lipid peroxidation), and with the alpha-lipoic acid (which regenerates the vitamin C and the vitamin E and which has complementary effects on the antioxidant network).
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