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In the form of Alpha-Tocopherol (the vitamin E form that acts like a vitamin) dosages of 50-75mg (or in the range of 150-200IU) appear to provide a good deal of benefit with little harm, although no ultimate conclusions can be drawn at this time.
Tocotrienols do not have enough information on them for an adequate dosage, but may be similar.
Vitamin E dosages, like all Essential Vitamin or Minerals, should be dosed by both supplements and food intake with normally no need to supplement for health or well being if food intake is sufficient.
Vitamin E can be quantified by weight (mg) or bioactivity (International Units, or IU); this is since not all forms of vitamin E (to be discussed) share the same bioactivity.
In regards to the form seen as a vitamin (alpha-tocopherol), 1mg of food-borne Alpha-tocopherol is approximately 1.49 IU while 1mg of the synthetic form (dl-alpha-tocopherol) is 2.22 IU.
The RDA (need to avoid deficiency for 97% of a population) for vitamin E is 15mg (or 22.5 IU) daily for both males and females above the age of 14. This requirement goes to 19mg (28.4 IU) in lactating individuals. The TUL (Tolerable Upper Intake) levels are 1,000mg (1,500IU) for both male and female adults and 800mg (1,200IU) for those between the ages of 14-18. No changes in the TUL occur for pregnancy or lactation.
It should be noted that some studies note side effects in the ranges of 400-800IU daily, and that consuming below the TUL may not be indicative of safety.
Alpha-Tocopherol is used as a signalling molecule and is able to inhibit smooth muscle cell proliferation, decrease PKC activity in cells, increase phosphoprotein phosphatase 2A activity, and regulate the the α-tropomyosin gene. The inhibition of PKC may be secondary to reducing levels of diacylglycerol (a PKC activator) leaked from the membrane and requires vitamin E to be a constituent of the membrane, which indicates a more chronic inhibition rather than acute.
Vitamin E can also regulate the expression of some pro-thrombrotic and artherogenic factors and may be secondary to upregulation of Phospholipase A2 and CycloOxygenase enzymes. These effects may be why vitamin E has been shown to dose-dependently increase prostacyclin levels in vivo.
Out of all forms, the liver tends to target α-tocopherol for incorporation into lipoproteins. This is also the specific isomer that reverses deficiency symptoms and has the highest bioavailability.
Deficiencies of Vitamin E tend to result in Myopathies and Neuromyopathies and forms of Ataxia. Overt deficiencies are rare, and usually only due to defects in the transport proteins responsible for Vitamin E or complete malabsorption secondary to alcoholism or intestinal diseases. Subclinical deficiencies may occur in response to excess oxidation and may diminish erythrocyte lifespan
Vitamin E is found in nature in 8 different forms. The tocopherols (of which exist alpha(α), beta(β), gamma(γ) and delta(δ)) and the tocotrienols (of which exist alpha(α), beta(β), gamma(γ) and delta(δ)). All forms are biologically active, although α-tocopherol is commonly seen as the most bioactive form.
γ-Tocopherol has been shown to exert a 'trapping' effect on nucleophilic mutagens (mutation causing agents) and aids in the chemoprotective properties of the anti-oxidant system Glutathione.
It appears to have its efficacy in chemoprotection reduced when paired with alpha-tocopherol.
Tocotrienols are named as such since they possess 3 double bonds in their isoprenoid side chains whereas tocopherols only possess two.
Tocotrienols can be seen as more potent than tocopherols in vitro in regards to their anti-oxidant properties directly and vicariously through selenoproteins, at inducing apoptosis and protecting against some forms of cancer, and at neuroprotection. In vivo, tocotrienols appear to be more potent than tocopherols at some cancer prevention, at antioxidation and anti-inflammation, and better protection of bone health.
However, the preference of the tocopherol transfer protein (TTP) for alpha-tocopherol still exists. thus in vitro results might be misleading if performed in non-hepatic tissue and in vivo results might be due to loading of tocotrienols (less efflux).
Tocotrienols may be the reason behind why natural vitamin E is sometimes seen as better than synthetic (as natural vitamin E is a mixture of various tocopherols and tocotrienols, as synthetic only aims to reproduce the alpha-tocopherol), but not much research has been conducted on tocotrienols relative to tocopherols.
Despite it's anti-clotting mechanisms, vitamin E supplementation (at 50mg) does not appear to protect the body significantly from strokes in normal populations but could potentially be of use in those with significantly high blood pressure. Those without high blood pressure may experience a greater risk for hemorrhagic stroke when exceeding the RDA with supplementation.
The pro-hemorrhagic effects may be more chronic than acute though, as even 800IU of vitamin E does not affect blood clotting factors for short durations (14 days).
As mentioned before, these effects may be throw increased oxidant protection of lipoproteins resulting in less artherogenic adhesion, or may be secondary to increases prostacyclin levels which are potent vasodilators and anti-artherogenic.
Vitamin E has the ability to act as a chain-breaking anti-lipid peroxidation agent, specifically in lipoproteins where it is incorporated by the liver. 'Chain-breaking' refers to being able to interrupt a series of oxidative events caused initially by oxidants. Vitamin E appears to be the central chain-breaker, as it still retains this ability even during deficiency states.
Supplemental vitamin E (as alpha-tocopherol) can alleviate mitochondrial dysfunction that is secondary to vitamin E losses.
In humans, supplementation of 400-800 IU of vitamin E in those with artherosclerotic buildup (artery plaque) was associated with a greatly reduced chance of a cardiac event from occurring. Doses of 300IU can improve markers of lipid peroxidaiton in humans. These events may be secondary to decreases in prothrombrotic factors.
Vitamin E is sometimes seen as synergistic with Selenium. In the process of protecting unsaturated lipids from oxidation, vitamin E forms hydroperoxides as byproducts which are readily reduced by selenoproteins. In this manner they can act together to alleviate oxidative stress.
Adequate vitamin E stores can reduce the amount of CoQ10 destroyed in oxidation as a result of exercise.|published=1995 Jan-Feb|authors=Fontana L, Rossi MA, Baccelliere L, Papagna D, Cottalasso D|journal=Minerva Cardioangiol]
Vitamin E works synergistically with Alpha-Lipoic Acid, as ALA recycles Vitamin E in the same manner as Vitamin E can recycle Vitamin C.|published=2008 Jan-Feb|authors=González-Pérez O, Moy-López NA, Guzmán-Muñiz J|journal=Rev Invest Clin] They also show synergy in anti-clotting of the blood, which could be cardioprotective or pro-hemorhhagic depending on dose.
Supplemental vitamin E at 300mg daily in uremic patients (tend to have elevated prolactin concentrations due to reduced clearance) has been noted to reduce circulating prolactin (50.8ng/mL down to 15.4ng/mL) without apparent influence on free testosterone. There are currently no studies investigating healthy controls and the influence of vitamin E supplementation.
At least one study has noted reductions in prolactin in uremic patients, although there is no evidence in healthy persons at this moment in time
One cohort study in china using a sample of 132,837 persons found that during follow-up that 267 persons (0.2%) developed cancer of the liver, and in comparing dietary information from the base sample against the cohort that developed liver cancer intake of Vitamin E was inversely related to cancer occurrence with a hazard ratio of 0.52 (almost half the risk) and a CI of 0.3-0.9.
Sesamin is a lignan from sesame seeds, and is an inhibitor of the process of Tocopherol-ω-hydroxylation (via CYP3A enzymes). This process metabolizes on the vitamin E vitamers, and works more readily on the gamma vitamers (γ-tocopherol and γ-tocotrienol) and thus inhibiting it with sesamin causes either inherent increases in plasma γ-tocopherol and γ-tocotrienol concentrations or it can augment a diet or supplement induced increases in plasma and tissue levels. This has been confirmed in humans given sesame oil (via food) conferring 94mg sesamin (and 42mg of the related lignan sesaminol) which halved the excretion of γ-tocopherol metabolites in the urine over the course of 72 hours in men.
Sesamin inhibits the metabolism of vitamin E vitamers (via inhibiting Tocopherol-ω-hydroxylation), and since this process works fastest on the gamma vitamers (γ-tocopherol and γ-tocotrienol) oral ingestion of sesamin will cause an increase in or augment the increase of plasma and tissue γ-tocopherol and γ-tocotrienol
When other factor are controlled for, high dosages of Vitamin E supplements (exceeding 400 IU daily) are associated with increase mortality from all causes, however these results have been contested by other analyses and counter points given in response to those. Independent of the epidemiological research, some researchers do suggest that dosages in this range exert no appreciable beneficial effect.
Tocotrienols might be seen as a safer alternative since they possess higher bioactivity (and thus less dosage needed to exert the same effect) and accumulate in tissues and tumors rather than in the blood, however this is a preliminary topic and not many assumptions can be made at this point in time.
(Common misspellings for Vitamin E include tokopherol, tokoferol, tokotrinol, tokotrienol, tocoferol, tocotrinol, vitmin)
(Common phrases used by users for this page include vit e pharmacodynamic, tocoferol bioactivity, profile vitamin e tokoferol, examine vitamina, examine vitamin e tocotrienols silverhyrda, alpha lipoic acid endothelium health)