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Vegetable oils, vegetable oil-based spreads, nuts, seeds, and egg yolk are

good food sources of vitamin E. The α-tocopherol content is highest in

sunflower oil followed by corn and rapeseed oil, olive oil, and soybean oil. In addition, vegetable oils contain variable amounts of other tocoph- erols and tocotrienols. Corn oil, soybean oil, and rapeseed oil are high in γ-tocopherol. On average, approximately half of the α-tocopherol in the diet of Finnish adults was provided by cereal and bakery products and fat spreads, oils, and dressings (7). Among the EPIC study participants from

the Nordic countries, added fats contributed the most to vitamin E (α-TE)

intake followed by cereal, cereal products, and cakes (8). Other important sources were fruits, vegetables, and fish and shellfish.

In recent dietary surveys from the Nordic countries, the mean dietary

intake of vitamin E (α-tocopherol) among adult populations varied between

7 mg and 10 mg per day (9–14). When expressed in relation to energy

intake, dietary intake of α-tocopherol by adults in the Nordic countries

ranges from 8 mg/10 MJ to 16 mg/10 MJ. During pregnancy, intake of vitamin E is higher and most of women use supplements containing vita-

min E (15–18). α-tocopherol intake by children ranges from 7 mg/10 MJ

to 11 mg/10 MJ and does not differ greatly from that of adults (18–20).

Physiology and metabolism

The uptake, transport, and tissue delivery of α-tocopherol involves mo-

lecular, biochemical, and cellular processes that are closely related with overall lipid and lipoprotein metabolism (21). The presence of bile salts and pancreatic enzymes and the formation of micelles are prerequisites for vitamin E absorption. In order to obtain maximal absorption, vitamin E should be given at meals. However, knowledge of vitamin E absorption is incomplete, and both the amount of fat and the food matrix influence

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vitamin E absorption. In balance studies with small radioactive doses of α-tocopherol, absorption in normal subjects has ranged between 55% and 79% (2, 22), whereas a much lower figure of 33% was reported based on

observed changes in plasma-labelled α-tocopherol after administration of

a stable isotope-labelled dose of α-tocopherol (23). Large individual varia- tion in vitamin E uptake has been reported.

Absorbed vitamin E is transported within chylomicrons or bound to

HDL in the liver where α-TTP preferentially binds α-tocopherol and is es-

sential for the selective resecretion of α-tocopherol (24). The metabolism of vitamin E is tightly regulated, and unlike other fat-soluble vitamins there is no toxic accumulation in the liver. α-tocopherol that is not released into circulation is excreted into the bile via transporters that are upregulated

in the presence of α-tocopherol or it is metabolized via the cytochrome

P450 system, also regulated with α-tocopherol, and excreted in bile or

urine. The major route of excretion of α-tocopherol is in the faeces with

small amounts excreted in urine (22). Turnover of vitamin E is slow; in a

kinetic study with tracer-marked RRR-α-tocopherol tracked for 460 days

in healthy men and women, the mean half-life of the dose was 44 days in plasma and 96 days in red blood cells (22).

Although no tissue serves to store vitamin E, depletion of body vitamin E

takes decades rather than weeks (25). Non-α-tocopherols and tocotrienols

are rapidly metabolized thereby preventing their tissue accumulation and limiting increases in their plasma concentrations (26). In human tissues, α-tocopherol is the most common tocopherol and contributes about 90% of the total amount of tocopherols and tocotrienols in plasma (27) and 50%–

80% in other tissues (4). Recently, water-soluble α-tocopheryl phosphate

has been shown to appear in minute amounts in foods and tissues (28).

The main biochemical function of α-tocopherol has been suggested to

be its antioxidant activity. As a chain-breaking antioxidant, α-tocopherol

might prevent the propagation of free radicals in membranes and in plasma lipoproteins (29). In addition, several other important biological functions, including modulation of cell signalling and gene expression, have been

ascribed to vitamin E (30). α-tocopherol might modulate the activity of

several enzymes. Most of these enzymes are membrane bound or activated by membrane recruitment, especially those affecting cell proliferation, membrane trafficking, and metabolism of xenobiotics (24). Genes involved

in the metabolism and excretion of vitamin E are regulated by α-tocopherol

itself. The ultimate biological function of vitamin E, however, remains to be elucidated (31).

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Vitamin E is suggested to affect health through its antioxidant activ- ity, immune system enhancement, inhibition of platelet aggregation, and anti-inflammatory function with much of this evidence coming from cell studies and the findings from animal experiments. Evidence for decreased

oxidative stress with α-tocopherol supplementation in humans is incon-

sistent (32). The effect of vitamin E on biomarkers of oxidative stress ap- pears to depend on the circumstances in which it is administered, most importantly on the level of baseline oxidative stress (33). Differences in

the individual responses to α-tocopherol are also suggested to arise due

to genetic factors (34, 35).

High vitamin E intake has been associated with prolonged bleeding suggesting that large amounts of vitamin E might interfere with the blood clotting system especially with simultaneous use of aspirin or treatment with anticoagulants (36, 37). It is hypothesized that vitamin E intake can affect vitamin K status because they share the same metabolic pathways (38, 39).