Summary of evidence for determining recommended nutrient intakes
In the chapter on antioxidants, it was decided that there was insufficient evidence to enable a recommended nutrient intake (RNI) to be based on the additional health benefits obtainable from nutrient intakes above those usually found in the diet. Even for vitamin E with its important biologic antioxidant properties, there was no consistent evidence for protection against chronic disease from dietary supplements.
Nevertheless, the main function of Vitamin E appears to be that of preventing oxidation of PUFAs, and this has been used by those bodies proposing RNIs for vitamin E because there is considerable evidence in different animal species that low vitamin E and PUFAs excess gives rise to a wide variety of clinical signs.
There is very little clinical evidence of deficiency disease in humans except in certain inherited conditions where the metabolism of vitamin E is disturbed. Even biochemical evidence of poor vitamin E status in both adults and children is minimal. Meta-analysis of data collected within European countries indicates that optimum intakes may be implied when plasma concentrations of vitamin E exceed 25–30 μmol/L of lipid-standardized α-tocopherol.
However, this approach should be treated with caution, as plasma vitamin E concentrations do not necessarily reflect intakes or tissue reserves because only 1 percent of the body tocopherol may be in the blood and the amount in the circulation is strongly influenced by circulating lipid. Nevertheless, the lipid-standardized vitamin E concentration (e.g., tocopherolcholesterol ratio) greater that 2.25 (calculated as μmol/mmol) is believed to represent satisfactory vitamin E status.
The erythrocytes of subjects with values below this concentration of vitamin E may show evidence of an increasing tendency to haemolyze when exposed to oxidizing agents and thus such values should be taken as an indication of biochemical deficiency. However, the development of clinical evidence of vitamin E deficiency (e.g., muscle damage or neurologic lesions) can take several years of exposure to extremely low vitamin E levels.
The main factor used to assess the adequacy of vitamin E intakes by the US and UK advisory bodies was the dietary intake of PUFAs. PUFAs are very susceptible to oxidation, and their increased intake without a concomitant increase in vitamin E can lead to a reduction in plasma vitamin E concentrations and to elevations in some indexes of oxidative damage in human volunteers.
Generally, however, diets high in PUFAs are also high in vitamin E, and to set a dietary recommendation based on extremes of PUFA intake would deviate considerably from median intakes of vitamin E in most Western populations. Hence ‘safe’ allowances for the United Kingdom (men 10 and women 7 mg/day) and ‘arbitrary’ allowances for the United States (men 10 and women 8 mg/day) for vitamin E intakes approximate the median intakes in those countries.
It is worth noting that there were only 11 (0.7 percent) subjects out of 1629 adults in the 1986–1987 British Nutrition Survey who had α-tocopherol – cholesterol ratios with its high content of γ-tocopherol substitutes for the intake of α-tocopherol in the British diet, a comparison of α-tocopherol-cholesterol ratios found almost identical results in two groups of randomly selected, middle-aged adults in Belfast (Northern Ireland) and Toulouse (France), two countries with very different intakes of α-tocopherol and cardiovascular risk.
It is suggested that when the main PUFA in the diet is linoleic acid, a d-α- tocopherol-PUFA ratio of 0.4 (expressed as mg tocopherol per g PUFA) is adequate for adult humans, and the ratio has been recommended in the United Kingdom for infant formulas. Use of this ratio to calculate the vitamin E requirements of men and women with energy intakes of 2550 and 1940 kcal/day containing PUFA at 6 percent of the energy intake (approximately 17 and 13 g, respectively) produced values of 7 and 5 mg/day of α-TEs, respectively. In both the United States and the United Kingdom, median intakes of α-TE are in excess of these amounts and the α-tocopherol-PUFA ratio is approximately 0.6, which is well above the 0.4 ratio which would be considered adequate.
The Nutrition Working Group of the International Life Sciences Institute Europe has suggested an intake of 12 mg α-tocopherol for a daily intake of 14 g PUFAs to compensate for the high consumption of soya oil in certain countries where over 50 percent of vitamin E intake is accounted for by the less biologically active γ form. As indicated above, however, plasma concentrations in France and Northern Ireland suggest that an increased amount of dietary vitamin E is not necessary to maintain satisfactory plasma concentrations.
At present, data are not sufficient to formulate recommendations for vitamin E intake for different age groups except for infancy. There is some indication that new-born infants, particularly if born prematurely, are vulnerable to oxidative stress because of low body stores of vitamin E, impaired absorption, and reduced transport capacity resulting from low concentrations at birth of circulating low-density lipoproteins.
However, term infants almost achieve adult plasma vitamin E concentrations in the first week and although the concentration of vitamin E in early human milk can be variable, after 12 days it remains fairly constant at 0.32 mg TE/100 ml milk. Thus a human-milk-fed infant consuming 850 ml would have an intake of 2.7 mg. It seems reasonable that formula milk should not contain less than 0.3 mg TE/100 ml of reconstituted feed and not less than 0.4 mg TE/g PUFA.
No specific recommendations concerning the vitamin E requirements in pregnancy and
lactation have been made by other advisory bodies (42, 43) mainly because there is no evidence
of vitamin E requirements different from those of other adults and presumably also as the
increased energy intake would compensate for the increased needs for infant growth and milk
synthesis.
Vitamin E appears to have very low toxicity, and amounts of 100–200 mg of the synthetic all-rac-α-tocopherol are consumed widely as supplements. Evidence of prooxidant damage has been associated with the feeding of supplements but usually only at very high doses (e.g., >1000 mg/day).
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