Objective: The intent of this review is to evaluate the scientific evidence for the assessment of adequacy of selenium status and of the requirements for selenium. From this evidence, attempts have been made to define levels of plasma selenium and dietary selenium intake, which could be used for the assessment of deficiency or adequacy of selenium status. Method: The first section briefly reviews the methods for assessment of selenium status. The second section outlines the requirements for selenium based on a number of criteria, and how these have been translated into recommended intakes of selenium. In the final section, levels of plasma selenium and dietary intake based on different criteria of adequacy have been proposed. Results and conclusion: The minimum requirement for selenium is that which prevents the deficiency disease, Keshan disease. The recommended intakes of selenium have been calculated from the requirement for optimum plasma glutathione peroxidase (GPx) activity that must, because of the hierarchy of selenoproteins, also take account of the amounts needed for normal levels of other biologically necessary selenium compounds. Whether optimal health depends upon maximization of GPx or other selenoproteins, however, has yet to be resolved, and the consequences of less-than-maximal GPx activities or mRNA levels need investigation. Intakes, higher than recommended intakes, and plasma selenium concentrations that might be protective for cancer or result in other additional health benefits have been proposed. There is an urgent need for more large-scale trials to assess any such beneficial effects and to provide further data on which to base more reliable estimates for intakes and plasma selenium levels that are protective.

An upper estimated requirement of 90 microgram Se/d was calculated as the intake necessary for maximization of plasma GSHPx activity, as used in the derivation of the US recommended daily allowance. Our lower estimated requirement of 39 microgram Se/d was the intake necessary to reach two-thirds of maximal GSHPx activity, as was used in calculating the World Health Organization normative requirement. The lower estimate is a realistic goal for New Zealand but the upper estimate could be achieved only with regular inclusion of high-selenium foods.

Thirty-three New Zealand women aged 18–23 years received daily for 32 weeks, 200 μg Se as Seenriched yeast (selenomethionine), or brewer's yeast mixed with selenate, or no added Se (placebo) in a double-blind trial. Se supplementation raised (P= 0.001), platelet glutathione peroxidase (EC1.11.1.9; GSHPx) activity, and also Se and GSHPx in whole blood, erythrocytes and plasma. Selenomethionine was more effective in raising blood Se concentrations than selenate, but both were equally effective in raising GSHPx activities in whole blood, erythrocytes and plasma, indicating a similar bioavailability for the two forms. These observations and those of gel filtration studies of erythrocytes and plasma proteins reported elsewhere (Butleret al.1991) are consistent with the incorporation of Se from selenomethionine into a general tissue protein pool while selenate is directly available for GSHPx synthesis, and explain the poorer correlation between Se and GSHPx in individuals with higher Se status. However, selenate raised platelet GSHPx activities to a greater extent than did selenomethionine suggesting some other effect of selenate on platelets which needs further investigation. A response of GSHPx activity in these New Zealand subjects indicates that their dietary Se intake is insufficient to meet recommended intakes based on the criterion of saturation of GSHPx activity, and could reflect a marginal Se status. The level of blood Se necessary for saturation of GSHPx of about 100 ng Se/ml whole blood confirms observations in earlier studies.

Consumption of 2 Brazil nuts daily is as effective for increasing selenium status and enhancing GPx activity as 100 mug Se as selenomethionine. Inclusion of this high-selenium food in the diet could avoid the need for fortification or supplements to improve the selenium status of New Zealanders.

Most New Zealand soils contain relatively low concentrations of the anionic trace elements F, I and Se. Some areas of Australia also have a history of I deficiency. In view of current interest in establishing nutrient reference intakes for Se and I in New Zealand and Australia, it is timely to review current understanding of the intakes and status of these two elements. In spite of a recent increase in Se status, the status of New Zealanders remains low compared with populations of many other countries and may still be considered marginal, although the clinical consequences of the marginal Se status are unclear. There are no recent reports of blood Se levels in Australia, but earlier reports indicate that they were generally greater than those of New Zealanders. Similarly, the consequences of decreasing I status in Australia and New Zealand are unclear. Mild I deficiency in New Zealand has resulted in enlarged thyroid glands indicating an increased risk of goitre. Currently there is little evidence, however, of any associated clinical disease. Public health recommendations to reduce salt intake, together with the reduction in I content of dairy products, are likely to result in further decreases in the I status of New Zealand and Australian residents. Some action is needed to prevent this decline and it may be necessary to consider other means of fortification than iodized salt. The consequences of possible interactions between Se and I in human nutrition are also unclear and no practical recommendations can be made.