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LETTER TO THE EDITOR |
Institute of Nutrition and Food Hygiene
Chinese Academy of Preventive Medicine
Beijing 100050
China
Anti-Epidemic Station of Mianning
Sichuan Province
China
Department of Biostatistics
Vanderbilt University School of Medicine
Nashville, TN
1030C Medical Research Building IV
Division of Gastroenterology, Hepatology, and Nutrition
Department of Medicine
Vanderbilt University School of Medicine
Nashville, TN 37232-0252 E-mail: raymond.burk{at}vanderbilt.edu
Dear Sir:
Wang raises the issue of which criteria should be used to determine the selenium requirement and argues that selenoprotein P might not be the best biomarker for this assessment. Considerable controversy exists over the selenium intake needed for optimal health, as indicated by Wang, and a framework for discussion of this topic is needed.
Many years ago, Keshan disease was shown by Chinese investigators to be a disease that required selenium deficiency for its occurrence (1). It was not reported from locations where selenium intakes were 
17 µg/d (2). Assertions have been made that other pathological conditions are related to selenium deficiency, but, so far, evidence for this remains circumstantial. Thus, available evidence supports the hypothesis that a selenium intake 
20 µg/d is required to prevent Keshan disease, the only known selenium-deficiency disease.
Inferences that much higher selenium intakes protect against cardiovascular disease and cancer have been drawn from results of epidemiologic studies. Intervention trials are needed (and some are underway) to assess these claims and to determine whether these high-selenium supplements are safe (3). This is an area of research that is active and important. At present, however, the data available are largely observational and do not allow firm recommendations for selenium intake.
Our study addressed the use of selenium biomarkers to assess selenium nutritional status (4). It is generally accepted that selenium exerts its biological actions through selenoproteins. Selenoproteins subserve many biochemical functions and are essential for life. As Wang points out, a hierarchy of the selenoproteins exists, and some are maintained better than others as the selenium supply diminishes (5). It appears that the selenoproteins most essential for life have higher positions in the hierarchy than do those that are less essential. Thus, the ideal biomarker by which to assess full expression of all selenoproteins would be the selenoprotein with the lowest position in the hierarchy. In studies conducted in rats, liver glutathione peroxidase appears to occupy the lowest position in the hierarchy and is therefore the ideal biomarker in that species (6).
Only a few selenoproteins are easily accessible for measurement in humans, and liver glutathione peroxidase is not among them. Plasma (or serum) contains 2 selenoproteins—glutathione peroxidase 3 and selenoprotein P—that are readily accessible and easy to measure, and that is why we compared those 2 selenoproteins. Our study showed that selenoprotein P was lower in the hierarchy of selenoproteins than was plasma glutathione peroxidase. Therefore, we concluded that selenoprotein P was a better biomarker for whole-body selenoprotein expression than was plasma glutathione peroxidase.
Two approaches are being used to determine the selenium nutritional requirement. One approach is disease-related and will require intervention trials to determine the selenium intake needed to prevent pathological conditions and ensure optimal health. At present, this approach supports an intake of 20 µg selenium/d to protect against Keshan disease. Intervention trials are being carried out to determine the effect of higher selenium supplements, and they may lead to an increase in this recommendation.
The second approach is the use of biomarkers for selenoproteins to assess the full expression of selenoproteins in the body. This approach was used in 2000 by the Institute of Medicine to support a dietary reference intake of 55 µg selenium/d, which is based on plasma glutathione peroxidase activity (7). The same glutathione peroxidase results were used by a Chinese panel to set a dietary reference intake of 50 µg selenium/d (8). When adequate data on optimization of selenoprotein P by selenium intake are available, the current recommendations will likely require an upward revision.
ACKNOWLEDGMENTS
None of the authors had any conflict of interest.
REFERENCES
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