Animal research showed that selenium (Se) was a dietary trace nutrient that would protect against disease, and that it often interacted with vitamin E in this protection. Studies reporting that Se was toxic and could cause cancer in animal models, however, prevented direct Se supplementation of animal feeds, and prevented recommendations for human diets. The key for Se’s emergence from the pool of other potentially essential trace elements was the discovery by John Rotruck and William Hoekstra of a biochemical role for Se as a cofactor in glutathione peroxidase (Gpx). Gpx activity falls in Se deficiency and rises to a plateau with Se supplementation, demonstrating that Gpx was an effective biomarker for Se deficiency, and supported dietary recommendations. There remain 8 or so potentially essential trace elements for higher animals that have been shown to result in abnormalities when lacking in the diet. It is very likely that future research will discover functional roles for the elements in humans as these elements are recognized by other living organisms for specific transport or incorporation into proteins or metalospecies. The identity of these processes in higher animals, and the challenge of finding good biomarkers for excess nutrient intake will provide ample opportunity for future trace element research.
Roger A. Sunde (Mon,) studied this question.