ABSTRACT
The trace element selenium (Se) appeared relatively late on the nutrition-health agenda. It was first reported in the 1930s to be the toxic principle involved in “blind staggers,” a neurological condition of horses and cattle grazing on seleniferous plants in the American Northern Plains (Franke, 1934a,b). It was not until the late 1950s that Se was found to prevent disorders of vitamin E deficiency (Schwarz and Foltz, 1957; Schwarz et al., 1957). This made Se the last nutrient to have been recognized as a dietary essential. Accordingly, the roles of Se in biology and health have been researched for less time than any other essential nutrient. Initial investigations of Se in animal nutrition spawned studies of its metabolic mechanisms starting in the 1960s. Then, suggestion that Se may have a role in cancer prevention (Shamberger and Frost, 1969; Shamberger and Willis, 1971) led to studies with a variety of tumor models starting in the late 1960s and, ultimately, to human clinical trials starting in the 1980s. This body of work addressed a sequence of central research questions. The resulting answers served, after the manner of scientific inquiry, to provoke additional questions. Accordingly, questions remain, the major one being who can benefit from increased Se intake? To address that, it is necessary to consider the answers to the progression of scientific questions that have led to it.
