100: Selenium

HISTORY AND EPIDEMIOLOGY

Selenium was discovered by Jöns Berzelius in 1817 as a contaminant in sulfuric acid vats that caused illness in Swedish factory workers. He originally believed it to be the element tellurium (from the Latin tellus, meaning “earth”); however, on finding it to be an entirely new, yet similar, element, he named it from the Greek selene, meaning “moon.” Selenium has unusual light-sensitive electrical conductive properties, leading to its widespread use in industry. The long-term health benefits and risks of selenium are the subject of much recent investigation. It is both an essential component of the human diet and a poison.

In the 1970s, the role of selenium as an essential cofactor of the enzyme glutathione peroxidase was discovered. Keshan disease, an endemic cardiomyopathy, was described in 1979 in Chinese women and children who chronically consumed a selenium-poor diet.¹¹ Kashin-Beck disease, a disease causing shortened stature from chondrocyte necrosis, is described in young children in Russia, China, and Korea; although other etiologies are also likely responsible, partial improvement results from selenium supplementation.^3,18 Selenium is currently being investigated for the prevention and treatment of a myriad of conditions, including autoimmune thyroiditis, cancer, Alzheimer disease, depression, and tropical leishmaniasis.³⁸­However, it is becoming more evident that “the moon” has two faces, as reports emerge that selenium supplementation may increase the risk of diabetes, amyotrophic lateral sclerosis, and some forms of malignancy.^20,46

The recommended daily allowance (RDA) in the United States of selenium for adults was established in 1980 at 55 μg/d. This was determined based on the degree of supplementation required to achieve optimal glutathione peroxidase activity in selenium-deficient study populations, and the amounts required to cause overt toxicity. Deficiency occurs when daily intake falls below 20 μg/d.¹¹

Chronic selenium toxicity, or selenosis, was first described in animals. It manifested as the acute syndrome of “blind staggers,” and the more chronic “alkali disease” affected livestock eating plants grown in highly seleniferous soil. Findings included blindness, walking in circles, anorexia, weight loss, ataxia, and dystrophic hooves. Humans in seleniferous areas of China and Venezuela develop similar integumentary symptoms (dermatitis, hair loss, and nail changes) at an intake of approximately 6000 μg/d.^5,41 In recent years, there have been several outbreaks of chronic selenium toxicity related to improperly formulated dietary supplements.^7,14,47

Selenium is widely distributed throughout the Earth’s crust, usually substituting for sulfur in sulfide ores such as marcasite (FeS₂), arsenopyrite (FeAsS), and chalcopyrite (CuFeS₂). It is found in the soil where it has leeched from bedrock, in groundwater, and in volcanic gas. The highest soil concentrations of selenium in the United States are in the Midwest and the West, specifically areas of the Dakotas, Wyoming, Nebraska, Kansas, Utah, Colorado, Arizona, and New Mexico.³ Dietary selenium ...