Abstract

Cobalt, atomic weight 58.9, is a metallic element and environmental substance found in the animal in microgram quantities, predominantly as vitamin B12, but is also a component of at least one mammalian enzyme unassociated with B12. Cobalt is a required trace mineral and has long been administered as a dietary supplement to humans and animals. Cobalt deficiency outside of its requirement in vitamin B12 has not been reported in humans. The administration of cobalt salts was once standard treatment for anaemia in humans, owing to its ability to stimulate red blood cell synthesis. Elemental cobalt acts by stabilising hypoxia inducible factor (HIF-1α), which activates the erythropoietin gene, which in turn increases haemoglobin/red blood cell synthesis, which had led to a presumption that cobalt may be performance enhancing in athletes. Administration of cobalt in amounts sufficient to significantly increase the haematocrit are associated with risk of toxicity in humans, and the only cobalt administration study in horses showed no effect on red blood cell parameters or toxicity. Because of the perception that cobalt administration may enhance athletic performance, racing regulators have recently begun to restrict cobalt use in horseracing which has led to the introduction of cobalt thresholds in several racing jurisdictions. The International Federation of Horseracing Authorities is considering an international regulatory threshold for cobalt of 100 ng/ml in urine, based on studies performed in five different countries. In the United States, the Racing Commissioners International has recently set a primary plasma threshold of 25 ng/ml and secondary threshold of 50 ng/ml. One New York and New Jersey racetrack owner has initiated testing for cobalt and has denied his facilities to trainers whose horses tested positive for excessive quantities of cobalt. This review seeks to summarise what is known about the use of cobalt in horse racing.

Document Type

Article

Publication Date

2016

Related Content

Published as paper # 419 from the Equine Pharmacology, Therapeutics and Toxicology Program at the Maxwell H. Gluck Equine Research Center and Department of Veterinary Science, University of Kentucky. The information reported in this paper is part of a project of the Kentucky Agricultural Experiment Station (Experiment Station Publication # 14-14-050) and is published with the approval of the Director. This work was made possible by research support from the United States Trotting Association, the National Horsemen’s Benevolent and Protective Association and the Alabama, Arizona, Arkansas, Canada, Charles Town (West Virginia), Florida, Iowa, Indiana, Kentucky, Louisiana, Michigan, Minnesota, Nebraska, Ohio, Oklahoma, Ontario (Canada), Oregon, Pennsylvania, Tampa Bay Downs (Florida), Texas, Washington State, and West Virginia Horsemen’s Benevolent and Protective Associations and the Florida Horsemen’s Charitable Foundation, the Oklahoma Quarter Horse Racing Association and Neogen Corporation.

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