One of the most potentially damaging drugs to hit the racetrack in recent years is erythropoietin, or EPO. A synthetic version of a naturally-occurring hormone which stimulates the bone marrow to make more red blood cells, EPO was designed to treat anemia in human chemotherapy patients, and those with severe renal disease.  It was considered a medical breakthrough when it was introduced in the 1980’s, and is still a valuable part of the drug arsenal for these conditions, with sales in the billions of dollars in 2002.

Unfortunately it wasn’t long before human athletes noticed the potential of EPO for performance enhancement. Cyclists, swimmers, and long-distance runners reasoned that more oxygen in the tissues meant more endurance–and the results bore them out, with an estimated 10-15% performance boost. But EPO administered to a human athlete prompts the release of so many red blood cells (RBCs) that the blood becomes thick and sludgy (a condition called polycythemia), and that may set athletes up for blood clots, strokes, and heart attacks. It’s estimated that EPO was a factor in the deaths of at least 15 European cyclists in the 1980s and 90s, and EPO scandals have plagued the Tour de France bicycle race and several Olympic events in the past decade or so.

In theory, EPO ought to work as a performance-enhancer in horses for the same reasons it does so in human athletes, but there’s some debate as to whether the drug actually functions this way in equines. Because horses are "natural blood dopers," with spleens that have the unique ability to dump up to 12 liters of extra RBCs into the bloodstream at times of stress, how much EPO might increase–or over-ride–their natural splenic contraction is a major question mark.

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