About the Author

Anthony Roberts holds a BA in both English and Philosophy, is the author of Anabolic Steroids: Ultimate Research Guide and Beyond Steroids, and is a staff writer for Muscle Evolution and a contributor to Muscle Insider. He’s a certified trainer and coach as well as having worked as a formulator in the nutritional industry. He is a member in good standing of the Society for Professional Journalists.

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Cobalt Chloride for increasing EPO

by: Anthony Roberts

Cobalt Chloride is currently available without a prescription, is untested for, not banned or illegal, and increases EPO (erythropoietin) as effectively as many prescription/banned/illegal alternatives. As you probably surmised by the name, it presents as a dark blue substance, although it reacts chemically with water (and other liquids) to change its appearance. If you ever had an "invisible ink" spy kit as a child (or adult, I suppose), you're probably familiar with the stuff already.

Cobalt is a constituent of vitamin B-12, and as a result, there is no RDA for it - but we'd be talking microgram amounts if we were discussing how much you could expect to find in your diet. Generally, you're not going to find the stuff listed on any multivitamins, and you'd be talking to a chemical supply house if you were trying to get your hands on it.

Cobalt also has another property which has gone relatively unnoticed by athletes: it increases EPO when taken orally. This ought to be somewhat obvious, as it has been used to treat certain types of anemia, which is characterized by a lowered red blood cell count. Here's how it works:

Hypoxia Inducible Factor and the HIF pathway are responsible for the expression of a variety of physiological responses to oxygen deprivation and conditions of lowered oxygen intake - similar to what would be seen with altitude training, which itself relies on adaptations mediated by this pathway to stimulate an increase in endogenous EPO and red blood cells.

Typically, the mediator of HIF undergoes rapid degredation under conditions of adequate oxygen intake. However, in an oxygen-deprived environment, it remains active for much longer and sets off a sequence of events that (among other benefits) activates the gene for producing EPO that promote efficient adaptation to hypoxia. Cobalt chloride appears to mimic the oxygen-deprived state at the genomic level, thereby causing the HIF mediator to remain stable enough to initiate increased EPO production.

In a rodent study published in 1947, a daily subcutaneous injection of 2.5 mg/kg of body weight, over 6 weeks, produced a 30% increase in the number of red blood cells and  hemoglobin. To mimic that effect orally, the scientists needed to bump the dose to 40 mg/kg (a dose that when administered subcutaneously resulted in death by day eight).(1)

However, a study published a few years later, by the same scientists in 1954, has suggested that polycythemia (an increase in the proportion of red blood cells) of up to 20% can be realized with a mere 120-150mgs/day. (2)

In terms of detection time, there is no current test for "cobalt doping" although we can reasonably expect that it would be a difficult one to engineer. Cobalt displays an absorptive half-life of 0.9 hrs, with an elimination phase half-life of 3.9 hrs and a terminal elimination half-life of 22.9 hrs. (3)

So it appears that Cobalt is an effective way to produce effects similar to EPO - a huge boost for endurance athletes or anyone needing increased stamina. Unfortunately, while it is legal and widely available, I don't know anyone who's experimented with it, and I'm hesitant to fully trust research from half a century ago.

Proc Soc Exp Biol Med. 1947 Oct;66(1):19.
Cobalt polycythemia relative effects of oral and subcutaneous administration of cobaltous chloride.

Am J Clin Pathol. 1954 Dec;24(12):1374-80.
Polycythemia induced by cobalt. III. Histologic studies with evaluation of toxicity of cobaltous chloride.

Ayala-Fierro F, Firriolo JM, Carter DE. Disposition, toxicity, and intestinal absorption of cobaltous chloride in male Fischer 344 rats. J Toxicol Environ Health A. 1999;56:571–591. doi: 10.1080/009841099157908.