Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
The threat of gene transfer technology to elite sport
The International Olympic Committee (IOC) recently released its new list of banned substances and methods. This list will be effective from 1 January 2003 and replaces the 1 September 2001 list. Amongst the important changes, the category of genetic doping as a banned method is listed for the first time. The current list can be easily accessed on both the IOC and World Anti-Doping Agency (WADA) websites (www.wada-ama.org or www.olympic.org)
The use of gene doping or gene transfer technology to improve athletic performance heralds a significant threat to the integrity of anti-doping initiatives. This approach has the potential to improve sporting performance far beyond “traditional” pharmacological means and in ways that make detection of use extremely difficult if not impossible at the present time. It sounds like the ultimate sporting nightmare come true.
There is also another side to gene transfer technology which is a more difficult ethical issue, namely the use of gene mapping in talent identification and the use of tissue engineering in the recovery from injury, such as muscle atrophy following cruciate ligament injury. Once such gene therapy is clinically available then can we deny its benefits to athletes?
HOW MAY GENE DOPING BE USED?
We have known for decades that genetic differences between athletes can result in markedly improved performance.1 At the 1964 Winter Olympics in Innsbruck, a Finnish competitor Eero Mäntyranta, won two gold medals in cross country skiing. Though his training programme wasn’t radically different from his rivals, Mäntyranta had a distinct advantage. He was born with a genetic mutation that increased the oxygen carrying capacity of his red blood cells by 25–50%. Mäntyranta had a mutation in the gene coding for the erythropoeitin (EPO) receptor which prevented the normal feedback control of red blood cell mass.2 This …