That an Olympic champion possesses a unique set of genes may seem only natural. But it’s scant consolation for the losers in the rarefied world of high-performance sport, where nature is often regarded as an obstacle to be overcome. And increasingly the natural advantage held by people like Mäntyranta is being imitated in laboratories around the world. The genetically engineered athlete, long an imagined creature, is slowly starting to emerge. Such athletes may already be here, and the sporting world appears ready to embrace them. Witness the experiment conducted by Dr. Lee Sweeney, a physiologist at the University of Pennsylvania, who started working on a cure for muscular dystrophy in the late 1990s. To reverse the disease’s muscle-wasting effects, he injected the gene that tells the body to grow new muscles into a single leg of his lab rats and put them on a weight-training regimen. Soon each rat had one leg that was nearly twice as big as the other.
When word of Sweeney’s rats spread in 2003, athletes, undeterred by the experimental nature of the science, came forward asking to serve as guinea pigs, leading Sweeney to predict that the superhuman of fiction was about to step onto the playing field. “The world,” he warned two months prior to the Athens Olympics in 2004, “may be about to watch one of its last Olympic Games without genetically enhanced athletes.”
Sweeney’s experiments are still being talked about in training camps around the world because of the relative ease with which he boosted the size of the leg muscles in his lab rats. He had injected them with the gene that triggers production of the insulin-like growth factor, igf-i. Before injecting it, Sweeney attached the gene to a harmless virus capable of moving through cell walls to deliver the gene to the targeted muscles. In effect, Sweeney gave the rats a genetic infection that took hold, producing a group of super-rats.
Now imagine the gruelling thirtykilometre cross-country ski race at the Turin Olympics. The winner, moving on genetically enhanced legs, wins by a wide margin, but a subsequent drug test fails to turn up any trace of a steroid or other performance-enhancing drug. wada officials, clearly concerned that such an incident could become a reality, are spending more than $4 million to develop a test for gene doping and have assembled a panel of eminent geneticists to oversee the project. Sweeney joined the panel, but he admitted that it may be difficult to catch gene-doped athletes. “If we [geneticists] do our jobs properly,” he said, “it [gene doping] will be impossible to detect.”
Pound’s attempt to stamp out gene doping at the Olympics will likely prove futile because for each medical breakthrough in gene therapy there seems to be an athletic application. Genetic science may soon advance beyond changing musculature and bloodoxygen levels to altering everything from limb proportion and heart size. Consider Lance Armstrong, the seventime winner of the Tour de France, whose heart is 30 percent larger than the average human’s and who produces one-third the usual amount of lactic acid under exertion, enabling his muscles to absorb oxygen at an extraordinary rate. Or the size seventeen feet of Australian Olympic swimmer Ian Thorpe, which act like flippers in the pool.
While athletes can’t train for genetic advantages, medical science may soon be able to create them. “You can deliver the [gene] to neonatal animals or in utero,” says Dr. Jeffrey Medin, a biochemist who runs a gene-therapy lab at the Ontario Cancer Institute in Toronto. “As the animal ages, that [gene] gets distributed very nicely. If you wanted to provide long-term gene doping, that would be the time to start.”
There are currently 1,100 human case studies chronicling the medical use of gene therapy. The first clinical trial was held in 1989 at the National Institute of Health in Bethesda, Maryland, and the first major success came in 2000 when eleven boys suffering from Severe Combined Immunodeficiency ( “bubble boy” disease ) underwent gene therapy at the Necker Children’s Hospital in Paris. This illness occurs when the body fails to produce a protein called interleukin-2, a critical component of the body’s immune-response system. In an experiment similar to Sweeney’s, the eleven children at Necker were injected with the interleukin-2 gene. The gene caught hold in nine of them and restored their immune systems to the point where they were able to lead almost normal lives.
When three of the nine children subsequently developed leukemia (one later died) the French government temporarily suspended all similar gene therapy trials. In the United States, the Food and Drug Administration had already shut down human trials at a gene therapy lab when a young man in treatment for a liver disorder died after his immune system failed. But despite the setbacks, gene therapy has produced far more successes than failures. “Gene therapy really hasn’t had that many negative effects,” notes Medin. “You look at bone-marrow- transplant patients in the 1970s, and until they figured it out everybody died. Here, we’ve had two or three patients out of 1,100 that have had severe consequences. If you’re looking at a new cancer drug, that’s an acceptable risk for a lot of people.”







Comments