Will It Ever Be Ethical for Athletes to Edit Their Genes?

At a small dinner party in London, England, the conversation has turned to one of my current favorite topics—using genome editing to build “better” humans. With considerable rhetorical flourish, my host Brian Semmens asks, “Why wouldn’t I want to be Usain Bolt?”

Indeed, why not? Bolt is an eight-time Olympic gold medalist and eleven-time world champion. He is widely considered to be the greatest sprinter of all time. Who wouldn’t want to run in his shoes?

My host is not a spry elite athlete who is looking for a competitive edge. He is an active, retired gentleman who used to participate in several amateur sports including climbing, fencing, and sailing. Like many of his generation, he is acutely aware of age-related muscle loss and increasingly limited mobility. He does not envision using genome editing technology to repair and strengthen his aged muscles, but rather imagines the life he or his children might have had (or the life his grandchildren or great-grandchildren might have) if the use of genome editing to maximize athletic performance were proven safe and effective.

If the answer to the rhetorical question “Why wouldn’t I want to be Usain Bolt?” is some version of “Yes, of course you would!,” what follows?

For some, the answer to this question is straightforward: train your body with intensive physical and mental conditioning. Take whatever supplements you can to grow your body to a level of invincibility. This website has many resources on such supplements. This is  a reasonable response, insofar as coaching, nutrition, personal drive, determination, and emotional fortitude are key to athletic success. But if human genome editing technologies are ever proven safe and effective, it may be reasonable to ask, “Why should someone who wants to increase speed, strength, power, and stability commit to a long, arduous training schedule and eat a carefully controlled diet (including vitamins and supplements), without at the same time embracing human genome editing?” If the desired athletic characteristics and capabilities are the result of complex environmental and genetic factors, why not try to make improvements on both fronts? Indeed, why shouldn’t those who want high-performance traits use human genome editing to enhance themselves?

Julian Savulescu and his colleagues Bennett Foddy and Megan Clayton believe that most elite athletes are born with a naturally occurring, unfair genetic advantage. Think, for example, of the retired American swimmer Michael Phelps, whose unusually long, thin torso, long wingspan, size 14 feet, double-jointed elbows and ankles, and natural, atypically low levels of lactic acid production helped make him the most decorated Olympic athlete of all time with a total of 28 medals. Or, think about the muscular physique of the tennis star Serena Williams, who currently holds 23 Grand Slam titles and four Olympic gold medals. Or think about the South African Olympic gold medalist Caster Semenya, a woman middle-distance runner with natural, atypically high levels of testosterone.

Savulescu and colleagues support efforts to genetically enhance athletic performance as a legitimate way to level the playing field. “Sport discriminates against the genetically unfit. Sport is the province of the genetic elite (or freak) . . . People do well at sport as a result of the genetic lottery that happened to deal them a winning hand.” In their view, “Performance enhancement is not against the spirit of sport; it is the spirit of sport. To choose to be better is to be human.”

Among those who disagree with Savulescu and his colleagues is the World Anti-Doping Agency (WADA). It bans “the use of gene editing agents designed to alter genome sequences and/ or the transcriptional, post-transcriptional or epigenetic regulation of gene expression,” as well as “the use of normal or genetically modified cells.” While WADA’s explicit concern about gene doping in sport dates back to the early 2000s, it is only now (some 20 years later), with the prospect of genome editing, that this has become a prominent concern. The worry is that cells could be removed from an athlete, genetically modified in the lab, and then returned to the athlete. Alternatively, genome editing could be done directly in the athlete’s body. At this time, there are no known efforts to improve athletic performance using human genome editing, but such efforts are anticipated.

Meanwhile, there are some coaches who already use genetic testing to improve athletic performance: to determine an athlete’s muscular endurance, muscular power, risk of injury, and metabolism. They then use this information to optimize that athlete’s training. Another use of genetic testing in sport is to identify talent based on genetic profile. A few companies claim that they can provide parents of young children with genetic information to help them choose sports at which their children may naturally excel.

Some years ago, one mother, Lori Lacy, suggested that this kind of genetic testing was inevitable, not necessarily because of any purported benefits, but because of peer pressure: “Parents will start to say, ‘I know one mom who’s doing the test on her son, so maybe we should do the test too . . .’ Peer pressure and curiosity would send people over the edge. What if my son could be a pro football player and I don’t know it?”

This marketing of genetic testing to parents is important because it begins the process of normalizing a role for genetic manipulation in sport.

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Athletic performance may be affected by as many as two hundred genes. Nonetheless, advocates of genome enhancement in sport are hopeful. One gene of interest is the MSTN gene that codes for the protein myostatin. Myostatin is a negative regulator of muscle growth. It acts like a brake on the production of muscle tissue so that the size and number of muscle cells stay within a certain range and the muscles don’t grow too big. When human or non-human animals have a faulty copy of the MSTN gene, the brakes are off. The muscle cells increase in size and number, and there is a gain in muscle mass.

This explains, for example, the naturally occurring increased muscle mass of the Belgian Blue and Piedmontese cattle breeds—which have what is known as “double muscling.” It also explains a natural variation among classes of whippets. In 2007, Dana Mosher and her colleagues reported that whippets with one normal and one faulty copy of the MSTN gene were the fastest of their breed. They had extra muscle (because of the one faulty copy of the MSTN gene), but they were not weighed down with too much muscle mass (because of the one normal copy of the MSTN gene).

Naturally occurring excessive muscling has also been observed in some humans. The first case recorded in 2000 was publicly reported in 2004. In humans, this muscle enlargement is a rare genetic condition called myostatin-related muscle hypertrophy. There are also anecdotal reports that some genetically gifted athletes, like champion bodybuilders, have naturally low levels of myostatin or deletions of the MSTN gene. These individuals are said to have as much as 50 percent more muscle mass and strength than the average person. Knowledge about the effects of myostatin on muscle growth have inspired some scientists to tinker with the MSTN gene. The earliest successful effort dates back to 1997, when Alexandra McPherron and her colleagues Ann Lawler and Se-Jin Lee produced “mighty mice” by disrupting the MSTN gene. These mice were stronger and more muscular than average mice. Since then, scientists have put their knowledge of myostatin to use in creating genome-edited farm animals and pets, including extra-muscular cows, sheep, goats, pigs, rabbits, and dogs.

These creations have had some problems, however, including in some instances a reduced lifespan. More recently, it has been reported that scientists have begun experimenting with genome editing in cloned horse embryos as part of an effort to design faster runners and better jumpers. Given these research efforts in non-human animals, it is reasonable to ask,“When will scientists try modifying the MSTN gene in humans to increase athletic performance?” Here it is perhaps worth remembering the self-experimentation by Josiah Zayner at the 2017 SynBioBeta conference, when he injected the CRISPR genome editing technology into himself to delete the MSTN gene in an attempt to grow bigger muscles in his forearm.

One hope for humans is that inactivating one copy of the MSTN gene would make for better sprinters. Studies in mice suggest otherwise, but that hasn’t dampened enthusiasm for the idea of genetically enhancing human athletic performance by manipulating that gene. Another thought is to make better bodybuilders and weight lifters by inactivating both copies of the MSTN gene.

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Many who debate the ethics of human genome editing fixate on the presumed distinction between treatment and enhancement—the difference, for example, between modifying the MSTN gene to treat muscular dystrophies versus modifying this same gene to improve athletic performance. They suggest that genome editing would be morally acceptable in the first case, but not in the second case, because of the difference in intent.

The professed distinction between treatment and enhancement is unhelpful, however. Descriptively all treatments are enhancements in the sense that all treatments aim to improve an individual by correcting an actual or perceived deficiency in relation to “normal” abilities (sometimes described as “normal species functioning” or “species-typical functioning”). As such, all human genome editing is a form of enhancement; it is just that some of the enhancements will be health-related and others not. And among those enhancements that are health-related, some will aim to “treat,” while others will aim to “prevent.”

The distinction between treatment and enhancement not only fails as a descriptive demarcation line, it also fails as a moral demarcation line. Consider, for example, somatic cell human genome editing to increase the height of young boys who are shorter than their peers. A young boy might be shorter because of a hormonal deficiency, or because his biological parents are short and thus he is genetically coded to be short. While some would describe human genome editing as an ethically acceptable treatment when used to correct a hormone deficiency, and an ethically unacceptable (or questionable) enhancement when used to correct inherited short stature, this categorization can be contested.

For example, it can be argued that both cases involve treatment, the goal being to improve health. In the first case, the treatment would be for a hormonal deficiency that not only affects height, but also is associated with various physiological abnormalities. In the second case—consistent with the World Health Organization definition of health as “a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity”—the treatment would be to improve mental health and well-being. Boys and girls with extreme shortness endure teasing and bullying; later in life, they may also experience height discrimination. These experiences have a negative effect on self-esteem that, in turn, interferes with psychological health and well-being.

Yet one could just as reasonably argue that both cases involve enhancement. The common goal is to increase height to within the range of “normal” for the community of belonging and thereby to reduce (if not eliminate) the social and psychological disadvantages commonly associated with short stature. From this perspective, both cases are ethically acceptable or unacceptable in equal measure.

In sharp contrast, it could reasonably be argued that efforts to use human genome editing to provide persons who are already at the tall end of the spectrum for height (or even within the range of “normal” height) with a few more inches so that they might outperform on the basketball court would be an ethically questionable (if not ethically unacceptable) form of enhancement. What matters ethically in this case is not that the planned genetic intervention can easily be categorized as a non-health-related enhancement, but that the intervention is likely to decrease equality, access, and fairness.

Consider next a different hypothetical scenario involving heritable genome enhancement where the goal is to increase equality, access, and fairness. An African-American couple, firm in the belief that they have an ethical obligation to give their children “the best life“  possible, decide they should use heritable genome editing to modify their future children’s skin color. They believe that white skin is desirable and black skin is undesirable, not for aesthetic reasons, but because of ongoing racism. They are also convinced that changing their children’s skin color will increase their children’s quality of life—for example, by giving them better access to educational and employment opportunities. Beyond this, given the high risk of death in the United States among young black men, they imagine this germline genetic modification might even increase the life expectancy of their male children.

Given the prevailing “system of attitudes and actions that are in fact unjust,” would it be ethically acceptable (or even obligatory) for these prospective parents to modify otherwise healthy embryos so that their children might not experience racism and might live longer?

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Francoise Baylis’ Altered Inheritance: CRISPR and the Ethics of Human Genome Editing is out now from Harvard University Press.