Extreme Exercise May Increase MND Risk in Genetically Vulnerable Athletes

Lewis Moody, the former England rugby captain known for his relentless pursuit and fearless play, revealed this week that he has been diagnosed with motor neurone disease. At 47, he is more than a decade younger than the typical person who receives this diagnosis. When he told his two sons—Dylan, 17, and Ethan, 15—about the news, he described it as the hardest thing he had ever done. "There's something about looking the future in the face and not wanting to really process that at the minute," he told the BBC, acknowledging both his understanding of where the disease leads and his reluctance to fully confront it.

Moody is not alone. In recent years, rugby has seen a cluster of similar diagnoses: Ed Slater of Gloucester, Doddie Weir of Scotland, and Rob Burrow of rugby league have all spoken publicly about their own MND diagnoses, with Weir and Burrow since deceased. Beyond MND itself, the toll of contact sport has become harder to ignore. Alix Popham, a former Wales international, and Steve Thompson, an England World Cup winner, have both been diagnosed with early-onset dementia linked to repetitive head injury. These cases have raised an uncomfortable question that has shadowed elite sport for years: could the physical extremes demanded by professional athletics carry a hidden neurological price?

Motor neurone disease is relatively rare, typically striking people over 50, with an average diagnosis age between 60 and 67. The condition begins subtly—stiff or weak hands, legs, or feet; twitches, spasms, or muscle cramps. It is progressive, and the specific subtype determines how quickly it advances. Moody has amyotrophic lateral sclerosis, or ALS, one of the most severe forms. Around 5,000 adults in the UK have MND at any given time. Researchers believe it stems from a combination of genetic factors (affecting about 20 percent of those diagnosed), environmental influences, and lifestyle choices. Understanding exactly which factors matter and why has become the work of scientists like Dr. Johnathan Cooper-Knock, a neurologist and geneticist at the University of Sheffield.

For years, suggesting a link between extreme sport and neurological disease was considered controversial. But over the past decade, Cooper-Knock's team, working alongside Professor Pam Shaw's internationally recognized MND research group, has uncovered something subtle but significant: extreme exercise can increase the risk of MND diagnosis, but only in a small subset of people with particular genetic profiles. "A lot of very athletic people were coming into clinic with motor neurone disease," Cooper-Knock explains. Initially, researchers wondered if this reflected survival bias—that fit people simply avoided cardiovascular disease and therefore were more likely to develop MND instead. The data, however, told a different story.

Cooper-Knock describes the mechanism using an analogy: every motor neurone in the body has a genetic safety brake designed to protect it. In some people, that brake is turned off. This genetic difference might allow them to perform at extraordinary levels of endurance and excel in sport. But it also means that each time they exercise, their system operates in a vulnerable state, without protection. Over years, this unguarded state might push certain neurons past their breaking point. A study of the Vasaloppet, a cross-country ski race in Sweden, found that participants in the top 5 percent—the most extreme exercisers—had roughly four times the background risk of developing MND. For everyone else in the race, the risk was actually lower than average. "It's that top sliver of intensity where we see something happening," Cooper-Knock says. "And even then, it's rare."

Understanding why this matters requires knowing what motor neurons do. According to Dr. Nick Cole, head of research for the MND Association, they function like electrical cables, carrying signals from the brain down the spinal cord to the muscles. When those cells die in MND—and unlike other tissues, they do not regenerate—the signal fails. Muscles waste away. Speech, swallowing, movement, and eventually breathing become impossible. The mind remains intact. "You become trapped in a failing body," Cole says. "It's devastating. It's also one of the biggest scientific puzzles of our time."

New research is beginning to illuminate the pathway. Last year, Professor Paul Chazot and his team at Durham University published findings from the UK Rugby Health Study, which examined the biological aftermath of concussion in professional rugby players. They sampled blood from players up to eight years after retirement and found something striking: those with a history of multiple concussions carried distinct patterns of proteins in their blood—the same proteins seen in people with brain diseases like MND. None had been diagnosed with neurological conditions, but the molecular changes suggested something subtle and long-lasting was happening inside the brain, long before symptoms appeared. Chazot's team believes this may involve damage to the brain-body barrier, the delicate protective membrane separating the brain's internal environment from the rest of the body. Even impacts that fall short of a full concussion, if repeated, could compromise this barrier and allow rogue proteins to leak in. "We think these biomarkers could be early indicators of trouble ahead," Chazot explains. "The hope is that by identifying these changes early, we can intervene before lasting damage takes hold."

There is genuine momentum in the research. More clinical trials are underway than at any point in Cooper-Knock's career. One recent breakthrough is a therapy for patients with SOD1 mutations that works by silencing the faulty gene and halting production of toxic protein—currently applicable to 1-2 percent of patients, but a solid foundation for developing treatments for the remaining 98 percent. Chazot's team has also been experimenting with red-light therapy for the past two decades, using near-infrared light on the gut and brain to target mitochondria and boost cell energy while reducing inflammation. Early clinical studies and case trials have shown patients with severe MND forms experiencing stabilization or even modest symptom improvement. "We're seeing encouraging effects in a number of people, though not everyone," Chazot says. The therapy has been used in Australia and the US with positive anecdotal results, though many neurologists say larger, blinded trials are needed before full endorsement. Chazot is pushing for exactly that: a major, multi-center study to test whether red-light treatment can genuinely slow or modify disease progression. "It's not a cure," he stresses, "but if we can buy people meaningful time, preserve their function, that's huge."

Everyone in the field agrees on one thing: awareness matters. Since the ice bucket challenge of the mid-2010s, public understanding has improved, and the last five years have seen an unprecedented surge of funding and interest. More is still needed. "MND is curable," Dr. Cole says flatly. "We just have to fund it long enough to find the cure." As Moody joins the growing line of athletes turned advocates—Weir, Burrow, Slater, and now him—each diagnosis underlines the urgency of a question that still looms over sport: how much do our games demand, and how do we mitigate that cost? Together, they are forcing science and sport alike to look harder and move faster toward a world where MND is no longer a life sentence.