By Zoë Beaty
Copyright independent
When Lewis Moody revealed this week that he had been diagnosed with motor neurone disease (MND), the reaction was instant, and visceral. Within hours, tributes flooded in for the former England captain once known as “Mad Dog” – a player revered for his fearlessness, humour and tireless chase. Columnists called him “the most determined kick-chaser” and “the noblest of gundogs”. Headlines described a man built for power now confronting a condition that slowly steals it away. Messages of solidarity poured in – all threaded with disbelief that yet another figure from Britain’s sporting elite had been struck by this devastating disease.
At just 47, Moody is more than a decade younger than the average person diagnosed with MND; he was “overcome with emotion” when he spoke about telling his sons – 17-year-old Dylan and 15-year-old Ethan – the news. “It was the hardest thing I’ve ever had to do,” he told reporters. “There’s something about looking the future in the face and not wanting to really process that at the minute,” Moody told the BBC on Monday. “It’s not that I don’t understand where it’s going. We understand that. But there is absolutely a reluctance to look the future in the face for now,” he admitted.
Heartbreakingly, rugby has seen this story play out before. Scotland’s Doddie Weir, England’s Rob Burrow and Gloucester’s Ed Slater (the first two sadly no longer with us) have all spoken about their own MND diagnoses in recent years, turning their grief into campaigns for awareness and research funding. Beyond MND itself, the toll of contact sport itself is becoming more difficult to ignore: former Wales international star Alix Popham and England World Cup winner Steve Thompson have both been diagnosed with early-onset dementia linked to repetitive head injury, while other athletes have faced diagnoses of Parkinson’s and related neurological decline. Moody’s latest diagnosis adds weight to an uneasy – and difficult to answer – question that has haunted elite sport for years: could the physical extremes demanded come with a hidden price?
MND is a relatively rare condition, most common in people over 50 – the average age for a diagnosis is 60-67. It’s not easy to spot or diagnose at first – sufferers may find they have stiff or weak hands, legs or feet, or begin to experience twitches, spasms or muscle cramps. It’s a progressive disease that is often separated into subtypes but symptoms frequently overlap.
Very loosely, the subtype diagnosed will determine the prognosis given. Amyotrophic lateral sclerosis (ALS) – the type Lewis Moody is suffering with – is one of the most severe, along with progressive bulbar palsy (PBP), which primarily affects the muscles controlling speech and swallowing, both of which have a more rapid progression than subtypes like primary lateral sclerosis (PLS) and progressive muscular atrophy (PMA).
Around 5,000 adults in the UK have the disease at any one time and it’s thought to be caused by a combination of genetics (affecting 20 per cent of those diagnosed), environmental and lifestyle factors. Identifying exactly what those factors are, and why they might contribute to the onset of MND, is the endeavour of researchers like Dr Johnathan Cooper-Knock.
Cooper-Knock, a neurologist and geneticist based at the University of Sheffield, has spent much of his career studying these missed connections. For a long time, drawing correlations between extreme sport and neurological conditions was considered controversial. But multiple studies have now begun to map the link between the two – something that Cooper-Knock spotted first hand.
“A lot of very athletic people were coming into clinic with motor neurone disease,” he tells me. “For a long time we wondered if it was just survival bias – that if you’re very fit and healthy, you don’t get cardiovascular disease, therefore you’re more likely to end up with motor neurone disease.” But the data started to tell a different story.
Over the last decade, his team – alongside Professor Pam Shaw’s internationally renowned MND group – has uncovered a subtle but important truth: that extreme exercise can increase the chance of being diagnosed with MND, but – crucially – only in a small subset of people with certain genetic make-ups.
“For the majority of us,” he stresses, “exercise is profoundly good – even protective. But for a few, those who push their bodies to molecular limits, something about the way their motor neurons fire might make them vulnerable.”
To better understand how it works, Cooper-Knock says, it’s useful to imagine that every motor neuron in our bodies has a safety brake to protect it – but in some people, the brake is genetically turned off. Having the brake off might mean that they’re able, then, to perform extraordinary levels of endurance and excel in sport. “But it also means that each time they exercise, their system is running in a vulnerable state, without protection,” he says. “Over years, that might tip certain neurons over the edge.”
He cites a study – the Vasaloppet cross-country ski race in Sweden – that found participants in the top five per cent (or the most extreme exercisers) had roughly four times the background risk of developing MND. As for everyone else in the race, their risk was actually lower than average. “It’s that top sliver of intensity where we see something happening,” he explains. “And even then, it’s rare.”
To understand why those “safety-off” neurons failing matters, you need to know what they do. “They’re like electrical cables,” explains Dr Nick Cole, head of research for the Motor Neurone Disease Association. “Signals travel from the brain down the spinal cord to the muscles. When you want to move your finger, that’s the current running down. But for reasons we don’t fully understand, those cells die in MND – and, unlike other tissues, they don’t regenerate.”
That failed signal causes muscles to waste; speech, swallowing, movement and eventually breathing becomes impossible. The mind’s function remains untouched, however. “You become trapped in a failing body,” says Cole. “It’s devastating. It’s also one of the biggest scientific puzzles of our time.”
New science is trying to solve it all the time. Last year, Professor Paul Chazot and his team at Durham University published findings from the UK Rugby Health Study, examining the biological aftermath of concussion and contact sport. They followed professional rugby players, sampling their blood up to eight years after retirement from sport – and found a striking revelation. Players 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 of them had actually been diagnosed with neurological conditions, but the presence of those molecular changes suggested something subtle (but long-lasting) was occurring inside the brain, long before any symptoms can be seen.
This could be key to understanding why, how and when to take preventative measures in the fight against MND. Chazot’s team believe it might be down to something called the “brain-body barrier” – the delicate protective membrane that separates the brain’s internal environment from the rest of the body. Even impacts that fall short of concussion but which are repetitive could contribute to damaging this barrier, allowing 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.”
It’s hopeful. In fact, there’s a lot of hope to be found in the excellent research being carried out in the UK, US and Australia in recent years. “There are more clinical trials happening now than at any point in my career,” Cooper-Knock says. One recent breakthrough is a therapy for patients with SOD1 mutations. It works by silencing the faulty gene and halting production of the toxic protein. Currently it’s only fit for 1-2 per cent of patients – but it’s a solid baseline to find therapies for the remaining 98 per cent.
There are also more unconventional therapies in the pipeline. For the last 20 years, Professor Chazot and his team have been experimenting with red-light therapy, using near-infrared light on the gut and brain to target mitochondria – “the battery of the cell” – and boost cell energy while reducing inflammation. The gut is crucial, he says, and often overlooked – last week a separate study found that researchers believe Parkinson’s disease actually begins in the gut microbiome.
Early clinical studies and case trials he has conducted have seen patients with severe forms of MND show stabilisation or even modest improvement in their symptoms. “We’re seeing encouraging effects in a number of people, though not everyone,” Chazot explains. “What’s exciting is that this could be a completely non-invasive, side effect-free, low-risk way to help the body heal itself.”
Still, the approach sits at the edge of mainstream neuroscience – and there’s plenty of scepticism about his findings. “Basically, ‘it can’t be that simple’ is the usual response,” he says. The therapy has been used in Australia and the US with positive anecdotal results, but many neurologists say larger, blinded trials are needed before the technique can be fully endorsed. Chazot is pushing for exactly that: a major, multi-centre study to test whether red-light treatment can genuinely slow or modify disease progression in MND. “It’s not a cure,” he stresses, “but if we can buy people meaningful time, preserve their function, that’s huge.”
If there’s one thing that everyone in the field agrees on, though, it’s that awareness matters. Since the infamous “ice bucket challenge” of the mid-2010s, that has improved. And, according to the MND Association, the last five years have seen an unprecedented surge of public interest and funding. More is still needed.
“MND is curable,” Cole says, bluntly. “We just have to fund it long enough to find the cure.”
There’s cautious optimism. “We’re making progress,” Cooper-Knock says. “Real progress. The more support we have, the faster it will come. What we all want – what Lewis and every patient deserves – is for the next diagnosis to come with a treatment that truly changes the outcome. That could be within reach.”
The hope is that as we understand more, tools for prevention will be found. In theory, one day, at-risk individuals – including elite athletes – could have their genetic and molecular profiles screened, long before any real damage occurs.
For now, Lewis Moody joins a long line of athletes turned advocates, their diagnoses already shifting the understanding and, hopefully, encouraging more funding and focus. Each name added to that list – Weir, Burrow, Slater and now Moody – underlines the urgency of the question that still looms over sport: how much do our games demand, and how do we mitigate that cost? Together, they’re forcing science and sport alike to look harder, dig deeper and move much faster towards a world where MND is not the life sentence it is now.