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Repeated blows to the head, including concussions, can leave a mark inside the brain that no scan or blood test picks up while a person is alive — it is found only after death. The disease defined by that mark has been argued over in American football for more than a decade. What had never been established was how common it actually is. A study released on Tuesday in the medical journal BMJ put a number on it, and the number points away from Sunday afternoons in the professional league.
Chronic traumatic encephalopathy, or CTE, is a neurodegenerative disease associated with repeated blows to the head. In the brain it shows up as an abnormal buildup of a protein called tau, and it is classified in four stages according to where the tau sits and how much of it has accumulated. In life, the symptoms attributed to it include memory loss, difficulty with attention, problems with impulse control, anxiety, depression, anger, headaches and dementia.
It is most often seen in people who play contact sports — American football, hockey, soccer — but it has also been detected in the brains of troops injured in explosions and in some people who experienced domestic violence.
The decisive limitation is the diagnosis itself: it can be made only after death. No living player can be told that they have it, or that they do not. Everything known about how widespread the disease is comes from brains donated for research — and that is exactly where the arithmetic has always broken down.
A separate recent analysis found CTE in 99% of the former National Football League players whose brains had been donated for research. The figure travelled far, but it carried a significant limitation: those brains were donated by families who, in many cases, had already noticed something wrong while the person was alive. The result described the donors, not the players.
Individual cases had done the same thing to the public debate. Junior Seau, Dave Duerson and Aaron Hernandez — all of whom took their own lives — were found to have had CTE when their brains were examined after death, and those names carried the subject for years without settling how frequent the disease is.
The new study, by researchers from Mass General Brigham, Boston University and the Concussion & CTE Foundation, many of whom worked on the earlier research, was built to get around that. Instead of starting from the donated brains, the team started from the deaths: it counted every former NFL player who died between 2008 and 2021, using death certificates, and compared that total against the donors with confirmed CTE. It then narrowed the window to 2016 through 2021, the period with the highest number of donations. Many of the brains were analysed at brain banks at Boston University and the University of California, San Francisco.
In that six-year window, 878 former players died. Of those, 235 donated their brains for research, and 215 of the donated brains were found to have CTE. That is the origin of the headline figure: at least one in four of the former players who died in that period had the disease. An editorial published alongside the study called it "one of the most informative estimates to date of CTE burden among former NFL players." Dementia, the researchers also found, was common among the donors.
Daniel Daneshvar, the study's lead author, is chair of physical medicine and rehabilitation at Mass General Brigham and an associate professor at Harvard Medical School. He said that repeated traumatic brain injuries are a known factor in elevated rates of neurodegenerative disease, and that "in NFL players, specifically, there is about a four times higher rate of death from neurodegenerative disease than the general population."
An NFL spokesperson said the league "continuously strives to make the game of football safer, including by implementing strategies to reduce concussions and head impacts", and that it remains committed to giving the NFL community access to a growing set of resources for physical and mental well-being, encouraging former players to use them when they are concerned about their health.
This is the part of the study that moves the conversation somewhere else. "The bulk of the head impacts that these former NFL players experienced didn't occur at the NFL level," Daneshvar said. "They occurred at the collegiate level, and at the high school level and in many cases the youth level. And all of those cumulative hits to the head added up to result in an increased risk."
And the impacts are not concentrated in matches. "We know that nearly 70% of head impacts are occurring in practice," he said. "So without changing a single minute of game time at any of those levels, we can be substantially reducing the cumulative head impact burden that these individuals are experiencing throughout their lives."
Rachel Grashow, director of research initiatives for the Football Players Health Study at Harvard University, who was not involved in the research, called the study important — and warned about how the figure will be read. A CTE diagnosis, she said, did not always correlate with symptoms.
"The scientific community looks at this paper and says, 'OK, now we've got a denominator. We know who's got these proteins. We know who doesn't. That's helpful,'" she said. "The worry is that the rest of the world will see this number and say 'that's symptoms.'"
Head injury, she added, is bad on its own terms: it causes low testosterone, sleep apnoea, depression, high blood pressure and tinnitus, and those conditions, left untreated, are themselves harmful to the brain. How much tau accumulates, and how it interacts with those injuries, she described as a big question mark.
The NFL's 2011 collective bargaining agreement limited the number of contact practices during the season; the current agreement was ratified in 2020 and runs through March 2031. The Ivy League, a conference of American universities, banned full-contact tackling in practice five years after that 2011 deal. In 2016, the US Supreme Court cleared the way for the NFL's settlement of concussion-related lawsuits brought by thousands of retired players.
What the study's authors argue is that the changes stopped at the top. "If the changes that have been implemented at the NFL level, including reducing the amount of contact in sports practices to less than one per week, were propagated at the collegiate, high school and youth levels, athletes would be better off," Daneshvar said.
If you played contact sports, or have a child playing now, the practical part of this study is not about the professional league. It is about practice sessions — the setting where, according to the researchers, nearly seven in ten head impacts occur, and which nobody watches on television.
That gives a concrete question to ask a school, a club or a youth league: how many full-contact practices are held per week, and whether the rule the NFL adopted in 2011 — fewer than one contact practice a week, in the version Daneshvar cited — exists there in any form. It is the kind of change that, by the authors' argument, does not require altering a single minute of game time.
The second point concerns symptoms. CTE cannot be confirmed in a living person, and Grashow's caution stands: the presence of tau in donated brains is not the same as a disease with symptoms, and several conditions caused by head injury — depression, sleep apnoea, high blood pressure among them — look similar from the outside and can be treated. Daneshvar urged current and former athletes who notice cognitive symptoms to get checked by a specialist in neurodegenerative disease. Persistent trouble with memory, mood or impulse control is the trigger to seek that evaluation, not a reason to assume the diagnosis.
And what remains open is worth keeping in view: the study establishes a proportion among those who died, not a prognosis for anyone alive, and the relationship between accumulated tau and the symptoms people actually experience is, in Grashow's words, still a big question mark.
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