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Content warning: This story includes references to death by suicide.
Evan Hansen was born to play football. A strong, rambunctious kid, he started playing sports year-round as early as he could. “He was very selfless, always willing to sacrifice himself for the betterment of the team,” says his father, Chuck Hansen. As a fearless linebacker at Wabash College in Indiana, the young player made 209 tackles in his first three seasons, and was hit far more than that during games and practices. Two days after winning the second game of his senior year, Evan died by suicide.
Searching for an explanation, Chuck Hansen pored through his son’s internet search history. One query popped out: “CTE.”
CTE stands for chronic traumatic encephalopathy, a neurodegenerative brain disease that causes symptoms like memory loss, depression, and emotional dysregulation. Since 2005, it has been linked to head trauma and to contact sports like football, where brains can get knocked around during tackles and collisions. In 2016, the National Football League acknowledged that the sport was linked to CTE after many retired players were diagnosed posthumously by researchers at the Boston University CTE Center.
Given the NFL-centered media coverage throughout the mid-aughts, “people have this impression that CTE is a disease of former NFL players,” says Julie Stamm, a clinical assistant professor of kinesiology at the University of Wisconsin-Madison. “But it’s not just a disease for professional athletes.”
Yet until recently, few studies focused on athletes like Evan, who never played professionally and died before developing age-related brain changes. (In older players, it can be challenging to separate signs of CTE from other kinds of neurodegeneration.) The Hansen family knew that Evan had only been diagnosed with one concussion in his 14 years of football—none since starting college. And although they knew that he’d had trouble doing schoolwork and experienced a bout of depression his junior year, his mental health seemed to have stabilized with therapy and medication.
While Evan’s search history suggests he suspected that these issues were signs of CTE, the disease can’t be diagnosed without examining the brain posthumously. So, like many other families seeking answers for unexplained changes in their loved ones’ behavior, the Hansens donated Evan’s brain to the Understanding Neurologic Injury and Traumatic Encephalopathy (UNITE) Brain Bank, run by the Boston University CTE Center.
Ann McKee, the center’s director, chose 152 of them to study. All were contact sports athletes who died under the age of 30, many by suicide or unintentional drug overdose. And as McKee’s team reported in August in JAMA Neurology, 41 percent of them already had CTE. One of them was Evan. Like him, of those diagnosed, most had only played sports at a high school or college level.
This study reveals that young, amateur athletes aren’t spared from the brain damage that comes with contact sports, even if they quit before going pro. And studying early-stage CTE in young, otherwise healthy brains, McKee says, “may give us clues as to how the disease is triggered.” To her, the takeaway is clear: “We need to reduce the number and the strength of head impacts in contact sports. If we don’t, we’re going to face consequences like this.”
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McKee, who is also the director of neuropathology for Veterans Affairs Boston, began studying the brains of former NFL players 15 years ago. She couldn’t believe what she saw: big lesions in the crevices of the brain, dotted with abnormal protein clusters. A huge Packers fan, McKee has watched a lot of football games. But, she recalls, until then, “it never occurred to me that they were damaging their brains, because you don’t see it on the field. They’ve got the helmets. They look invincible.”
Researchers now know more about what is happening to the brain beneath the helmet. The jostling of the brain tugs at neural tissue, placing cells and blood vessels under stress. Tau proteins, which stabilize the scaffolding that gives neurons their structure, fall off when a cell is stressed. These fallen proteins pile up inside the cell, “a sort of toxic clump,” as McKee describes it. Eventually, the pileup overwhelms and kills the cell, leaving neurofibrillary tangles, which appear as ominous dark smears under a microscope. These tangles, which also appear in Alzheimer’s disease, make it harder for neurons to communicate with each other, causing memory problems.
Meanwhile, injured blood vessels compromise the sacred blood-brain barrier that normally protects sensitive neural tissue from irritating molecules flowing through the rest of the body. The resulting irritation causes inflammation, which induces more tau clumping, initiating a downward spiral of neurodegeneration.
To screen the donated young athletes’ brains for CTE, the researchers looked for tau, as well as signs of larger-scale problems like inflammation, hardening or deterioration of blood vessels, and changes to white matter, which contains the connections between neurons. They also interviewed the donors’ loved ones to learn more about their behavior and cognitive symptoms while they were alive. All of them had experienced issues like memory loss, depression, and impulsive behavior.
Of the 152 brains examined, 63 were posthumously diagnosed with CTE. The vast majority were still in early stages of neurodegeneration, but three of them—one belonging to a former NFL player, one to a college football player, and one to a professional rugby player—had reached the third of CTE’s four stages. Notably, another brain with CTE belonged to a 28-year-old women’s collegiate soccer player—the first case of its kind.
The youth of these players also allowed the research team to rule out aging as the cause of the damage. Aging, as well as high blood pressure, cardiac disease, and other neurodegenerative problems, can all damage brain tissue. But in the sample used for the new study, all of the athletes died between the ages of 13 and 29. “These are pristine, beautiful brains,” McKee says.
The fact that so many of the donors’ families had noticed mood and memory changes—regardless of whether their child was ultimately diagnosed with CTE—might be an artifact of the study’s sample pool. Families were simply more likely to donate to the brain bank if they had noticed unusual behavior in their child. But McKee says this also suggests that some of the symptoms experienced by these young athletes are not always caused by CTE, but may still reflect the aftermath of head trauma. Chris Nowinski, a study coauthor and CEO of the nonprofit Concussion Legacy Foundation, remembers struggling with chronic symptoms after the concussion that ended his pro wrestling career in his twenties. In cases like his, concussion-related problems like sleep impairments, or the difficulties of coming to terms with life as an injured or retired athlete, are likely the root cause of the mental health issues—not necessarily tau pathology.
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The new study’s results build upon a mountain of evidence connecting contact sports to CTE. One 2017 study of 202 deceased football players found that 87 percent had CTE, including 110 of the 111 brains belonging to retired NFL players. Other studies revealed that CTE is more prevalent in athletes than non-athletes, and is specifically tied to experience playing contact sports, not one-off traumatic brain injuries. Ongoing studies are developing ways to diagnose CTE while people are alive, in the hopes of finding ways to intervene while the disease is still in its earliest stages.
A common misconception is that a one-time impact can lead to neurodegeneration. The real problem is getting hit in the head over and over, for years and years. “A tennis player who had five concussions is not going to get CTE,” says Nowinski. “There’s something about getting hundreds or thousands of head impacts a year. That’s what triggers it, whether you have concussion symptoms or not.”
Like many kids in the United States, Evan Hansen started playing tackle football in third grade. “He was in his 14th year of football, a senior in college, when he died,” says his dad. The number of years he played, and the age he was when he started facing regular blows to the head, likely contributed to developing CTE, according to McKee’s findings. When he signed his son up for football, Hansen recalls, “It was just pure ignorance. I didn’t know what I didn’t know.”
While his son’s diagnosis wasn’t made until after his death, Chuck Hansen suspects that Evan’s fear of the disorder, and what it meant for his future, weighed on him heavily. “I believe that he thought he had CTE, and had never talked about it,” Hansen says. “Maybe he thought it was a terminal thing that would only get worse, and that there was no hope.”
While there is no medical treatment for CTE yet, McKee and Nowinski recommend that young athletes focus on seeking treatment for individual mental health symptoms, like insomnia or depression. The Concussion Legacy Foundation runs a HelpLine for those who are struggling with post-concussion symptoms, or who are worried about CTE. The Hansen family also started a foundation to promote mental health awareness and CTE research, and to fund scholarships for medical students.
But CTE is preventable. Small changes to practice drills and gameplay could make a huge difference for young athletes, says Nowinski. The playbook for prevention is simple: Reduce the number of hits to the head, and reduce the strength of those hits. Most happen during practice, so by reducing the number of drills involving head impacts and choosing ones that are less likely to cause high-magnitude blows, coaches can spare their players unnecessary danger. “You can’t get rid of CTE in tackling sports,” adds Nowinski, “but you can get rid of most cases of CTE.”
Reducing the length of each game and the number of games per season can minimize the likelihood of head injuries, and banning brain-jostling events, like fighting in hockey or heading in soccer, can make games safer, he continues. Perhaps most importantly, youth sports leagues can raise the age at which kids are first exposed to preventable head impacts. “With tackle football before 14, the risks are not worth the benefits,” Nowinski says. “You don’t become a better football player from playing young.” In one case study reported by the US Centers for Disease Control and Prevention, transitioning from tackle to flag football would reduce a young athlete’s median number of head impacts per season from 378 to eight.
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But, Nowinski points out, there is no central governing body in charge of youth sports leagues, leaving it largely up to individual coaches to make changes to their practice drills and recruitment strategies. “The opportunity is right in front of our faces,” says Nowinski. “I remember being told how much football makes you a leader. But right now, on this issue, there’s a black hole of leadership.”
McKee doesn’t think that parents should take their kids out of sports—far from it. “We just need to change the rules and our thinking about these games, so that CTE isn’t a consequence of playing contact sports,” McKee says.
And for young athletes concerned about CTE, she urges them to seek help for mental health symptoms, build personal support systems, and keep moving forward with their lives. “Individuals like Evan need to be seen, because in all likelihood, we can treat their symptoms and help them feel less hopeless,” she says. “It’s not a time to despair. It’s a time to come in, be evaluated, and be treated.”
If you or someone you know needs help, call 1-800-273-8255 for free, 24-hour support from the National Suicide Prevention Lifeline. You can also text HOME to 741-741 for the Crisis Text Line. Outside the US, visit the International Association for Suicide Prevention for crisis centers around the world.
