Can contact sports lower your intelligence?
Originally published in Discover.
Linebacker Harry Carson (left) was an honorary team captain for the New York Giants during the 2008 National Football Conference championship game in Green Bay, Wisconsin. (The other honorary captain was Army Lt. Col. Greg Gadson, who lost both legs in Iraq and is shown here with his son Jaelen.) Carson attributes his slew of health problems, including depression, to his many football concussions. Photo by Jerry Pinkus/NYG, published under a Creative Commons license.
SOME 20 YEARS AGO, IN FRONT OF A FRENZIED and antagonistic crowd, Harry Carson hurled his entire bulk—240 pounds—into an equally massive human body racing toward him across the field at Washington’s RFK Stadium. A middle linebacker with the New York Giants, Carson was a celebrated defensive football player, smart and agile, selected for the Pro Bowl even during years his team couldn’t eke out a winning season. Above all, he was known for aggression. Once, walking off the field after a game, Carson felt a tug on his jersey, turned around, and found himself eye to eye with O. J. Simpson. “Man, I’ve been hit by some of the best,” the running back told him. “But I’ve never been hit as hard as you hit me today.”
That day at RFK Stadium, Carson’s quarry was John Riggins, a Washington Redskins fullback with a similar reputation. Helmet against helmet, shoulder against shoulder, the players crashed with a concussion—producing impact that Carson would remember for decades. “It was like two trains colliding,” he would later say. Dazed, Carson dusted himself off and walked back into the Giants’ huddle—and as he stood holding his teammates’ hands, everything went black. He didn’t faint. He didn’t stop playing. For a few minutes, though, he found himself unable to interpret his coach’s signals from the sidelines. He couldn’t call the next play, as the middle linebacker is expected to do. He just remained in the game, doing the best he could until he regained his wits.
Blackouts like these were becoming familiar sensations for Carson. Over 13 seasons, he estimates he received between 15 and 18 concussions. It was only toward the end of his career that he began to exhibit the cumulative effects of all these hits, signaling what his doctors would later call postconcussion syndrome. Carson developed headaches and muscle twitches. He grew sensitive to bright lights and loud noises, making it difficult for him to sit in a busy restaurant or do a television interview. He’d lose track of time: “It’d be Monday, and before I knew it, it’d be Thursday afternoon, and I didn’t fully understand what had transpired.” And then came the depression, hitting once or twice a month for no obvious reason. One day, while approaching New York’s Tappan Zee Bridge on his way to Giants Stadium, Carson’s mind took a macabre turn. “I should just drive the car right off the bridge,” he thought to himself. “All I have to do is just accelerate, go right through the guardrail, and that would be it.”
Until recently, athletes like Carson—alive and able bodied—were of little interest to scientists. With dozens of football fatalities each year in the 1960s, particularly at the high school level, researchers were much more concerned with on-field catastrophes. “When someone dies, that catches everyone’s attention,” says neurosurgeon Robert Cantu, medical director of the National Center for Catastrophic Sports Injury Research. “It’s not surprising that fatalities in football have been tracked since 1931.”
Thanks to better protective equipment and safer coaching techniques, football deaths have now dropped to single digits each year. The decline has allowed scientists to focus on more subtle traumas, and concussions are chief among them. For decades, neurologists and sports-medicine researchers considered their long-term effects negligible, but recently they’ve discovered that these “mild” injuries aren’t so mild after all. Preliminary results show that even a minor ding can trigger a neurological cascade that can eventually cause cognitive dysfunction and mental illness. Among retired football players who have sustained three or more concussions, 20 percent have been diagnosed with clinical depression—more than three times the rate of players who never got a concussion. Almost half of those are taking antidepressant medications, and most report that the condition impedes their normal daily activities, such as shopping for groceries and going to work.
All of this begs the question: Are the country’s most popular sports a hazard to brains as well as bodies? Every year, millions of children join Pee Wee football and soccer programs. For them, are the exercise and camaraderie of contact sports worth the risk of lifelong depression and mental disability?
DURING THE 1970S AND 1980S, scientists knew little about what happened inside the brain during assaults like those Harry Carson sustained. Now the picture is starting to come into focus. At the UCLA Brain Injury Research Center, neuropsychologist David Hovda spent much of the 1990s examining rat brains in an effort to understand what happens after traumas that leave brain cells alive and the animals conscious. Immediately after a concussion, all the cells in the brain fire at once—a massive electrical discharge “like a miniseizure,” he says—indiscriminately releasing an excitatory neurotransmitter called glutamate, which in turn triggers brain cells to release potassium. As potassium rushes out of the cells, calcium rushes in and takes up residence in the mitochondria, the cells’ power centers. To restore imbalances, the brain needs considerable energy, which comes in the form of glucose (sugar). But the mitochondria, which are essential to glucose metabolism, have become impaired as a result of the excess calcium. This leads to what Hovda calls a “cellular energy crisis.” Just as the brain needs the fuel that glucose provides, that glucose has become less available.
An injured athlete may be oblivious to the neurochemical cascade inside his brain. “You can see a broken arm,” says Carson. “You can see a torn ligament in the knee. But with a concussion, you don’t see it.” The effects show up in statistical research.
In 2001 Kevin Guskiewicz, research director of the Center for the Study of Retired Athletes at the University of North Carolina at Chapel Hill, sent a 10-page questionnaire to 3,500 retirees, asking about medical conditions from asthma to schizophrenia. Twenty-six hundred forms were completed, an unusually high response rate.
Guskiewicz knew the athletic community was eager to know whether there was a link between head injuries and Alzheimer’s disease. As he crunched the numbers, he noted that only 33 former players reported an Alzheimer’s diagnosis. Most of the players had suffered at least one concussion during their careers, however, and athletes with three or more concussions were considerably more likely to have been diagnosed with mild cognitive impairment—a condition that sometimes signals the approach of Alzheimer’s disease. Guskiewicz says the word “mild” is misleading: “This is significant memory impairment, deteriorating cognitive function, but not at the level that they would be classified as being demented.” Guskiewicz now plans to track 90 retired players, most with cognitive problems, to determine whether head injuries accelerate the onset of dementia. “If we find that players with three or four concussions are at risk for Alzheimer’s,” he says, “they might realize, ‘This is the point where I need to end my career.'”
Guskiewicz was even more surprised by the depression statistics. Athletes with no concussions had a lifetime diagnosis rate of 6.6 percent, in line with the male population as a whole. Once they suffered three or more traumas, however, the rate skyrocketed to 20.2 percent. What’s particularly pernicious about retired football players’ depressions, Guskiewicz says, is that they can interact with other health problems to destroy the former athletes’ lives: “It’s sort of a snowball effect. You retire from football. You’re told at age 35 that you can’t do something you’ve been doing your entire life. You’re overweight. You are already beginning to develop musculoskeletal problems—sore knees, ankles, hips. Therefore, you begin thinking, ‘How am I going to take this weight off?’ But you’re depressed, you’re not eating right, your diet’s bad. You’re not exercising. You don’t have a strength coach now, a conditioning coach, a nutritionist overseeing your well-being. And, you know, things start to go downhill.”
IN THE LATE 1990S, AFTER HOVDA’S GROUNDBREAKING WORK on neurological cascades, other scientists at the UCLA Brain Injury Research Center continued to use laboratory rats to refine their knowledge of what happens inside a traumatized brain. To test the animals’ mental capacities after a concussion, the researchers used a Morris water maze, a tank the size of a kiddie pool filled with water made opaque with white organic paint. Just below the surface sat a hidden platform. The quicker the rat found the platform, the quicker (to its relief) it could stop swimming. Early tests showed that adults found it harder to find the platform after concussions, but with juveniles it made no difference at all. This suggested that youngsters have pliable brains that can function well even after suffering a trauma—relief for parents whose children sustain concussions on the Pee Wee league football field.
It wasn’t long, though, before these findings were cast in doubt. In 1998 neurologist Christopher Giza came aboard the center and soon found a flaw in the experimental design. “Young rats have a hard time learning this task without injury,” Giza says. “It’s like saying you have a head-injured 6-year-old and your test to determine if he’s impaired is algebra. Nobody can do it, so they all look the same. And you say, ‘Well, the injury didn’t have an effect.’ But it’s not really true.”
So Giza modified the experiment. He returned some of the young rats—both head-injured and not—to a large communal cage filled with wheels and ladders and tubes to play with. Experiments done as early as the 1960s had shown that spending time in an enriched environment helps an animal’s cerebral cortex grow thicker and increases the number of synaptic contacts in its brain, augmenting the animal’s intelligence. Giza figured that a rat that spent time in an enriched enclosure should gain a competitive advantage in the water maze over one living in an ordinary cage.
Giza introduced the rats to the maze a month after the concussions. The uninjured animals from the enriched cages indeed proved wizards at finding the hidden platform. But the injured ones performed exactly the same regardless of which cage they lived in. Their brains, in other words, were incapable of benefiting from the extra mental stimulation of the wheels and ladders.
To understand what was happening anatomically, Giza began dissecting injured and uninjured rats and examining their cortices. The uninjured rats, he found, had thickened their cortices by about 15 percent after a month in the enriched cages. The injured rats, on the other hand, had the same cortical thickness as their counterparts in barren cages. Their brains didn’t atrophy; they just didn’t achieve their potential. In a later experiment—in which they used computers to trace digitally the neurons in the rats’ brains—Giza and his colleagues discovered that head injuries also stunted the branching of the dendrites, the fibers that conduct information from one nerve cell to another.
These findings dovetailed perfectly with Hovda’s work on neurological cascades. Remember how part of the cascade is the haphazard release of the neurotransmitter glutamate? One of the consequences of this glutamate release is the overstimulation of the brain’s N-methyl-D-aspartate (NMDA) receptor. Normal stimulation of the NMDA receptor is essential to brain development and plasticity, but too much can have negative effects. Giza believes that traumatic injuries may overstimulate the NMDA receptor, rendering it less responsive to physiological stimulation, like the enriched environment.
The same could be true of humans, especially children, with head injuries from playing sports, Giza adds. A month of a rat’s life translates into years in a human’s—years in which classroom education might not be helping to thicken the cortex or accelerate the dendritic branching of a child’s brain. “Maybe at 6 years of age, you can’t do algebra,” Giza says. “But if your brain doesn’t grow a certain way between 6 and 15, you may never be able to do algebra very well.”
FOOTBALL IS HARDLY THE ONLY SPORT that knocks its athletes’ heads around. Hockey and baseball players also have their share of concussions, but the one that batters the most brains in the world is probably soccer. A soccer ball can travel as fast as 70 miles per hour in a professional game, and when players hit it with their heads they usually do so as hard as possible. An estimated 12.4 million children under the age of 18 now play soccer in America, and the explosion of interest has been most noticeable among girls. What do Giza’s findings mean for their developing brains? Can heading a soccer ball repeatedly cause brain injury?
Over the past six years, neuropsychologists Erik Matser of St. Anna Hospital in Geldorp, the Netherlands, and Muriel D. Lezak of Oregon Health and Sciences University in Portland have studied the cognitive performance of Dutch amateur and professional soccer players. In one study, 33 amateur players (seven of whom had sustained two or more concussions) underwent a battery of interviews and neurological tests. Matser and Lezak compared the results with those of 27 swimmers and runners and found the soccer players were three to four times more likely to show deficits in memory and planning skills. The more concussions players suffered, the lower their scores on three of the 16 tests.
Researchers elsewhere have come up with similar results. Two Florida Institute of Technology researchers looked at male players from high school through the professional leagues. They reported that the more someone heads a soccer ball, the lower that player will score on tests measuring attention, concentration, and general intellectual functioning. Lezak is unsurprised. “I know what happens when you bat on the brain,” she says. “Given what we know about boxing, it would have been surprising if we hadn’t found anything. In soccer, people are punishing themselves in much the same way boxers do.”
When the Dutch findings came out, it sent shock waves through youth soccer leagues in the United States, Kevin Guskiewicz says. “I had every mother and father calling me, asking if their son or daughter shouldn’t be playing soccer.” So Guskiewicz and his colleagues at the University of North Carolina conducted their own study. They took 91 college students who had played an average of more than 15 seasons of soccer apiece and compared them with 149 students with no soccer experience. On average, they found, the players performed no differently on neurocognitive tests or Scholastic Aptitude Tests (SATs) than nonplayers, even when the former had suffered concussions.
When Donald Kirkendall, assistant director for prevention research at the National Center for Health Promotion and Disease Prevention, reviewed all the research done on the topic, he likewise concluded that children under 12 faced the smallest risk, because they don’t play with nearly as much power: Children rarely kick a soccer ball faster than 40 mph. “Heading in children’s games tends to be a novelty, usually off a bounced or thrown ball, and kids just can’t kick the ball that hard,” Kirkendall told a reporter. Most head injuries, he concluded, came from running into goalposts, colliding into other players, and other mishaps unrelated to heading.
These findings came as a relief to Guskiewicz. “We already have enough obesity and inactivity in American society, and here’s a sport that gets kids out there moving,” he says. Even Lezak concedes that youth-league soccer probably won’t create a generation of brain-impaired children. “If a kid’s been playing soccer for a couple or three years, he may not have been in a vulnerable position where he does much heading,” she says.
FOR PROFESSIONAL ATHLETES, THOUGH, the risk is clear. Harry Carson lives in suburban New Jersey these days, in a comfortable home filled with helmets and photos from his football days. He spends much of his time making speeches, doing celebrity endorsements, and writing his autobiography. But he relies heavily on notepads and calendars to jog his memory, and he gives few firm RSVPs, knowing he might not be able to tolerate the camera flashes and noisy conversations of the charity dinners. Carson knows he’s luckier than other athletes with postconcussion syndrome. “I have a friend who talks about wanting to just sit in a dark room away from everyone, just to be at peace,” he says. “I’ve never been to that point. I’ve learned how to just encapsulate myself, and just be by myself, even if I’m in a crowded room.”
At 51, Carson still has broad shoulders and sinewy arms and gives the impression that the brutality of football always felt like anathema to him. “I was never a violent person,” he says. “Even as a kid, when my father would go fishing, he’d bring fish home and they’d still be alive. I’d run water and put the fish in the tub.” Once during a game he slammed into a Seattle Seahawks running back. “I guess he tore up his knee,” he recalls. “After the game, I went to the Seattle locker room to see how he was doing, but he’d already gone to the hospital. It just ate me up that I’d hurt this guy.”
Still, looking back, he understands that football had a few unspoken rules. No. 1: Never let an injury keep you off the field. “Other people got hurt,” Carson says. “I didn’t get hurt. Even if I got hurt, I played through my hurt. The nature of the game, the culture of the game, is that you have to be tough to play it.”
