“A long time ago, someone suggested that the [C.T.E. rate] in boxers was twenty per cent,” McKee told me. “I think it’s probably higher than that among boxers, and I also suspect that it’s going to end up being higher than that among football players as well. Why? Because every brain I’ve seen has this. To get this number in a sample this small is really unusual, and the findings are so far out of the norm. I only can say that because I have looked at thousands of brains for a long time. This isn’t something that you just see. I did the same exact thing for all the individuals from the Framingham heart study. We study them until they die. I run these exact same proteins, make these same slides—and we never see this.”

McKee’s laboratory occupies a warren of rooms, in what looks like an old officers’ quarters on the V.A. campus. In one of the rooms, there is an enormous refrigerator, filled with brains packed away in hundreds of plastic containers. Nearby is a tray with small piles of brain slices. They look just like the ginger shavings that come with an order of sushi. Now McKee went to the room next to her office, sat down behind a microscope, and inserted one of the immunostained slides under the lens.

“This is Tom McHale,” she said. “He started out playing for Cornell. Then he went to Tampa Bay. He was the man who died of substance abuse at the age of forty-five. I only got fragments of the brain. But it’s just showing huge accumulations of tau for a forty-five-year-old—ridiculously abnormal.”

She placed another slide under the microscope. “This individual was forty-nine years old. A football player. Cognitively intact. He never had any rage behavior. He had the distinctive abnormalities. Look at the hypothalamus.” It was dark with tau. She put another slide in. “This guy was in his mid-sixties,” she said. “He died of an unrelated medical condition. His name is Walter Hilgenberg. Look at the hippocampus. It’s wall-to-wall tangles. Even in a bad case of Alzheimer’s, you don’t see that.” The brown pigment of the tau stain ran around the edge of the tissue sample in a thick, dark band. “It’s like a big river.”

McKee got up and walked across the corridor, back to her office. “There’s one last thing,” she said. She pulled out a large photographic blowup of a brain-tissue sample. “This is a kid. I’m not allowed to talk about how he died. He was a good student. This is his brain. He’s eighteen years old. He played football. He’d been playing football for a couple of years.” She pointed to a series of dark spots on the image, where the stain had marked the presence of something abnormal. “He’s got all this tau. This is frontal and this is insular. Very close to insular. Those same vulnerable regions.” This was a teen-ager, and already his brain showed the kind of decay that is usually associated with old age. “This is completely inappropriate,” she said. “You don’t see tau like this in an eighteen-year-old. You don’t see tau like this in a fifty-year-old.”

McKee is a longtime football fan. She is from Wisconsin. She had two statuettes of Brett Favre, the former Green Bay Packers quarterback, on her bookshelf. On the wall was a picture of a robust young man. It was McKee’s son—nineteen years old, six feet three. If he had a chance to join the N.F.L., I asked her, what would she advise him? “I’d say, ‘Don’t. Not if you want to have a life after football.’ ”

At the core of the C.T.E. research is a critical question: is the kind of injury being uncovered by McKee and Omalu incidental to the game of football or inherent in it? Part of what makes dogfighting so repulsive is the understanding that violence and injury cannot be removed from the sport. It’s a feature of the sport that dogs almost always get hurt. Something like stock-car racing, by contrast, is dangerous, but not unavoidably so.

In 2000 and 2001, four drivers in Nascar’s élite Sprint Cup Series were killed in crashes, including the legendary Dale Earnhardt. In response, Nascar mandated stronger seats, better seat belts and harnesses, and ignition kill switches, and completed the installation of expensive new barriers on the walls of its racetracks, which can absorb the force of a crash much better than concrete. The result is that, in the past eight years, no one has died in Nascar’s three national racing series. Stock-car fans are sometimes caricatured as bloodthirsty, eagerly awaiting the next spectacular crash. But there is little blood these days in Nascar crashes. Last year, at Texas Motor Speedway, Michael McDowell hit an oil slick, slammed head first into the wall at a hundred and eighty miles per hour, flipped over and over, leaving much of his car in pieces on the track, and, when the vehicle finally came to a stop, crawled out of the wreckage and walked away. He raced again the next day. So what is football? Is it dogfighting or is it stock-car racing?

Football faced a version of this question a hundred years ago, after a series of ugly incidents. In 1905, President Theodore Roosevelt called an emergency summit at the White House, alarmed, as the historian John Sayle Watterson writes, “that the brutality of the prize ring had invaded college football and might end up destroying it.” Columbia University dropped the sport entirely. A professor at the University of Chicago called it a “boy-killing, man-mutilating, money-making, education-prostituting, gladiatorial sport.” In December of 1905, the presidents of twelve prominent colleges met in New York and came within one vote of abolishing the game. But the main objection at the time was to a style of play—densely and dangerously packed offensive strategies—that, it turns out, could be largely corrected with rule changes, like the legalization of the forward pass and the doubling of the first-down distance from five yards to ten. Today, when we consider subtler and more insidious forms of injury, it’s far from clear whether the problem is the style of play or the play itself.

Take the experience of a young defensive lineman for the University of North Carolina football team, who suffered two concussions during the 2004 season. His case is one of a number studied by Kevin Guskiewicz, who runs the university’s Sports Concussion Research Program. For the past five seasons, Guskiewicz and his team have tracked every one of the football team’s practices and games using a system called HITS, in which six sensors are placed inside the helmet of every player on the field, measuring the force and location of every blow he receives to the head. Using the HITS data, Guskiewicz was able to reconstruct precisely what happened each time the player was injured.

“The first concussion was during preseason. The team was doing two-a-days,” he said, referring to the habit of practicing in both the morning and the evening in the preseason. “It was August 9th, 9:55 A.M. He has an 80-g hit to the front of his head. About ten minutes later, he has a 98-g acceleration to the front of his head.” To put those numbers in perspective, Guskiewicz explained, if you drove your car into a wall at twenty-five miles per hour and you weren’t wearing your seat belt, the force of your head hitting the windshield would be around 100 gs: in effect, the player had two car accidents that morning. He survived both without incident. “In the evening session, he experiences this 64-g hit to the same spot, the front of the head. Still not reporting anything. And then this happens.” On his laptop, Guskiewicz ran the video from the practice session. It was a simple drill: the lineman squaring off against an offensive player who wore the number 76. The other player ran toward the lineman and brushed past him, while delivering a glancing blow to the defender’s helmet. “Seventy-six does a little quick elbow. It’s 63 gs, the lowest of the four, but he sustains a concussion.”

“The second injury was nine weeks later,” Guskiewicz continued. “He’s now recovered from the initial injury. It’s a game out in Utah. In warmups, he takes a 76-g blow to the front of his head. Then, on the very first play of the game, on kickoff, he gets popped in the earhole. It’s a 102-g impact. He’s part of the wedge.” He pointed to the screen, where the player was blocking on a kickoff: “Right here.” The player stumbled toward the sideline. “His symptoms were significantly worse than the first injury.” Two days later, during an evaluation in Guskiewicz’s clinic, he had to have a towel put over his head because he couldn’t stand the light. He also had difficulty staying awake. He was sidelined for sixteen days.

When we think about football, we worry about the dangers posed by the heat and the fury of competition. Yet the HITS data suggest that practice—the routine part of the sport—can be as dangerous as the games themselves. We also tend to focus on the dramatic helmet-to-helmet hits that signal an aggressive and reckless style of play. Those kinds of hits can be policed. But what sidelined the U.N.C. player, the first time around, was an accidental and seemingly innocuous elbow, and none of the blows he suffered that day would have been flagged by a referee as illegal. Most important, though, is what Guskiewicz found when he reviewed all the data for the lineman on that first day in training camp. He didn’t just suffer those four big blows. He was hit in the head thirty-one times that day. What seems to have caused his concussion, in other words, was his cumulative exposure. And why was the second concussion—in the game at Utah—so much more serious than the first? It’s not because that hit to the side of the head was especially dramatic; it was that it came after the 76-g blow in warmup, which, in turn, followed the concussion in August, which was itself the consequence of the thirty prior hits that day, and the hits the day before that, and the day before that, and on and on, perhaps back to his high-school playing days.