This week’s New Yorker has an article in it by Malcolm Gladwell that, apparently prompted by the return of QB Michael Vick to the NFL after his prison term for dogfighting, asks how similar football and dogfighting are.
He argues that they are similar in that both dogs trained to fight and NFL players are “selected for gameness” (along with Marines and physicians) — their respective systems weed out those unwilling to continue trying to persevere even in the face of great pain and suffering. The dogs do it out of love for and devotion to their owners, which is why during dogfights, the owners maneuver around the pit to stay within their dogs’ fields of vision. The players do it for more complicated reasons — a mix of love of the game itself, camaraderie, money and a long list of other enticements, tangible and intangible.
The difference, of course, is that NFL players 1) have a choice and 2) are highly compensated — even those making the league minimum are making substantially more money than most Americans.
Until recently, or at least so we thought, there was one other difference: No dog, no matter how aggressive and well-trained, will live forever. Sooner or later, it will age or slow or just catch a bit of bad luck and go down to another dog. NFL players, on the other hand, almost all walk away from the game relatively intact, or so most fans think. (The less glamorous reality, which the NFL doesn’t talk much about, is that a large percentage of NFL players who play in the league any length of time leave with some sort of permanent injury or disability.)
And although there’s no conclusive proof, Gladwell writes, there is some disturbing evidence that NFL players as a group may be at far greater risk than the general population for a form of brain damage called chronic traumatic encephalopathy (C.T.E.) because of the pounding their heads take during the course of a career. C.T.E. presents, as the doctors say, a lot like Alzheimer’s, but it’s caused by brain injury and the brain cells of its victims look different from those of Alzheimer’s patients. It gets worse over time. And as with Alzheimer’s, there’s no cure.
Two neuropathologists are looking at this particular question. One is Dr. Ann McKee, who is doing the neuropathology research associated with the long-running Framingham heart-disease study, which has been following a large group of patients for decades. She also is involved with the New England Centenarian Study, which looks at the brains of people who lived an extraordinarily long time. (“I’m looking at brains constantly,” McKee says.) In the course of her work, she has run across close to two dozen brains of former athletes — mostly football players, a couple of boxers.
The other is Dr. Bennet Omalu, who has found cases of C.T.E. in several former NFL players. Both are disturbed by their findings, although both also say they haven’t seen enough cases yet to decide anything.
The league also has been looking, and what it has found is disturbing:
… late last month the University of Michigan’s Institute for Social Research released the findings of an N.F.L.-funded phone survey of just over a thousand randomly selected retired N.F.L. players—all of whom had played in the league for at least three seasons. Self-reported studies are notoriously unreliable instruments, but, even so, the results were alarming. Of those players who were older than fifty, 6.1 per cent reported that they had received a diagnosis of “dementia, Alzheimer’s disease, or other memory-related disease.” That’s five times higher than the national average for that age group. For players between the ages of thirty and forty-nine, the reported rate was nineteen times the national average. …
“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 [damage]. 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 [a protein that damages brain cells, found in both Alzheimer’s and C.T.E. patients and detectable only at autopsy — Lex] 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?
(I should point out that both researchers say that other factors, such as genetics and steroid use, may well figure into this phenomenon — neither is drawing any straight-line conclusions at this point.)
As it happens, I read this article just last night, so it was still very much on my mind as I watched today’s Panthers-Buccaneers game.
Just seconds before halftime, the Panthers punted, and the Bucs’ returner, Clifton Smith, signaled for a fair catch. When a punt returner signals for a fair catch, that means he’s supposed to be allowed to catch the ball, and then his team starts its next play from that spot — he doesn’t run with it once he catches it. In return for his not running, not only is the punting team not allowed to tackle that returner, for the past few years they haven’t even been allowed within a 3-yard “halo” around such a returner.
But on this play, the Panthers’ Dante Wesley, the “gunner” (first guy to sprint downfield on punts to try to tackle the returner), launched himself into Clifton Smith, who, having signaled for a fair catch, was watching the ball coming down out of the sky and had no idea what Wesley was doing. Wesley slammed into him at full speed, appearing to catch him under the chin with his shoulder pad and knocking him out cold. (You can see the play here.)
Smith suffered a concussion — he “got his bell rung,” as the players sometimes say — and did not return. Wesley was ejected and likely will be fined by the league. For such a blatant and excessive hit — not only running into Smith, but also leaving his feet to do so, an additional violation of the rules — he might even be suspended. (I hope he is. What he did came as close to assault with a deadly weapon as an unarmed man is ever likely to come without martial-arts training.)
Now, you might suppose that it’s hits like that that cause the kind of brain trauma these researchers are finding. And they can. But research just down the road in Chapel Hill suggests a more disturbing problem for those of us who play and/or love football:
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.
In technological terms, C.T.E. ain’t a bug, it’s a feature.
What football must confront, in the end, is not just the problem of injuries or scientific findings. It is the fact that there is something profoundly awry in the relationship between the players and the game.“Let’s assume that Dr. Omalu and the others are right,” Ira Casson, who co-chairs an N.F.L. committee on brain injury, said. “What should we be doing differently? We asked Dr. McKee this when she came down. And she was honest, and said, ‘I don’t know how to answer that.’ No one has any suggestions—assuming that you aren’t saying no more football, because, let’s be honest, that’s not going to happen.”
I hope we fans — and I am definitely including myself when I say “we” because I love pro football, ran a fantasy-league team for 18 years and am probably overly invested in how well the Panthers do — are going to be able to live with the knowledge I expect we’ll be getting as this research progresses. Because based on what we’ve seen so far, we’re likely to come to two conclusions: The players we love to watch will be at substantially, if not hugely, increased risk for dementia as they age, and the damage won’t stop until we stop paying to watch what causes it.