In childhood football games in American Samoa, Reagan Maui'a, now an NFL fullback most recently with the Cardinals, would pretend to be Junior Seau. Actually, he says, everyone pretended to be Junior Seau. "It didn't matter if you were playing quarterback, you were Junior Seau," Maui'a says, reflecting on the stature of the revered linebacker who retired in 2010 and who, last May, committed suicide by shooting himself in the chest at age 43.
So it is easy to understand why, after last week's report that Seau's dissected brain had the tau protein splotches indicative of chronic traumatic encephalopathy (CTE), the phrase on the lips of broadcasters and radio hosts was tipping point. As in: Is this the tipping point beyond which we decide that football is simply too dangerous?
The recent spotlight on brain trauma in football has shown the sports media at its best, elevating awareness of a public health issue endemic in the country's favorite sport. But the media in general is far less equipped to put the suicide of a famous player in the proper context.
Junior Seau's damaged brain is a harrowing symbol, but it is also only a single data point in the study of brain trauma in football. For scientists, its value as evidence is not at all weighted by Seau's nine All-Pro selections, two Super Bowl appearances or status as a football icon. "It's one more case in a series of case studies that's now added to the data," says Kevin Guskiewicz, a neuroscientist, athletic trainer and director of North Carolina's Center for the Study of Retired Athletes. Seau's CTE has no more scientific claim to being a tipping-point moment than the CTE found five months earlier in the brain of less-heralded former Falcons safety Ray Easterling, who also shot himself.
January 21, 2013
One of the most prominent postsuicide CTE findings turned up in the brain of Owen Thomas, a 21-year-old Penn defensive end who killed himself in 2010. In that instance Dr. Robert Cantu, codirector of Boston University's Center for the Study of Traumatic Encephalopathy, surmised that "not enough [CTE] was there to affect behavior." Cantu's conscientious assessment underscores how little is known about the link between CTE, which is associated with dementia in ex--NFL players, and depression.
Independent studies have found that retired NFL players do indeed have higher rates of depression than their peers of the same age in the general public, but not dramatically so. The most popular current narrative says that CTE is a degenerative illness that, like Alzheimer's, inevitably gets worse with age. But the depression gap between ex--NFL players and the general public actually decreases in middle age.
According to work that Guskiewicz has led on nearly 3,000 former players, the highest incidence of depression is in the 35-to-44 age group—13.5% compared with 8% in the general population. For the 45-to-54 set of former players, the incidence is 11%, only three percentage points higher than the general population. "Some of it may be from effects of concussions," Guskiewicz says, "but I think it's multifactorial. The withdrawal from the sport is a big factor, otherwise you wouldn't see the disparity in that [35--44] window as opposed to when we move further out in time."
Separately, a study by the National Institute for Occupational Safety and Health found fewer than half as many suicides among a cohort of 3,439 retired players as would be expected in a similar group from the general population.
Still, in Guskiewicz's work former players who reported three or more confirmed concussions were much more likely to have had a bout of depression than were players who had fewer concussions. After Seau's death his former teammate Gary Plummer made headlines with his specious assertion that Seau suffered 1,500 concussions over his career. But even the link between concussions and CTE is murky.
Many, if not most, of the brains that have shown evidence of CTE came from linemen, who are little affected by football's rule changes and who rarely suffer concussions. Simple tallies of concussions may turn out to be peripheral to the central point of the safety discussion. A growing body of work suggests that the accumulation of smaller hits, those that do not cause concussion, may be as important or more so to the total damage. Researchers in the Purdue Neurotrauma Group, who have been studying brain injury in high school players, now recommend that coaches think of hits the way baseball managers think of pitches and impose strict weekly limits.
In that light Seau, who never had a diagnosed concussion but played 20 seasons as a battering-ram middle linebacker, is probably the least surprising CTE case in the history of football. If this is a tipping point, it's only because of his Q rating; we were already there as far as the science. The urgent need is to study what doctors call the "dose-response" relationship between hits and brain problems—the connection between the number and force of hits and the specific damage to the brain. "That's been neglected," says Guskiewicz. "It can't just be 'got [CTE] or don't got it.' My guess is you and I probably have tau protein somewhere in our brain. A little may mean nothing."
Once we know how much tau is too much, the next step is to couple that with real time detection, looking at the brains of living former players. In a study published by the Journal of the American Medical Association three days before the Seau/CTE news, researchers used imaging technology that shows the flow patterns of water over the brain to detect damage to cerebral white matter in former players who are cognitively impaired.
At this point, it is pretty much a given that the dissected brain of someone who played football for a living and had cognitive impairment will show tau protein. But it's up to the scientists, rather than writers, broadcasters and pundits, to determine the connection between head hits, brain injury and damaged lives. Until that becomes clearer, talk of a tipping point is meaningless.
SIGN OF THE APOCALYPSE
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